Height is typically a predestined characteristic in most people. According to Medical News Today, up to 80% of someone's height is based on their DNA. If you come from a tall or short family, you are more likely to be taller or shorter. Yet despite baseline genetics, there are a variety of actions to take during childhood and teen years to ensure that your reach your maximum potential height according to your DNA.

Basically, it's the health advice you've likely heard several times before but not everyone follows. Obey a nutritious dietby eating lots of fruits and veggies every day. Make sure you have enough calcium to grow healthy bones as well as plenty of protein. Get adequate exercise to strengthen bones and muscles.

One of the biggest things teens need to reach optimal height is sleep. A growth hormone is released while you're in certain sleep stages (via Verywell Health). If sleep is insufficient, a body won't likely reach maximum growth.

There are numerous ways to predict how tall a boy will be as he grows. The Mayo Clinic outlines two different techniques. In the first prediction, add the mother's height to the father's height and then add 5 inches for boys. (Subtract 5 inches for girls). Then just divide by two. The second way to estimate height is to find a boy's height at age 2 and then double it. (For girls, do the same at age of 18 months.)

As a general rule, men stop growing when they're 18. There is a slight possibility that if a teen boy began puberty late, he may grow a bit in his early 20s, but that is unusual. The reason is simple and it has to do with growth plates (via Healthline). That's the area of the bone made of cartilage that continues to grow. However, they meld together right after puberty, meaning there is no more potential to grow once they have fused.

Over the years the average height of men has grown and that's because men are now getting better nutrition, exercise, and sleep both as children and teens. In the early 1900s, men were averaging 5 feet, 8 inches tall (via A Hundred Years Ago). Currently, in the United States, the average height for men is approximately 5 feet, 9 inches tall, according to the Centers for Disease Control and Prevention (CDC)while the average weight for menrests at 197.9 pounds.

Oddly enough, there are certain states where heights differ. According to the World Population Review, the U.S. states with the tallest men, averaging 5 feet, 10.8 inches or more, are Alabama, Iowa, Kentucky, Montana, Nebraska, North Dakota, South Dakota, Tennessee, Utah, West Virginia, and Wyoming. The states with the shortest average male heights, averaging below 5 feet, 10 inches, are New York, New Jersey, California, Nevada, New Mexico, Hawaii, and Texas. All the remaining states lie somewhere in between.

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What Is The Average Height For Men In The US? - The List

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Participants

For factor analyses, we restricted our analyses to autistic individuals from the SSC and SPARK cohorts. Participants had to have completed the two phenotypic measures (details are below) to be included in the factor analyses. We also excluded autistic individuals with incomplete entries in either of the two measures (n=5,754 only in the SPARK cohort). This resulted in 1,803 participants (n=1,554 males) in the SSC, 14,346 participants (n=11,440 males) in SPARK version 3 and 8,271 participants (n=6,262 males) in extra entries from SPARK version 5 (SSC, mean age=108.75 months, s.d.=43.29 months; SPARK version 3, mean age=112.11 months, s.d.=46.43 months; SPARK version 5, mean age=111.22 months, s.d.=48.19 months). Only the SCQ was available for siblings in the SPARK study.

We conducted analyses using data from four cohorts of autistic individuals: the SSC (n=8,813)30, the Autism Genetic Resource Exchange (AGRE, CHOP sample) (nmax=1,200)64, the AIMS-2-TRIALS Longitudinal European Autism Project (LEAP) sample (nmax=262)65 and SPARK (n=29,782)31. For sibling comparisons, we included siblings from the SSC (n=1,829) and SPARK (n=12,260) cohorts. For trio-based analyses, we restricted to complete trios in the SSC (n=2,234) and SPARK (n=4,747) cohorts. For all analyses, we restricted the sample to autistic individuals who passed genetic quality control (QC) and who had phenotypic information.

We conducted factor analyses using the SCQ29 and the RBS28. The SCQ is a widely used caregiver report of autistic traits capturing primarily social communication difficulties and, to a lesser extent, repetitive and restricted behaviors29. There are 40 binary (yes-or-no) questions in total, with the first question focusing on the individuals ability to use phrases or sentences (total score, 039). We used the Lifetime version rather than the current version as this was available in both the SPARK and SSC studies. Of note, in the Lifetime version, questions 119 are about behavior over the lifetime, while questions 2040 refer to behavior between the ages of 4 to 5 years or in the last 12 months if the participant is younger. We excluded participants who could not communicate using phrases or sentences (n=217 in the SSC and n=17,092 in SPARK) as other questions in the SCQ were not applicable to this group of participants. The RBS is a caregiver-reported measure of presence and severity of repetitive behaviors over the last 12 months. It consists of 43 questions assessed on a four-point Likert scale (total score, 0129). Higher scores on both measures indicate greater autistic traits.

We conducted exploratory factor analysis on a random half of the SSC (n=901 individuals, of which 782 were males) using promax rotation to identify correlated factors as implemented by psych (ref. 66) in R. We conducted three sets of exploratory correlated factor analyses: for all items, for social items and for non-social items. Previous studies have provided support for a broad dissociation between social and non-social autism features12,23 and have conducted separate factor analyses of social (for example, refs. 67,68) and non-social autism features (for example, refs. 69,70). Thus, we reasoned that separating items into social and non-social categories might aid the identification of covariance structures that may not be apparent when analyzing all items together. We divided the data into social (all of the SCQ except item 1 and nine other items and item 28 from the RBS) and non-social (nine items from the SCQ (items 8, 11, 12 and 1418) and all items from RBS except item 28) items, which was carried out after discussion between V.W. and X.Z. The ideal number of factors to be extracted was identified from examining the scree plot (Supplementary Fig. 2), parallel analyses and theoretical interpretability of the extracted factors. However, we examined all potential models using confirmatory factor analyses as well to obtain fit indices, and the final model was identified using both exploratory and confirmatory factor analyses.

We then applied the model configurations from promax rotated exploratory factor analysis for bifactor models to explore the existence of general factor(s). In addition to a single general factor bifactor model, we divided the data into social and non-social items as mentioned earlier and applied bifactor models separately for the social and non-social items. Hierarchical values and explained common variances were then calculated for potential models as extra indicators of the feasibility of bifactor models, but hierarchical values were not greater than 0.8 for most of the models tested, and explained common variances were not greater than 0.7 (refs. 71,72,73) for any of the models tested (Supplementary Table 2).

Three rounds of confirmatory factor analyses were conducted: first for the second half of the SSC, followed by analysis of SPARK participants whose phenotypic data were available in version 3 of the data release and, finally, analysis of SPARK participants whose phenotypic data were available only in version 4 or version 5 of the data release and not in the earlier releases. To evaluate the models, multiple widely adopted fit indices were considered, including the comparative fit index (CFI), the TLI and the root mean square error of approximation. In CFA, items were assigned only to the factor with the highest loading to attain parsimony. We conducted three broad sets of confirmatory factor analyses: (1) confirmatory factor analyses of all correlated factor models, (2) confirmatory factor analyses of the autism bifactor model and (3) confirmatory factor analyses of social and non-social bifactor models. For each of these confirmatory factor models, we limited the number of factors tested based on the slope of the scree plots and based on the number of items loading onto the factor (five or more). For the confirmatory factor analyses of social and non-social bifactor models, we iteratively combined various numbers of social and non-social group factors. In bifactor models, items without loading onto the general factor in the correspondent EFA were excluded. Items were allocated to different group factors, which were identified based on the highest loading (items with loading <0.3 were excluded). Due to the ordinal nature of the data, all CFAs were conducted using the diagonally weighted least-squares estimator (to account for the ordinal nature of the data) in the R package lavaan 0.6-5 (ref. 74). We identified the model most appropriate for the data at hand with TLI and CFI>0.9 (TLI and CFI>0.95 for bifactor models), low root mean square error of approximation and good theoretical interpretability based on discussions between V.W. and X.Z. Additionally, as sensitivity analyses, the identified model (correlated six-factor model) was run again with two orthogonal method factors mapping onto SCQ and RBS-R to investigate if the fit indices remained high after accounting for covariance between items derived from the same measure, as these measures vary subtly during the period of time evaluated. We also reanalyzed the identified model after removing items that were loaded onto multiple factors (>0.3 on two or more factors) to provide clearer theoretical interpretation of the model. For genetic analyses, we used factor scores from the correlated six-factor model without including the orthogonal method factors and without dropping the multi-loaded items.

QC was conducted for each cohort separately by array. We excluded participants with genotyping rate <95%, excessive heterozygosity (3s.d. from the mean), non-European ancestry as detailed below, mismatched genetic and reported sex and, for families, those with Mendelian errors >10%. SNPs with genotyping rate <10% were excluded, or they were excluded if they deviated from HardyWeinberg equilibrium (P<1106). Given the ancestral diversity in the SPARK cohort, HardyWeinberg equilibrium and heterozygosity were calculated in each genetically homogeneous population separately. Genetically homogeneous populations (corresponding to five super-populations: African, East Asian, South Asian, admixed American and European) were identified using the five genetic principal components calculated using SPARK and 1000 Genomes Phase 3 populations75 and clustered using UMAP76. Principal components were calculated using linkage disequilibrium-pruned SNPs (r2=0.1, window size=1,000kb, step size=500 variants, after removing regions with complex linkage disequilibrium patterns) using GENESIS77, which accounts for relatedness between individuals, calculated using KING78.

Imputation was conducted using the Michigan Imputation Server79 with 1000 Genomes phase 3 version 5 as the reference panel49 (for AGRE and SSC), with the HRC r1.1 2016 reference panel80 (for AIMS-2-TRIALS) or using the TOPMed imputation panel81 (for both releases of SPARK). Details of imputation have been previously reported82. SNPs were excluded from polygenic risk scores if they had minor allele frequency <1%, had an imputation r2<0.4 or were multi-allelic.

We restricted our PGS associations to four GWAS. First, we included a GWAS of autism from the latest release from the iPSYCH cohort (iPSYCH-2015)83. This includes 19,870 autistic individuals (15,025 males and 4,845 females) and 39,078 individuals without an autism diagnosis (19,763 males and 19,315 females). All individuals included in this GWAS were born between May 1980 and December 2008 to mothers who were living in Denmark. GWAS was conducted on individuals of European ancestry, with the first ten genetic principal components included as covariates using logistic regression as provided in PLINK. Further details are provided elsewhere49. We additionally included GWAS for educational attainment (n=766,345, excluding the 23andMe dataset)35, intelligence (n=269,867)34, ADHD (n=20,183 individuals diagnosed with ADHD and 35,191 controls)36 and schizophrenia (69,369 individuals diagnosed with schizophrenia and 236,642 controls)37. These GWAS were selected given the relatively large sample size and modest genetic correlation with autism. Additionally, as a negative control, we included PGS generated from a GWAS of hair color (blonde versus other, n=43,319 blondes and n=342,284 others) from the UK Biobank, which was downloaded from https://atlas.ctglab.nl/traitDB/3495. This phenotype has SNP heritability comparable to that of the other GWAS used (h2=0.15, s.e.=0.014), is unlikely to be genetically or phenotypically correlated with autism and related traits, and has a sample size large enough to be a reasonably well-powered negative control.

PGS were generated for three phenotypes using polygenic risk scoring with continuous shrinkage (PRS-CS)84, which is among the best-performing polygenic scoring methods using summary statistics in terms of variance explained85. In addition, this method bypasses the step of identifying a P-value threshold. We set the global shrinkage prior () to 0.01, as is recommended for highly polygenic traits. Details of the SNPs included are provided in Supplementary Table 3.

De novo variants were obtained from Antaki et al.19. De novo variants (structural variants and SNVs) were called for all SSC samples and a subset of the SPARK samples (phase 1 genotype release, SNVs only). To identify high-impact de novo SNVs, we restricted data to variants with a known effect on protein. These are damaging variants: transcript_ablation, splice_acceptor_variant, splice_donor_variant, stop_gained, frameshift_variant, stop_loss, start_loss or missense variants with MPC86 scores >2. We further restricted data to variants in constrained genes with a LOEUF score <0.37 (ref. 87), which represent the topmost decile of constrained genes. For SVs, we restricted data to SVs affecting the most constrained genes, that is, those with LOEUF score <0.37, representing the first decile of most constrained genes. We did not make a distinction between deletions or duplications. To identify carriers, non-carriers and parents, we restricted our data to samples from the SPARK and SSC studies that had been exome sequenced and families in which both parents and the autistic proband(s) passed the genotyping QC.

For genes associated with severe developmental disorders, we obtained the list of constrained genes that are significant genes associated with severe developmental disorders from Kaplanis et al.27. To investigate the association of this set of genes with autism and developmental disorders, we first identified autistic carriers with a high-impact de novo variant and then divided this group into carriers who had at least one high-impact de novo variant in a DD gene and carriers with high-impact de novo variants in other constrained genes.

Only individuals with undiagnosed developmental disorders are recruited into the Deciphering Developmental Disorders study, and, as such, known genes associated with developmental disorders that are easy for clinicians to recognize and diagnose may be omitted from the genes identified by Kaplanis et al.27. To account for this bias, we ran sensitivity analyses using a larger but overlapping list of genes identified from the Developmental Disorder Gene-to-Phenotype database (DDG2P). From this database, we used constrained genes that are either confirmed or probable developmental disorder genes and genes for which heterozygous variants lead to developmental phenotypes (that is, mono-allelic or X-linked dominant).

We identified 19 autism core and associated features that (1) are widely used in studies related to autism; (2) are a combination of parent-, self- and other-reported and performance-based measures to investigate if reporter status affects the PGS association; (3) are collected in all three cohorts; and (4) cover a range of core and associated features in autism. The core features are

ADOS88: social affect

ADOS88: restricted and repetitive behavior domain total score

ADI89: communication (verbal) domain total score

ADI89: restricted and repetitive behavior domain total score

ADI89: social domain total score

RBS28

Parent-reported Social Responsiveness Scale-2 (ref. 90): total raw scores

SCQ29

Insistence of sameness factor (F1)

Social interaction factor (F2)

Sensorymotor behavior factor (F3)

Self-injurious behavior factor (F4)

Idiosyncratic repetitive speech and behavior (F5)

Communication skills factor (F6).

The associated features are

Vineland Adaptive Behavior Scales91: composite standard scores

Full-scale IQ

Verbal IQ

Nonverbal IQ

Developmental Coordination Disorders Questionnaire92.

Measures of IQ were quantified using multiple methods across the range of IQ scores in the AGRE, SSC and LEAP studies. In the SPARK study, IQ scores were available based on parent reports on ten IQ score bins (Fig. 1c). We used these as full-scale scores. For analyses involving the SPARK and SSC cohorts, we converted full-scale scores from the SSC into IQ bins to match what was available from the SPARK study and treated them as continuous variables based on examination of the frequency histogram (Supplementary Fig. 8). For the six factors, we excluded individuals who were minimally verbal (Factor analyses), but these individuals were not excluded for analyses with other autism features.

We identified seven questions relating to developmental delay in the SPARK medical screening questionnaire. These are all binary questions (yes or no). Summed scores ranged from 0 to 7. The developmental phenotypes include the presence of

ID, cognitive impairment, global developmental delay or borderline intellectual functioning

Language delay or language disorder

Learning disability (learning disorder, including reading, written expression or math; or nonverbal learning disability)

Motor delay (for example, delay in walking) or developmental coordination disorder

Mutism

Social (pragmatic) communication disorder (as included in DSM IV TR and earlier)

Speech articulation problems.

We included the age of first words and the age of walking independently for further analyses. This was recorded using parent-reported questionnaires in the SPARK study and in ADI-R89 in the SSC study. While other developmental phenotypes are available, we focused on these two, as they represent major milestones in motor and language development and are relatively well characterized.

Before any statistical analyses, we visually inspected the distributions of the variables. All continuous variables were approximately normally distributed with the exception of the age of first words, the age of walking independently and the count of co-occurring developmental disabilities. For these three variables, we used quasi-Poisson or negative binomial regression to account for overdispersion in the data and because the variance was much greater than the mean. These models produced the same estimate but modestly different standard errors. Both have two parameters. However, while quasi-Poisson regression models the variance as a linear function of the mean, the negative binomial models the variance as a quadratic function of the mean. The model that produced the lower residual deviance was chosen between the two. For all other continuous variables, we used linear regression and parametric tests. For binary data, we used logistic regression as there was not a large imbalance in the case:control ratio.

For each cohort, PGS and high-impact de novo variants were regressed against the autism features with sex and the first ten genetic principal components as covariates in all analyses, with all continuous independent variables standardized. In addition, array was included as a covariate in SSC and AGRE datasets. This was performed using linear regression for standardized quantitative phenotypes, logistic regression for binary phenotypes (for example, association between PGS and the presence of a high-impact de novo variant), Poisson regression for count data (number of developmental disorders or delays, not standardized) and negative binomial regression for the age of walking independently or the age of first words (not standardized; MASS93 package in R).

For the association between genetic variables and core and associated autism phenotypes, we first conducted linear regression analyses for the four PGS first using multivariate regression analyses with data from SPARK (waves 1 and 2), SSC, AGRE and AIMS-2-TRIALS LEAP. This is of the form:

$$yapprox {textrm{PGS}}_{textrm{autism}} + {textrm{PGS}}_{textrm{schizophrenia}} + {textrm{PGS}}_{textrm{EA}} + {textrm{PGS}}_{textrm{intelligence}} + {textrm{sex}} + {textrm{age}} + 10 {textrm{PCs}},$$

(1)

where EA is educational attainment and 10PCs are ten principal components. For the negative control, we added the negative control as an additional independent variable in equation (1):

$$begin{array}{lll}yapprox {textrm{PGS}}_{textrm{autism}} + {textrm{PGS}}_{textrm{schizophrenia}} + {textrm{PGS}}_{textrm{EA}} + {textrm{PGS}}_{textrm{intelligence}} \+ {textrm{PGS}}_{textrm{hair color}} + {textrm{sex}} + {textrm{age}} + 10{textrm{PCs}}.end{array}$$

(2)

For the AGRE and SPARK studies, we ran equivalent mixed-effects models with family ID modeled as random intercepts to account for relatedness between individuals. This was carried out using the lme4 (ref. 94) package in R.

For high-impact de novo variants, we included the count of high-impact de novo variants as an additional independent variable in equation (1) and ran regression analyses for SPARK (wave 1 only) and SSC. To ensure interpretability across analyses, we retained only individuals who passed the genotypic QC, which included only individuals of European ancestries. Family ID was included as a random intercept:

$$begin{array}{l}yapprox {textrm{PGS}}_{textrm{autism}} + {textrm{PGS}}_{textrm{schizophrenia}} + {textrm{PGS}}_{textrm{EA}} + {textrm{PGS}}_{{mathop{{{rm{intelligence}}}}} } \+ {textrm{high-impact de novo count}} + {textrm{sex}} + {textrm{age}} + 10{textrm{PCs}.}end{array}$$

(3)

Effect sizes were meta-analyzed across the three cohorts using inverse-variance-weighted meta-analyses with the following formula:

$$begin{array}{l} {w_{i}} = {{mathrm{SE}}_{i}^{-2}} \ {{mathrm{SE}}_{mathrm{meta}}} = {surd}left(left({Sigma}_{1} w_{i}right)^{-1}right)\ {{beta}_{mathrm{meta}} = {Sigma}_{i}{{beta}_{i}}{{w}_{i}}{left({{Sigma}_{i}}{{w}_{i}}right)}^{-1}},end{array}$$

(4)

where i is the standardized regression coefficient of the PGS, SEi is the associated standard error and wi is the weight. P values were calculated from Z scores. Given the high correlation between the autism features and phenotypes, we used BenjaminiYekutieli false discovery rates to correct for multiple testing (corrected P<0.05). We calculated heterogeneity statistics (Cochrans Q and I2 values) for the PGS meta-analyses but not for the associations with high-impact de novo variants, as the latter were calculated using only two datasets (SSC and SPARK).

For the SPARK and SSC studies, we investigated the association between PGS (equation (1)) and being a carrier of a high-impact de novo variant (equation (3)) and the age of first walking and first words using negative binomial regression and conducted inverse-variance meta-analyses (equation (4)). We ran the same analyses for the SPARK study to investigate the association between PGS (equation (1)) and high-impact de novo variants (equation (3)) and counts of co-occurring developmental disabilities (quasi-Poisson regression). Leave-one-out analyses were conducted by systematically excluding one of seven co-occurring developmental disabilities and reconducting the analyses.

To investigate additivity between common and high-impact de novo variants, we conducted logistic regression with carrier status as a dependent binary variable and all PGS included as independent variables and genetic principal components, sex and age included as covariates. This was carried out separately for SPARK (wave 1) and SSC and meta-analyzed as outlined earlier.

Statistical significance of differences in factor scores between sexes were computed using t-tests. Associations with age and IQ bins were conducted using linear regressions after including sex as a covariate.

Matrix equivalency tests were conducted using the Jennrich test in the psych66 package in R. Power calculations were conducted using simulations. Statistical differences between pairwise correlation coefficients (carriers versus non-carriers) in core and associated features were tested using the package cocor95 in R. Using scaled existing data on full-scale IQ, adaptive behavior and motor coordination, we generated correlated simulated variables at a range of correlation coefficients to reflect the correlation between the six core factors and the three associated features. We then ran regression analyses using the simulated variable and high-impact de novo variants as provided in equation (3). We repeated this 1,000 times and counted the fraction of outcomes for which the association between high-impact de novo variant count and the simulated variable had P<0.05 to obtain statistical power. Differences in the age of walking and the age of first words between groups of autistic individuals and siblings were calculated using Wilcoxon rank-sum tests.

Polygenic transmission deviation was conducted using polygenic transmission disequilibrium tests14. To allow comparisons with midparental scores, residuals of the autism PGS were obtained after regressing out the first ten genetic principal components. These residuals were standardized by using the parental mean and standard deviations. We obtained similar results using PGS that had not been residualized for the first ten genetic principal components. We defined individuals without co-occurring ID as individuals whose full-scale IQ is above 70 the SSC and SPARK studies. Additionally, in the SPARK cohort, we excluded any of these participants who had a co-occurring diagnosis of intellectual disability, cognitive impairment, global developmental delay or borderline intellectual functioning. Analyses were conducted separately in the SSC and SPARK cohorts and meta-analyzed using inverse-variance-weighted meta-analyses. We additionally conducted pTDT analyses on non-autistic siblings to investigate differences between males and females.

For sex differences in high-impact de novo variants, we calculated relative risk in autistic females versus males based on (1) all carriers, (2) carriers of DD genes and (3) carriers of non-DD genes (SPARK wave 1 and SSC). For sensitivity analyses, we conducted logistic regression with sex as the dependent variable and carrier status for DD genes and either full-scale IQ and motor coordination scores (in SPARK wave 1 and SSC) or number of developmental disorders (only in SPARK wave 1) as covariates. For each sensitivity analysis, we provide the estimates of the unconditional analysis as well (that is, without the covariates).

We opted to conduct heritability analyses using unscreened population controls rather than family controls (that is, pseudocontrols or unaffected family members), as this likely reduces SNP heritability96 owing to parents having higher genetic likelihood for autism compared to unselected population controls55 and due to assortative mating97. Casecontrol heritability analyses were conducted using the ABCD cohort as population controls; specifically, the ABCD child cohort in the USA, recruited at the age of 9 or 10 years. This cohort is reasonably representative of the US population in terms of demographics and ancestry. As such, it represents an excellent comparison cohort for the SPARK and SSC cohorts. The ABCD cohort was genotyped using the Smokescreen genotype array, a bespoke array designed for the study containing over 300,000 SNPs. Genetic QC was conducted identically as for SPARK. Genetically homogeneous groups were identified using the first five genetic principal components followed by UMAP clustering with the 1000 Genomes data. We restricted our analyses to 4,481 individuals of non-Finnish European ancestries in the ABCD cohort. Scripts for this are available at https://github.com/vwarrier/ABCD_geneticQC. Imputation was conducted, similar to the analysis of SPARK data, using the TOPMed imputation panel.

For casecontrol heritability analyses, we combined genotype data from the ABCD cohort and from autistic individuals from the SPARK and SSC cohorts. We restricted the analysis to 6,328,651 well-imputed SNPs (r2>0.9) with minor allele frequency >1% in all datasets. Furthermore, we excluded multi-allelic SNPs and SNPs with minor allele frequency difference of >5% between the three datasets and, in the combined dataset, were not in HardyWeinberg equilibrium (P>1106) or had genotyping rate <99%. We additionally excluded related individuals, identified using GCTA-GREML, and individuals with genotyping rate <95%. We calculated genetic principal components for the combined dataset using 52,007 SNPs with minimal linkage disequilibrium (r2=0.1, 1,000kb, step size of 500 variants, removing regions with complex long-range linkage disequilibrium). Visual inspection of the principal-component plots did not identify any outliers (Supplementary Fig. 9). While our QC procedure is stringent, we note that there will be unaccounted-for effects in SNP heritability due to fine-scale population stratification, differences in genotyping array and participation bias in the autism cohorts. However, our focus is on the differences in SNP heritability between subgroups of autistic individuals, and unaccounted-for casecontrol differences will not affect this.

We calculated SNP heritability for autism and additionally in subgroups stratified for the presence of ID, sex, sex and ID together, and the presence of high-impact de novo variants. We also conducted SNP heritability in subgroups of autistic individuals with scores >1s.d. from the mean for each of the six factors, autistic individuals with F1 scores>F2 scores and autistic individuals with F2 scores>F1 scores.

We calculated the observed-scale SNP heritability (baseline and subgroups) using GCTA-GREML52,53 and, additionally, using PCGC54. In all models except for the sex-stratified models, we included sex, age in months and the first ten genetic principal components as covariates. In the sex-stratified models, we included age in months and the first ten genetic principal components as covariates. For sex-stratified heritability analyses, both case and control data were from the same sex. For GCTA-GREML, the observed-scale SNP heritability was converted into liability-scale SNP heritability using equation (23) from Lee et al.98. PCGC estimates SNP heritability directly on the liability scale using the prevalence rates from Maenner et al.99. For all analyses, we ensured that the number of cases did not exceed the number of controls, with a maximum case:control ratio of 1.

We used prevalence rates from Maenner et al.99, which provides prevalence of autism among 8 year olds (1.8%). The study also provides prevalence rates by sex and by the presence of ID. However, there is wide variation in autism prevalence. We thus recalculated the SNP heritability across a range of state-specific prevalence estimates obtained from Maenner et al.99. For estimates of liability-scale heritability for subtypes defined by factor scores >1s.d. from the mean, we estimated a prevalence of 16% of the total prevalence. For F1>F2 and F2>F1, prevalence was estimated at 50% of the total autism prevalence. Estimating approximate population prevalence of autistic individuals with high-impact de novo variant carriers is difficult due to ascertainment bias in existing autism cohorts. However, a previous study has demonstrated that the mutation rate for rare protein-truncating variants is similar between autistic individuals and siblings from the SSC and autistic individuals and population controls from the iPSYCH sample in Denmark, which does not have a participation bias100, implying that the de novo mutation rate in autistic individuals from the SPARK and SSC cohorts may be generalizable. Using the sex-specific proportion of de novo variant carriers and autism prevalence, we calculated a prevalence of 0.2% for being an autistic carrier of a high-impact de novo variant.

For sex-stratified SNP heritability analyses, we additionally calculated SNP heritability for a range of state-specific prevalence estimates to better model state-specific factors that contribute to autism diagnosis. In addition, using a total prevalence of 1.8%, we estimated SNP heritability using a male:female ratio of 3.3:1 (ref. 51) to account for diagnostic bias that may inflate the ratio.

We used GCTA-GREML to also estimate SNP heritability for the six factors, full-scale IQ and the bivariate genetic correlation between them. We used the same set of SNPs used in the casecontrol analyses. We were unable to conduct bivariate genetic correlation for the casecontrol datasets due to limitations of sample size.

We received ethical approval to access and analyze de-identified genetic and phenotypic data from the three cohorts from the University of Cambridge Human Biology Research Ethics Committee.

Further information on research design is available in the Nature Research Reporting Summary linked to this article.

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Genetic correlates of phenotypic heterogeneity in autism - Nature.com

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Among neurologic complaints, migraines are the most common cause of productivity loss and emergency room visits. Migraines may be the most painful type of headache, increasing stroke, and heart attack risk in men.

While migraines tend to affect more women, migraines in men do happen. About 9% of men are regular sufferers (vs. 17% of women), and certain types of headaches like cluster headaches are more common in men. Genetics also play a role since approximately 70% of sufferers have a close relative with the problem.

Today, some consider chronic migraine (>15 migraine days per month) as an individual and societal burden as it is more disabling than episodic migraine. A hypothesis to this higher probability of progression could be that men are often not diagnosed or misdiagnosed. The theory may be that they are less likely to report or seek medical treatment for migraines.

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Ginger prevents nausea that can occur in many migraine patients.

Yoga and biofeedback help many patients cope with pain along with complimentary as well as medication management.

There are many migraine-specific vitamins that your migraine neurologist can recommend along with treatment.

There are also devices for migraines that attempt to interrupt pain signals, more specifically an external trigeminal nerve stimulation (eTNS) unit. The premise of the Cefaly is similar to that of other neurostimulators being tested for migraine treatment. SpringTM may be another option. You hold this device at the back of your head at the first sign of a headache, and it gives off a magnetic pulse that stimulates part of the brain. In addition, there is a noninvasive vagus nerve stimulator called gammaCore. When placed over the vagus nerve in the neck, it releases a mild electrical stimulation to the nerve's fibers to relieve pain. Nerivio is a wireless remote electrical neuromodulator.

Avoid certain foods. Diet plays a vital role in preventing migraine attacks. Your diet plays a part, too. In about 10% of people with these headaches, food is a trigger. Choose better food. Eat as much wholesome, fresh food, like fruits and vegetables, as you can. Avoid processed and packaged foods.

Some common trigger foods include:

Tyramine is a natural compound that forms in protein-rich foods as they age. It's also a trigger for migraines. These cheeses are high in tyramine:

Chemicals added to food to enhance their flavor or help them stay fresh longer may bring on a headache:

Limit stress as tension's a common trigger. Using mediation, music, meditation, yoga, and massage to relieve tension can help. There are many evidence-based complementary techniques. Along with your prescribed treatment, you might want to try one of these to help prevent migraines, such as acupuncture, massage & cognitive behavioral therapy

It is wise to avoid a drop in blood sugar which can set off a migraine. My patients know to drink at least 4-5 glasses of water to avoid dehydration, which can trigger headaches.

Exercise regularly, many of my patients are afraid it might trigger a migraine. Overdoing a workout may trigger a headache for some people, but research suggests regular, moderate aerobic exercise may make migraines shorter, less severe, and happen less often for many people. Vigorous exercise might be a trigger in migraineurs, but overall the benefits of physical activity far outweigh the risk for people with migraine.

Regular exercise is associated with a reduction in the frequency and intensity of migraines, says. Avoid exercise if you're in the middle of a migraine attack, as it can make the pain worse. When you're exercising it can help keep future away attacks by relieving stress, a common migraine trigger.

Exercise also stimulates the release of feel-good hormones called endorphins and enkephalins which are our natural painkillers and natural antidepressants. Migraines share brain receptors with serotonin responsible for our mood.

Preventive or good habits can go a long way to prevent migraines. Yet, it is not a substitute for a proper evaluation by a migraine neurologist. Good sources of information are the American Headache Society (AHS) and the American Migraine Foundation (AMF). The most important thing I keep in mind when treating my patients is that everyone is unique and the approach is never a one size fits all solution. Be aware of overusing over-the-counter pain relievers as they can actually trigger medication overuse headaches and cause stomach upset and ulcers. There is hope for your pain and you do not have to suffer in silence. And to protect your life and the lives of others, don't visit any of these 35 Places You're Most Likely to Catch COVID.

Shae Datta, MD, co-director, NYU Langone's Concussion Center, and director of cognitive neurology at NYU Langone HospitalLong Island.

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Best Habits to Prevent a Migraine, Says Neurologist Eat This Not That - Eat This, Not That

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Research News

The subfossil jawbone of a polar bear that lived 115,000 to 130,000 years ago in Norways Svalbard archipelago. A genomic study includes an analysis of DNA extracted from a tooth attached to this jawbone, which is now housed at the Natural History Museum at the University of Oslo. Photo: Karsten Sund, Natural History Museum, University of Oslo

By CHARLOTTE HSU

A new study is providing an enhanced look at the intertwined evolutionary histories of polar bears and brown bears.

Becoming separate species did not completely stop these animals from mating with each other. Scientists have known this for some time, but the new research draws on an expanded data set including DNA from an ancient polar bear tooth to tease out more detail.

The story that emerges reveals complexities similar to those that complicate human evolutionary history.

The formation and maintenance of species can be a messy process, says Charlotte Lindqvist, associate professor of biological sciences, College of Arts and Sciences, and an expert on bear genetics. Whats happened with polar bears and brown bears is a neat analog to what were learning about human evolution: that the splitting of species can be incomplete.

As more and more ancient genomes have been recovered from ancient human populations, including Neanderthals and Denisovans, were seeing that there was multidirectional genetic mixing going on as different groups of archaic humans mated with ancestors of modern humans. Polar bears and brown bears are another system where you see this happening.

We find evidence for interbreeding between polar bears and brown bears that predates an ancient polar bear we studied, she says. And, moreover, our results demonstrate a complicated, intertwined evolutionary history among brown and polar bears, with the main direction of gene flow going into polar bears from brown bears. This inverts a hypothesis suggested by other researchers that gene flow has been unidirectional and going into brown bears around the peak of the last ice age.

A mother polar bear and her 2-year-old cubs in northwestern Greenland. Photo: ystein Wiig

The study was published June 6 in the Proceedings of the National Academy of Sciences. It was led by Lindqvist; Luis Herrera-Estrella at the National Laboratory of Genomics for Biodiversity (LANGEBIO) in Mexico and Texas Tech University; and Kalle Leppl at the University of Oulu in Finland. Tianying Lan, a former UB postdoctoral researcher now at Daicel Arbor Biosciences, was co-first author with Leppl.

The concept of Arctic-adapted polar bears capturing genetic material from brown bears, which are adapted to life in lower latitudes, is one of several findings of possible interest for scientists concerned with climate change impacts on threatened species.

As the world warms and Arctic sea ice declines, polar bears and brown bears may run into each other more frequently in places where their ranges overlap. This makes their shared evolutionary history a particularly intriguing subject of study, Lindqvist says.

An adult male polar bear in northwestern Greenland. Photo: ystein Wiig

Splitting of species can be messy process

As Lindqvist explains, scientists once thought modern humans and Neanderthals simply split into separate species after evolving from a common ancestor. Then, researchers found Neanderthal DNA in modern Eurasian people, implying that modern human populations received an influx of genes from Neanderthals at some point in their shared evolutionary history, she says.

Only later did scientists realize that this genetic intermingling also supplemented Neanderthal populations with modern human genes, Lindqvist adds. In other words, interbreeding can be complex, not necessarily a one-way street, she says.

The new study on bears reveals a remarkably similar story: The analysis finds evidence of hybridization in both polar bear and brown bear genomes, with polar bears in particular carrying a strong signature of an influx of DNA from brown bears, researchers say. Earlier research proposed the inverse pattern only, Lindqvist says.

Its exciting how DNA can help reveal ancient life history. Gene flow direction is harder to determine than merely its presence, but these patterns are vital to understanding how past adaptations have transferred among species to give modern animals their current features, says Leppl, postdoctoral researcher in the research unit of mathematical sciences at the University of Oulu.

Population genomics is an increasingly powerful toolbox to study plant and animal evolution, and the effects of human activity and climate change on endangered species, says Herrera-Estrella, Presidents Distinguished Professor of Plant Genomics and director of the Institute of Genomics for Crop Abiotic Stress Tolerance in the Texas Tech Department of Plant and Soil Science. He is also a professor emeritus at LANGEBIO. Bears dont provide simple speciation stories any more than human evolution has. This new genomic research suggests that mammalian species groups can hide complicated evolutionary histories.

The subfossil jawbone of a polar bear that lived 115,000 to 130,000 years ago in Norways Svalbard archipelago. Photo: Karsten Sund, Natural History Museum, University of Oslo

Evidence from modern bear genomes and DNA from an ancient tooth

The study analyzed the genomes of 64 modern polar and brown bears, including several new genomes from Alaska, a state where both species are found.

The team also produced a new, more complete genome for a polar bear that lived 115,000 to 130,000 years ago in Norways Svalbard archipelago. DNA for the ancient polar bear was extracted from a tooth attached to a subfossil jawbone, which is now housed at the Natural History Museum at the University of Oslo.

Using this data set, researchers estimate that polar bears and brown bears started to become distinct species about 1.3 to 1.6 million years ago, updating prior assessments made by some of the same scientists. The age of the split has been and remains a topic of scientific debate, with past interbreeding and limited fossil evidence for ancient polar bears among factors that make the timing hard to pinpoint, Lindqvist says.

In any case, after becoming their own species, polar bears endured dramatic population decline and a prolonged genetic bottleneck, leaving these bears with much less genetic diversity than brown bears, the new study concludes. The findings confirm past research pointing to the same trends, and add evidence in support of this hypothesis.

Genomes analyzed in a new study on bears include that of this bear, pictured here in 1995 on Alaska's North Slope. Scientists had wondered if this bear might be a brown bear-polar bear hybrid, but the new research finds that, This bear is not a hybrid, but simply a light-colored brown bear, says UB biologist Charlotte Lindqvist. Photo: Richard Shideler, Division of Wildlife Conservation, Alaska Department of Fish and Game

Together with the analysis of gene flow, these findings are providing new insights into the messy, intertwined evolutionary history of polar bears and brown bears.

The international research team included scientists from UB, LANGEBIO, Texas Tech, the University of Oulu, the Far Northwestern Institute of Art and Science, the Alaska Department of Fish and Game, the Natural History Museum at the University of Oslo, Nanyang Technological University, University of Helsinki and Aarhus University.

The research was funded by the National Fish and Wildlife Foundation, U.S. National Science Foundation, Alaska Department of Fish and Game, and U.S. Geological Survey.

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Study offers better look at tangled evolutionary histories of polar bears, brown bears - UB Now: News and views for UB faculty and staff - University...

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TWH Extreme weather sometimes reveals unknown or unexplored archaeological sites. A prolonged drought in Iraq has threatened its harvest and resulted in authorities releasing water from the Mosul reservoir for crop irrigation.

As the waters receded, the ruins of a Bronze Age, Mitanni city emerged. Archaeologists excavated the site and found defensive walls, towers, a multi-story warehouse and more than 100 cuneiform boards.

Archaeologists have dated the ruins to around 1400 B.C.E. The ruins are those of Zakhiku, a city in the Mitanni Empire. That empire controlled parts of northern Syria and Mesopotamia from 1550 to 1350 B.C.E.

In 2018, when an earlier drought had lowered the water height in the reservoir, the palace of Zakhiku emerged. Archaeologists seized the opportunity to examine its ruins.

In 2019, The University of Tbingen reported that this palace had walls up to seven meters tall (22.9 feet). They partially excavated eight rooms of the palace. Its inner, plastered walls had heights and thicknesses of up to two meters (6.6 feet). Vivid reds and blue murals covered those walls. Archaeologists think that such murals would have been common. Few Mitanni buildings, however, have survived.

Only three other Mitanni palaces have ever been found, but they were all from the outskirts of the empire. In contrast, Zakhiku lies close to the Mitanni heartland.

They also found ten cuneiform tablets. One of these tablets identified the site as the ancient city of Zakhiku. Other Mitanni records from 1800 B.C.E. refer to Zahiku. As these ruins date to roughly 1400 B.C.E, Zakhiku lasted for, at least, four-hundred years.

The palace had stood on an elevated platform, 20 meters (65.6 feet) from the east bank of the Tigris. The city lay to the palaces north.

In 2021, the waters of the reservoir had receded enough to expose the ruins of Zakhiku. Archaeologists knew that the water levels in the reservoir would begin to rise soon. They decided to excavate the ruins while they were above water. Kurdish archaeologist, Dr. Hasan Ahmed Qasim, joined two German archaeologists, Professor Dr. Ivana Puljiz of the University of Freiburg, and Professor Dr. Peter Pflzner of the University of Tbingen. Oasim chairs the Kurdistan Archaeology Organization.

In their excavations, they found a massive fortification with walls and towers, as well as a multi-story warehouse, and a complex of workshops.

In 2022, the University of Tbingen reported on the significance of that warehouse. The size of the warehouse indicated that it stored a large number of goods. For Qasim, this capacity showed that the site was an important center in the Mitanni Empire.

Inside the warehouse, excavators found five ceramic jars containing more than 100 cuneiform tablets. These tablets do not date from the Mitanni period. They date from the latter Middle Assyrian period from 1350 to 1100 B.C.E.

The Mitanni Empire collapsed around 1350 B.C.E., and Zakhiku fell under Assyrian control. The cuneiform tablets may contain information about that transition.

A strong earthquake struck the region around 1350 B.C.E. which destroyed the city. The upper walls of buildings collapsed and buried the lower parts of the building which may have helped to preserve the structures.

Dried bricks formed the main building material in Zakhiku. The lack of water damage stunned the research team.

After excavation, archaeologists covered most of the site in tight-fitting plastic. Then they covered the buildings with gravel. The Mosul reservoir has returned to capacity. Now, water covers Zakhiku once more, at least until the next drought strikes.

The Mitanni Empire extended from the eastern Mediterranean to northern Iraq. Its center lay in northeastern Syria.

Egyptian texts record that Mitanni had a similar status to that of Babylon, Egypt, and the Hittites. Mitanni rulers intermarried with Egyptian pharaohs.

The Smithsonian Magazine reported that the Mitanni produced the worlds oldest horse training manual. Masters of horsemanship, the Mitanni developed improved wheel technology for their war chariots.

Of all the kingdoms of the Bronze Age in Anatolia, Mesopotamia, and the Levant, the Mitanni Empire remains one of the least known. Very few of their records have survived and their religion left few remains. Surviving mentions of the Mitanni Empire mainly occur in treaties with Egypt, the Hittite Empire, or Assyria. Their Empire combined elements of the indigenous Hurrian culture with migrating or invading Indo-Aryan culture.

Map of Eastern Mediterranean and Middle East in 14th century Image credit: Alexikoua, CC BY-SA 3.0

Indo-Aryan refers to a branch of the Indo-European languages. That branch spread from the steppe region of Eurasia into south and western Asia. Another branch of that language spread into Europe.

Humans being human, people mix genetics and cultures. Languages can spread from one population to another, without one genetic population replacing another. Indo-European is a linguistic, not a genetic concept.

In their paper, About the Mitanni-Aryan Gods, Arnaud Fournet argued that Indo-Aryan words appear in surviving Mitanni texts. Those tablets include what may be the worlds oldest horse training manuals. Two surviving Hittite-Mitanni treaties mention major gods of the RigVeda, and specifically name Mitra, Varuna, Indra, and the Nasatya.

Other words in other surviving texts appear to be Hurrian. That language has no relation to any Indo-European or Semitic languages.

In The Storm-Gods of the Ancient Near East: Summary, Synthesis, Recent Studies, Daniel Schwemer argues for the prominence of storm gods in Upper Mesopotamia. Among the Hurrians, the major storm god had the name, Teub. [Variations on spellings include: Teshub which is also written as Teshup,Teup, orTeup] Schwemer called Teub, the head of the Hurrian pantheon, a divine king.

Chamber A, main scene depicting (left to right) the God Kumarbi (chief god of the Hurrians), the weather and storm god Teshuba, the earth goddess Hepat, Sharumma (son of Teshuba & Hepat) and Alanzu (daughter of Teshup Hepat), Yazlkay in Hittite capital city of Hattusa, Image credit: Carole Raddato, FRANKFURT, Germany CC BY-SA 2.0

The main, barely-surviving Hurrian myth involves generational conflict. It only survives in fragments, mostly written in Hittite. The sky god, Anu, deposes his father, the primeval god, Alahu.

Kumarbi, of the same generation as Anu, then fights Anu and overthrows him. In that fight, Kumarbi bites off (and maybe eats) Anus genitals. That act of castration and absorption brings the divine line into the usurper, Kumarbi.

Anu, apparently still male, gives birth to a new generation of gods, including Tessub. His children, including Tessub, defeat Anu. Tessub becomes the new King of the Gods. Kumarbi returns and makes an alliance with the sea and underworld gods. Tessub eventually defeats that alliance.

This mythic complex has obvious parallels with the Uranus-Cronus-Zeus cycle. Modern Pagans may choose to view this myth cycle through a genderqueer lens. Scholars have studied its fragmentary sources, however, through a reconstructed language. A certain humility is in order. Some things are forever lost in the past, and we may never know.

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Mitanni City emerges from the Mosul Reservoir - Middle East, News, Paganism, Science, US, Uncovering the Past, World - The Wild Hunt

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Mice receiving a gene for a telomere-building enzyme have had their lifespan extended by 41%. Treatment with another gene, this time for follistatin (FST), extended their lives by 36%. Both treatments significantly boosted glucose tolerance, physical performance and stalled body mass decline and fur loss.

The life extension came as a surprise to the researchers. We wanted to see what the effects were [of the gene therapy], explains Hua Zhu at Rutgers New Jersey Medical School. In the meantime, we saw that the [24] control mice died, whereas all [36]experimental mice were still alive, so the treatment clearly was significantly increasing the lifespan of the mice.

Telomeres are repetitive DNA sequences that cap chromosomes and tend to shorten with ageing. Efforts to extend the healthy lifespan of people is an active area of research, and features a range of techniques such as caloric restriction and small molecules that target metabolic pathways linked to ageing.

The researchers delivered the gene for telomerase reverse transcriptase, which activates and encourages telomere lengthening, and FST, a secretory protein with an important role in muscle development and maintenance, using a herpes virus.

Monthly treatment began in mice aged 18 months. After two months, the treated mice looked stronger and had shinier, healthier fur than controls, which started to lose their fur and suffered declining body weight, notes Zhu. Injections were repeated monthly to sustain high levels of the protein. All mice in control groups died by 29 months, while the mice in the experimental groups died between 38 and 42 months.

Liz Parrish, chief executive of the biotech firm BioViva that provided funding for the research, notes that the next step will be to test the safety and efficacy of the gene therapy in monkeys using weakened strains of a rhesus virus. Based on the result of the monkey studies, we will submit our report to the [US Food and Drug Administration] to give us permission to start clinical trials in humans, she explains.

There are major hurdles for anyone wishing to treat ageing with a gene therapy approach, says Ilaria Bellantuono, a professor of muscular ageing at the University of Sheffield, UK. We find difficulties proposing a drug approach, which is far less expensive and risky, so a gene therapy approach would encounter [a] higher level of resistance.

Bellantuono says that it is still hard for any treatment for ageing to compete with diet and exercise. Therefore, the best approach would be to target an age-related condition such as muscle loss or dementia, she says. This would require a clinical trial to test whether the intervention prevents such conditions.

A preventive trial is very complex. You need to give the treatment. Then wait for the disease to manifest, says Bellantuono. You would need biomarkers, which would tell us within three to six months whether an intervention gene therapy or drug is working.

Peter Lansdorp, a molecular biologist at the University of British Columbia in Canada, notes that ageing is multi-factorial and it seems unlikely that a single protein could have such a large impact on lifespan. He notes also that side effects from repeated activation of the immune system by viral vector infection are of concern in humans, but not so much in mice. First, possible effects of the transgene on viral virulence need to be excluded, Lansdorp says. Next this study needs to be reproduced in mice by other, independent groups.

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Gene therapy showcases technique to extend life in mice - Chemistry World

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Space junk sounds like a cyberpunk problem but is very much a real-world issue today. A couple of months ago, the European Space Agency had to take emergency debris collision avoidance action for its Sentinel-1A satellite, part of the Copernicus radar observatory program.

Japanese space technology company Astroscale is working to solve the problem of orbital space objects in conjunction with Ansys Government Initiatives (AGI). We spoke with Cody Short, AGIs principal astrodynamicist, to learn more about this space safety project.

According to NASA, there are more than 27,000 pieces of space debris being tracked, but that is only a small amount of what is really out there. Space debris orbits around the Earth at about 15,700 mph in low Earth orbit. It could cause significant damage to a satellite or a spacecraft in case of a collision.

Some measures have been taken to attempt to resolve the issue, including coating for satellites, but a coordinated approach is needed and fast.

According to Short,

Space is big, but particular orbital slots, especially those of high value, are crowded and becoming increasingly so. As a result, satellite operators must burn expensive fuel meant to sustain the delivery of services and profits to instead move their satellites to safer or more advantageous orbits. Up until now, the way we have operated in space has been bad for the space environment, and bad for space business. But its on this unsustainable foundation that we are trying to build a trillion-dollar space economy.

Astroscale and Ansys are working together to increase space safety and solve the problem of space debris. Their collaboration includes improving situational awareness, enabling life extension and other on-orbit servicing, and offering end-of-life options with active debris removal. The project is called ELSA (The End-of-Life Services by Astroscale).

Short explains:

By focusing on developing the technologies, informing the international policies, and building the economics for orbital sustainability, Astroscale is reorienting governments and businesses long-term decisions. In the end, it is building a sustainable space infrastructure in the process.

Astroscale is taking two key approaches to the space debris problem.

The first approach is about mitigation and preparation. The idea is to stack a common docking plate so that servicer satellites can remove them at the end of their useful life or in the event of a launch failure.

The second approach is to coordinate removals, in partnership with national governments and space agencies. The idea is to find and target larger pieces of debris that pose some of the highest risks. This might include upper-stage rocket bodies, for example.

A great part of this work depends on a digital mission engineering application, Ansys Systems Tool Kit, or STK, by engineering company Ansys. According to Short, this digital tool is

an indispensable digital mission engineering application for the aerospace, defense, telecommunications, and other industries. It features an accurate, physics-based modeling environment to analyze platforms and payloads in a realistic mission context.

Short adds that Ansys Systems Tool Kit enables the simulation of

multidomain scenarios that extend simulation beyond systems to an interactive model of the operational environment.

Fundamentally, this means that four-dimensional three-dimensional, plus time models can be built up to include terrain, imagery, RF environments, and other elements of the environment.

Short told us more about this digital mission:

STK extends digital engineering to the mission the operational environment in which your systems and systems of systems must succeed. While it feels like something that comes at the end of your projects life cycle once your system is designed its more than that. Digital mission engineering should be applied early and often, from design through development, test, operations, and sustainment. Uncover problems sooner rather than later and youll have a design that excels against your adversaries, ready to deploy far quicker than your competition.

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Space Safety: How to Solve the Problem of Orbital Debris? - DirectIndustry News - DirectIndustry e-Magazine

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MSM IS FOCUSED ON TURNAROUND PLAN AMIDST THE

RISING MAIN PRODUCTION COST

KUALA LUMPUR, JUNE 8, 2022 - MSM Malaysia Holdings Berhad (MSM) remains focused on sustaining its turnaround plan amidst the rising main production cost elements namely raw sugar, freight, natural gas and foreign exchange. The producer of the national refined sugar brand "Gula Prai" has turnaround with improved financial performance since 2020 despite market challenges.

Relatively, MSM recorded an improved profit before tax (PBT) of RM81 million for FY2021, against RM36 million in FY2020. The Group also recorded 3% increase in revenue of RM2.26 billion for 12 months FY2021 compared to RM2.18 billion in the last financial year. During FY2021, gain from disposal of MSM Perlis Sdn Bhd amounting to RM91.8 million has contributed to the Group recording a total consolidated PBT of RM170 million.

Within a continually challenging environment, MSM key focus for 2021 was on the execution of the turnaround plan through reorganisation and asset optimisation, staying resilient with strengthened income streams and building integration for sustainable performance.

"For financial year 2021 (FY2021), MSM recorded a revenue of RM2.3 billion with a profit before tax (PBT) of RM81 million on the back of total assets of RM2.87 billion. This is an encouraging improvement from 2020 despite challenges faced throughout the year. MSM also has returned to a dividend-paying stock where we declared a dividend of 3 sen per share for FY2021," said MSM Group Chief Executive Officer, Syed Feizal Syed Mohammad during the 11th Annual General Meeting that was held virtually today attended by 1,057 shareholders online.

MSM produced close to 900,000 tonnes of refined sugar that is sold under "Gula Prai" brand amidst slower domestic and competitive international markets in 2021 due to the COVID-19 pandemic and the movement control order. MSM was challenged by many different factors in 2021 but appropriate mitigation measures were taken to address them.

MSM has a dynamic 3-year strategic blueprint with 2021 being Turnaround, 2022 Resilient and 2023 Integration. MSM Johor remains a key focus of MSM Group on the ramp-up programme and achieving profitability while MSM Prai will be undergoing a rejuvenation process with a 30-year life extension in sweating the assets.

"We will work to increase our domestic market share while opening up new market channels through Last Mile general trades, HORECA and small SKU packaging suited for convenient chains. MSM shall continue to gain greater market share within Asia Pacific and penetrate Singapore retail segment viewed from a domestic lens and logistics strategy. We shall also increase more volumes of value-added products such as liquid sugar and premix which has higher margins and great demand in markets like China. As part of strengthening Johor, MSM remains open to have a right fit partner with strong export market and operational experience," Syed Feizal said.

As for financial year 2022 (FY2022), MSM foresees greater challenges with rising main production cost. For first quarter (1Q) FY2022, MSM posted an expected loss after tax (LAT) of RM28 million as compared to profit after tax (PAT) of RM31 million for 1Q2021. This was largely due to higher production cost largely 29% higher NY11, 57% increase in freight cost and weaker Ringgit. The Group's refining cost also recorded an increase of 28%, largely driven by 86% increase in gas cost. In response to cost pressures, MSM as a joint industry has engaged the government on the need to revise the controlled ceiling prices for the retail segment. The sugar refining price has had a net increase of only 1 sen/kg since 2011.

"We strived to reinforce our brand positioning, stayed on track for current and long-term targets maximising our capabilities through market expansion and greater outreach. Critically, we continued to strengthen our balance sheet and enhanced liquidity. MSM has a healthy gearing ratio of 26% in FY2021 versus 33% in FY2020. In initiatives, we stepped-up with acceleration our ESG journey and kicked-off digitalisation towards IR 4.0 during the year," Syed Feizal added.

Moving forward, MSM will further exploring strategic partnership to strengthen export segment and to further unlock synergistic value in 2022 in ensuring consistent returns and greater shareholder value as the nation's leading premium sugar refiner.

-ENDS-

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About MSM Malaysia Holdings Berhad (MSM)

MSM Malaysia Holdings Berhad (MSM) is Malaysia's leading refined sugar producer and one of the biggest sugar refiners in Asia. MSM is involved in producing, marketing and selling refined sugar products under the "Gula Prai" brand. The company conducts its business principally through two operating subsidiaries, MSM Prai Berhad and MSM Sugar Refinery (Johor) Sdn Bhd. In addition, MSM also operates a logistics company - MSM Logistics Sdn Bhd.

At present, MSM's annual production capacity is up to 2.05 million tonnes of refined sugar. In 2021, MSM produced 895,222 tonnes of refined sugar, of which 246,101 tonnes are catered for the export market. Currently, MSM corroborates up to 60% of the domestic market share. MSM has been listed on the Main Market of Bursa Malaysia since 2011 and has a market capitalisation of RM900 million as at 31 December 2021. MSM combines economic success with environmental protection and social responsibility for a sustainable future.

MSM offers a variety of products ranging from white refined sugar of various grain sizes to soft brown sugar. These are marketed and sold in a variety of packaging options under its flagship brand - Gula Prai. MSM also sells molasses, a by-product of the refining process, to distilleries and producers of ethanol, animal feed and yeast, among other products. Aside from household consumers, MSM sells to a wide range of customers in Malaysia and in other countries directly and indirectly through traders, wholesalers and distributors. Its customers include major companies in the beverage and confectionery industries, hotels, restaurants and food outlets.

For more information, please visit http://www.msmsugar.com

Forward Looking Statements

Certain statements in this media release regarding MSM's operations may constitute forward-looking statements. These statements can be identified by key words such as "believes", "estimates", "anticipates", "expects", "intends", "may", "will", "plans", "outlook" and other words of similar meaning in connection with a discussion of future operating or financial performance. These statements relate to the plans, objectives, goals, strategies, future operations and performance of MSM. Actual results and outcomes may differ materially from those projected in any forward-looking statements due to various events, risks, uncertainties and other factors. We neither intend to nor assume any obligation to update or revise any forward-looking statements, whether as a result of new information, future events or otherwise.

For media enquiries, please contact:

Siti Noorbaya Mohd Yunus

Syahidah Ismail

+603 2181 5018 ext. 158

+603 2181 5018 ext. 154

+6016 677 6118

+6019 225 9705

noorbaya.my@msmsugar.com

syahidah.i@msmsugar.com

3

Disclaimer

MSM Malaysia Holdings Bhd published this content on 08 June 2022 and is solely responsible for the information contained therein. Distributed by Public, unedited and unaltered, on 08 June 2022 08:31:07 UTC.

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MSM Malaysia Berhad : IS FOCUSED ON TURNAROUND PLAN AMIDST THE RISING MAIN PRODUCTION COST - Marketscreener.com

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Anti-submarine warfare capability, or ASW, is one of the U.S. Navys top priorities. After all, adversary submarines such as the Russian Typhoon class and Red Chinas Type-093A Shang-II Class pose arguably the deadliest threat to American carriers. To counter the threat of silent submersible stalkers, the Navy continues to use an aerial platform that has served faithfully for over 50 years: the Lockheed Martin P-3 Orion.

Still Going Strong

Though the P-3 Orion is slowly but surely being replaced by the Boeing P-8 Poseidon for ASW work, the transition is far from complete. The older Orion unlike other famous Cold War-era Navy warplanes such as the F-14 Tomcat, A-6 Intruder, and A-7 Corsair IIhas definitely not been retired yet. The P-3 is currently being used by two Navy Reserve patrol squadrons, VP-62 and VP-69. It also lives on as a land-based multi-intelligence reconnaissance variant, the EP-3E Aries II.

And thats without even counting the 16 foreign countries that still fly the Orion.

The P-3 was based on a commercial airliner, the Lockheed L-188 Electra, that was first flown in 1957. This is somewhat akin to how the E-3 Sentry AWACS plane was based on the commercial Boeing 707. The militarized Orion variant made her maiden flight in November 1959 and officially entered service in August 1962a mere two months before the Cuban Missile Crisis. Thus, in 2012, the P-3 joined the pantheon of military aircraft that the U.S. has used for 50-plus years, joining the B-52, the KC-135, the C-130, and the U-2.

The keydistinguishing feature of the P-3 that you wont see on the civilian L-188 is the Magnetic Anomaly Detection boom at the tail end of the fuselage. This feature makes the P-3s submarine-hunting mission feasible in the first place. Needless to say, the Cold War never went hot, so the Orion never got to put its sub-killing potential to the test in the real world. But that doesnt mean the Orion didnt get battle-tested.

P-3 Orions over Afghanistan, Iraq, and the Balkans

Indeed, it was during 2002s Operation Anaconda in Afghanistan that the P-3 pulled off what is arguably its most remarkable wartime feat. As noted by the official Lockheed Martin website, During a key battle in the Shah-e-Kot Valley, P-3 crews scouted the rugged valleys below and radioed in movement of enemy vehicles, allowing Special Operations Forces soldiers on the ground to set up strategic ambushes and save countless lives. Not bad for a fifty-year-old sea-searching aircraft design on duty in the middle of the desert.

Rewind 11 years to 1991s Operation Desert Storm: It was here that the P-3 first showed its potential as a land surveillance aircraft, monitoring Iraqi troop activities and providing battle-damage assessments on the ground. The introduction of new long-range video cameras for use over the skies of Bosnia allowed these planes to provide real-time combat intelligence for NATO commanders, a tactical advantage that proved equally useful during Operation Deliberate Force in 1995.

The P-3 Orion: A Versatile Plane

One characteristic shared by all the planes that have reached a half-century of service is versatility, and the P-3 Orion is no exception in this regard. Beside the military applications weve already covered, this old warbird has also proven adaptable for civilian law enforcement, namely anti-narcotics smuggling and anti-illegal immigration missions. It is flown by the intrepid aircrews of the Air and Marine Operations component of one of my former employers, the U.S. Customs & Border Protection. The CBP dubs its P-3 variant the Long Range Tracker.

Like its fellow 50-somethings, the P-3 hasnt failed to keep up with technological advances. To quote the Lockheed Martin folks one more time, The P-3 MLU [Mid-Liffe Upgrade] Program is the answer to maintaining effectiveness and reliability in a critical global economy. It consists of a life extension kit replacing the aircraft outer wings, center wing lower section and horizontal stabilizer with new production components.

MLU removes all current P-3 airframe flight restrictions and provides 15,000 additional flight hours, greatly enhancing capability leveraged with cost-effectiveness. The design replaces all fatigue-life-limiting structures on the aircraft with enhanced-design components and new improved corrosion-resistant materials that will greatly reduce the cost of ownership over the aircrafts remaining service life. This is an affordable solution that Lockheed Martin has proven can be installed in 11 months.

Specifications/General Characteristics

Primary Function:Anti-Submarine warfare and Anti-Surface Warfare

Contractor:Lockheed Martin Aeronautical Systems Company

Propulsion:Four Allison T-56-A-14 turboprop engines (4,600 hp each)

Length:116.7 feet (35.57 meters)

Height:33.7 feet (10.27 meters)

Wingspan:99.6 feet (30.38 meters)

Weight:Maximum takeoff, 139,760 pounds (63,394 kilograms)

Airspeed:411 knots; Cruise, 328 knots

Ceiling:28,300 feet (8,626 meters)

Range:2,380 nautical mile radius; for three hours on station at 1,500 feet, 1,346 nautical miles

Crew:Three pilots, two naval flight officers (NFOs), two flight engineers, three sensor operators and one in-flight technician

Armament:AGM-84 Harpoon, AGM-84K SLAM-ER, AGM-65F Maverick missiles, Mk46/50/54 torpedoes, rockets, mines and depth bombs

Christian D. Orr is a former Air Force officer, Federal law enforcement officer, and private military contractor (with assignments worked in Iraq, the United Arab Emirates, Kosovo, Japan, Germany, and the Pentagon). Chris holds a B.A. in International Relations from the University of Southern California (USC) and an M.A. in Intelligence Studies (concentration in Terrorism Studies) from American Military University (AMU). He has also been published in The Daily Torch and The Journal of Intelligence and Cyber Security.

Go here to see the original:
P-3 Orion: The Plane Built to Hunt and Kill Russia's Submarines - 19FortyFive

Recommendation and review posted by Bethany Smith

USS Vicksburg, a Ticonderoga-class guided-missile cruiser, passes through the Strait of Gibraltar on March 31, 2015. The House Armed Services Committees subpanel on seapower and projection forces plans to prohibit the Navy from cutting the Vicksburg as well as four landing dock ships from its fleet, according to committee aides. (Anthony Hilkowski/U.S. Navy)

WASHINGTON House lawmakers will push to save five ships that the Navy is slating for retirement, rejecting the service branchs proposal to decommission 24 ships in its fiscal 2023 budget.

The House Armed Services Committees subpanel on seapower and projection forces plans to prohibit the Navy from cutting the cruiser USS Vicksburg as well as four landing dock ships from its fleet, according to committee aides. Lawmakers will recommend the changes to the full House committee this week as it drafts the National Defense Authorization Act, an annual sweeping military policy and funding bill.

Theres consensus that USS Vicksburg should be retained, an aide said, speaking on condition of anonymity. With respect to [landing dock ships], theres strong support for the commandant of the Marine Corps assessment that he needs no fewer than 31 amphibious ships so prohibiting the retirement of the [landing dock ships] certainly gets after that.

The USS Vicksburg, a Ticonderoga-class guided missile cruiser that launched in 1991, is nearing the end of a nearly $500 million modernization overhaul in Virginia that began in 2020. Rep. Kay Granger, the ranking Republican of the House Appropriations Committee, admonished Navy officials at a hearing last month for seeking to decommission the cruiser.

At a time when the ship is still in its maintenance period, the Navy is proposing to scrap it, the Texas congresswoman said. If the Navy experts expect Congress to support its vision for this fleet, it must do a much better job of managing the inventory it has. We will not stand idly by as valuable taxpayer funds are wasted.

Other cruisers on the Navys chopping block include USS Bunker Hill, USS Mobile Bay, USS San Jacinto and USS Lake Champlain.

Retirements are also planned for two Los Angeles-class submarines, two oilers, two expeditionary transfer docks and all nine of the Navys Freedom-class littoral combat ships, some of which have been in service less than five years. One of the four landing dock ships that lawmakers are hoping to keep the Whidbey Island-class USS Tortuga is undergoing the same service-life extension repairs as the USS Vicksburg.

Navy officials said decommissioning will save about $3.6 billion in the next five years, allowing the Navy to get rid of aging ships and systems that are expensive to maintain and instead invest in unmanned platforms and other technology. The divest to invest strategy has repeatedly frustrated lawmakers who are warily eyeing Chinas rapidly growing fleet.

Congress last year reversed the Navys plan to retire seven cruisers, forcing the service to hang on to two, and ordered the Navy to build 13 ships instead of a requested eight. Next years proposed $180 billion Navy budget also calls for building eight ships a plan that Rep. Elaine Luria, a retired Navy commander, described as anemic.

The Navy has no strategy, Luria, D-Va., tweeted in March. Stop saying you do, because if you did you would be able to explain how this fleet size will allow us to defend Taiwan.

Rep. Rob Wittman, the ranking Republican on the seapower subcommittee, noted last month that the Navy is congressionally mandated to have 355 ships. The Navys proposed cuts would immediately shrink the current 298-ship fleet to 285 ships, he said.

We dont expand our naval capacity and capabilities by subtracting more than we add, the Virginia congressman said. The budget request definitely does not support [Defense] Secretary [Lloyd] Austins stated intent of pacing the Chinese naval capabilities whose force is expected to exceed 460 ships by the turn of this decade, at which point our fleet will be only two-thirds the size of the Peoples Liberation Army Navy.

Despite the criticism, the subcommittee will recommend sticking to the Navys shipbuilding plan, committee aides said. The Navy is aiming to acquire two Virginia-class attack submarines, two Arleigh Burke-class destroyers, one frigate, one amphibious transport dock, one oiler and one towing, salvage and rescue ship.

House lawmakers will also seek to set a statutory floor of 31 amphibious ships and require the Navy secretary to consult with the Marine Corps commandant on all major decisions concerning amphibious force structure and capability, committee aides said.

Other recommendations by the subcommittee include allowing the Air Force to retire eight of its C-130 transport aircraft and 13 of its air-refueling tanker aircraft and authorizing the Navy secretary to enter into procurement contracts for up to 15 guided-missile destroyers and up to 25 Ship-to-Shore connector crafts, according to aides.

The House Armed Services Committee will announce parts of its legislative agenda for the 2023 NDAA during six subcommittee markups this week, with a full committee markup scheduled for June 22. The Senate Armed Services Committee will begin unveiling its version of the bill next week.

See original here:
House panel aims to save five ships from retirement, rejecting Navy's plan to decommission them - Stars and Stripes

Recommendation and review posted by Bethany Smith

When the MiG-25 Foxbat entered service with the Soviet Union in 1970, it gave NATO airpower planners plenty to worry about. The Foxbat was the fastest interceptor in the world at the time, and the ever-pervasive fear of the unknown flew alongside it. However, much of that fear dissipated after the defection of MiG-25 pilot Lt. Viktor Belenko in 1976. Belenko helped to eliminate the aura of mystery that had surrounded this high-speed aircraft.

But the Soviet war machine didnt let Belenkos defection deter them from improving on the concept. Thus the MiG-31 Foxhound was born.

From Foxbat to Foxhound

The Foxhound made her maiden flight in September 1975 and officially entered into service with the Soviet PVO (voyska protivovozdushnoy oborony, or Anti-Air Defense Troops) in 1981.

The MiG-31 bears a striking cosmetic resemblance to the MiG-25, which probably explains at least in part why NATO retained the Fox portion when assigning its codename to the successor aircraft. However, look beneath the surface and you will find the Foxhound equipped with state-of-the-art digital avionics that its older foxy sibling lacked.

For one thing, the MiG-31 was the first Soviet fighter aircraft to have true look-down/shoot-down capability, thanks to its phased array radar. Earlier USSR fighter radars had a tendency to run afoul of ground clutter. In addition, the Foxhound can work efficiently in all weather conditions while fulfilling visual flight rules and instrument flight rules, day and night.

Yet another improvement was the newer planes extended range, which increased to 1,900 miles (3,000 kilometers) upon initial takeoff, and further bolstered to 3,400 miles (5,400 kilometers) with one aerial refueling. By contrast, the gas-guzzling Foxbat bore the curse of a relatively short range: 1,160 miles (1,860 kilometers) at Mach 0.9 and 1,013 miles (1,630 kilometers) when zipping along at Mach 2.35. This underscored how lucky the aforementioned Belenko was to make his initial escape from Vladivostok to Hokkaido, Japan. (In retrospect, perhaps NATO shouldve codenamed the MiG-25 the Cheetah. It can pursue its prey at tremendous speeds, but only for short distances.)

The Foxhounds pilots also enjoyed a reduced likelihood of failure to communicate. As my 1945 colleague Caleb Larson explains,MiG-31s can network with other airplanes in their sortie, relaying information on enemy aircraft locations and thus covering a much wider area than unnetworked groups of airplanes.

Foxhound Flies On

Five hundred and nineteen Foxhounds have been produced so far, out of which 370 were delivered to the Russian Air Force and 30 are in service with Kazakh air force. In July 2020, Russias Defense Ministry announced its intention to invest in modernization and life extension programs for its MiG-31 fleet.

MiG-31 customers outside of the former Soviet republics have been few and far between. In 1992, right on the heels of the collapse of the Soviet Union, the cash-starved post-Soviet Russian arms industry offered the Mig-31 to Finland, but the Finns turned it down. Meanwhile, Syria ordered eight MiG-31E airframes for its own air force in 2007, but the order was suspended in May 2007. Six of these MiGs may or not have been delivered to Syria as of August 2015, depending on whether you choose to believe the Turkish or the Russian media.

What is not in dispute is that the Russians themselves have deployed the MiG-31 in missions over Syria. In addition, the Foxhound has been blooded in Vladimir Putins so-called special military operation in Ukraine. On March 18, a MiG-31K variant launched a strike on a Ukrainian arms depot near the Polish border, evidently using a Kh-47M2 Kinzhal hypersonic missile. In turn, on April 26, the Ukrainians managed to shoot down a Foxhound with a British-made Starstreak missile.

Specifications

General Characteristics

Crew: Two (pilot and weapons system officer)

Length: 22.69 m (74 ft 5 in)

Wingspan: 13.46 m (44 ft 2 in)

Height: 6.15 m (20 ft 2 in)

Wing area: 61.6 m (663 ft)

Empty weight: 21,820 kg (48,100 lb)

Armament

1 GSh-6-23 23 mm cannon with 260 rounds.

Fuselage recesses for 4 R-33 (AA-9 Amos) (or for MiG-31M/BM only 6 R-37 (AA-X-13 Arrow) long-range air-to-air missiles)

4 underwing pylons for a combination of:

Christian D. Orr is a former Air Force officer, Federal law enforcement officer, and private military contractor (with assignments worked in Iraq, the United Arab Emirates, Kosovo, Japan, Germany, and the Pentagon). Chris holds a B.A. in International Relations from the University of Southern California (USC) and an M.A. in Intelligence Studies (concentration in Terrorism Studies) from American Military University (AMU). He has also been published in The Daily Torch and The Journal of Intelligence and Cyber Security.

Continue reading here:
MiG-31 Foxhound Is One Really Fast Russian Jet - 19FortyFive

Recommendation and review posted by Bethany Smith

The National Aerospace Laboratories (NAL) in Bengaluru on Sunday marked 55 years of the 1.2mm trisonic wind tunnel, the only industrial wind tunnel providing the high-speed aerodynamic data for national aerospace programmes, both in the civil and military sectors.

Wind tunnels are used for simulating flight conditions in the laboratory. The NAL stated that the facility will continue to meet the experimental aerodynamic data requirement of future programmes.

Council of Scientific and Industrial Research (CSIR)-NAL is currently working towards setting up a continuous wind tunnel facility to meet the increased demand for high speed experimental aerodynamic data. Practically each and every indigenously developed aerospace vehicle in the country has graduated out of this facility. To cater to the emerging requirements of the country, continual upgrades of the facility have been implemented in CSIR-NAL, leading to many state-of-the-art techniques related to high-speed wind tunnel testing mainly to improve the data quality, productivity and life extension of various components of the wind tunnel, a statement from CSIR-NAL read.

The 1.2m trisonic wind tunnel was built by the CSIR between 1963 and 1967. The first blow-down (test) was conducted on May 29, 1967. The vision of the late Dr P Neelakantan, the first Director of CSIR-NAL, enabled the realisation of this facility, which is the major workhorse for all the national aerospace programmes. The highest speed of this tunnel is Mach 4.0 which is four times the speed of sound, the release said.

The mission of this facility is to provide advanced technology solutions to national aerospace programs, fighter aircraft, defence systems, launch vehicles and satellites and space systems.

This wind tunnel was primarily conceived for research and development in experimental aerodynamics. Subsequently, as the Indian Space Research Organization (ISRO) and Defence Research and Development Organization (DRDO) started the development of launch vehicles, missiles and aircraft, the need for high-speed wind tunnel tests in the 1.2m wind tunnel increased. To name a few, DRDOs missiles such as Agni, Akaash, Prithvi, Pralay, SRSAM, LRSAM, ASTRA, NAG, LRAShM, BrahMos, Nirbhay, Unmanned Aerial Vehicles, etc. were characterized in this facility.

Similarly, aerodynamic characterisation of the ISROs launch vehicles such as ASLV, PSLV, SLV, SSLV, GSLV, RLV and GAGANYAAN programmes were carried out extensively. The nations first Light Combat Aircraft (LCA-TEJAS) was conceived at this facility and now it is flying in the sky. Many weapon integration programmes on LCA, Mirage-2000, Sukhoi-30, Jaguar, MiG aircraft etc., were successfully carried out in this facility.

More here:
Bengaluru: NAL marks 55 years of 1.2m trisonic wind tunnel - The Indian Express

Recommendation and review posted by Bethany Smith

Dive Brief:

Though small in scope, Immatics and Editas deal adds to a flurry of recent activity involving treatments that harness gamma delta T cells, rare white blood cells with unique tumor-fighting capabilities.

Unlike the T cells used in Novartis, Gilead and Bristol Myers Squibbs treatments, gamma delta cells have elements of both innate and adaptive immunity, which could enable them to generate a broader response against cancers. These cells also have key differences that make them less likely to trigger graft-versus-host disease, give them the potential to persist in the body for years, and to recognize a range of targets.

Those traits have already prompted drugmakers including Takeda, Johnson & Johnson, Bristol Myers and Regeneron to make investments. Clinical data presented at the American Society of Clinical Oncology has further elevated the profile of gamma delta cell therapy, as a treatment from Adicet Bio has shown early promise against non-Hodgkins lymphoma.

Immatics has already capitalized on the momentum, turning its alliance with Bristol Myers into a new, lucrative deal. Now Immatics is bringing gene editing tools in as well.

Genetic engineering is already part of many cell therapies, as CAR-T treatments involve modifications that help T cells recognize cancer. But CRISPR and other gene editing approaches could help do more. Allogene Therapeutics, for example, uses gene editing to make changes aimed at reducing the risk of graft-versus-host disease. Nkarta and CRISPR Therapeutics plan to give treatments involving natural killer cells, which share some similarities with gamma delta T cells, more tumor-killing punch.

Immatics and Editas appear to share a similar goal, saying in a statement that they want to make gamma delta cells with enhanced tumor recognition and destruction. Those potential benefits do come with added risk, however. U.S. regulators halted testing of Allogenes programs last year to investigate whether the gene editing involved in its treatment led to a chromosomal abnormality in a treated patient. Follow-up investigation exonerated Allogenes treatment, but the setback led to a lengthy delay.

For Editas, the deal adds to multiple other partnerships involving cell therapy. The company is already working with Bayer's Bluerock Therapeutics subsidiary on natural killer cell therapies for solid tumors, and with Bristol Myers on so-called alpha-beta T cell treatments.

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Immatics and Editas join up to bring CRISPR to 'gamma delta' cell therapy - BioPharma Dive

Recommendation and review posted by Bethany Smith

CRISPR Therapeutics (NASDAQ:CRSP Get Rating) and Inhibrx (NASDAQ:INBX Get Rating) are both medical companies, but which is the superior business? We will compare the two companies based on the strength of their valuation, earnings, dividends, institutional ownership, profitability, analyst recommendations and risk.

Earnings and Valuation

This table compares CRISPR Therapeutics and Inhibrxs revenue, earnings per share and valuation.

Profitability

This table compares CRISPR Therapeutics and Inhibrxs net margins, return on equity and return on assets.

Analyst Recommendations

This is a summary of recent ratings and recommmendations for CRISPR Therapeutics and Inhibrx, as reported by MarketBeat.

CRISPR Therapeutics presently has a consensus price target of $114.71, indicating a potential upside of 70.25%. Inhibrx has a consensus price target of $44.33, indicating a potential upside of 291.64%. Given Inhibrxs stronger consensus rating and higher possible upside, analysts plainly believe Inhibrx is more favorable than CRISPR Therapeutics.

Insider & Institutional Ownership

56.1% of CRISPR Therapeutics shares are owned by institutional investors. Comparatively, 59.6% of Inhibrx shares are owned by institutional investors. 10.7% of CRISPR Therapeutics shares are owned by company insiders. Comparatively, 25.8% of Inhibrx shares are owned by company insiders. Strong institutional ownership is an indication that large money managers, endowments and hedge funds believe a stock will outperform the market over the long term.

Volatility & Risk

CRISPR Therapeutics has a beta of 2.04, suggesting that its stock price is 104% more volatile than the S&P 500. Comparatively, Inhibrx has a beta of 3.1, suggesting that its stock price is 210% more volatile than the S&P 500.

Summary

CRISPR Therapeutics beats Inhibrx on 8 of the 14 factors compared between the two stocks.

About CRISPR Therapeutics (Get Rating)

CRISPR Therapeutics is a gene-editing company focused on developing transformative gene-based medicines for serious diseases using its proprietary CRISPR/Cas9 platform. CRISPR/Cas9 is a revolutionary gene-editing technology that allows for precise, directed changes to genomic DNA. CRISPR Therapeutics has established a portfolio of therapeutic programs across a broad range of disease areas including hemoglobinopathies, oncology, regenerative medicine and rare diseases. To accelerate and expand its efforts, CRISPR Therapeutics has established strategic collaborations with companies including Bayer, Vertex Pharmaceuticals and ViaCyte, Inc. CRISPR Therapeutics AG is headquartered in Zug, Switzerland, with its wholly-owned U.S. subsidiary, CRISPR Therapeutics, Inc., and R&D operations based in Cambridge, Massachusetts, and business offices in San Francisco, California and London, United Kingdom. For more information, please visit http://www.crisprtx.com.

About Inhibrx (Get Rating)

Inhibrx, Inc., a clinical-stage biotechnology company, focuses on developing a pipeline of novel biologic therapeutic candidates. The company's therapeutic candidates include INBRX-109, a tetravalent agonist of death receptor 5, which is in Phase 2 clinical trials to treat cancers, such as chondrosarcoma, mesothelioma, and pancreatic adenocarcinoma; INBRX-105, a tetravalent conditional agonist of programmed death-ligand 1 and a conditional agonist of 4-1BB that is in Phase 1 clinical trials to treat patients with locally advanced or metastatic solid tumors; and INBRX-101, an alpha-1 antitrypsin (AAT)-Fc fusion protein therapeutic candidate, which is in Phase 1 clinical trials for use in the treatment of patients with AAT deficiency. It also provides INBRX-106, a hexavalent agonist of OX40 for a range of oncology indications. The company was founded in 2010 and is headquartered in La Jolla, California.

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Analyzing CRISPR Therapeutics (NASDAQ:CRSP) and Inhibrx (NASDAQ:INBX) - Defense World

Recommendation and review posted by Bethany Smith

- Vertex announces three additional abstracts on the burden of beta thalassemia and sickle cell disease accepted for poster presentation

BOSTON & ZUG, Switzerland & CAMBRIDGE, Mass., June 02, 2022--(BUSINESS WIRE)--Vertex Pharmaceuticals Incorporated (Nasdaq: VRTX) and CRISPR Therapeutics (NASDAQ: CRSP) today announced new late-breaking clinical data accepted for oral presentation at the 2022 European Hematology Association (EHA) Congress. Vertex also announced three abstracts accepted for poster presentation at EHA.

Late-breaking abstract #LB2367 entitled "Efficacy and Safety of A Single Dose of CTX001 For Transfusion-Dependent eta-Thalassemia and Severe Sickle Cell Disease," will be an oral presentation on Sunday, June 12 at 09:4511:15 CEST. The abstract from Vertex and CRISPR Therapeutics includes data on patients treated in CLIMB111 and CLIMB121 and followed in CLIMB131 with CTX001, now known as exagamglogene autotemcel (exa-cel). This abstract has been selected for the media briefing program and is therefore embargoed until Saturday, June 11 at 09:00 am CEST.

In addition, three real-world evidence and health economics abstracts from Vertex have been accepted for poster presentation.

Abstract #P1704 entitled "Projected Lifetime Economic Burden of Severe Sickle Cell Disease in the United States," will be a poster presentation on Friday, June 10 at 16:3017:45 CEST. The abstract posted online projects the per-patient lifetime direct health care cost of severe sickle cell disease (SCD) from a U.S. health care payer perspective using an economic model developed based on published model frameworks.

Abstract #P1703 entitled "Economic Burden of TransfusionDependent BetaThalassemia in the United States," will be a poster presentation on Friday, June 10 at 16:3017:45 CEST. The abstract posted online estimates the economic burden of transfusion-dependent beta thalassemia (TDT) using administrative claims data to estimate the costs and health care utilization associated with disease management in the U.S.

Abstract #P1482 entitled "Patients With Severe Sickle Cell Disease on Standard-of-Care Treatment Are Very Unlikely to Become VOCFree for One Year: A Cohort Study of Medicaid Enrollees," will be a poster presentation on Friday, June 10 at 16:3017:45 CEST. The abstract posted online contextualizes the efficacy of exacel in eliminating vasoocclusive crises (VOCs) in patients with SCD using nationwide U.S. Medicaid claims data from 2000 to 2014 to assess the proportion of patients with recurrent VOCs who became VOCfree during a 1year follow up on standard of care.

Story continues

The accepted abstracts are now available online on the EHA website.

Exacel is being investigated in multiple ongoing clinical trials as a potential one-time therapy for patients with either TDT or SCD.

About exagamglogene autotemcel (exa-cel)

Exacel, formerly known as CTX001, is an investigational, autologous, ex vivo CRISPR/Cas9 geneedited therapy that is being evaluated for patients with TDT or SCD characterized by recurrent VOCs, in which a patients own hematopoietic stem cells are edited to produce high levels of fetal hemoglobin (HbF; hemoglobin F) in red blood cells. HbF is the form of the oxygencarrying hemoglobin that is naturally present during fetal development, which then switches to the adult form of hemoglobin after birth. The elevation of HbF by exacel has the potential to alleviate transfusion requirements for patients with TDT and reduce painful and debilitating sickle crises for patients with SCD. Earlier results from these ongoing trials were published in The New England Journal of Medicine in January of 2021.

Based on progress in this program to date, exacel has been granted Regenerative Medicine Advanced Therapy (RMAT), Fast Track, Orphan Drug, and Rare Pediatric Disease designations from the U.S. Food and Drug Administration (FDA) for both TDT and SCD. Exa-cel has also been granted Orphan Drug Designation from the European Commission, as well as Priority Medicines (PRIME) designation from the European Medicines Agency (EMA), for both TDT and SCD.

Among geneediting approaches being evaluated for TDT and SCD, exacel is the furthest advanced in clinical development.

About CLIMB111 and CLIMB121

The ongoing Phase 1/2/3 openlabel trials, CLIMB111 and CLIMB121, are designed to assess the safety and efficacy of a single dose of exacel in patients ages 12 to 35 years with TDT or with SCD, characterized by recurrent VOCs, respectively. The trials are now closed for enrollment. Patients will be followed for approximately two years after exacel infusion. Each patient will be asked to participate in CLIMB131, a longterm followup trial.

About CLIMB-131

This is a longterm, openlabel trial to evaluate the safety and efficacy of exacel in patients who received exacel in CLIMB111, CLIMB121, CLIMB141 or CLIMB151. The trial is designed to follow participants for up to 15 years after exacel infusion.

About CLIMB141 and CLIMB151

The ongoing Phase 3 open-label trials, CLIMB141 and CLIMB151, are designed to assess the safety and efficacy of a single dose of exacel in patients ages 2 to 11 years with TDT or with SCD, characterized by recurrent VOCs, respectively. The trials are now open for enrollment and currently enrolling patients ages 5 to 11 years of age and will plan to extend to ages 2 to less than 5 years of age at a later date. Each trial will enroll up to 12 patients. Patients will be followed for approximately two years after infusion. Each patient will be asked to participate in CLIMB-131, a longterm followup trial.

About the GeneEditing Process in These Trials

Patients who enroll in these trials will have their own hematopoietic stem and progenitor cells collected from peripheral blood. The patients cells will be edited using the CRISPR/Cas9 technology. The edited cells, exacel, will then be infused back into the patient as part of an autologous hematopoietic stem cell transplant (HSCT), a process which involves a patient being treated with myeloablative busulfan conditioning. Patients undergoing HSCT may also encounter side effects (ranging from mild to severe) that are unrelated to the administration of exacel. Patients will initially be monitored to determine when the edited cells begin to produce mature blood cells, a process known as engraftment. After engraftment, patients will continue to be monitored to track the impact of exacel on multiple measures of disease and for safety.

About the VertexCRISPR Collaboration

Vertex and CRISPR Therapeutics entered into a strategic research collaboration in 2015 focused on the use of CRISPR/Cas9 to discover and develop potential new treatments aimed at the underlying genetic causes of human disease. Exacel represents the first potential treatment to emerge from the joint research program. Under an amended collaboration agreement, Vertex now leads global development, manufacturing and commercialization of exacel and splits program costs and profits worldwide 60/40 with CRISPR Therapeutics.

About Vertex

Vertex is a global biotechnology company that invests in scientific innovation to create transformative medicines for people with serious diseases. The company has multiple approved medicines that treat the underlying cause of cystic fibrosis (CF) a rare, life-threatening genetic disease and has several ongoing clinical and research programs in CF. Beyond CF, Vertex has a robust pipeline of investigational small molecule, cell and genetic therapies in other serious diseases where it has deep insight into causal human biology, including sickle cell disease, beta thalassemia, APOL1mediated kidney disease, pain, type 1 diabetes, alpha1 antitrypsin deficiency and Duchenne muscular dystrophy.

Founded in 1989 in Cambridge, Mass., Vertex's global headquarters is now located in Boston's Innovation District and its international headquarters is in London. Additionally, the company has research and development sites and commercial offices in North America, Europe, Australia and Latin America. Vertex is consistently recognized as one of the industry's top places to work, including 12 consecutive years on Science magazine's Top Employers list and one of the 2021 Seramount (formerly Working Mother Media) 100 Best Companies. For company updates and to learn more about Vertex's history of innovation, visit http://www.vrtx.com or follow us on Facebook, Twitter, LinkedIn, YouTube and Instagram.

(VRTX-GEN)

Vertex Special Note Regarding Forward-Looking Statements

This press release contains forward-looking statements as defined in the Private Securities Litigation Reform Act of 1995, as amended, including, without limitation, our plans and expectations to present clinical data from the ongoing exa-cel clinical trials during the EHA Congress, expectations regarding the abstracts that will be made available on the virtual platform and the clinical data that will be presented during the EHA Congress, including anticipated projections and estimates related to the various economic impacts of SCD and TDT, the potential benefits, efficacy, and safety of exa-cel, including the potentially transformative nature of the therapy and the potential of the treatment for patients, our plans and expectations for our clinical trials and pipeline products, the status of our clinical trials of our product candidates under development by us and our collaborators, including activities at the clinical trial sites, patient enrollment and expectations regarding clinical trial follow-up. While Vertex believes the forward-looking statements contained in this press release are accurate, these forward-looking statements represent the company's beliefs only as of the date of this press release and there are a number of risks and uncertainties that could cause actual events or results to differ materially from those expressed or implied by such forward-looking statements. Those risks and uncertainties include, among other things, that data from a limited number of patients may not be indicative of final clinical trial results, that data from the company's development programs, including its programs with its collaborators, may not support registration or further development of its compounds due to safety and/or efficacy, or other reasons, that internal or external factors that could delay, divert, or change our plans and objectives with respect to our research and development programs, that future competitive or other market factors may adversely affect the commercial potential for exa-cel, and other risks listed under the heading "Risk Factors" in Vertex's most recent annual report and subsequent quarterly reports filed with the Securities and Exchange Commission (SEC) and available through the company's website at http://www.vrtx.com and on the SECs website at http://www.sec.gov. You should not place undue reliance on these statements or the scientific data presented. Vertex disclaims any obligation to update the information contained in this press release as new information becomes available.

(CRSP-GEN)

About CRISPR Therapeutics

CRISPR Therapeutics is a leading gene editing company focused on developing transformative gene-based medicines for serious diseases using its proprietary CRISPR/Cas9 platform. CRISPR/Cas9 is a revolutionary gene editing technology that allows for precise, directed changes to genomic DNA. CRISPR Therapeutics has established a portfolio of therapeutic programs across a broad range of disease areas including hemoglobinopathies, oncology, regenerative medicine and rare diseases. To accelerate and expand its efforts, CRISPR Therapeutics has established strategic collaborations with leading companies including Bayer, Vertex Pharmaceuticals and ViaCyte, Inc. CRISPR Therapeutics AG is headquartered in Zug, Switzerland, with its wholly-owned U.S. subsidiary, CRISPR Therapeutics, Inc., and R&D operations based in Cambridge, Massachusetts, and business offices in San Francisco, California and London, United Kingdom. For more information, please visit http://www.crisprtx.com.

CRISPR Therapeutics Forward-Looking Statement

This press release may contain a number of "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995, as amended, as well as statements regarding CRISPR Therapeutics expectations about any or all of the following: i) the safety, efficacy and clinical progress of the ongoing exa-cel clinical trials, including expectations regarding the abstract that will be made available on the virtual platform and our plans to present and the clinical data that are being presented during the EHA Congress; and (ii) the therapeutic value, development, and commercial potential of CRISPR/Cas9 gene editing technologies and therapies. Without limiting the foregoing, the words "believes," "anticipates," "plans," "expects" and similar expressions are intended to identify forward-looking statements. You are cautioned that forward-looking statements are inherently uncertain. Although CRISPR Therapeutics believes that such statements are based on reasonable assumptions within the bounds of its knowledge of its business and operations, existing and prospective investors are cautioned that forward-looking statements are inherently uncertain, are neither promises nor guarantees and not to place undue reliance on such statements, which speak only as of the date they are made. Actual performance and results may differ materially from those projected or suggested in the forward-looking statements due to various risks and uncertainties. These risks and uncertainties include, among others: the potential for initial and preliminary data from any clinical trial and initial data from a limited number of patients (as is the case with exa-cel at this time) not to be indicative of final or future trial results; the potential that the exa-cel clinical trial results may not be favorable or may not support registration or further development; that future competitive or other market factors may adversely affect the commercial potential for exa-cel; CRISPR Therapeutics may not realize the potential benefits of its collaboration with Vertex; potential impacts due to the coronavirus pandemic, such as to the timing and progress of clinical trials; uncertainties regarding the intellectual property protection for CRISPR Therapeutics technology and intellectual property belonging to third parties; and those risks and uncertainties described under the heading "Risk Factors" in CRISPR Therapeutics most recent annual report on Form 10-K, quarterly report on Form 10-Q, and in any other subsequent filings made by CRISPR Therapeutics with the U.S. Securities and Exchange Commission, which are available on the SEC's website at http://www.sec.gov. CRISPR Therapeutics disclaims any obligation or undertaking to update or revise any forward-looking statements contained in this press release, other than to the extent required by law.

View source version on businesswire.com: https://www.businesswire.com/news/home/20220601006221/en/

Contacts

Vertex Pharmaceuticals Incorporated Investors: Michael Partridge, +1 617-341-6108OrManisha Pai, +1 617-961-1899OrMiroslava Minkova, +1 617-341-6135

Media: mediainfo@vrtx.com orU.S.: +1 617-341-6992orHeather Nichols: +1 617-839-3607orInternational: +44 20 3204 5275

CRISPR Therapeutics Investors: Susan Kim, +1 617-307-7503susan.kim@crisprtx.com

Media: Rachel Eides, +1-617-315-4493.rachel.eides@crisprtx.com

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Vertex and CRISPR Therapeutics Announce Acceptance of Late-Breaking Abstract for CTX001 at the 2022 Annual European Hematology Association (EHA)...

Recommendation and review posted by Bethany Smith

The latest competent intelligence report published by WMR with the title An increase in demand and Opportunities for Global CRISPR-Cas9 Market 2022 provides a sorted image of the CRISPR-Cas9 industry by analysis of research and information collected from various sources that have the ability to help the decision-makers in the worldwide market to play a significant role in making a gradual impact on the global economy. The report presents and showcases a dynamic vision of the global scenario in terms of market size, market statistics, and competitive situation.

At present, the CRISPR-Cas9 market is possessing its presence over the globe. The Research report presents a complete judgment of the market which consists of future trends, growth factors, consumption, production volume, CAGR value, attentive opinions, profit margin, price, and industry-validated market data. This report helps the individuals and the market competitors to predict future profitability and to make critical decisions for business growth.

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Scope of CRISPR-Cas9 Market:

Emerging trends, The report on the CRISPR-Cas9 market givesa complete picture of demands and opportunities for the future that are beneficial for individuals and stakeholders in the market. This report determines the market value and the growth rate based on the key market dynamics as well as the growth improving factors. The entire study is based on the latest industry news, market trends, and growth probability. It also consists of a deep analysis of the market and competing scenario along with the SWOT analysis of the well-known competitors.

The Leading Players involved in the global CRISPR-Cas9 market are:

Editas Medicine CRISPR Therapeutics Horizon Discovery Sigma-Aldrich Genscript Sangamo Biosciences Lonza Group Integrated DNA Technologies New England Biolabs Origene Technologies Transposagen Biopharmaceuticals Thermo Fisher Scientific Caribou Biosciences Precision Biosciences Cellectis Intellia Therapeutics

Segmentation by Type:

Biotechnology Companies Pharmaceutical Companies Others

Segmentation by Applications:

Genetic Engineering Gene Library Human Stem Cells Others

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Global CRISPR-Cas9 Market Regional Analysis:

The research study has segregated the global CRISPR-Cas9 industry into segments, including product type, application, and vertical, to broaden the overall understanding of the industry. This assessment has been carried out on the basis of size, share, and CAGR. Additionally, regional analysis has been done by the experts stressing the growth potential of the key regions and countries. The report also encompasses accurate and reliable figures based on the CRISPR-Cas9 consumption and production in key regions.

North America: USA, Canada, Mexico, etc.Asia-Pacific: China, Japan, Korea, India, and Southeast AsiaThe Middle East and Africa: Saudi Arabia, the UAE, Egypt, Turkey, Nigeria, and South AfricaEurope: Germany, France, the UK, Russia, and ItalySouth America: Brazil, Argentina, Columbia, etc.

The report helps in providing a wider introduction to the market and also helps in dealing with the detailed methodology of research for the calculation of the size and forecasts of the market. The sources of secondary data are used and the primary inputs are taken for the validation of data. This section also helps in the outlines of the several segments that have also been covered as being a part of the report. Additionally, the Research Methodology reviews tend of providing the calculation for determining the inclinations of the global market.

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Some of the Major Points of TOC cover:

Chapter 1: Techniques & Scope

1.1 Definition and forecast parameters1.2 Methodology and forecast parameters1.3 Information Sources

Chapter 2: Latest Trends Summary

2.1 Regional trends2.2 Product trends2.3 End-use trends2.4 Business trends

Chapter 3: CRISPR-Cas9 Industry Insights

3.1 Industry fragmentation3.2 Industry landscape3.3 Vendor matrix3.4 Technological and innovative landscape

Chapter 4: CRISPR-Cas9 Market, By Region

Chapter 5: Company Profiles

5.1 Company Overview5.2 Financial elements5.3 Product Landscape5.4 SWOT Analysis5.5 Systematic Outlook

Chapter 6: Assumptions and Acronyms

Chapter 7: Research Methodology

Chapter 8: Contact (Continue . . .)

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Finally, the report CRISPR-Cas9 Market 2022 provides an industry development game plan, the industry information source, research findings, an appendix, and a conclusion. The report offers precise clarification of the market by highlighting the market manufacturing procedure, market competitors, sellers and merchants classification, the implementation of innovation, and business improvement designs. All these details will reassure clients of future plans and actions intended to compete with other players in the market. Further, the most recent improvements in the market are displayed.

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Worldwide Market Reports,Tel: U.S. +1-415-871-0703U.K. +44-203-289-4040Japan +81-50-5539-1737Email: [emailprotected]Website: https://www.worldwidemarketreports.com/

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CRISPR-Cas9 Market: Established Keyplayers Will Try to Generate New Growth Opportunities in the Upcoming Years: Editas Medicine, CRISPR Therapeutics,...

Recommendation and review posted by Bethany Smith

With a targeted disruptive innovation biotechnology-related exchange traded fund strategy, investors can focus on companies driving change in targeted therapeutics, bioinformatics, CRISPR technology, and more.

In the recent webcast, Change the DNA of Your Portfolio: Growth Opportunities Through Genomics, Nicholas Grous, associate portfolio manager at ARK Invest, highlighted five innovation platforms that will experience long-term growth, including artificial intelligence, energy storage, robotics, DNA sequencing, and blockchain technology. These five sub-categories are expected to enjoy long-term growth. For instance, gene sequencing is expected to expand to $3.6 trillion in 2030 from $125 billion in 2020. Overall, ARK Invest projects disruptive innovation technologies could grow to $210 trillion by 2030, compared to $14 trillion in 2020.

The increased adoption of disruptive innovation technologies will not just be a one-off event as these innovative ideas will cover a broad swathe of industries and touch upon many facets of the global economy. For example, Grous believed that the convergence of next-generation DNA sequencing, artificial intelligence, and gene therapies should boost returns on investment significantly, potentially creating a golden age of health care likely to rival that of the 1980s and 1990s.

Simon Barnett, research analyst at ARK Invest, explained that researchers had historically been forced to choose between accuracy with short-read sequencing or comprehensiveness with long-range sequencing to break the genome into smaller segments to analyze with high-resolution optics, which is then reassembled with computer algorithms. According to Wrights Law, for every cumulative doubling in data produced on its reinstalled base, the cost of synthesis-based LRS has declined and will continue to decline by 28%. Looking ahead, ARK projects the cost to sequence a whole human genome with long-read technology will drop to $100-$200 and its accuracy will be superior to SRS across all variant types by the end of 2025.

According to our research, gene editing breakthroughs are creating more effective therapies at a faster rate than historically has been the case, Barnett said.

For example, compared to zinc finger nucleases (ZFNs), which moved from discovery to the first human dose in roughly eight years, the relatively new CRISPR technology took less than half the time, three years, and can address 48% of known diseases, or almost twice ZFNs 28%. Prime and base editing CRISPR derivatives address even more diseases, 79% and 59%, respectively. Consequently, Barnett argued that CRISPR may be seen as a superior gene-editing method going forward, and it already shows as CRISPR has been dominating recent academic research and clinical trials.

Looking ahead, ARK expects gene editing and gene therapy companies to grow to $1.1 trillion in market capitalization by 2026. Given potential cures for diseases, the share of research and development funding for gene therapy innovations should continue to rise. By 2026, the share of total R&D spending devoted to gene editing and therapy companies could grow from 3% to 17%.

Additionally, Barnett noted that routine blood-based, multi-cancer screening combined with improvements in single-cancer screening could prevent 40% of metastatic diagnoses and increase loco-regional diagnoses by 10%. Even without improvements in cancer therapy, ARK estimates that earlier intervention could prevent 66,000 cancer deaths per year in the US alone.

The Central Dogma could help describe how biotechnology moves forward. The Central Dogma states that DNA (the genome) is transcribed into RNA (the transcriptome), which ultimately is translated into protein (the proteome). Proteins carry out virtually all critical-to-life functions but, when altered, can cause disease.

Understanding the interactions between and among the pillars of the Central Dogma, we will improve our ability to make predictions, diagnoses, and leaps of fundamental, biological insight, Barnett said.

We believe the future of molecular biology is based on multi-omics techniques that integrate pillars of the Central Dogma. Based on our research, multi-omics including life science tools, basic and translational research, population health efforts, and molecular diagnostics could impact oncology, organ health, and population health, scaling from $110 billion to roughly $300 billion during the next five years, he added.

As a way to capture this potential growth opportunity, investors can turn to theARK Genomic Revolution Multi-Sector Fund (NYSEArca: ARKG), an actively managed strategy that seeks long-term growth of capital by investing in domestic and foreign equity securities of companies across multiple sectors, including health care, information technology, materials, energy, and consumer discretionary, that are relevant to the funds investment theme of the genomics revolution.

ARKG aims for thematic multi-cap exposure to innovative elements including gene therapy bio-informatics, bio-inspired computing, molecular medicine, and pharmaceutical innovations. The ETF aims to capture long-term growth with a low correlation of relative returns to traditional growth strategies and a negative correlation to value strategies. Additionally, the fund offers a tool for diversification due to little overlap with traditional indices. It can be a complement to traditional value/growth strategies.

Financial advisors who are interested in learning more about growth opportunities in the biotech segment can watch the webcast here on demand

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An Innovative ETF Opportunity That Taps Into Our Increased Understanding of the Human Genome - ETF Trends

Recommendation and review posted by Bethany Smith

CAMBRIDGE, Mass., June 08, 2022 (GLOBE NEWSWIRE) -- Intellia Therapeutics, Inc. (NASDAQ:NTLA), a leading genome editing company focused on developing potentially curative therapies leveraging CRISPR-based technologies, today announced that interim clinical data from the Phase 1 study of NTLA-2001, an investigational therapy in development for the treatment of transthyretin (ATTR) amyloidosis, will be shared in an oral presentation at the European Association for the Study of the Livers International Liver Congress 2022, taking place June 22 26 in London.

We are pleased to be presenting longer-term, follow-up data from the first-in-human study of NTLA-2001, which is designed to potentially halt progression and reverse ATTR amyloidosis, said Intellia President and Chief Executive Officer John Leonard, M.D. We look forward to sharing interim data we believe demonstrates the potential of our CRISPR-based investigational therapy to be a single-dose treatment that provides a deep and durable response.

The presentation will include new data from the ongoing Phase 1 study evaluating NTLA-2001 in people living with hereditary ATTR amyloidosis with polyneuropathy (ATTRv-PN). These include additional results from all four dose-escalation cohorts in Part 1, highlighting the durability of response after a single dose of NTLA-2001. Data supporting the fixed dose selection for Part 2, the single-dose expansion cohort of the polyneuropathy arm, will also be presented.

The presentation will build upon interim data presented in February, which showed significant reductions in serum TTR levels from baseline in a dose-dependent manner in 15 patients with ATTRv-PN. At the highest dose tested, 1.0 mg/kg, the mean and maximum serum TTR reductions were 93% and 98%, respectively, by day 28 across the six patients treated. The Company also previously announced it is now evaluating a fixed dose of 80 mg in Part 2 of the Phase 1 study, which is expected to deliver a similar exposure to the 1.0 mg/kg dose in the ATTRv-PN target population, and that the first patient has been dosed in the expansion cohort in the polyneuropathy arm. Intellia also continues to dose patients in the cardiomyopathy arm of the Phase 1 study, which is evaluating NTLA-2001 in dose-escalation cohorts of people with ATTR amyloidosis with cardiomyopathy (ATTR-CM).

Presentation Details

Title: In vivo CRISPR/Cas9 editing of the TTR gene with NTLA-2001 in patients with transthyretin amyloidosis dose selection considerations

Session: Rare liver diseases (including paediatric and genetic)

Date and Time: Friday, June 24, 2022 from 10:00-11:30 a.m. BST

Presenter: Dr. Edward J. Gane, MBChB, MD, FRACP, MNZM, Professor of Medicine at the University of Auckland, New Zealand and Chief Hepatologist, Transplant Physician and Deputy Director of the New Zealand Liver Transplant Unit at Auckland City Hospital, the trials national investigator in New Zealand

Intellia Therapeutics Investor Event and Webcast Information

Intellia will host a live webcast on Friday, June 24, 2022 at 8:00 a.m. ET to review the presented data. To join the webcast, please visit this link, or the Events and Presentations page of the Investors & Media section of the companys website at http://www.intelliatx.com. A replay of the webcast will be available on Intellias website for at least 30 days following the call.

About Transthyretin (ATTR) AmyloidosisTransthyretin amyloidosis, or ATTR amyloidosis, is a rare, progressive and fatal disease. Hereditary ATTR (ATTRv) amyloidosis occurs when a person is born with mutations in theTTRgene, which causes the liver to produce structurally abnormal transthyretin (TTR) protein with a propensity to misfold. These damaged proteins build up as amyloid in the body, causing serious complications in multiple tissues, including the heart, nerves and digestive system. ATTRv amyloidosis predominantly manifests as polyneuropathy (ATTRv-PN), which can lead to nerve damage, or cardiomyopathy (ATTRv-CM), which can lead to heart failure. Some individuals without the genetic mutation produce non-mutated, or wild-type TTR proteins that become unstable over time, misfolding and aggregating in disease-causing amyloid deposits. This condition, called wild-type ATTR (ATTRwt) amyloidosis, primarily affects the heart. There are an estimated 50,000 people worldwide living with ATTRv amyloidosis and between 200,000 and 500,000 people with ATTRwt amyloidosis.

About NTLA-2001Based on Nobel Prize-winning CRISPR/Cas9 technology, NTLA-2001 could potentially be the first single-dose treatment for ATTR amyloidosis. NTLA-2001 is the first investigational CRISPR therapy candidate to be administered systemically, or through a vein, to edit genes inside the human body. Intellias proprietary non-viral platform deploys lipid nanoparticles to deliver to the liver a two-partgenome editingsystem: guide RNAspecific to the disease-causing gene and messenger RNAthat encodes the Cas9 enzyme, which carries out the precision editing. Robust preclinical data, showing deep and long-lasting transthyretin (TTR) reduction following in vivo inactivation of the target gene, supports NTLA-2001s potential as a single-administration therapeutic. Intellia leads development and commercialization of NTLA-2001 as part of a multi-target discovery, development and commercialization collaboration with Regeneron. The global Phase 1 trial is an open-label, multi-center, two-part study of NTLA-2001 in adults with hereditary transthyretin amyloidosis with polyneuropathy (ATTRv-PN) or transthyretin amyloidosis with cardiomyopathy (ATTR-CM). Visitclinicaltrials.gov(NCT04601051) for more details.

About Intellia TherapeuticsIntellia Therapeutics, a leading clinical-stage genome editing company, is developing novel, potentially curative therapeutics leveraging CRISPR-based technologies. To fully realize the transformative potential of CRISPR-based technologies, Intellia is pursuing two primary approaches. The companys in vivo programs use intravenously administered CRISPR as the therapy, in which proprietary delivery technology enables highly precise editing of disease-causing genes directly within specific target tissues. Intellias ex vivo programs use CRISPR to create the therapy by using engineered human cells to treat cancer and autoimmune diseases. Intellias deep scientific, technical and clinical development experience, along with its robust intellectual property portfolio, have enabled the company to take a leadership role in harnessing the full potential of genome editing to create new classes of genetic medicine. Learn more at intelliatx.com. Follow us on Twitter@intelliatx.

Forward-Looking Statements This press release contains forward-looking statements of Intellia Therapeutics, Inc. (Intellia or the Company) within the meaning of the Private Securities Litigation Reform Act of 1995. These forward-looking statements include, but are not limited to, express or implied statements regarding Intellias beliefs and expectations concerning: its ability to successfully extend its leadership position and harness the full potential of genomic medicines to bolster its genome editing capabilities and pipeline; the safety, efficacy, success and advancement of its clinical programs for NTLA-2001 for the treatment of transthyretin amyloidosis pursuant to its clinical trial applications (CTA), including the expected timing of data releases, regulatory filings, and the initiation, enrollment, and completion of clinical trials; the expansion of its CRISPR/Cas9 technology and related technologies to advance additional development candidates and timing expectations of advancing such development candidates; its ability to maintain and expand its related intellectual property portfolio; expectations of the potential impact of the coronavirus disease pandemic, including the impact of any variants, on strategy, future operations and timing of its clinical trials; its ability to optimize the impact of its collaborations on its development programs, including, but not limited to, its collaboration with Regeneron Pharmaceuticals, Inc.

Any forward-looking statements in this press release are based on managements current expectations and beliefs of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by such forward-looking statements. These risks and uncertainties include, but are not limited to: risks related to Intellias ability to protect and maintain its intellectual property position; risks related to Intellias relationship with third parties, including its licensors and licensees; risks related to the ability of its licensors to protect and maintain their intellectual property position; uncertainties related to the authorization, initiation and conduct of studies and other development requirements for its product candidates, including uncertainties related to regulatory approvals to conduct clinical trials; the risk that any one or more of Intellias product candidates will not be successfully developed and commercialized; the risk that the results of preclinical studies or clinical studies will not be predictive of future results in connection with future studies; the risk that clinical study results will not be positive; and the risk that Intellias collaborations with Regeneron or its other collaborations will not continue or will not be successful. For a discussion of these and other risks and uncertainties, and other important factors, any of which could cause Intellias actual results to differ from those contained in the forward-looking statements, see the section entitled Risk Factors in Intellias most recent annual report on Form 10-K, as well as discussions of potential risks, uncertainties, and other important factors in Intellias other filings with the Securities and Exchange Commission (SEC). All information in this press release is as of the date of the release, and Intellia undertakes no duty to update this information unless required by law.

Intellia Contacts:

Investors:Ian KarpSenior Vice President, Investor Relations and Corporate Communications+1-857-449-4175ian.karp@intelliatx.com

Lina LiDirector, Investor Relations and Corporate Communications+1-857-706-1612lina.li@intelliatx.com

Media:Matt CrensonTen Bridge Communications+1-917-640-7930media@intelliatx.com mcrenson@tenbridgecommunications.com

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Intellia Therapeutics to Present Updated Interim Clinical Data from Ongoing Phase 1 Study of NTLA-2001 for the Treatment of Transthyretin (ATTR)...

Recommendation and review posted by Bethany Smith

ByKen Heydon*

Trade is a key multiplier in spreading the technology vital to the climate transition. But protectionist tendencies embedded in the implementation of the climate transition pose a major threat to the global trading system.

Technological innovation backed by a carbon tax to make it competitive is the essential requirement for transition to net-zero carbon emissions by 2050. And trade, by stimulating competition, is a catalyst of innovation.

Three areas of technological transformation stand out. Australia and its Asia Pacific neighbours have a stake in each of them.

The first is solar photovoltaic technology that uses solar panels to convert sunlight into electricity. Over the past decade, solar photovoltaic has become a pillar of the low-carbon sustainable energy system with installed capacity increasing 100-fold and costs declining by 77 per cent. Some 40 per cent of the decline in the cost of solar photovoltaic modules since 2001 isattributableto trade.

With the highest solar radiation per square meter of any continent, Australia is particularly well placed to profit from solar photovoltaic technology, as testified by the proposed DarwinSingapore undersea renewables-generated electricity cable. Malaysia, Vietnam, Thailand and the Philippines rank among the top 10 global exporters of selected solar photovoltaic goods.

The second area of trade-augmented innovation is the export of low-carbonhydrogen, important in hard-to-electrify sectors like steel production and facing a potential six-fold increase in demand by 2050.

Australia is at the forefront in using renewable energy to produce zero-emissions ammonia a low-cost carrier for hydrogen and no less than six Japanese corporations havehydrogen development projects in Australia.

The third area of innovation is CRISPR (clustered regularly interspaced short palindromic repeats). This gene-editing helps countries decarbonise their food systems by making export crops that are resistant to disease or bad weather, reducing the need for increased farmland via deforestation the source of 10 per cent of global carbon emissions.

For example, CRISPR-based genome editing of oil palm to eradicate Basal Stem Rot will significantly reduce plant loss and subsequent compensatory deforestation in Indonesia and Malaysia the leading exporters of palm oil. A switch to trade in gene-edited palm oil promises major environmental benefits.

Beyond trades multiplier role in spreading the benefits of specific technologies, it also has a more general function in stimulating the economic growth necessary to fund the energy transformation.

Yet despite trades role in the climate transition, the transition itself threatens trade. As countries environmental commitment varies, pressure mounts fortariff restrictionson imports of carbon-intensive products, like steel, from perceived environmental free riders.

The difficulty of identifying carbon intensity and free riding fuels the view that such penalties are simply disguised protectionism. The resulting tensions augmented by the climate transitions emotive power and by broader protectionist tendencies, including as countries favour their own climate technologies pose a major threat to the trading system.

In each of the three areas of technological promise there are strong contradictory forces of trade restriction.

Trade in solar photovoltaic technology is subject to both tariff and non-tariff barriers. For example, 31 WTO members apply tariffs over 10 per cent to certain essential solar photovoltaic materials such as polysilicon. Australia scores an own-goal by imposing duties (both dumping and countervailing) on solar equipment imports thus raising the costs of renewable electricity.

The threat to trade in hydrogen comes from a call by competition-fearing European Union electricity groups for a carbon tariff on EU hydrogen imports. Though the case for Australias blue hydrogen using brown coal and carbon capture and storage is controversial, a Carbon Border Adjustment Mechanism tax risks application to all hydrogen imports and a setback to carbon capture and storage, without which net zero will be impossible.

The threat to CRISPR gene-editing is a repeat of the type of regulatory barriers that invoke health and environmental concerns to hinder the development and trade of genetically modified organisms. Many countries farming regulations, including those of New Zealand, constrain both GMOs and CRISPR, even though CRISPR does not introduce DNA from other species.

The challenge is real. Protectionism risks hobbling trades role in fostering the technological promise of the climate transition raising the level of the carbon tax needed to effect that transition and weakening public support for it.

Resisting protectionist forces will require action at all levels. Domestically, by improving coherence in national policy, including in Australia in respect to solar equipment. Regionally, with a key role for APEC in respect to bothenvironmental goodsandservices. And multilaterally, where Australia is among 13 countries (including the United States and Canada) that have submitted to the WTO that gene-edited products should be regulated in the same way as conventional ones.

The stakes are particularly high for theWTO, which is about to face via the climate transition one of the most severe systemic challenges in its history.

*About the author: Ken Heydon is Visiting Fellow at the London School of Economics and Political Science. He is a former Australian trade official and senior member of the OECD secretariat.

Source: This article was published by East Asia Forum

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Protectionism Threatens The Climate Transition Analysis Eurasia Review - Eurasia Review

Recommendation and review posted by Bethany Smith

If you've experienced gender dysphoria the distressing feeling that occurs when your gender identity differs from the one you were assigned at birth you might have considered hormone-replacement therapy. Originally, HRT referred to the process of prescribing sex hormones like estrogen to people going through menopause as a way of treating symptoms such as hot flashes (a practice that has since been the subject of some controversy). But today, the term "HRT" is commonly used to describe "gender affirming hormone therapy" for "individuals who are seeking to alter their secondary sex characteristics for a more 'masculine' or more 'feminine' gender presentation," as defined by Folx, an online health and wellness provider for the LGBTQ+ community. At Folx and other gender-affirming-therapy providers, HRT involves using hormones like estrogen or testosterone to give the body a more traditionally feminine or masculine appearance to match one's gender identity.

While many trans and nonbinary people describe the medicine as life-saving, the process isn't for everyone, nor is it a requirement for trans and nonbinary people. "HRT does not make a trans person trans," stresses TikToker and professional actor Dylan Mulvaney, a trans woman who has been chronicling her self-described girlhood on the app. "If there is a trans person out there, and for whatever reason, they don't think HRT is right for them right now, or ever, we need to see them as such and respect their pronouns as such," Mulvaney adds.

The decision to start HRT is individual and can be complex. Sade Bolger, a Vermont-based activist and public-affairs organizer for Planned Parenthood, started HRT specifically testosterone therapy (or T) in May of 2017. But when he began, the decision was one of uncertainty. "When I did start T, I didn't really actually fully feel like I did know that for certain this is going to be the right thing," Bolger says. "I stepped into T in an explorative way, having seen other people who had gone through that process, and utilized it as a tool for self-discovery and self-exploration."

California-based Mulvaney echoes a similar sentiment: "The initial reason for going on HRT was just to sort of explore what that side to me was." Before beginning HRT, the actor had considered themself nonbinary for about 18 months. "But I always knew that I wanted to be more feminine," she says. "And even while I was nonbinary I knew that I loved the features on a woman, that I would love to have." Even so, she tells POPSUGAR, "I was so nervous to start [HRT] because it really is a huge decision to be potentially altering your body."

Josie Moon, another trans TikToker, also described her decision to start HRT as a tough one. Moon says she didn't know what the word "trans" meant until she was late into high school. The Nashville-based content creator got married at 24 years old, came out to her now-ex-wife as trans about two years into their marriage, and decided to get divorced just before the 2020 COVID lockdown. Through her own research, she discovered that some trans people don't take hormones. When making the choice for herself, she considered how it would affect her. "I was very concerned that even if I went on hormones at 29, it wasn't going to be enough for me to feel comfortable in my body," Moon tells POPSUGAR.

So she gathered more information, reading relevant threads on Reddit and Twitter and speaking to others in the trans community to make sure HRT was the right decision for her. "There's a subreddit called Trans timelines which shows pictures of mostly trans women but also trans men, really trans people in general before and after hormones," Moon says. "And I was like, wow, these people are the same age as me . . . and they look amazing. The results are amazing. So maybe this could work for me too." It had gotten to the point, Moon says, where she was constantly looking at these pictures and "imagining just feeling comfortable in my body and what that would look like." Now, two years on HRT, Moon is happy with her decision to start the therapy. So are Mulvaney and Bolger. "I look at myself in the mirror now and every day I get a little bit closer to finding myself to be a beautiful woman," Mulvaney says. "I think it was through the process of experiencing the changes that came alongside taking T that really kind of confirmed for me that this was what I wanted to do and who I wanted to be on the planet," says Bolger.

If you're still trying to figure out whether HRT is right for you, this explainer will help answer some of your questions, including what to ask your doctor, when to expect changes, and what side effects to be aware of.

Masculinizing or feminizing hormone therapy, also commonly referred to as hormone-replacement therapy or HRT, is a process used to "induce the physical changes in your body" caused by male or female hormones "to promote the matching of your gender identity and body (gender congruence)," per the Mayo Clinic.

Someone transitioning from male to female (MTF) would typically use feminizing hormone therapy and "be given medication to block the action of the hormone testosterone. You'll also be given the hormone estrogen to decrease testosterone production and induce feminine secondary sex characteristics," the Mayo Clinic states. In a female to male (FTM) transition with hormone therapy, "you'll be given the male hormone testosterone, which suppresses your menstrual cycles and decreases the production of estrogen from your ovaries."

The method in which those hormones are administered can vary, says Dave Usman, nurse practitioner at Radiant Health Centers, a California-based LGBTQIA+ Health and HIV care center. "It depends on the comfortability of the individual that's seeking hormone therapy," he says. For those receiving masculinizing HRT through testosterone, there are two options, Usman says. The most common route is injection. "It can be self-administered or office-administered," he says. There's also a topical gel option. For estrogen therapy, there's a pill, injectable, or patch.

Not every hospital or clinic provides gender-affirming healthcare. There are some instances in which medical providers can get exceptions, specifically hospitals and clinics with religious affiliations. It's important to do your research beforehand to ensure that you can get the care you need.

Bolger was referred to an endocrinologist after expressing to his therapist that he was considering HRT. Mulvaney recommends going to a queer health center in your area. "The great part is that they focus primarily on queer trans clients, so they are very in the know as far as treatment plans," she explains. Another good option? An informed-consent clinic, which means that a referral or therapy note is not required to receive care. (Planned Parenthood is an informed-consent clinic.) You can also receive hormone therapy online through services like Folx and Plume.

As far as cost goes, many insurance plans cover hormone therapy. For those who are uninsured or have trouble accessing hormone therapy, health centers like Radiant Health rely on contracted pharmacies that provide the medication at a low out-of-pocket cost for patients. Brands like Folx also offer an HRT care fund which distributes financial resources to an annual grant covering 12 months of hormone-replacement therapy, including prescription medication, unlimited clinical visits and messaging, and labs. Eighty percent of the Folx HRT grants are reserved for BIPOC. Eligibility starts at 18 years old, and you must live in a state where Folx is currently available.

"The first visit is mainly educating the patient, asking questions, and telling them what is expected," Usman says. "And then, once they have all the questions answered, they feel like they're ready, they're mentally and physically ready, that's when we start initiating therapy." That initiation point can be that day or weeks later. It's really about the patient's comfortability level.

Mulvaney first went to get information and ask questions about the process and then was prescribed spironolactone and estradiol. Spironolactone is a testosterone blocker and estradiol is a form of estrogen. "I went for the information, I got it, I got my mind put at ease. And then I started [the hormones] a few weeks later," Mulvaney says. She adds that she started out with a low dosage "because I was still new to it. I was nervous. I just didn't want to throw myself into it too fully quite yet."

One major conversation you should have with your provider, Mulvaney stresses, is about reproductive options, which will change during hormone therapy. Testosterone and estrogen therapy can lower your sperm count or egg production and may permanently change or stop your body's production of eggs and/or sperm altogether. So if someone is planning to undergo hormone therapy and they may want to conceive a child in the future, Usman says it's encouraged to do egg or sperm retrieval or freezing. "I actually didn't start the spironolactone until recently because I wanted to freeze my sperm first," Mulvaney says. "Being in my 20s, I just wanted to keep all my options open for the future and family planning because I don't know what that's going to look like when I'm older." But Bolger adds that not knowing what you want your reproductive options to be is OK, too. They started T when they were 19 years old. "I didn't know what I wanted to do reproduction wise I still don't. I'm 23 now, and I'm still figuring it out." But it's important that you know all of your options and make the decision that's best for you.

Everyone's timeline of changes is different, but Usman says you can start to see small physical changes as early as a month in.

"My first sort of notice was stretch marks on my booty," says Mulvaney. It was an unexpected surprise to her less than three months on HRT, in addition to a smoothing of her face and the loss of muscle mass in the chest. "I never had hard nipples before," Mulvaney says. "And now they are starting to bud."

For Bolger, the most notable initial changes were voice deepening, peach-fuzz hairs on the lip, and clitoral enlargement, which is commonly referred to as bottom growth. In terms of mood, Bolger says, "My libido pretty greatly increased and stayed kind of intense for the first couple of months into that first year." They also dealt with recurring mood swings. But this was predominantly "just during the period of time where my hormone balance was off because I was transitioning between estrogen and testosterone. And once I kind of plateaued with the T in my body, and that became the main hormone in my body, then all that stuff kind of settled out."

What's important to note is that the mental and emotional changes are just as important to address as the physical ones, and they may hit you sooner. "The first two weeks, I'm not gonna lie, were tough. I didn't feel like myself in some ways. My mind was foggy, I felt very emotional, I had some anxiety," says Mulvaney. These changes ultimately went away, or Mulvaney became accustomed to them. "I think my body learned to accept that this was the new normal and I started to feel like myself again," she says.

Therapy also helped, she adds. "I'm in therapy once a week and I have been with the same therapist for two years, it's changed my whole life and outlook on things." With HRT, you're seeing a doctor every three months or so for check-ins. "But you also need to have a support system in place that can help you with the day-to-day, because it can get pretty overwhelming," says Mulvaney.

Moon agrees that at times, the emotional aspects of HRT can become overwhelming. "When I was younger, I used to say I had three emotions angry, happy, neutral and that was just how it was," says Moon. But in starting HRT, she unlocked a new range of emotions with various depths and layers. "Angry is actually, 'I'm a little bit hungry, but I feel hurt and misunderstood and just sad in general.' And then when I was happy, I'm not just happy or euphoric, it's like, 'I'm excited about this and there's a little bit of joy about this.'" The whole process is "also a little bit bittersweet, because in transitioning, I get to be myself, but I also lost so, so much and had to rebuild," Moon says. "I think emotionally, it took me off guard."

One change that Bolger says he was the most unprepared for is the way others perceive him. "I absolutely took on male privilege," he says. "I noticed that I was being treated differently. The men in the room would shake my hand before they left. I was listened to more. There was more of a platform in a space, people kind of waited for me to have something to say." Emotionally, Bolger says it was "so weird." Because they don't identify as a man, "it was like switching from feeling misgendered on one side to feeling misgendered on the other side." He also says the transition between living the first 18 years experiencing sexism against women only then to be welcomed and respected by sexist men was "not ever in my intentions." There's this layer of complexity for nonbinary individuals, Bolger says, because T or no T, "we live in a society where people assume that you're either a man or a woman."

Another unexpected change? Anecdotally, many people on T have said that it changes their sexual attraction, especially as it pertains to men. Bolger says that being on T hasn't necessarily changed his attraction level to men but rather his comfortability level being with a man. "I felt really uncomfortable being with men, for example, when I was younger, because I knew that that would make people see me as a girl," Bolger says. Being on T changed the way people perceived them and how Bolger perceived himself. Ultimately, "T didn't make me stop loving women. T didn't make me start loving men. T didn't change anything about who I loved or who I f*cked. It changed my comfort, being in those relationships and having those experiences because of how I was feeling and perceiving myself."

Yes. "That's why we screen people initially for their past medical history and family history, because both [hormones] have side effects and adverse effects that can affect their overall health," says Usman. Hormone therapy can aggravate pre-existing depression and anxiety. Other complications include developing diabetes, high cholesterol, high blood pressure, and blood clots. If you're a chronic smoker in particular and you're on estrogen, "there's higher risk of developing blood clots," Usman says. So be sure to be honest about all of your lifestyle habits within that first meeting so that your provider can assess your needs and design a hormone-therapy plan that works best for you.

Bolger, for example, is neurodivergent. "I have ADHD. I sometimes struggle with routine, like hygiene care, because of that," Bolger says, and talking to his provider about that openly was "really important" in figuring out which form of T was right for them. For example, the topical gel has to be applied once a day. "It has to be a part of your routine and for me with my ADHD, that wasn't something that I really thought was going to be plausible," Bolger says. So he went with the weekly injections instead. Even so, Bolger experienced health complications, including ovarian cysts, which were caused by going off schedule on T, a diversion caused by his ADHD. That's why Bolger emphasizes the importance of seeking out a provider who can assess and treat your whole self someone who will be looking our for your mental, physical, and emotional health not just you as a trans person, but you as a whole human, too.

Image Source: Getty Images

Originally posted here:
Hormone-Replacement Therapy Is Life-Changing: What to Consider Before Getting Started - POPSUGAR

Recommendation and review posted by Bethany Smith

Its probably not an exaggeration to say that every woman on the planet has, at one point or another, heard someone say, Oh, its probably just your hormones. People seem to be inclined to blame just about everything from headaches to hot flashes and all kinds of conditions in between on good old hormones.

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Sometimes itisyour hormones, though. Andhormonal imbalancescan mean more for your health than just a grumpy day or a few zits before your period. So, how can you tell when its hormones and when its something else?

Womens health specialistPelin Batur, MD, talks about a few types of hormonal imbalances commonly seen in women, including symptoms you shouldnt ignore and when to see a medical professional.

To decide whether you need hormone testing (and if so, what kind), your doctor will likely start by asking you lots of questions about your symptoms. This will help them put together the puzzle pieces of what might be going on.

The workflow in my head focuses on three questions, Dr. Batur says. First, do these symptoms sound hormonal? If so, do they sound like theyre related to estrogen, progesterone, testosterone or some other type of hormone? And finally, is it because theyre too low or too high?

Once your doctor has a sense of what might be happening, theyll figure out which tests to (or not to) run.

One symptom that indicates that you may need testing is irregular periods.

If youre having regular menstrual cycles and not having symptoms throughout the month, I dont usually start with lots of estrogen, progesterone or testosterone tests, Dr. Batur says. But if youre experiencing a lot of irregularities in your cycle, Im likely to do more testing.

We have at least 50 different hormones in our body, and very complex symptoms can arise from them, Dr. Batur says. Having too much or too little of certain hormones causes symptoms and issues with your health.

Here are some of the most common hormonal imbalances seen in people assigned female at birth (AFAB).

There are less-common hormonal imbalances, too, likeCushings syndromeandAddisons disease. Only a doctor can help identify which hormonal imbalance youre experiencing and what course of treatment is best.

Heres the thing: Hormonal imbalances can have a lot of symptoms and they can have a lot ofdifferentsymptoms, depending on which ones are at the root of your issues. Those symptoms may seem muddled or initially unrelated, and theyre not always related to hormones at all.

Hormones can cause so many symptoms, but that doesnt mean theyre always the cause of your symptoms, Dr. Batur says, so its really important to be seen by a doctor for an individualized assessment.

Here are some common symptoms of hormonal imbalances in women and what theymight signify.

Weird periods are a key sign of a hormonal imbalance.Irregular menstruationcan be a sign of perimenopause but can have a number of other causes, too, especially if youre not yet nearing menopausal age.

If your menstrual cycles are disrupted or if youre going through menopause, you should definitely come in to be seen and to talk things out, Dr. Batur advises.

If a woman comes in complaining of acne, Im concerned about potentially high levels of hormones such as testosterone, Dr. Batur says. We see this in women withpolycystic ovary syndrome. PCOS causes higher levels of male hormones called androgens (including testosterone), which can lead to acne.

If you start to notice differences in your hair whether on your head, face or someplace else, like your arms and legs it could be a sign of a hormone imbalance.

Starting to see chin hairs or a bit of a mustache? Increased testosterone can cause excess hair growth (hirsutism). This can be a symptom of PCOS or menopause, but it has other causes, too.

On the flip side, hormonal imbalances can also cause thinning hair on your head, legs and pubic region.During menopause, a drop in estrogen can lead to slower hair growth, or cause it to fall out more easily.Hypothyroidism and hyperthyroidism can cause hair loss, too. Or your hair loss may be related to something else entirely something nonhormonal.

It can be really complex to figure out, Dr. Batur says. You might assume hair loss is hormonal, but it can be related to high or low thyroid level, low estrogen, high testosterone or something else, like vitamin deficiency or lifestyle stressors.

These symptoms usually indicate that a womans hormones are lower, like the kind of dropping estrogen levels we see in perimenopause or postmenopause, Dr. Batur says. They can alsobe a side effect of some medications and treatments.

Your doctor can help you find ways tomanage your hot flashesso they dont negatively affect your quality of life.

Weight gain can be a symptom of a variety of hormonal imbalances, as well as lifestyle-related factors, so doctors use other clues about your health to get a sense of whats going on.

Difficulty losing weight is a very common problem in the United States, and its often blamed on hormones, Dr. Batur says. Sometimes, its related to high testosterone levels, like with PCOS, and menopause is associated with weight gain, too. But if you have weight gain with regular menstrual cycles, its more likely to be related to something likecortisol, thyroid, insulin or lifestyle habits.

Havent changed your lifestyle habits but have suddenly dropped 15 lbs.? This symptom is often a sign of an overactive thyroid, orhyperthyroidism. When your body produces too much thyroid hormone, your metabolism speeds up, which can cause weight loss along with rapid heartbeat, an intolerance to heat and other symptoms.

Althoughvaginal drynesscan be a sign of a few issues, its one of the most common symptoms of menopause. Your estrogen levels drop during menopause, which can to lead vaginal dryness that causesdiscomfort during sex.

The vagina is quite sensitive to lack of estrogen, Dr. Batur says. About 50% of women have vaginal dryness that may get in the way of intercourse, and it tends to get worse over time.

While its important to advocate for your health, try not to be swayed by broad, overarching claims (looking at you, social media) that insist thateveryoneneeds hormone testing or that every symptom youre experiencing is related to your hormones.

Just because youre experiencing symptoms of a hormonal imbalance doesntmean you haveahormonal imbalance. Nearly every symptom of a hormonal imbalance can have other causes, as well.

Its important to not lump everything together under hormones, and to instead break down each symptom individually, Dr. Batur advises. We have to take a deep dive to make sure were not missing anything, whether its lifestyle factors or another medical condition.

More here:
Do You Need Hormone Testing? - Health Essentials from Cleveland Clinic

Recommendation and review posted by Bethany Smith

Ascendis Pharma

Late-breaker oral presentation of TransCon PTH Phase 3 PaTHway Trial data in adult hypoparathyroidism on Tuesday, June 14

Oral presentation of TransCon PTH Phase 2 PaTH Forward Trial Open-Label Extension Data in adult hypoparathyroidism on Monday, June 13

PaTHway Trial results represent the second consecutive successful pivotal Phase 3 trial of a TransCon product candidate

COPENHAGEN, Denmark, June 07, 2022 (GLOBE NEWSWIRE) -- Ascendis Pharma A/S (Nasdaq: ASND) today announced that its presentations at ENDO 2022 will include oral presentations of Phase 2 and Phase 3 data for its investigational product candidate TransCon PTH in adult hypoparathyroidism (HP). During the meeting, which will be held in-person and virtually June 11-14 in Atlanta, Dr. Aliya Khan, M.D., Clinical Professor of Medicine at McMaster University and Director of the Calcium Disorders Clinic at McMaster University Medical Center, will give a late-breaker oral presentation of Phase 3 PaTHway Trial data for TransCon PTH in adult HP.

This is the first Phase 3 trial in adult hypoparathyroidism in which the majority of treated patients achieved real control of their disease that is, normalization of serum calcium, independence from conventional therapy, and a more normal patient-reported quality of life, said Dr. Khan. Additionally, TransCon PTH was generally well-tolerated with no discontinuations related to study drug, and TransCon PTH-treated patients showed a mean decrease in 24-hour urine calcium excretion into the normal range. I am hopeful that, with these encouraging results, we are closer to changing the treatment paradigm for patients living with this under-recognized and often debilitating disease.

An additional Ascendis oral presentation at ENDO 2022 will include a review of Phase 2 TransCon PTH long-term data by Dr. Bart Clarke, Professor of Endocrinology at Mayo Clinic, showing durable benefit for adult hypoparathyroidism patients treated with TransCon PTH through Week 84 of the Pathway Trial. Additionally, Ascendis posters will present new data showing the continued safety and efficacy of once-weekly TransCon hGH in children with growth hormone deficiency treated for 2.5 years in the EnliGHten Trial, and, for adults with growth hormone deficiency, new research showing low treatment rates, increased medical risks, and higher healthcare costs.

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Ascendis will also host a Medical Affairs booth (#1515) at ENDO 2022, as well as a separate booth (#1415) and events showcasing SKYTROFA (lonapegsomatropin-tcgd), the companys once-weekly treatment for pediatric growth hormone deficiency.

ENDO is one of the largest endocrine health symposiums, and we are especially pleased this year to be providing a comprehensive review of data from our second consecutive successful Phase 3 trial, said Jan Mikkelsen, Ascendis Pharmas President and Chief Executive Officer. Ascendis is deeply committed to developing products that deliver value for patients, payers and society, and we are honored to be able to partner with patients, physicians, and other specialists in our work to advance understanding and treatment of rare endocrine diseases.

Ascendis Pharma presentations and educational sessions at ENDO 2022 will include:

Hypoparathyroidism

Tuesday, June 149:45 11:15am

Late-BreakerPhase 3 PaTHway Trial: Participants Treated with TransCon PTH Achieved Independence from Conventional Therapy While Maintaining Normal Serum CalciumPresented by: Aliya Khan, M.D.

Monday, June 1311:30am 1:00pm

Oral PresentationThe PaTH Forward Trial: Efficacy and Safety of TransCon PTH Through Week 84 for Adults with HypoparathyroidismPresented by: Bart Clarke, M.D.

Saturday, June 111:00 2:00pmProduct Theater #2

EducationManaging Patients with Hypoparathyroidism: A Healthcare Professional and Patient PartnershipSpeaker: John P. Bilezikian, M.D.

Growth Hormone Deficiency

Monday, June 1312:30 2:30pmOn-site and on-demand for virtual attendees

Rapid Fire e-PosterSafety and Efficacy of Treatment with Lonapegsomatropin in Children with Growth Hormone Deficiency at Week 130 in the EnliGHten TrialPresented by: Paul Saenger, M.D.

On-site and on-demand for virtual attendees

Poster PlusEconomic Burden of Growth Hormone Deficiency in a U.S. Adult PopulationAuthored by: Alden Smith, Janna Manjelievskaia, et al

Saturday, June 1110:15 11:15amProduct Theater #3

EducationSKYTROFA (Lonapegsomatropin-tcgd): The First FDA-Approved Once-Weekly Treatment for Pediatric Growth Hormone DeficiencySpeaker: Aristides Maniatis, M.D.

About Ascendis Pharma A/SAscendis Pharma is applying its innovative platform technology to build a leading, fully integrated biopharma company focused on making a meaningful difference in patients lives. Guided by its core values of patients, science and passion, the company uses its TransCon technologies to create new and potentially best-in-class therapies. Ascendis is headquartered in Copenhagen, Denmark, and has additional facilities in Heidelberg and Berlin, Germany; Palo Alto and Redwood City, California; and Princeton, New Jersey. Please visit http://www.ascendispharma.com to learn more.

Forward-Looking Statements This press release contains forward-looking statements that involve substantial risks and uncertainties. All statements, other than statements of historical facts, included in this press release regarding Ascendis future operations, plans and objectives of management are forward-looking statements. Examples of such statements include, but are not limited to, statements relating to (i) Ascendis expectations regarding the potential for TransCon PTH to be a replacement therapy for adult hypoparathyroidism, (ii) Ascendis ability to apply its platform technology to build a leading, fully integrated biopharma company, and (iii) Ascendis use of its TransCon technologies to create new and potentially best-in-class therapies. Ascendis may not actually achieve the plans, carry out the intentions or meet the expectations or projections disclosed in the forward-looking statements and you should not place undue reliance on these forward-looking statements. Actual results or events could differ materially from the plans, intentions, expectations and projections disclosed in the forward-looking statements. Various important factors could cause actual results or events to differ materially from the forward-looking statements that Ascendis makes, including the following: dependence on third party manufacturers and distributors to supply TransCon hGH, the SKYTROFA Auto-Injector and other study drug for commercial sales in the U.S. and clinical studies; unforeseen safety or efficacy results in its oncology programs, TransCon hGH, TransCon PTH and TransCon CNP or other development programs; unforeseen expenses related to commercialization of lonapegsomatropin-tcgd in the U.S., the co-pay program, and the further development of TransCon hGH, expenses related to the development and potential commercialization of its oncology programs, TransCon hGH, TransCon PTH and TransCon CNP or other development programs, selling, general and administrative expenses, other research and development expenses and Ascendis business generally; delays in the development of its oncology programs, TransCon hGH, TransCon PTH and TransCon CNP or other development programs related to manufacturing, regulatory requirements, speed of patient recruitment or other unforeseen delays; dependence on third party manufacturers to supply study drug for planned clinical studies; Ascendis ability to obtain additional funding, if needed, to support its business activities and the effects on its business from the worldwide COVID-19 pandemic. For a further description of the risks and uncertainties that could cause actual results to differ from those expressed in these forward-looking statements, as well as risks relating to Ascendis business in general, see Ascendis Annual Report on Form 20-F filed with the U.S. Securities and Exchange Commission (SEC) on March 2, 2022 and Ascendis other future reports filed with, or submitted to, the SEC. Forward-looking statements do not reflect the potential impact of any future licensing, collaborations, acquisitions, mergers, dispositions, joint ventures, or investments that Ascendis may enter into or make. Ascendis does not assume any obligation to update any forward-looking statements, except as required by law.

Ascendis, Ascendis Pharma, the Ascendis Pharma logo, the company logo, TransCon, and SKYTROFA are trademarks owned by the Ascendis Pharma Group. June 2022 Ascendis Pharma A/S.

Read more:
Ascendis Pharma A/S Announces Two Oral Presentations Highlighting the Potential for TransCon PTH to be a Replacement Therapy for Adult...

Recommendation and review posted by Bethany Smith

Adults with obesity who undergo bariatric surgery to lose weight may roughly halve their risk of dying of cancer, a new study suggests.

For the study, researchers compared the risk of cancer diagnosis and death for more than 30,000 people with obesity, including more than 5,000 individuals who had bariatric surgery. Surgery was associated with a 32 percent lower risk of cancer and a 48 percent decreased chance of cancer-related death.

Patients can lose 20 to 40 percent of their body weight after surgery, and weight loss can be sustained over decades, said the lead study author,Ali Aminian, MD, the director of the Bariatric & Metabolic Institute at the Cleveland Clinic in Ohio, in a statement.

The striking findings of this study indicate that the greater the weight loss, the lower the risk of cancer, Dr. Aminian said.

About two in five American adults have obesity, according to the Centers for Disease Control and Prevention (CDC). And obesity increases the risk of 13 types of cancer that together account for 40 percent of all tumors diagnosed each year in the United States, according to the CDC.

In the study, those who underwent bariatric surgery lost an average of 25.5 kilograms (kg) (61 pounds [lb]) after 10 years of follow-up, compared with 2.7 kg (6 lb) without these operations.

Surgery was associated with a significantly lower risk of obesity-related cancers, including malignancies of the breast, ovaries, uterine lining, colon, liver, pancreas, and thyroid. Overall, 2.9 percent of people who had weight loss surgery developed these tumors, compared with 4.9 percent of those who didnt have operations.

Bariatric surgery was also tied to a significantly lower risk of diagnosis and death from all cancers, including tumors unrelated to obesity, the researchers reported June 3 in JAMA. After a decade, 0.8 percent of patients who had surgery died of cancer, compared with 1.4 percent in the nonsurgical group.

One limitation of the study is that the majority of the participants were female and white, so it's possible the results might be different for men and individuals of other racial and ethnic groups.

The study also wasnt a controlled experiment designed to prove whether or how weight loss surgery might directly reduce cancer risk.

Its possible that excess weight accelerates tumor growth because it causes inflammation, impairs the bodys ability to use the hormone insulin to turn sugars from food into energy, and increases the production of sex hormones that play a role in the growth of some cancers, the study team writes.

But its also possible that people who underwent surgery were healthier in other ways that helped prevent cancer, the researchers noted. They might have had healthier diets, exercised more, or been less likely to smoke than people who didnt have bariatric procedures, for example.

Original post:
Weight Loss Surgery Tied to Lower Risk of Obesity-Related Cancers - Everyday Health

Recommendation and review posted by Bethany Smith

Cancer impacts people all over the world. Experts are constantly evaluating how different treatments can eliminate or slow the spread of cancer

Each type of cancer is different, leading to the development of various treatment and detection methods.

A recent study that appears in The Lancet found that a specific combined treatment therapy may improve the survival rate for men with prostate cancer.

Prostate cancer is one of the most common types of cancer among men. As noted by the Centers for Disease Control and Prevention (CDC), in 2018, there were over 210,000 new cases of prostate cancer, and almost 31,500 of those with prostate cancer died of it.

As noted by the American Cancer Society, a few different methods can help detect prostate cancer. One is to do a prostate-specific antigen (PSA) blood test.

If the PSA level is higher than a specific reference point, it can indicate prostate cancer. However, there are other reasons for the PSA level to be high, so this is not a definitive diagnostic tool.

Doctors can also do a digital rectal exam to feel the prostate and note abnormal lumps. To confirm the findings of an elevated PSA or an abnormal digital rectal exam, doctors will order a biopsy of the prostate. If this confirms the presence of prostate cancer, treatment can begin.

Treatment for prostate cancer may include one or several options, such as surgery, radiation, cryotherapy, hormone therapy, immunotherapy, and chemotherapy. Researchers are still working to improve the treatment options and survival rate for people with prostate cancer.

The study in The Lancet was a randomized controlled trial. Researchers divided men with prostate cancer into three distinct treatment groups.

The study included participants that had previously had to have their prostate removed and had a certain PSA level after prostate removal. A total of 1,792 participants enrolled in the study.

Researchers sought to discover if using a specific, combined treatment method increased survival rates and decreased severe cancer progression.

They used the label freedom from progression. The three treatment groups included the three different treatment methods:

The study found that freedom from progression after 5 years was highest for those in group 3. In group 1, almost 71% of the group had freedom from progression. In group 3, the percentage was 87.4%.

These results indicate that adding short-term androgen deprivation therapy and pelvic lymph node radiotherapy to salvage prostate bed radiotherapy can help to improve survival rates among those with prostate cancer.

Study author Dr. Alan Pollack noted the following highlights to Medical News Today:

This is the first randomized study to demonstrate the incremental benefit of adding pelvic lymph node treatment to androgen deprivation therapy and standard prostate bed treatment. This is a three-arm study designed to test the intensification of treatment from standard of care prostate bed RT (PBRT), PBRT plus short term androgen deprivation therapy (STADT), and PBRT plus STADT plus pelvic lymph node treatment (PLNRT). The primary endpoint was 5-year freedom from progression [and the study] showed that overall there were incremental gains with the addition of ADT and then further gains with PLNRT.

The study authors do note that using this combined treatment method is not without risks. They point out that it could increase the risk for certain bone marrow problems. They also note that a longer follow-up time would be necessary to confirm the full effectiveness of the treatment.

Dr. Kelvin Moses, director of the Comprehensive Prostate Cancer Clinic at Vanderbilt University Medical Center, who was not involved in this study, agreed that more follow-up research is needed, but said that the results so far are promising.

He explained for MNT that [t]his study reinforces the importance of control of the pelvic lymph nodes either at the time of surgery, or in the setting of post-prostatectomy recurrence.

He added that [i]t remains to be seen if the progression benefit translates to a reduction in metastasis or death from prostate cancer, but these results are promising and can change the paradigm for treatment of biochemical recurrence.

The study authors further note that, as imaging of the prostate improves, it will impact how this treatment method is applied. But the research provides overall encouraging results that survival rates can improve for those with prostate cancer with the right kind of treatment.

Dr. Hayley Whitaker, a cancer expert at the University College of London, who was not involved in this study, was enthusiastic regarding its results:

There are several ways to treat patients with prostate cancer, but the order that different treatments are used or combining different treatments offers huge potential to prolong [the] life of men by many years.

According to her, [t]his is groundbreaking research that has the potential to make a real impact on men being treated for prostate cancer by making significant advances in combining surgery, radiotherapy, and hormone treatments.

More here:
Prostate cancer: Combination therapy shows high success rate - Medical News Today

Recommendation and review posted by Bethany Smith

Photo-Illustration: Josiah Whitfield; Photos: Getty

When Michelle went in for an egg-freezing consultation at a Sacramento, California, fertility clinic in February 2021, she was, in most ways, the typical egg-freezing patient. She was 36, a college-educated professional, and had spent much of her 20s and 30s focusing on her career and traveling to more than four dozen countries. Like the majority of women who seek out elective egg freezing, she was single and thought it would lighten the anxiety she felt while dating. So that its not like, Hi, okay, when do you wanna have a baby, you know? she says.

Nine months later, after a five-month recovery from ankle surgery, Michelle was ready to start the process, which entails hormone injections to stimulate egg-follicle growth; regular monitoring; and a short, 15- to 30-minute egg retrieval, during which a needle guided by ultrasound is used to gently suction out the eggs from their follicle sacs. The procedure is done underanesthesia, and after a few hours rest, patients can go home (clinics recommend doing so while accompanied by a friend or family member, to be safe). In the interim, she also had her hormone levels measured and learned that her anti-Mllerian hormone (AMH) level was lower than average for her age, a possible sign that her ovarian reserve was depleted. She was anxious to get going.

After a few false starts on the first two attempts at getting an appointment, communication and scheduling mishaps pushed her start date back by a month each time the busy clinic finally slotted her in for March, and called her back to the clinic in January to update her vitals. But just as she was gearing up to begin, she hit an unexpected roadblock. A few lines into a longemail from the nurse coordinatorin which she instructed Michelle on which vitamins and supplements to take, discussed the timing of the cycle, and counseled her to abstain from unprotected sex during the course of treatment, lay an unexpected ask: Dr. Lovely wants you to loose [sic] 9 more lbs before you can proceed with the treatment, we would like you under 262 lbs.

Michelle pushed the nurse for more information. She felt healthy and strong: She works out three to five times a week, eats nutritious food, and is a longtime member of a competitive traveling roller-derby team. The nurse pointed her to a practice bulletin from the American College of Obstetricians and Gynecologists on the management of obesity during pregnancy, of which only the abstract is visible without a subscription. The nurse also cited the bed-weight capacity in the clinics operating rooms, which Michelle found dubious (standard hospital beds support between 350 and 450 pounds.)

Put bluntly, Michelle was told she was too fat to continue.

Egg freezing today is sold as an empowering option for everyone. Fertility clinics and egg-freezing studios hammer this message home through social-media advertising aimed at under-40 women, promotional vans offering free fertility tests to passersby on the street, and wine-and-cheese informational nights held at clinics and egg-freezing studios across the country. But when it comes to women in larger bodies, some clinics draw the line, turning away patients over a certain body mass index, or BMI. Although there is no national data kept on this phenomenon, an estimated 11.7 percent of American women are considered severely obese, with a body mass index of 40 or higher.

There is little, if any, research evidence on egg freezing and weight. The vast majority of studies examine BMI and in vitro fertilization, and results from these are mixed. Some have linked overweight and obesity with fewer eggs retrieved and lower rates of pregnancy and live births, while others find no impact of a high BMI on IVF outcomes. Dr. Nicole Noyes, a reproductive endocrinologist who has published extensively on egg freezing and helped establish the egg-freezing program at NYU Langone Fertility Center, notes that higher BMIs are linked to more health risks in general. For egg freezing in particular, she cites risks such as those related to anesthesia; increased difficulty in performing the egg-retrieval procedure because of technical issues (such as suboptimal visualization on the ultrasound machine due to fatty tissue, which increases the risk of inadvertently piercing adjacent pelvic structures and causing internal bleeding); and a still rare but greater likelihood of needing surgery such as laparoscopy in case of complications.These risks combine with the potential for lower egg quality in obese women, something Noyes suspects may be due to theinfluence of an abnormal hormonal environment surrounding the developing egg, although she admits there is no known explanation for this.

The messaging is that this is the responsible thing to do, the thing that they should be doing to preserve their fertility, says Nicola Salmon, a U.K.-based fertility coach who specializes in working with larger patients. Salmon, whose job includes assuring her clients that they are worthy of care, engaging with clinicians and presenting them with research and evidence on caring for larger bodies, and screening clinics to ensure theyll provide sensitive and individualized care, is currently working with an egg-freezing patient in Texas. Salmons client, like Michelle, is ready to begin the egg-freezing process. But, by Salmons estimates, theyve reached out to at least eight or nine fertility clinics in the Texas areaabout their BMI guidelines, and none will work with them, typically citing BMI cutoffs of 40 (her clients BMI is 42). This has been a real blow to their body confidence, to how they feel in their body, Salmon says, because they feel that this option this thing that should be available to everybody has been taken away from them.

In general, complications from egg freezing for larger-bodied patients are rare: Noyes estimates she has done at least 20,000 egg retrievals in her 30-year career, and had fewer than ten bleeding-complication cases, none of which were in overweight or obese patients. In some cases, she has performed egg retrievals on larger-bodied women without anesthesia, either because the patient exceeded the anesthesiologists threshold for providing anesthesia or in order to avoid anesthesia risks. (She likens the procedure without anesthesia to having blood drawn; the puncture of the needle through the vaginal wall hurts, but most patients do well if they are prepared for that moment.) Ultimately, she says, medicine is about weighing risk versus benefits, and when risks creep up and the benefits are potentially lower, doctors ask themselves, Is the outcome worth it?

Dr. Lynn Westphal, chief medical officer at Kindbody, a national chain of fertility and womens healthcare clinics, suggests a simpler reason many freestanding fertility clinics are only accredited to perform anesthesia on patients classified by the American Society of Anesthesiologists as having a risk score of I (a normal healthy patient) or II (a patient with mild systemic disease). People with BMIs between 30 and 40 are considered obese and fall into category II; those with BMIs over 40 are considered morbidly obese and have a risk score of III. This is why, Westphal explains, anesthesiologists at manyclinics use 40 as the cutoff for who they can and cant treat. Fertility clinics based in hospitals, which have different accreditation, have more leeway to treat a broader range of patients. For example, they are able to intubate patients if there is any airway problem, Westphal says, which is something that should not be done in a procedure room.

Michelle wasnt told any of this. Instead, the nurse suggested a change in diet for weight loss, without knowing anything about what Michelle currently eats, a clear sign, Michelle says, that this person has assumptions because of your size.

The weight loss itself didnt trouble her as much as the lack of context or at least context she found plausible for their request. Nine pounds on a large body is not a lot. I could lose nine pounds overnight if I wanted to, she says. I wasnt concerned about the amount of pounds; I was more concerned about the way they talked to me about it without any kind of explanation. She eventually got so fed up with the nurses communications that she stopped responding. By then, shed lost three months (most of December, January, and February) to their unhelpful back-and-forth. Because this process had already taken so long, it was a big risk for me to completely let go of this group that I had already worked with, Id already paid the consult for. Id have to do all of that again, she says.

This is what advocates for body-positive fertility care say is really at issue here: stigma. Jen McLellan, a childbirth educator who blogs at PlusSizeBirth.com, notes that many of the same risk factors doctors cite for high BMI are also present in women of advanced maternal age (35 and older), yet that patient population is targeted for fertility care all the time. Similarly, people with normal or low BMIs may be poor egg-freezing candidates for other reasons. Instead of using a single number as a cutoff, she advocates for evaluating patients on an individualized basis, especially in facilities that are equipped to handle patients with higher ASA scores. To make these blanket statements, when we dont have evidence to point to dramatic increased risks, to me points to a lot of weight bias, says McLellan.

Furthermore, weight stigma, and the stress experienced by people of size during their encounters with the medical system and in the world more generally, can also create unhealthy physical reactions, such as higher stress and cortisol levels, which in turn affect hormones and inflammation. Anyone who is in a bigger body that has been to their doctor, they will tell you how stressful that situation is, Salmon says. When you look at the research around weight stigma, a lot of health-care risks associated with being fat can be explained by this weight-stigma phenomenon.

Candace, a freelance web developer in San Diego, had been hoping to do IVF in Mexico, where the procedure is less expensive than in the U.S. The clinics she called, though, all had BMI limits lower than her BMI of 44. (She recalls the cap being around 35.) She called local clinics in Southern California, and eventually went in for a consultation at one for a 20-minute appointment that cost $195. The doctor took one look at her, she says, and told her she was a poor candidate for IVF. Instead he recommended she get weight-loss surgery. When she suggested freezing eggs to buy her some time to lose weight before carrying a pregnancy, he said her eggs would probably be poor quality and doing it would be a waste of money. He spent the remainder of their consult talking nonstop about her weight. Candace had brought a notebook filled with questions she had written down that she opened up at the beginning of the consultation. Once she realized she wasnt going to get any of the answers she hoped for, she closed it and resigned herself to enduring the rest of his lecture. Like Michelle, she left that appointment out her consultation fee and no closer to getting her eggs frozen.

Im receptive, because I am trying to lose weight, says Candace. It was just how it was presented to go to a fertility appointment and spend so much time on my weight. Certain people, you can just see their bias. It was less about what he said; he was being professional. It was how he was saying it.

The advice to come back after losing weight is particularly vexing for patients who feel the clock is ticking on their fertility. Especially if youre older, delaying treatment in order to lose weight is going to lower your chance of success because of the delay, says Dr. Peter Klatsky, a reproductive endocrinologist at Spring Fertility, which has locations in California, New York City, and Vancouver. At Spring Fertility, patients with BMIs over 40 may need an additional anesthesia consultation, and at 45 or over, will require the approval of a physician review committee to ensure the patients safety during the procedure. This is because it becomes harder to protect and maintain a patients airway under anesthesia, and there may be other medical risks like diabetes and cardiovascular disease that must be assessed before undergoing anesthesia, adds Klatsky.

For Beth, a 35-year-old attorney in New York City who asked that her real name not be used, weight loss had been on the agenda since she was in her 20s. She had always had irregular periods, and a series of ob-gyns told her that losing weight could help regulate her cycle. When she reached her early 30s, it occurred to her that her irregular cycle could affect her ability to get pregnant, so in the fall of 2020 she arranged to see an ob-gyn at New York University who specializes in fertility. The doctor confirmed she had polycystic ovary syndrome (PCOS), which is linked to irregular periods and weight gain. The conversation got her thinking that times a-ticking, especially because one complication of PCOS is infertility. We need to start taking a little bit of ownership here, she told herself. But when she asked about egg freezing, thats when the BMI thing became an issue. She doesnt remember what the BMI limit was, but it was far below her BMI at the time (NYU Langone Fertility Center confirmed to the Cut that 42 is the cutoff, citing anesthesia guidelines). She called around to other clinics an additional one in New York, one in Miami, one in Connecticut, and one in Utah, and was told the same thing. The first time I heard it, I dismissed it, because, like, the lawyer-asshole in me didnt really believe it. I was like, oh, its just what they said, Beth recalls. The second time I heard it, my heart definitely sank.

Beth wishes someone had warned her earlier on that her weight might be a barrier to accessing care. Its kind of the fourth quarter here, or the end of the third. To find out that theres this huge obstacle now had I known this at 30, I could have made different changes or choices, she says. But to find out now that theres a years worth of self-work that I have to do before I can even get to the plate to talk about egg quality, to even get to the plate to talk about fertility, I think thats what frustrated me. I wasnt depressed. I was mad.

Now Beth is focusing on losing weight in a healthy, sustainable way. She has stopped eating as much takeout and is snacking less often, and has dropped about 50 pounds since August. But it hasnt been an enjoyable process. I eat a ton of vegetables and bad-tasting food, she says. Im always a little bit hungry. She is giving herself until the end of this year to lose more weight, and will revisit the egg-freezing process then.

The question of whether to lose weight is itself a tricky one. Salmon notes that if losing weight were easy, many larger patients would have already done so. Going on crash diets by, say, cutting out entire food groups, is also unhealthy and may lead to poor fertility outcomes, she adds.

After her discouraging experience with the Sacramento clinic, Michelle had a lucky break. Her sister, who is also of size, referred her to Dr. Geoffrey Sher, a fertility specialist in New York, with whom shed undergone IVF (and who had never mentioned her weight during treatment). Michelle traveled to New York for the retrieval in March. At the recommendation of Sher, she chose to have the eggs fertilized with donor sperm, since frozen embryos are believed to survive the freezing and thawing process better than eggs. Although she is relieved to have two embryos frozen, when she looks back at her experience with the first clinic, Im like, Oh, yeah, that was wrong like, everything about the way that they interacted with me was wrong, she says. She worries that the bias and obstacles she encountered might discourage other larger patients altogether. What if they never get the memo that there might be better, more responsive care options out there?

If I didnt have my sister encouraging me I think some people would just let it go, says Michelle. They would just let it go because they couldnt lose the amount of weight that they were asked to, or they would let it go because they were like, I wasnt anticipating being fat-shamed today, and I dont want to deal with this.

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Behind BMI Limits in Egg-Freezing Procedures - The Cut

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