Archive for September, 2020

A study which appeared in the journal Oncotarget sheds light on why people with Down syndrome are at higher risk of Leukemia. Researchers pinpointed a new set of genes overexpressed in endothelial cells of individuals with Down syndrome, thus creating an environment conducive for leukemia.

Down syndrome occurs in approximately in one in 700 babies, and individuals with the syndrome not only development physical impairments, they have a greatly augmented risk of developing leukemia. Specifically, people with Down syndrome have a 500-fold risk of developing acute megakaryoblastic leukemia (AMKL) and a 20-fold risk of being diagnosed with acute lymphoblastic leukemia (ALL).

In this study, researchers used skin samples from patients with Down syndrome to create induced pluripotent stem cells (iPSC). They subsequently differentiated the iPSC cells into that were then endothelial cells. The researchers observed that the endothelial cell genetic expression produced altered endothelial function throughout cell maturation. We found that Down syndrome, or Trisomy 21, has genome-wide implications that place these individuals at higher risk for leukemia, says co-lead author Mariana Perepitchka, BA, Research Associate at the Manne Research Institute at Lurie Childrens via a press release. We discovered an increased expression of leukemia-promoting genes and decreased expression of genes involved in reducing inflammation. These genes were not located on chromosome 21, which makes them potential therapeutic targets for leukemia even for people without Down syndrome.

Our discovery of leukemia-conducive gene expression in endothelial cells could open new avenues for cancer research, said co-lead author Yekaterina Galat, BS, Research Associate at the Manne Research Institute at Lurie Childrens.

Fortunately, advances in iPSC technology have provided us with an opportunity to study cell types, such as endothelial cells, that are not easily attainable from patients, stated senior author Vasil Galat, PhD, Director of Human iPS and Stem Cell Core at Manne Research Institute at Lurie Childrens and Research Assistant Professor of Pathology at Northwestern University Feinberg School of Medicine. If our results are confirmed, we may have new gene targets for developing novel leukemia treatments and prevention.

Excerpt from:
Study Identifies New Set of Genes That May Explain Why People with Down Syndrome Have a Higher Risk of Leukemia - DocWire News

The study of Cosmetic Skin Care market is a compilation of the market of Cosmetic Skin Care broken down into its entirety on the basis of types, application, trends and opportunities, mergers and acquisitions, drivers and restraints, and a global outreach. The detailed study also offers a board interpretation of the Cosmetic Skin Care industry from a variety of data points that are collected through reputable and verified sources. Furthermore, the study sheds a lights on a market interpretations on a global scale which is further distributed through distribution channels, generated incomes sources and a marginalized market space where most trade occurs.

Along with a generalized market study, the report also consists of the risks that are often neglected when it comes to the Cosmetic Skin Care industry in a comprehensive manner. The study is also divided in an analytical space where the forecast is predicted through a primary and secondary research methodologies along with an in-house model.

Download PDF Sample of Cosmetic Skin Care Market report @ https://hongchunresearch.com/request-a-sample/77005

Key players in the global Cosmetic Skin Care market covered in Chapter 4:HenkelNatura & CoKaoLaboratories IPRADMary KayBeiersdorfEste Lauder CompaniesCotyColgate-PalmoliveUnileverP&GShiseidoChanelJohnson & JohnsonAmorepacificRevlonKoseAvonLVMHL BrandsLOreal

In Chapter 11 and 13.3, on the basis of types, the Cosmetic Skin Care market from 2015 to 2026 is primarily split into:Anti-Aging Cosmetic ProductsSkin Whitening Cosmetic ProductsSensitive Skin Care ProductsAnti-Acne ProductsDry Skin Care ProductsWarts Removal ProductsInfants Skin Care ProductsAnti-Scars Solution ProductsMole Removal ProductsMulti Utility Products

In Chapter 12 and 13.4, on the basis of applications, the Cosmetic Skin Care market from 2015 to 2026 covers:Stem Cells Protection Against UVFlakiness ReductionRehydrate the Skin SurfaceMinimize wrinklesIncrease the viscosity of Aqueous

Geographically, the detailed analysis of consumption, revenue, market share and growth rate, historic and forecast (2015-2026) of the following regions are covered in Chapter 5, 6, 7, 8, 9, 10, 13:North America (Covered in Chapter 6 and 13)United StatesCanadaMexicoEurope (Covered in Chapter 7 and 13)GermanyUKFranceItalySpainRussiaOthersAsia-Pacific (Covered in Chapter 8 and 13)ChinaJapanSouth KoreaAustraliaIndiaSoutheast AsiaOthersMiddle East and Africa (Covered in Chapter 9 and 13)Saudi ArabiaUAEEgyptNigeriaSouth AfricaOthersSouth America (Covered in Chapter 10 and 13)BrazilArgentinaColumbiaChileOthers

For a global outreach, the Cosmetic Skin Care study also classifies the market into a global distribution where key market demographics are established based on the majority of the market share. The following markets that are often considered for establishing a global outreach are North America, Europe, Asia, and the Rest of the World. Depending on the study, the following markets are often interchanged, added, or excluded as certain markets only adhere to certain products and needs.

Here is a short glance at what the study actually encompasses:Study includes strategic developments, latest product launches, regional growth markers and mergers & acquisitionsRevenue, cost price, capacity & utilizations, import/export rates and market shareForecast predictions are generated from analytical data sources and calculated through a series of in-house processes.

However, based on requirements, this report could be customized for specific regions and countries.

Brief about Cosmetic Skin Care Market Report with [emailprotected] https://hongchunresearch.com/report/cosmetic-skin-care-market-size-2020-77005

Some Point of Table of Content:

Chapter One: Report Overview

Chapter Two: Global Market Growth Trends

Chapter Three: Value Chain of Cosmetic Skin Care Market

Chapter Four: Players Profiles

Chapter Five: Global Cosmetic Skin Care Market Analysis by Regions

Chapter Six: North America Cosmetic Skin Care Market Analysis by Countries

Chapter Seven: Europe Cosmetic Skin Care Market Analysis by Countries

Chapter Eight: Asia-Pacific Cosmetic Skin Care Market Analysis by Countries

Chapter Nine: Middle East and Africa Cosmetic Skin Care Market Analysis by Countries

Chapter Ten: South America Cosmetic Skin Care Market Analysis by Countries

Chapter Eleven: Global Cosmetic Skin Care Market Segment by Types

Chapter Twelve: Global Cosmetic Skin Care Market Segment by Applications12.1 Global Cosmetic Skin Care Sales, Revenue and Market Share by Applications (2015-2020)12.1.1 Global Cosmetic Skin Care Sales and Market Share by Applications (2015-2020)12.1.2 Global Cosmetic Skin Care Revenue and Market Share by Applications (2015-2020)12.2 Stem Cells Protection Against UV Sales, Revenue and Growth Rate (2015-2020)12.3 Flakiness Reduction Sales, Revenue and Growth Rate (2015-2020)12.4 Rehydrate the Skin Surface Sales, Revenue and Growth Rate (2015-2020)12.5 Minimize wrinkles Sales, Revenue and Growth Rate (2015-2020)12.6 Increase the viscosity of Aqueous Sales, Revenue and Growth Rate (2015-2020)

Chapter Thirteen: Cosmetic Skin Care Market Forecast by Regions (2020-2026) continued

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List of tablesList of Tables and FiguresTable Global Cosmetic Skin Care Market Size Growth Rate by Type (2020-2026)Figure Global Cosmetic Skin Care Market Share by Type in 2019 & 2026Figure Anti-Aging Cosmetic Products FeaturesFigure Skin Whitening Cosmetic Products FeaturesFigure Sensitive Skin Care Products FeaturesFigure Anti-Acne Products FeaturesFigure Dry Skin Care Products FeaturesFigure Warts Removal Products FeaturesFigure Infants Skin Care Products FeaturesFigure Anti-Scars Solution Products FeaturesFigure Mole Removal Products FeaturesFigure Multi Utility Products FeaturesTable Global Cosmetic Skin Care Market Size Growth by Application (2020-2026)Figure Global Cosmetic Skin Care Market Share by Application in 2019 & 2026Figure Stem Cells Protection Against UV DescriptionFigure Flakiness Reduction DescriptionFigure Rehydrate the Skin Surface DescriptionFigure Minimize wrinkles DescriptionFigure Increase the viscosity of Aqueous DescriptionFigure Global COVID-19 Status OverviewTable Influence of COVID-19 Outbreak on Cosmetic Skin Care Industry DevelopmentTable SWOT AnalysisFigure Porters Five Forces AnalysisFigure Global Cosmetic Skin Care Market Size and Growth Rate 2015-2026Table Industry NewsTable Industry PoliciesFigure Value Chain Status of Cosmetic Skin CareFigure Production Process of Cosmetic Skin CareFigure Manufacturing Cost Structure of Cosmetic Skin CareFigure Major Company Analysis (by Business Distribution Base, by Product Type)Table Downstream Major Customer Analysis (by Region)Table Henkel ProfileTable Henkel Production, Value, Price, Gross Margin 2015-2020Table Natura & Co ProfileTable Natura & Co Production, Value, Price, Gross Margin 2015-2020Table Kao ProfileTable Kao Production, Value, Price, Gross Margin 2015-2020Table Laboratories IPRAD ProfileTable Laboratories IPRAD Production, Value, Price, Gross Margin 2015-2020Table Mary Kay ProfileTable Mary Kay Production, Value, Price, Gross Margin 2015-2020Table Beiersdorf ProfileTable Beiersdorf Production, Value, Price, Gross Margin 2015-2020Table Este Lauder Companies ProfileTable Este Lauder Companies Production, Value, Price, Gross Margin 2015-2020Table Coty ProfileTable Coty Production, Value, Price, Gross Margin 2015-2020Table Colgate-Palmolive ProfileTable Colgate-Palmolive Production, Value, Price, Gross Margin 2015-2020Table Unilever ProfileTable Unilever Production, Value, Price, Gross Margin 2015-2020Table P&G ProfileTable P&G Production, Value, Price, Gross Margin 2015-2020Table Shiseido ProfileTable Shiseido Production, Value, Price, Gross Margin 2015-2020Table Chanel ProfileTable Chanel Production, Value, Price, Gross Margin 2015-2020Table Johnson & Johnson ProfileTable Johnson & Johnson Production, Value, Price, Gross Margin 2015-2020Table Amorepacific ProfileTable Amorepacific Production, Value, Price, Gross Margin 2015-2020Table Revlon ProfileTable Revlon Production, Value, Price, Gross Margin 2015-2020Table Kose ProfileTable Kose Production, Value, Price, Gross Margin 2015-2020Table Avon ProfileTable Avon Production, Value, Price, Gross Margin 2015-2020Table LVMH ProfileTable LVMH Production, Value, Price, Gross Margin 2015-2020Table L Brands ProfileTable L Brands Production, Value, Price, Gross Margin 2015-2020Table LOreal ProfileTable LOreal Production, Value, Price, Gross Margin 2015-2020Figure Global Cosmetic Skin Care Sales and Growth Rate (2015-2020)Figure Global Cosmetic Skin Care Revenue ($) and Growth (2015-2020)Table Global Cosmetic Skin Care Sales by Regions (2015-2020)Table Global Cosmetic Skin Care Sales Market Share by Regions (2015-2020)Table Global Cosmetic Skin Care Revenue ($) by Regions (2015-2020)Table Global Cosmetic Skin Care Revenue Market Share by Regions (2015-2020)Table Global Cosmetic Skin Care Revenue Market Share by Regions in 2015Table Global Cosmetic Skin Care Revenue Market Share by Regions in 2019Figure North America Cosmetic Skin Care Sales and Growth Rate (2015-2020)Figure Europe Cosmetic Skin Care Sales and Growth Rate (2015-2020)Figure Asia-Pacific Cosmetic Skin Care Sales and Growth Rate (2015-2020)Figure Middle East and Africa Cosmetic Skin Care Sales and Growth Rate (2015-2020)Figure South America Cosmetic Skin Care Sales and Growth Rate (2015-2020)Figure North America Cosmetic Skin Care Revenue ($) and Growth (2015-2020)Table North America Cosmetic Skin Care Sales by Countries (2015-2020)Table North America Cosmetic Skin Care Sales Market Share by Countries (2015-2020)Figure North America Cosmetic Skin Care Sales Market Share by Countries in 2015Figure North America Cosmetic Skin Care Sales Market Share by Countries in 2019Table North America Cosmetic Skin Care Revenue ($) by Countries (2015-2020)Table North America Cosmetic Skin Care Revenue Market Share by Countries (2015-2020)Figure North America Cosmetic Skin Care Revenue Market Share by Countries in 2015Figure North America Cosmetic Skin Care Revenue Market Share by Countries in 2019Figure United States Cosmetic Skin Care Sales and Growth Rate (2015-2020)Figure Canada Cosmetic Skin Care Sales and Growth Rate (2015-2020)Figure Mexico Cosmetic Skin Care Sales and Growth (2015-2020)Figure Europe Cosmetic Skin Care Revenue ($) Growth (2015-2020)Table Europe Cosmetic Skin Care Sales by Countries (2015-2020)Table Europe Cosmetic Skin Care Sales Market Share by Countries (2015-2020)Figure Europe Cosmetic Skin Care Sales Market Share by Countries in 2015Figure Europe Cosmetic Skin Care Sales Market Share by Countries in 2019Table Europe Cosmetic Skin Care Revenue ($) by Countries (2015-2020)Table Europe Cosmetic Skin Care Revenue Market Share by Countries (2015-2020)Figure Europe Cosmetic Skin Care Revenue Market Share by Countries in 2015Figure Europe Cosmetic Skin Care Revenue Market Share by Countries in 2019Figure Germany Cosmetic Skin Care Sales and Growth Rate (2015-2020)Figure UK Cosmetic Skin Care Sales and Growth Rate (2015-2020)Figure France Cosmetic Skin Care Sales and Growth Rate (2015-2020)Figure Italy Cosmetic Skin Care Sales and Growth Rate (2015-2020)Figure Spain Cosmetic Skin Care Sales and Growth Rate (2015-2020)Figure Russia Cosmetic Skin Care Sales and Growth Rate (2015-2020)Figure Asia-Pacific Cosmetic Skin Care Revenue ($) and Growth (2015-2020)Table Asia-Pacific Cosmetic Skin Care Sales by Countries (2015-2020)Table Asia-Pacific Cosmetic Skin Care Sales Market Share by Countries (2015-2020)Figure Asia-Pacific Cosmetic Skin Care Sales Market Share by Countries in 2015Figure Asia-Pacific Cosmetic Skin Care Sales Market Share by Countries in 2019Table Asia-Pacific Cosmetic Skin Care Revenue ($) by Countries (2015-2020)Table Asia-Pacific Cosmetic Skin Care Revenue Market Share by Countries (2015-2020)Figure Asia-Pacific Cosmetic Skin Care Revenue Market Share by Countries in 2015Figure Asia-Pacific Cosmetic Skin Care Revenue Market Share by Countries in 2019Figure China Cosmetic Skin Care Sales and Growth Rate (2015-2020)Figure Japan Cosmetic Skin Care Sales and Growth Rate (2015-2020)Figure South Korea Cosmetic Skin Care Sales and Growth Rate (2015-2020)Figure Australia Cosmetic Skin Care Sales and Growth Rate (2015-2020)Figure India Cosmetic Skin Care Sales and Growth Rate (2015-2020)Figure Southeast Asia Cosmetic Skin Care Sales and Growth Rate (2015-2020)Figure Middle East and Africa Cosmetic Skin Care Revenue ($) and Growth (2015-2020) continued

About HongChun Research:HongChun Research main aim is to assist our clients in order to give a detailed perspective on the current market trends and build long-lasting connections with our clientele. Our studies are designed to provide solid quantitative facts combined with strategic industrial insights that are acquired from proprietary sources and an in-house model.

Contact Details:Jennifer GrayManager Global Sales+ 852 8170 0792[emailprotected]

NOTE: Our report does take into account the impact of coronavirus pandemic and dedicates qualitative as well as quantitative sections of information within the report that emphasizes the impact of COVID-19.

As this pandemic is ongoing and leading to dynamic shifts in stocks and businesses worldwide, we take into account the current condition and forecast the market data taking into consideration the micro and macroeconomic factors that will be affected by the pandemic.

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Impact Of Covid-19 on Cosmetic Skin Care Market 2020 Industry Challenges, Business Overview and Forecast Research Study 2026 - Owned

SOUTH SAN FRANCISCO, Calif.--(BUSINESS WIRE)--Genentech, a member of the Roche Group (SIX: RO, ROG; OTCQX: RHHBY), today announced new data that show Ocrevus (ocrelizumab) is a highly effective treatment option for people with relapsing-remitting multiple sclerosis (RRMS) who experienced a suboptimal response to their prior disease modifying therapy (DMT). Subgroup analysis from the two-year open-label Phase IIIb CASTING study also demonstrates that patients benefit across a wide range of disease related and demographic subgroups, regardless of prior treatment background. Findings will be presented at MSVirtual2020, the 8th Joint Meeting of the Americas Committee for Treatment and Research in Multiple Sclerosis (ACTRIMS) and the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS).

For a wide range of people with MS who experienced a suboptimal response to prior treatment, we continue to see evidence that Ocrevus provides significant benefit in slowing disease progression, said Levi Garraway, M.D., Ph.D., chief medical officer and head of Global Product Development. New real-world Ocrevus data show high persistence and adherence to the only B-cell therapy with a twice-yearly dosing schedule, which we know can be very important to both people with MS and their physicians.

Phase IIIb open-label CASTING study

Approximately 75% of RRMS patients (492/658) had no evidence of disease activity (NEDA; brain lesions, relapses and worsening of disability) two years after switching to twice-yearly Ocrevus treatment (with prespecified MRI re-baselining at 8 weeks) in the primary analysis of the CASTING study. Patients enrolled in the study had prior suboptimal response to at least six months of treatment with up to two DMTs. The analysis also showed the proportion of patients achieving NEDA remained consistently high across all measured patient subgroups, including baseline MRI activity, relapse activity, disability level, age and the number of prior DMTs. Further, 78% of patients treated with only one prior DMT compared with 70% of patients treated with two prior DMTs achieved NEDA.

Additionally, patients treated with Ocrevus experienced an improvement in the majority of symptoms measured by SymptoMScreen after two years. SymptoMScreen is a patient-reported outcome tool to assess symptom severity across twelve domains. The most pronounced significant improvements (p<0.001) were seen in sensory symptoms, fatigue and vision, which are important for daily living.

CONFIDENCE real-world safety study

A 97% treatment persistence for Ocrevus patients at 18 months, and strong adherence to infusions every six months, was seen in an interim analysis of more than 1,600 patients in the ongoing German CONFIDENCE study. Separate data from a U.S. commercial claims database that support high persistence and sustained adherence to Ocrevus treatment will also be presented.

Ocrevus longer-term safety data

New safety data as of January 2020 will be presented, representing 5,680 patients with RMS and PPMS and 18,218 patient-years of exposure to Ocrevus, across all Ocrevus clinical trials. These findings further demonstrate the consistently favorable benefit:risk profile of Ocrevus over seven years.

With rapidly growing real-world experience and more than 170,000 people treated globally, Ocrevus has twice-yearly (six-monthly) dosing and is the first and only therapy approved for RMS (including relapsing-remitting MS [RRMS] and active, or relapsing, secondary progressive MS [SPMS], in addition to clinically isolated syndrome [CIS] in the U.S.) and primary progressive MS (PPMS). Ocrevus is approved in 92 countries across North America, South America, the Middle East, Eastern Europe, as well as in Australia, Switzerland and the European Union.

About multiple sclerosis

Multiple sclerosis (MS) is a chronic disease that affects nearly one million people in the United States, for which there is currently no cure. MS occurs when the immune system abnormally attacks the insulation and support around nerve cells (myelin sheath) in the brain, spinal cord and optic nerves, causing inflammation and consequent damage. This damage can cause a wide range of symptoms, including muscle weakness, fatigue and difficulty seeing, and may eventually lead to disability. Most people with MS experience their first symptom between 20 and 40 years of age, making the disease the leading cause of non-traumatic disability in younger adults.

Relapsing-remitting MS (RRMS) is the most common form of the disease and is characterized by episodes of new or worsening signs or symptoms (relapses) followed by periods of recovery. Approximately 85 percent of people with MS are initially diagnosed with RRMS. The majority of people who are diagnosed with RRMS will eventually transition to secondary progressive MS (SPMS), in which they experience steadily worsening disability over time. Relapsing forms of MS (RMS) include people with RRMS and people with SPMS who continue to experience relapses. Primary progressive MS (PPMS) is a debilitating form of the disease marked by steadily worsening symptoms but typically without distinct relapses or periods of remission. Approximately 15 percent of people with MS are diagnosed with the primary progressive form of the disease. Until the FDA approval of Ocrevus, there had been no FDA approved treatments for PPMS.

People with all forms of MS experience disease activity inflammation in the nervous system and permanent loss of nerve cells in the brain even when their clinical symptoms arent apparent or dont appear to be getting worse. An important goal of treating MS is to reduce disease activity as soon as possible to slow how quickly a persons disability progresses. Despite available disease-modifying treatments (DMTs), some people with RMS continue to experience disease activity and disability progression.

About Ocrevus (ocrelizumab)

Ocrevus is the first and only therapy approved for both RMS (including clinically isolated syndrome, RRMS and active, or relapsing, SPMS) and PPMS, with dosing every six months. Ocrevus is a humanized monoclonal antibody designed to target CD20-positive B cells, a specific type of immune cell thought to be a key contributor to myelin (nerve cell insulation and support) and axonal (nerve cell) damage. This nerve cell damage can lead to disability in people with MS. Based on preclinical studies, Ocrevus binds to CD20 cell surface proteins expressed on certain B cells, but not on stem cells or plasma cells, suggesting that important functions of the immune system may be preserved.

Ocrevus is administered by intravenous infusion every six months. The initial dose is given as two 300 mg infusions given two weeks apart. Subsequent doses are given as single 600 mg infusions.

Important Safety Information

What is Ocrevus?

Ocrevus is a prescription medicine used to treat:

It is not known if Ocrevus is safe or effective in children.

Who should not receive Ocrevus?

Do not receive Ocrevus if you have an active hepatitis B virus (HBV) infection.

Do not receive Ocrevus if you have had a life threatening allergic reaction to Ocrevus. Tell your healthcare provider if you have had an allergic reaction to Ocrevus or any of its ingredients in the past.

What is the most important information I should know about Ocrevus?

Ocrevus can cause serious side effects, including:

These infusion reactions can happen for up to 24 hours after your infusion. It is important that you call your healthcare provider right away if you get any of the signs or symptoms listed above after each infusion.

If you get infusion reactions, your healthcare provider may need to stop or slow down the rate of your infusion.

Before receiving Ocrevus, tell your healthcare provider about all of your medical conditions, including if you:

Tell your healthcare provider about all the medicines you take, including prescription and over-the-counter medicines, vitamins, and herbal supplements.

What are the possible side effects of Ocrevus?

Ocrevus may cause serious side effects, including:

Most common side effects include infusion reactions and infections.

These are not all the possible side effects of Ocrevus.

Call your doctor for medical advice about side effects. You may report side effects to the FDA at 1-800-FDA-1088.

For more information, go to http://www.Ocrevus.com or call 1-844-627-3887.

For additional safety information, please see the full Prescribing Information and Medication Guide.

About Genentech in neuroscience

Neuroscience is a major focus of research and development at Genentech and Roche. Our goal is to pursue groundbreaking science to develop new treatments that help improve the lives of people with chronic and potentially devastating diseases.

Genentech and Roche are investigating more than a dozen medicines for neurological disorders, including multiple sclerosis, stroke, Alzheimers disease, Huntingtons disease, Parkinsons disease, Duchenne muscular dystrophy and autism spectrum disorder. Together with our partners, we are committed to pushing the boundaries of scientific understanding to solve some of the most difficult challenges in neuroscience today.

About Genentech

Founded more than 40 years ago, Genentech is a leading biotechnology company that discovers, develops, manufactures and commercializes medicines to treat patients with serious and life-threatening medical conditions. The company, a member of the Roche Group, has headquarters in South San Francisco, California. For additional information about the company, please visit http://www.gene.com.

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New Data Further Reinforce Genentech's Ocrevus (ocrelizumab) as a Highly Effective Treatment for People With Multiple Sclerosis - Business Wire

If you were to ask an ancient Greek how it is determined that a baby is born a boy or a girl, they would have had some interesting and very compelling theories to offer you. One camp held that it was determined by which of the males testes the child originated from, while another believed that what really matters is what side of the womb the fetus develops in, until Aristotle put everybody on notice by declaring once and for all, and definitively, that it is temperature that makes the difference, because men are governed by the element fire, and women by the cooler element water.

For two millennia, our ideas about sex determination were little more advanced than those of the ancient Greeks, with pre-natal environment considered the most important factor for determining whether a child, sexless at conception, emerged a boy or a girl. Temperature continued to be sited as an important factor, but also the nutrition consumed by the mother was deemed to be crucial, and such was the common wisdom until 1905, when a Bryn Mawr cytologist by the name of Nettie Stevens (1861-1912) published Studies in Spermatogenesis with Especial Reference to the Accessory Chromosome,' a daring paper that smashed all previous theories and established on a definite basis the chromosomal, hereditary nature of gender.

For the importance of her work, we know astonishingly little about her life. She was born three months after the start of the US Civil War in Vermont to Julia and Ephraim Stevens, one of four children of whom only two survived to adulthood. Julia Stevens died in 1863 and Nettie was raised primarily by her stepmother, whom her father married in 1865. The year of Stevenss birth put her firmly between two generations of expectations and opportunities. Born two decades earlier, and her career would have firmly been that of a gifted and vastly overqualified governess or school teacher. Born two decades later, and her talents would have opened a series of doors that would have resulted in their steady and early development.

Nettie Stevens would author 38 papers in under a decade, one of which describing the results of her investigations into sex determination ranks among the most important genetic works of the 20th Century

As it stood, Stevens underwent several starts and stops to her career as she attempted to navigate her way through the grey area of the late nineteenth century educational system. She attended public school in Westford, Massachusetts and her academic performance there allowed her to continue on as one of the rare women students attending Westford Academy, where she graduated in 1880. Stevens had clear gifts, but she was also driven by the need to be financially independent, and in 1880 that meant finding a job as a teacher, as paying research positions for women interested in biology were not, as of yet, an option. She took up a position as a Latin, English, mathematics, and biology teacher in Lebanon, New Hampshire and furthered her scientific education as best she could at Westfield Normal School, where she graduated at the top of her class in 1883.

The next thirteen years, then, were devoted to the sort of necessary, money-earning work that would allow her to maintain what she prized most of all, her independence. She worked as a librarian and a teacher in three different cities while waiting for an opportunity to take the next step in her education. That opportunity arose in 1896 when she heard about a new university on the West Coast, founded in 1891 and open to women applicants Leland Stanford Junior University.

In a move that seems doubly bold in view of her history of cautious and pragmatic career decisions, she decided to move out to California in 1896 and join Stanford as a special-case student preparatory to earning her full freshman status in 1897, and an advanced status a few months after that. She worked at Stanford with Frank Mace MacFarland, a nudibranch authority who steered Stevens towards histology, the study of organic tissues by microscope. She earned her bachelors degree in 1899 and her Masters in 1900 with her thesis Studies on Ciliate Infusoria.

1900 was a crucial year not only for Nettie Stevens, when she earned her Masters and settled in to the work at Bryn Mawr College that was to define the rest of her life, but for biology generally. This was the year that the genetic work of Gregor Mendel was rediscovered and verified in a paper by German botanist Carl Correns, kickstarting a new wave of investigations that would come to define modern biology. By 1903 Walter Sutton and Theodor Boveri had established that chromosomes were the carriers of genetic material, thereby providing the locus of study for any researchers interested in questions of heredity.

Stevens had a chance to study with Boveri himself at the University of Wrzberg at precisely the time that he was carrying out his important investigations of chromosomal regularity in sea urchins, furthering concentrating her interest from cytology generally to chromosomal research. She received her PhD in 1903 for her dissertation Further Studies on the Ciliate Infusoria, Licnophor and Boveria, which focused on morphology and particularly the regenerative processes of those organisms. Her interest, however, was turning towards a new investigation of the possible hereditary basis of sex determination, work which she would need funding to carry out. She applied for a Carnegie stipend to supplement her meager salary as a reader in experimental morphology at Bryn Mawr, and received it in 1904.

Stevens would author thirty-eight papers over the next eight years of life left to her, but it was to be the paper published in 1905 describing the results of her investigations into sex determination that would earn her a pedestal in the scientific pantheon. The majority opinion of the scientific community in the early 1900s was that environmental factors determined the evolution of a fetuss sex in the womb. In 1901 Clarence McClung, working with the grasshoppers that were readily available around the University of Kansas, had hypothesized that gender was determined by the presence or absence of a second X chromosome in the cell, an observation which is true enough in grasshoppers, where females have two X chromosomes while males only have one, but was, unfortunately for McClung, not true of the larger animal kingdom.

Stevens worked with the meal worm Tenebrio molitor and noted that while eggs always possessed ten full sized chromosomes, that sperm gametes contained either ten full chromosomes or nine full chromosomes and one smaller chromosome (what we now call the Y chromosome). When an egg was fertilized by a sperm with the larger tenth chromosomes, it developed into a female, and when it was fertilized by a sperm with the smaller tenth chromosome, it developed into a male. This was the death knell of the environmental hypothesis for sex determination, and also of McClungs theory that sex was caused generally by the presence of an extra accessory chromosome. In later studies, she expanded her research to ensure that her results were true for other species besides Tenebrio molitor (in particular aphids, beetles, and flies), while her results were confirmed independently by influential biologist EB Wilson, and in his paper on the topic he acknowledged Stevenss priority in a footnote.

Though she was first in the discovery of the hereditary basis of sex determination, she was not invited to a conference in 1906 where Wilson and her superior at Bryn Mawr (though her junior in age), Thomas Hunt Morgan, were slated to speak about their research in that topic. Morgan then compounded this omission in his official obituary of Stevens, which conveniently mis-stated the year of her work with Tenebrio molitor as 1906 instead of 1904 to make the case that Wilson and she essentially co-discovered the XY principle.

Morgans willingness to muddy the chronology on Stevenss work to give more credit to a male colleague was mirrored in his unwillingness to credit Stevens as an early researcher in the organism that he later won the Nobel Prize for genetically describing, Drosophila melanogaster. This was a species of fly first bred by C.W. Woodworth and used in genetics research at Harvard by William E. Castle as a model organism for genetics studies, and it was one of the species that Stevens included in her researches, several years before Morgan began making it the centerpiece of his genetics experiments in 1909. In his obituary of Stevens, written in 1912, mention is made of the fact that she worked with flies generally, but the fact that she worked with that particular species is not present. This is not to say that Morgan stole the idea of working with Drosophila from Stevens the account given in his Nobel biography states that the idea was suggested to him by entomologist Frank Eugene Lutz but it is all the same a curious missed opportunity to recognize a predecessor in the research of his preferred organism upon the occasion of her death.

Nettie Stevens was granted less than a decade of professional work in the field she had finally found her place in at the age of forty. It was only at the end of her life that Bryn Mawr offered to create a research professorship position for her so that she would not have to expend energy scrapping up funding to supplement her official position as Associate in Experimental Morphology, and she died of breast cancer before the new title and salary could be conferred upon her. There are so many What Ifs that accumulate about her person and career What if she had started sooner? What if she had been given a position equal to her abilities earlier? What if those best placed to assure her legacy had worked more assiduously towards that end? It is easy to get lost in those What Ifs, and to fail to see what is right before us 38 papers in under a decade, one of which ranks among the most important genetic works of the Twentieth Century, produced by an individual only three years into her second, mid-life, career. We know far too little of her character and voice, but the work remains, and in it we find the building blocks of our destinies, writ small but distinct, in the cells of our cousin and sometimes friend, the humble meal worm.

FURTHER READING: Marilyn Ogilvie devotes a good amount of space to Stevens in her classic Women in Science (1986) but there is no stand alone biography of her life and work. The best source is, ironically, a French article from 2008 by Simone Gilgenkrantz which places Stevens within the context of her fellow chromosomal researches. Thomas Hunt Morgans obituary of Stevens can still be found online, which is a good source for details about her work that most authors gloss over, though of course it needs to be approached skeptically.

Lead image: Nettie Stevens (circa 1909); by Bryn Mawr College Special Collections source, Public Domain

Link:
Where Sex Begins: The Chromosomal Investigations Of Nettie Stevens - Women You Should Know

Galanin is known to be associated with mental health. People born with genetically low levels of galanin face an uncommonly high risk of depression and anxiety disorders.

Multiple studies show that exercise increases production of the substance. In the rat experiments, some of which were conducted at Dr. Weinshenkers lab, researchers found that exercise led to a surge in galanin production in the animals brains, particularly in a portion of the brain that is known to be involved in physiological stress reactions. Perhaps most interesting, they also found that the more galanin there, the greater the rats subsequent stress resilience.

For the new research, they gathered healthy adult male and female mice and gave some of them access to running wheels in their cages. Others remained inactive. Mice generally seem to enjoy running, and those with wheels skittered through multiple miles each day. After three weeks, the scientists checked for genetic markers of galanin in the mouse brains and found them to be much higher in the runners, with greater mileage correlating with more galanin.

Then the scientists stressed out all of the animals by lightly shocking their paws while the mice were restrained and could not dash away. This method does not physically harm the mice but does spook them, which the scientists confirmed by checking for stress hormones in the mice. They had soared.

The next day, the scientists placed runners and inactive animals in new situations designed to worry them again, including cages with both light, open sections and dark, enclosed areas. Mice are prey animals and their natural reaction is to run for the darkness and then, as they feel safe, explore the open spaces. The runners responded now like normal, healthy mice, cautiously moving toward the light. But the sedentary animals tended to cower in the shadows, still too overwhelmed by stress to explore. They lacked resilience.

Finally, the researchers confirmed that galanin played a pivotal role in the animals stress resilience by breeding mice with unusually high levels of the substance. Those rodents reacted like the runners to the stress of foot shocks, with full-body floods of stress hormones. But the next day, like the runners, they warily braved the well-lit portions of the light-and-dark cage, not recklessly but with suitable prudence.

The upshot of these experiments is that abundant galanin seems to be crucial for resilience, at least in rodents, says Rachel P. Tillage, a Ph.D. candidate in Dr. Weinshenkers lab who led the new study. And exercise increases galanin, amplifying the animals ability to remain stalwart in the face of whatever obstacles life and science places before them.

See more here:
Exercise May Make It Easier to Bounce Back From Stress - The New York Times

As Covid-19 cases keep rising in the country, a pattern is emerging: a disproportionately high number of men are being infected.

At the beginning of April, truck drivers and their associates (turn boys, off-loaders, and delivery men) were a risk factor in the spread of the disease. Now, however, with the number of community transmissions rising, the same pattern is persisting.

On August 31, statistics on the Uganda Covid-19 Response Info Hub showed that the country has 3037 cumulative coronavirus cases. Of those who were still hospitalised, 85.2 per cent (950) were men, while 14.8 per cent (165) were female.

Last month, Mr George Bagala, an accountant working in Kampala, tested positive for the coronavirus. Like many who have recently tested positive, Bagala was surprised at the results.

I rarely go downtown, and I always wear a mask in public. But I remember, at the beginning of the month I visited a friend. When I entered his office, I removed my mask. My friend had flu and he was drinking lemon tea. It was a hot afternoon and the air conditioner was on, he says.

Downtown Kampala, with its open air markets, shopping arcades, and business hubs, is a hotspot for the virus because of overcrowding and lax adherence to the wearing masks and social distancing.Two days later, an ambulance ferried Bagalas friend to Mulago National Referral Hospital after he tested positive for Covid-19.

By then, I was not well. I had a feeling of blood rushing to my head all the time. I was fatigued all the time, had muscle aches and pain in my eyes. But I put this down to stress, until my wife advised me to take a test, he says.After a mass test at his workplace, Bagala and 10 of his male workmates tested positive for the virus. Role of gender in mortality and morbidity according to a paper, Gender Differences in patients with Covid-19: Focus on Severity and Mortality, published in April 2020 on Frontiers in Public Health, of the 2,442 people who died on the Chinese mainland from the coronavirus, two-thirds were men.

The World Health Organisation Covid-19 weekly surveillance report indicates that 63 per cent of the Covid-19 related deaths in Europe have been among men. The study also adds that according to clinical classification of severity, men tended to develop more serious cases than women.Dr Monica Musenero, the senior presidential advisor on epidemics, says these statistics are being replicated all over the world.

It is a global fact that Covid-19 is infecting and killing more men than women. We dont know why, but in Uganda we are looking at different reasons. It could be that men have more core morbidities (other chronic diseases), or it could be age or genetics. By mid September, we will have a desegregation of the data from the community transmission cases, she says.

Men more exposedStatistics from the Response Info Hub show that the most affected age group were those between 30 and 39, closely followed by those in the 20 and 29 age group.For instance, by August 31, 350 men aged between 30 and 39 had been infected with the virus, yet only 35 women in the same age group had been affected.

In the 20 to 29 age group, 268 were men while 71 were female. By the same date, 17 men had died from Covid-19 compared to nine women.Dr Alex Ndyabakira, an epidemiologist with Uganda Public Health Fellowship Programme, says more men are infected by virtue of being breadwinners.

The 20 to 39 age group is a mobile population. Men are the majority in the open struggle for survival because they work away from home. You will find that most people in Kikuubo (business hub) and taxi parks are young men. The women in this age group are in their child-bearing years and they tend to be stay-at-home mothers or work in less risky places, he says.Dr Ndyabakira adds that the risk of exposure through travel cannot be under looked.

Public transport is a risk factor. How many taxi drivers and conductors are women? Even the length of exposure matters. A passenger is less likely to be infected than the conductor who spends the entire day in the taxi. Besides, we are in a political season, and most people gathering in rallies and political meetings are men, he added.

It is also true that the majority of rapid response health workers and burial teams are men. Both occupations are high risk factors for contracting the virus.

However, Ivan Bamweyana, a member of the Kampala Capital City Authoritys Covid-19 taskforce, says in the medical profession more women have been impacted.

Many female nurses are on the frontlines, treating people who have tested positive. We cannot conclusively say men are more exposed because we do not yet have the statistics on which people are being tested. If you are testing more men because they are the ones in the trading centre, it is obvious more men will turn up positive, he says.

A man without a mask buys bananas from a street vendor without a mask near Jinja Road traffic lights on August. PHOTO | KELVIN ATUHAIRE

Poor medical seeking behaviourGenerally, as a nation, voluntary health seeking behaviour is still a challenge. For many men, going to hospital is a sign of weakness.

When a woman has a persistent headache, she will go to a clinic for treatment. On the other hand, a man will take a panadol and dismiss the disease. But even if he goes to hospital, when he is referred to another hospital, he is less likely to comply with the referral, Dr Musenero says.It could also be that because of poor health seeking behaviour, most men are not aware of underlying medical conditions they might have that could predispose them to the virus.

Women, on the other hand, during their childbearing years always get maternity reviews that bring these conditions to light.Bamweyana says women have a more responsible attitude towards the coronavirus.

Women having a better health seeking behaviour compared to men. As a result, they tend to take Covid-19 related messaging very seriously. Men, though, will tend to think that Covid-19 is nothing to them. I have heard people say that they have survived being shot at or have lived through hellish situations and survived, so how can Covid-19 affect them. They think it is a simple flu, he says.

Risky lifestylesPoverty and neglect for a healthy lifestyle have seen many Ugandans unable to eat a balanced diet. One of the keys to fighting the virus is to boost immunity levels by eating fruits and vegetables.

In an effort to maintain a minimum weight or to lose weight, a number of women in the most affected age group (20-39) will try to maintain healthy lifestyles, which includes eating lots of fruits and vegetables.Covid-19 affects the respiratory system and lifestyle behaviour such as smoking that impact lung health are more predominant in men.

In Uganda, smoking is largely a male habit. The Global Adult Tobacco Survey: Country Report 2013 showed that 7.9 per cent of adults in Uganda aged 15 and above (1.3 million) use tobacco products. The rates are higher among males than women, with 11.6 per cent of men and 4.6 per cent of women using tobacco products.

According to a WHO publication, although there are currently no peer-reviewed studies that directly estimate the risk of hospitalisation with Covid-19 among smokers, 27 observational studies found that smokers constituted 1.4 per cent to 18.5 per cent of hospitalised adults.

The studies done in Europe have not been conclusive. However, smoking is a sever risk factor for any respiratory disease, but even with that, if you have a male smoker and a female smoker, the man is likely to die from Covid-19 than the woman, Dr Musenero says.

Another reason could be that women are more likely than men to adhere to wearing masks. Because of high testosterone levels, men are alpha risk takers and tend to believe they cannot be infected with the virus.

The psychological effectAlthough a conclusive study is yet to be done, the effects of the lockdown and the subsequent downward economic effect seem to be affecting more men than women. Since July, seven men between the ages of 29 and 40 have been known to have committed suicide.

Dr Musenero says this is because women cope better than men when it comes to stress.Men tend to want to work through their problems and show that they are in charge. A woman, on the other hand, will call up a friend, narrate her problems, cry about it and will feel better. Ordinarily, a man would go to a bar to socialise with friends but now, those places are closed, she says.

The way forwardSince the data is still being analysed, there is no guarantee that broadcast messages targeted at men will change the trend.A proper data analysis must be done before a message targeting men can go out. Otherwise, you might cause relaxation of the standard operating procedures among women, Bamweyana says.

Another disturbing detail that is being analysed, according to Dr Musenero, is that most of those who have died never reaced the stage of needing a ventilator, as has been the case in Europe and the USA. Here, the progression from flu and cough to respiratory distress has been alarmingly quick less than five days.

It is a global fact that Covid-19 is infecting and killing more men than women. We dont know why, but in Uganda we are looking at different reasons. It could be that men have more core morbidities (other chronic diseases), or it could be age or genetics. By mid September, we will have a desegregation of the data from the community transmission cases, Dr Monica Musenero, the senior presidential advisor on epidemics.

Many female nurses are on the frontlines, treating people who have tested positive. We cannot conclusively say men are more exposed because we do not yet have the statistics on which people are being tested. If you are testing more men because they are the ones in the trading centre, it is obvious more men will turn up positive, Mr Ivan Bamweyana, member of KCCA Covid-19 Taskforce,

gnantume@ug.nationmedia.com

See more here:
Covid-19 taking a greater toll on men than women - reports - Daily Monitor

Many people are surprised to learn how many decisions need to be made throughout pregnancy. Where do I want to receive my prenatal care? What lifestyle changes am I going to make to stay as healthy as possible?

Another big decision that needs to be made is about genetic screening during pregnancythere are so many options, and it can feel overwhelming. But take heart, mama. We promise you'll figure it out. Especially because you don't have to do it alone.

It's important to know that genetic screening is optional during pregnancy. Whatever feels right for you and your baby is usually best. New information on genetics comes out all the time. If you are thinking about having prenatal genetic screening or testing, talk to your provider first for the most up-to-date information and specific guidance based on your personal story.

According to the American College of Obstetricians and Gynecologists (ACOG), "prenatal genetic screening gives parents-to-be' information about whether their fetus has a certain genetic disorder."

Screenings are not diagnostic. This means that the results are not definitive ("The baby does or does not have Down syndrome,") but rather a prediction of chance ("There is a higher or lower than normal chance that the baby could have Down syndrome.")

If tests come back indicating that there is a high chance of abnormality, your provider may recommend diagnostic testing which can give a definitive yes or no result (more on that soon).

There are two main types of prenatal genetic testing: prenatal screening test and prenatal diagnostics test.

Prenatal screening tests:

Prenatal genetic screening tests can identify whether your baby is more or less likely to have certain birth defects, most stemming from genetic disorders. These are not definitive tests, they just tell you the chances. If results indicate an increased risk, your provider may talk to you about doing a diagnostic test.

Here are some common prenatal genetic screening tests:

Noninvasive prenatal testing (NIPT), also called cell-free fetal DNA testing. This can be done between weeks 10 and 20. It assesses the chances of chromosomal abnormalities, such as Down syndrome (trisomy 21), Patau syndrome (trisomy 13), Edwards syndrome (trisomy 18) and certain single-gene disorders associated with abnormalities of the skeleton, bones or heart. This test can also determine the sex of your baby if you'd like to know. The results take about a week to come in.

First-trimester combined screening. This is an optional test that is offered between weeks 11 and 14. The test involves taking a blood sample from you along with doing an ultrasound that looks at certain aspects of the baby's development. Specifically, the ultrasound looks at the clear space in the tissue at the back of the baby's neckthe size of this space, along with the information provided by the blood test, can help identify a higher chance for Down syndrome.

Second Trimester screening. Similar to the first trimester screening, your provider will take a blood test called a quad screen. This will measure four substances in your blood which indicate the chance of carrying a baby with chromosomal defects like Down syndrome, as well as neural tube defects.

Here are some common prenatal diagnostic tests:

Your provider may recommend a diagnostic test if your screening indicates an elevated chance of abnormality, or if other factors like family and medical history warrant it. These are more invasive and the only way to be sure of a diagnosis.

Chorionic Villus Sampling (CVS). CVS tests for certain disorders and chromosomal abnormalities in the fetus by looking at the chorionic villi, which are wisps of placental tissue that contain your baby's DNA. It can be done as early as 10 weeks. Placental tissue is extracted from your uterus by a catheter inserted into your cervix or by needle into the abdomen. The tissue will be genetically analyzed for certain disorders.

The procedure carries a small (0.35%) risk of miscarriage. It may sting and induce some cramping, but after a day of rest, you are cleared to resume normal activity. The benefit of CVS is that it can be done earlier in the pregnancy than an amniocentesis.

Amniocentesis. An amniocentesis (often called an amnio) is a procedure to sample the fluid that surrounds the baby. This amniotic fluid contains your baby's DNA, so it can be used to test for genetic disorders. It is usually performed between weeks 15 and 20 and does carry some risks, so it is important to be informed about them. According to the Society for Maternal-Fetal Medicine, amniocentesis is associated with a miscarriage rate of 1 in 300 to 500.

With most tests, there is a potential for false-positive results (when a positive test is wrong) and false-negative results (when a negative test is wrong). We recommend reaching out to your provider, they can give you more information on the rates of false-positive and false-negative test results and compare other options.

The risk associated with genetic testing can depend on the test you get. For the prenatal screening tests, the risks are limited due to its less invasive process (blood test and ultrasound). Many of the risks associated with genetic testing involve emotional, social and financial consequences of the test results. These are just as important to keep in mind (more on these in a bit).

For diagnostic screening, there is a small but real risk of miscarriage due to it being a more invasive procedure. This is because they need a sample of amniotic fluid or tissue from the fetus.

If you are trying to decide if you'd like to have genetic screening or testing, here are some questions to ask your provider:

There are also genetic specialists who may have even more information about the prenatal genetic testing than your provider does. Do not hesitate to request an appointment with a genetic specialist to discuss any of your questions further.

Mama, trust yourself. People are going to have all kinds of advice regarding genetic screeningsand it's okay to listen if you want to. But ultimately, you have to make the best decision for you. This is a great time to tune out the noise, get evidence-based and personalized information from your provider, and then listen to your gut. There is no right answer here, so doing what feels right is totally appropriate.

Some women choose to have all the available tests done, while others decline all of them. The majority of women probably fall somewhere in the middle.

Mama, it's all okay.

Here's a way to make the decision: Think about what you are going to do with the information you receive. Consider this:

If the test comes back saying your baby has a very low chance of having a chromosomal abnormality, will that help you to feel more relaxed during your pregnancy? Or would you rather not think about this knowledge one way or the other?

If the test comes back saying that your baby has a high chance of having a chromosomal abnormality, will you then choose to have an amniocentesis to get more reliable information?

If you do choose an amniocentesis, and it reveals that your baby does indeed have a chromosomal abnormality, does that impact your decision-making moving forward? Will you, for example, appreciate knowing this information so you can begin to make special plans for caring for the baby? Will you choose to terminate the pregnancy? If the answer to both of those questions is no, perhaps you may not want to have the testing at all.

Again, it's complicated. But just like with all of pregnancy and parenting, there is no one right way to do things. The world is full of ideas and judgment, but in these moments, focus on your needs and desires and your provider's guidance.

A portion of this article has been excerpted from The Motherly Guide to Becoming Mama.

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Should I get prenatal genetic screening? The most common questions, answered. - Motherly Inc.

While identifying new genetic targets and developing novel drugs is important for the future of non-small cell lung cancer (NSCLC), more emphasis should be put on improving patient access to existing targeted treatments, according to Dr. Nathan A. Pennell.

In an interview with OncLive, CUREs sister publication, Pennell, an associate professor in thedepartment of medicine and director of the lung cancer medical oncology program at theTaussig Cancer Institute of Cleveland Clinic,spoke about current and emerging treatment options in NSCLC, including immunotherapy combinations and personalized treatments involving T cells.

But when it comes to the future, Pennell said, identifying targetable genetic alterations in patients and treating them with existing drugs should be a key area of focus.

Studies have shown that probably fewer than half of people with targetable genetic alterations in lung cancer are being identified and never receiving treatment for this, Pennell said, and I think before we move on to the next exciting drug or the next exciting marker, we should spend a little time making sure that every patient is identified and gets access to the treatments that we already have.

Transcription:

We've made such tremendous progress over the last decade. And just it seems like every year, new targets are emerging and new drugs are getting approved. And so, the speed with which we're moving from discovery to actually treating people has been staggering, and I hope that continues.

There continue to be very promising emerging biomarkers including KRAS mutations, again, HER2 mutations. There certainly is lots of room for improving the efficacy of immunotherapy, which can be tremendously life changing and potentially even curative in patients with metastatic disease. But unfortunately, it's only really working in a minority of patients and so lots of room to be improved in that.

I think combinations of immunotherapy and perhaps even more personalized immunotherapy, using T-cells that recognize individual patients tumors, may be the future for this, or personalized tumor vaccines.

But honestly, instead of just focusing on discovering new treatments and new targets, I think we should focus more on applying what we already know. So, we have tremendous treatments for patients with specific subgroups of lung cancer, but studies have shown that probably fewer than half of people with targetable genetic alterations in lung cancer are being identified and never receiving treatment for this. And I think before we move on to the next exciting drug or the next exciting marker, we should spend a little time making sure that every patient is identified and gets access to the treatments that we already have.

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Personalized Medicine, Genetic Testing Could Shape the Future of Non-Small Cell Lung Cancer - Curetoday.com

An employee works in a protective suit in a laboratory of the biotech company Qiagen in Germany, September 8, 2020.

Fabian Strauch | picture alliance | Getty Images

German genetic testing companyQiagenannounced Tuesday that it plans to launch a new antigen test for the coronavirus that it says could eventually be deployed in airports and stadiums if it receives the appropriate authorizations.

The company said it plans to launch two versions of the antigen test in the U.S. later this year: one version that's meant to be processed in a clinical laboratory and another that's portable and can be processed at point of care. The company has not yet applied for emergency use authorization from the Food and Drug Administration but said it plans to.

If the test, called theAccess Antigen Test, is granted FDA authorization for point-of-care use and if it's waived from the requirements under the Clinical Laboratory Improvement Amendments, Qiagen said, the test could be used in high-volume settings such as airports and stadiums to test people with symptoms. Rapidly testing symptomatic people could become increasingly important in the fall and winter as seasonal influenza, which causes many of the same early symptoms as seen in Covid-19, spreads in the Northern Hemisphere.

"The portable test offers a new combination of speed and scale that marks an important step towards decentralized mass testing that health authorities all over the world have been urgently seeking," the company said in a release.

The test, which wasdeveloped in collaboration withAustralian diagnostics company Ellume, can screen up to eight nasal-swab samples simultaneously, the company said. Administrators of the test use a small digital platform, called an eHub, which was launched in August with Qiagen's antibody test, to process the nasal swabs.

The platform can yield results in less than 15 minutes, the company said, and can process an average of about 30 swab samples every hour. Qiagen added that the test correctly diagnoses a positive coronavirus infection 90% of the time and correctly diagnoses a negative result 100% of the time. The company did not elaborate on the methods used to arrive at the accuracy conclusions.

The company has not yet disclosed a price point for the test, but Qiagen CEO Thierry Bernard called the tests "cost-effective." Qiagen also did not disclose details on how many tests it will be able to manufacture.

In a statement, Bernard added that the antigen tests are meant to supplement, not replace, the molecular, or PCR, tests, which are the most accurate tests on the market. PCR tests, however, are dependent on a strained supply chain of technical laboratory equipment, need to be processed by trained scientists and can take hours or days to yield results.

The company added that it will also apply for certification in Europe.

"The Access Antigen Test is fast, easy to use and cost-effective and will be a valuable tool to address the so far unmet high-volume testing needs for SARS-CoV-2 antigens in situations where time is of the essence," Bernard said in a statement. "It will deliver highly accurate results and will complement the gold-standard PCR tests used for detection of active COVID-19 infection. PCR tests offer a high level of diagnostic accuracy but are time-consuming and lab-bound."

CNBC's Meg Tirrell contributed to this report.

See the original post:
Qiagen to launch rapid coronavirus test it says could be used in airports and stadiums - CNBC

Fort Collins, Colorado The Global Breast Cancer Predictive Genetic Testing Market research report offers insightful information on the Global Breast Cancer Predictive Genetic Testing market for the base year 2019 and is forecast between 2020 and 2027. Market value, market share, market size, and sales have been estimated based on product types, application prospects, and regional industry segmentation. Important industry segments were analyzed for the global and regional markets.

The effects of the COVID-19 pandemic have been observed across all sectors of all industries. The economic landscape has changed dynamically due to the crisis, and a change in requirements and trends has also been observed. The report studies the impact of COVID-19 on the market and analyzes key changes in trends and growth patterns. It also includes an estimate of the current and future impact of COVID-19 on overall industry growth.

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In market segmentation by applications of the Global Breast Cancer Predictive Genetic Testing, the report covers the following uses-

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(Covid-19 Impact)Breast Cancer Predictive Genetic Testing Market Size is Thriving Worldwide 2020 | Growth and Profit Analysis, Forecast by 2027 - The...

New Jersey, United States, The Preimplantation Genetic Testing Market report 2020 provides a detailed impression, describe the product industry scope and the market expanded insights and forecasts up to 2027. It shows market data according to industry drivers, restraints and opportunities, analyzes the market status, the industry share, size, future Trends and growth rate of the market. The Preimplantation Genetic Testing Market report is categorized by application, end user, technology, product / service types, and other, as well as by region. In addition, the report includes the calculated expected CAGR of chitosan acetate-market derivative from the earlier records of the Preimplantation Genetic Testing Market, and current market trends, which are organized with future developments.

Preimplantation Genetic Testing Market was valued at USD 401.49 million in 2019 and is projected to reach USD 796.89 million by 2027, growing at a CAGR of 9.65% from 2020 to 2027.

1.Preimplantation Genetic Testing Market, By Technology:

Next-Generation Sequencing Polymerase Chain Reaction Fluorescence in Situ Hybridization Comparative Genomic Hybridization Single-Nucleotide Polymorphism

2.Preimplantation Genetic Testing Market, By Procedure Type:

Preimplantation Genetic Screening Preimplantation Genetic Diagnosis

3.Preimplantation Genetic Testing Market, By Application:

Aneuploidy Structural Chromosomal Abnormalities Translocations Deletions Duplications Inversions Single Gene Disorders X-Linked Disorders HLA Typing Gender Identification

4.Preimplantation Genetic Testing Market, By Products And Services:

Reagents and Consumables Instruments Software and Services

5.Preimplantation Genetic Testing Market, By End User:

Maternity Centers & Fertility Clinics Hospitals, Diagnostic Labs, and Service Providers Research Laboratories & Academic Institutes

The report provides detailed coverage of the Preimplantation Genetic Testing Market, including structure, definitions, applications, and Industry Chain classifications. The Preimplantation Genetic Testing Market analysis is provided for the international markets including development trends, competitive landscape analysis, investment plan, business strategy, opportunities and development status of key regions. Development policies and plans are discussed and manufacturing processes and cost structures analyzed. This report also includes information on import / export consumption, supply and demand, costs, industry share, policy, Price, Sales and gross margins.

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The Preimplantation Genetic Testing Market was created on the basis of an in-depth market analysis with contributions from industry experts. The report covers the growth prospects in the coming years and the discussion of the main providers.

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Preimplantation Genetic Testing Market is Thriving Worldwide 2020 | Trends, Growth and Profit Analysis, Forecast by 2027 - The Daily Chronicle

As Marina Giokas sails the Strait of Georgia off the southwestern coast of B.C., her phone rings. Despite being on the high seas, the West Vancouver communications and finance consultants cell signal is clear as a bell.

Youve got to love technology, she quips.

Giokas means that in more ways than one. Since 2018, Giokas has depended on nutrigenomics the way genes interact with different foods and nutrients to personalize her diet.

Story continues below advertisement

Since taking a DNA test through Vancouver company dnaPower Inc., Giokas has been using the companys resulting personalized report to discover the best diet for her genetic makeup.

It goes deep, she says of the service. Its about what your body does not tolerate and what it needs more of.

Marina Giokas, pictured here with her boat in West Vancouver, uses a personalized nutrigenomics report to guide her diet choices.

Darryl Dyck / THE GLOBE AND MAIL

Giokas now eats more fruit and vegetables, washing them thoroughly to remove any pesticides or chemicals. And shes said goodbye to supplements. Instead, Giokas has replaced them with the B vitamins the report said she needed.

After a tough year of treatment for breast cancer in 2017/2018, shes hoping these simple changes to her diet and exercise regime will keep her feeling healthier.

Personalized diet and wellness plans based on DNA have grown in popularity in recent years as Canadians look for new, tech-savvy ways to improve their health. According to Statistics Canada, 63.1 per cent of Canadians are now considered either overweight or obese.

Health experts have long known that a one-size-fits-all approach to diet doesnt work. One person might drop 20 pounds on a high fat diet or low carb diet, while the scales needle doesnt budge for someone else who eats the same foods. So how can we know in advance which side of the equation someone will land on?

Clients of dnaPower Inc. receive a swab to collect their DNA, then send it back through the mail.

Darryl Dyck / THE GLOBE AND MAIL

Lois Nahirney, president and founder of dnaPower, says she gets asked that question all the time, particularly in relation to the popular low-carb, high-fat Ketogenic diet. When people ask her if its right for them, she responds, It depends.

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Im looking at a report right now that shows this person has a problem with dietary saturated fats. Thats someone who would have some challenges on a Keto diet, she explains. Based on this persons DNA, the company would likely recommend eating unsaturated fats found in flaxseed oil, hemp seed and walnuts. Leafy greens would get a thumbs up too, while dairy and fatty meats would go on the no-no list.

The idea behind nutrigenomics is that by understanding your unique DNA, you can match your diet choices to how your body processes nutrients. For example, research has linked specific genes, or groups of genes, to conditions like lactose sensitivity, food allergies, gluten intolerance and caffeine sensitivity. Nutrigenomics may reveal that someone should stay away from too much coffee, eat more healthy fats or specific vitamin-rich foods, for example.

Taking a DNA test is as easy as sticking a swab in your cheek and then mailing it back, says Nahirney. Results still come back within two to six weeks, and clients then can go over the results with a dnaPower dietitian. The cost is $299. (DNA-based reports addressing other wellness areas like exercise and brain health are also available for an added fee.)

Lois Nahirney, founder and CEO of dnaPOWER, at her home office in Vancouver.

Darryl Dyck / THE GLOBE AND MAIL

dnaPower is only one of many companies using biometric readings to create targeted health and diet plans. Theres DNAfit from the U.K. which provides everything from sleep and stress reports to personalized diets and meal plans. Milwaukee, WI-based GenoPalate offers personalized recipes built from clients genetic results, and Torontos Nutrigenomix promises a way to eat according to your genes.

But the question for most potential clients might be: Does it work?

Kristin Kirkpatrick, a registered dietitian and wellness manager for the Cleveland Clinic Wellness Institute, says she has seen firsthand how personalized nutrigenomic testing has helped patients commit to their diet once they understand which diets and exercise programs may work best for them. Some have switched from a Keto diet to a Mediterranean-based one. Others have swapped resistance training for more aerobic exercise.

Still, while DNA testing for wellness offers the potential for addressing more serious health conditions in the future, theres more research to be done first, she says.

Though DNA-based diets are trending and gaining valuable evidence through studies, we are not ready for prime time quite yet for recommending to all populations, she says, mentioning that people may also be unable to afford genetic testing since it is not typically covered by insurance.

But Giokas is glad she took the plunge and shelled out for the test, even if she falls off the wagon from time to time, tempted by cheese and popcorn. Having her DNA-based health plan gives her the motivation to get back on track.

Im amazed just how simple it is to take control of your health once you have the information, she says.

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Diet by DNA: How tech is changing what it means to eat healthy - The Globe and Mail

New Jersey, United States, The Direct-To-Consumer (DTC) Genetic Testing Market report 2020 provides a detailed impression, describe the product industry scope and the market expanded insights and forecasts up to 2027. It shows market data according to industry drivers, restraints and opportunities, analyzes the market status, the industry share, size, future Trends and growth rate of the market. The Direct-To-Consumer (DTC) Genetic Testing Market report is categorized by application, end user, technology, product / service types, and other, as well as by region. In addition, the report includes the calculated expected CAGR of chitosan acetate-market derivative from the earlier records of the Direct-To-Consumer (DTC) Genetic Testing Market, and current market trends, which are organized with future developments.

Global Direct-to-Consumer (DTC) Genetic Testing Market was valued at USD 789.92 Million in 2018 and is projected to reach USD 2,361.12 Billion by 2026, growing at a CAGR of 14.59% from 2019 to 2026.

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Global Direct-to-Consumer (DTC) Genetic Testing Market, By Test Type

Predictive Testing Carrier Testing Nutrigenomics Testing Others

Global Direct-to-Consumer (DTC) Genetic Testing Market, By Technology

Single Nucleotide Polymorphism Chips Whole Genome Sequencing Targeted Analysis

The report provides detailed coverage of the Direct-To-Consumer (DTC) Genetic Testing Market, including structure, definitions, applications, and Industry Chain classifications. The Direct-To-Consumer (DTC) Genetic Testing Market analysis is provided for the international markets including development trends, competitive landscape analysis, investment plan, business strategy, opportunities and development status of key regions. Development policies and plans are discussed and manufacturing processes and cost structures analyzed. This report also includes information on import / export consumption, supply and demand, costs, industry share, policy, Price, Sales and gross margins.

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Direct-To-Consumer (DTC) Genetic Testing Market forecast up to 2027, with information such as company profiles, product picture and specification, capacity production, price, cost, revenue, and contact information. Upstream raw materials and equipment as well as downstream demand analyses are also carried out. The Direct-To-Consumer (DTC) Genetic Testing Market size, development trends and marketing channels are analyzed. Finally, the feasibility of new investment projects is assessed and general research results are offered.

The Direct-To-Consumer (DTC) Genetic Testing Market was created on the basis of an in-depth market analysis with contributions from industry experts. The report covers the growth prospects in the coming years and the discussion of the main providers.

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Direct-To-Consumer (DTC) Genetic Testing Market is Thriving Worldwide 2020 | Trends, Growth and Profit Analysis, Forecast by 2027 - The Daily...

The GlobalGenetic Testing Market report contains a complete analysis of the different aspects of the market such as the market size, key marketing regions, key players, leading firms, market structure, segmentation, revenue generation, demand, research, and development, and top marketing strategies. The Genetic Testing Market report provides comprehensive data for the latest market entrants. Furthermore, the explosion delivers a market summary, SWOT analysis, and total market share.

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List ofTop Key Playersof Genetic Testing Market:

HI GeneRegulatoryAnnoroadSinoGenoMaxGenePlanetCounsyl, Inc.RepconexNatera, IncBiomarkerGeeppine360Jiyin23andMe, IncCapitalBioBiomedlabGene by GeneUnited GeneGeneDxFind Bio-TechAiyin GeneCourtagen Life SciencesAgenGeneTestsAsper BiotechPathway GenomicsNovogeneBGIGene KangBerry GenomicsAijiyin

Genetic Testing Market report also covers a comprehensive analysis of the competitive landscape, upcoming development trends, and key manufacturers of the industry. The recovery from COVID-19 is likewise being shared through this report discussed with the expertise in the industry. Besides the summary, the report shares a huge region of knowledge that has comprehensive evolution, definitions & classifications, with expert opinion. Also, itll mention Capacity, Amount, Revenue, Cost, and Gross margin of profit, growth rate, Import, Export, Market Share, and Technological Developments.

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Genetic Testing Market Segment by Type:

CancerCystic fibrosisSickle cell anemiaDuchenne muscular dystrophyAlzheimer diseaseThalassemiaHuntington diseaseOthers

Genetic Testing Market segment by Application:

Newborn screeningDiagnostic testingCarrier testingPreimplantation genetic diagnosisPrenatal diagnosisPredictive and presymptomatic testingPharmacogenomics

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The Genetic Testing Market Research report delivers an all-inclusive overview of the competitive landscape along with an in-depth analysis of the company profiles, revenue estimation, and gross margin profits, and market size and share. Furthermore, the report studies the strategic initiatives taken by the companies to expand their customer base, market size. It also evaluates key industry trends and sales and distribution channels.

The Genetic Testing Market Report Can Answer The Following Questions:

Reasons To Buy Genetic Testing Market Research Report:

Table of Contents

1. Research Methodology 2. Executive Summary 3.Market Overview 3.1. Definition 3.2. Genetic Testing Industry Market Value Chain Analysis 3.3. Porters 5 Forces 3.4. Regulations 4. Market Dynamics 4.1. Introduction 4.2. Drivers 4.3. Constraints 4.4. Trends 5. Global Genetic Testing Market Segmentation, Forecasts, and Trends by Application 6. Global Genetic Testing Market Segmentation, Forecasts, and Trends by Technology 7. Global Genetic Testing Market Segmentation, Forecasts, and Trends by Region 8. Competitive Intelligence 8.1. Company Market Share Analysis 9. Company Profiles 10. Investment Opportunities

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Global Genetic Testing Market By Covid-19 Impact Analysis, Global Industry Report: Overview with Product Scope, Opportunities Risk, Top Participants,...

Trusted Business Insights answers what are the scenarios for growth and recovery and whether there will be any lasting structural impact from the unfolding crisis for the Direct-to-Consumer Genetic Testing market.

Trusted Business Insights presents an updated and Latest Study on Direct-to-Consumer Genetic Testing Market 2019-2029. The report contains market predictions related to market size, revenue, production, CAGR, Consumption, gross margin, price, and other substantial factors. While emphasizing the key driving and restraining forces for this market, the report also offers a complete study of the future trends and developments of the market.The report further elaborates on the micro and macroeconomic aspects including the socio-political landscape that is anticipated to shape the demand of the Direct-to-Consumer Genetic Testing market during the forecast period (2019-2029).It also examines the role of the leading market players involved in the industry including their corporate overview, financial summary, and SWOT analysis.

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Abstract, Snapshot, Market Analysis & Market Definition: Direct-to-Consumer Genetic Testing MarketIndustry / Sector Trends

Direct-to-Consumer Genetic Testing Market size was valued at USD 831.5 million in 2018 and is expected to witness 15.2% CAGR from 2019 to 2025.

U.S. DTC Genetic Testing Market Size, By Test Type, 2018 & 2025 (USD Million)

Rising prevalence of genetic diseases such as cystic fibrosis and Alzheimers globally is one of the major factors fostering direct-to-consumer genetic testing market growth. According to Global Genes, over 300 million people globally suffer from rare diseases. Recently developed DTC genetic tests allows consumer to identify probability of acquiring a specific genetic disease. Therefore, increasing adoption of DTC genetic testing for early disease detection and identification of genetic diseases will boost the industry growth over forecast timeline.

Increasing demand for personalized medications to treat genetic diseases will positively impact industry growth in forthcoming years. Individuals genome must be tested to develop personalized medicines. This increases the demand for DTC genetic kits since, it provides detailed information about individuals genetic predisposition. As detailed information regarding genetic makeup of individuals is easily available with the use of DTC genetic kits, researchers can easily design and develop personalized medicine that would help in faster patient recovery. Aforementioned factor is expected to drive the industry growth. However, high cost of DTC genetic testing kits may hamper industry growth to some extent during the forecast period.

Market Segmentation, Outlook & Regional Insights: Direct-to-Consumer Genetic Testing Market

Direct-to-Consumer Genetic Testing Market, By Test Type

Predictive testing segment will experience around 17% growth throughout the analysis period. Considerable segmental growth can be associated with rising prevalence of genetic diseases. Recently developed DTC genetic tests help to identify mutations that increase the chances of acquiring specific disease accurately. Surging awareness regarding benefits of such presymptomatic testing has reduced the mortality rates by enabling effective management of disease. Above mentioned factors have stimulated the segmental growth that is predicted to continue over the forecast timeframe.

Ancestry and relationship testing segment accounted for over 43% revenue share in 2018. Increasing awareness regarding ethnicity tests amongst the American and European population has increased the demand for DTC genetic tests. Accuracy and efficiency possessed by these tests has fostered segmental growth. Moreover, ancestry tests developed by companies such as Ancestry.com are user friendly. Availability of robust DTC ancestry tests providing meaningful clinical, genealogical and even forensic information will positively impact the segment growth.

Direct-to-Consumer Genetic Testing Market, By Technology

Targeted analysis segment was valued over USD 310 million in 2018. Targeted analysis is utilized for determining the defects in genes that are responsible for a particular disorder. Targeted genotyping can accurately measure an individuals gene pool that encodes important information regarding various diseases. Targeted analysis can be conducted at significant low cost compared to other available techniques that should augment its adoption rate over forecast timeframe.

Single nucleotide polymorphism segment will experience around 15% growth throughout the forecast period. Single nucleotide polymorphism chips specifically detect changes in single nucleotide that increases the efficiency of tests. For instance, SNP chips utilized for diagnosing hereditary cancers have detected 1300 mutations in BRCA2 genes. Various companies such as Ancestry.com and Color Genomics utilize SNP arrays that analyse gene sequences at a specific resolution and reveal detailed analysis about the defective genes that may in future cause certain disease. Increasing adoption of such advanced SNP chips in DTC testing kits will trigger the segmental growth.

Germany DTC Genetic Testing Market Size, By Technology, 2018 (USD Million)

Direct-to-Consumer Genetic Testing Market, By Region

North America direct-to-consumer genetic testing market accounted for around 39% regional share in 2018. Regional market growth can be attributed to increasing prevalence of genetic diseases. Rare genetic diseases such as thalassemia, hemophilia and anaemia require continuous and critical monitoring. According to CDC, every year more than 1,000 people are affected by thalassemia. Furthermore, American population has higher literacy rate and also, awareness regarding DTC tests is high amongst the American population that augments demand for DTC genetic tests.

Europe is estimated to experience around 15% growth over the coming years. European direct-to-consumer genetic testing market is highly regulated and for carrying out some of the genetic tests through DTC kits, customers are required to have physicians prescription. However, currently, European regulatory bodies are working on improving regulations set on DTC tests due to improved accuracy and efficiency possessed by them. Thus, improvement in regulatory scenario will positively impact regional market growth.

Latin America DTC Genetic Testing Market Size, By Country, 2025 (USD Million)

Key Players, Recent Developments & Sector Viewpoints: Direct-to-Consumer Genetic Testing Market

Few of the eminent industry players operating in direct-to-consumer genetic testing market are Ancestry, 23andMe, Color, Family Tree DNA, EasyDNA, Helix, Identigene, Full Genomes, Genesis HealthCare, Karmagenes, MyHeritage, MapMyGenome, Living DNA and Pathway Genomics. Chief industry players implement numerous initiatives such as mergers, acquisitions and new product launch to maintain their market position. Receiving approvals from regulatory bodies for new products will also foster companys revenue share. For instance, in October 2018, 23andme received first U.S. FDA approval for de novotechnology utilized in pharmacogenomic tests. This approval will enable company to launch innovative products, thereby fostering companys growth.

Direct-to-Consumer (DTC) Genetic Testing Industry Viewpoint

Direct-to-consumer genetic testing industry can be traced back to early 2000s. Earlier DTC tests were thought to be convenient as they would allow the patients to access their genetic information without involvement of physician. Although, DTC genetic testing kits had several benefits, in the initial days, they were stringently regulated by regulatory bodies. Regulatory scenario has always been stringent since the introduction of DTC genetic kits in European countries. Currently, there has been change in the regulatory scenario and European countries have started receiving approval for DTC genetic kits. Defects in the DTC kits have been reduced and people have started relying on these kits. DTC genetic testing market is sort of matured in North America due to numerous technological advancements and is still in developing phase in Asian countries. With further advancements in technology, DTC genetic tests industry will experience numerous growth opportunitie

Key Insights Covered: Exhaustive Direct-to-Consumer Genetic Testing Market1. Market size (sales, revenue and growth rate) of Direct-to-Consumer Genetic Testing industry.2. Global major manufacturers operating situation (sales, revenue, growth rate and gross margin) of Direct-to-Consumer Genetic Testing industry.3. SWOT analysis, New Project Investment Feasibility Analysis, Upstream raw materials and manufacturing equipment & Industry chain analysis of Direct-to-Consumer Genetic Testing industry.4. Market size (sales, revenue) forecast by regions and countries from 2019 to 2025 of Direct-to-Consumer Genetic Testing industry.

Research Methodology: Direct-to-Consumer Genetic Testing Market

Looking for more? Check out our repository for all available reports on Direct-to-Consumer Genetic Testing in related sectors.

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Direct-to-Consumer Genetic Testing Market: Trends, Applications, Industry Competitive Analysis, Growth,Forecast: 2019 to 2029 - The News Brok

We're so close to eradicating polio. Here's why we need $1.5 billion more to finish the job.

By Ryan Hyland and Erin Biba

When was polio last in Europe? If you guessed 2002, the year the region was certified polio-free, youre wrong.

The last time polio affected a child in Europe was 2015. Two Ukrainian children were diagnosed with paralytic polio, and that likely means that many more were infected and didnt show symptoms. At least one Western news outlet deemed the outbreak crazy but the reality is that no place on Earth is safe from polio until the disease is eradicated everywhere.

Ukraine had fully vaccinated only 50 percent of its children against polio, and low immunization rates are a recipe for an outbreak. In this case, a rare mutation in the weakened strain used in the oral polio vaccine was able to spread because so many children had not been vaccinated. To stop it from progressing, the country needed to administer 6 million vaccines through an emergency program.

Rotary was there at the beginning of the global effort to eradicate polio, says International PolioPlus Committee Chair Michael K. McGovern. It would be unfortunate if Rotary isnt there at the finish line. Weve done too much; weve made too much progress to walk away before we finish.

Finding poliovirus outside Afghanistan, Nigeria, and Pakistan, the only countries that have yet to eradicate it, is not unusual. In 2014, just before the World Cup brought travelers from all over the planet to Brazil, poliovirus was detected in the sewage system at So Paulos Viracopos International Airport. Using genetic testing, officials traced its origin to Equatorial Guinea. Brazils regular vaccination efforts kept the disease from showing up beyond the airport doors.

Those are frustrating examples for the thousands of people around the world working to eradicate polio. The fight has come a long way, but it is far from over. And while many involved in the effort say we may detect the final naturally occurring case of polio this year, getting to that point and ensuring that the disease remains gone will continue to require money, hard work, and the support of Rotarians around the world.

Here are the steps needed to ensure polio is truly gone forever:

One of the most important aspects of the fight to eradicate polio is detection. This requires continuous surveillance that is complicated and costly. Polio surveillance consists of two parts. First, doctors and community health workers monitor children for acute flaccid paralysis. The second part of the process involves local authorities collecting samples from sewage systems or in places that don't have adequate sanitation facilities, including rivers or bodies of water near a large group of residents.

Ninety percent of people infected with the virus show no symptoms, and those who do usually have mild symptoms such as fever, fatigue, and headaches. Only one in every 200 cases of the illness results in paralysis, which means that for every child who is paralyzed, several hundred are carrying the disease and may not show it.

And not every case of paralysis is caused by polio. Other viruses that can cause the polio-like symptoms known as acute flaccid paralysis include Japanese encephalitis, West Nile, and Zika. To determine if a patient has polio, health workers must collect two stool specimens 14 days apart and send them to a lab for testing.

To find the patients who don't present symptoms or don't make it to a clinic, Rotary and its partners in the Global Polio Eradication Initiative (GPEI) --- composed of the World Health Organization, the U.S. Centers for Disease Control and Prevention (CDC), UNICEF, and the Bill & Melinda Gates Foundation --- have set up environmental sampling sites in the areas that are most susceptible to the disease.

Fifteen to 20 countries are still at high risk despite having eradicated the illness. Because the poliovirus is most easily detected, and most easily contracted, through stool, researchers take samples from sewage systems and, in places that don't have sewer infrastructure, from rivers and open gutters.

GPEI has developed a network of 145 laboratories around the world that can identify the disease, and Rotary has played a leading role in supporting these facilities.

But regular environmental surveillance is "logistically not so easy to do and it's relatively expensive. It adds a considerable burden to the labs to process the sewage samples," says Stephen Cochi, senior adviser to the director, Global Immunization Division, at the CDC. "It costs real money to keep that network operational, and this lab network is the most highly sophisticated, state-of-the-art infectious-disease network in the world. Rotarians should be proud of that --- it's the No. 1 network, bar none."

As part of this system of labs, Rotary has helped fund small, sophisticated local laboratories to track genetic variations of the disease. All viruses mutate to confuse the human immune system, but the poliovirus is notorious for doing so at a rapid rate.

One of these labs allowed Brazilian authorities to trace the virus at So Paulo airport to Equatorial Guinea more than 6,400 kilometers (4,000 miles) away.

Vigilance is key to successful surveillance, says Michel Zaffran, director of polio eradication at WHO. "This is a hidden cost to the program that people don't realize is absolutely necessary to maintain," he said.

The GPEI is providing surveillance in about 72 countries, RI President John F. Germ said at Rotary's World Polio Day event on 24 October 2016. "It's an expensive fight," he said.

The appearance of polio in Ukraine in 2015 is a perfect example of why continued vaccination campaigns are essential --- and not only in Afghanistan, Nigeria, and Pakistan. Large-scale vaccinations are enormous undertakings that require money as well as thousands of volunteers on the ground. And in places where the vaccination programs have been successful, the challenge is now to locate and vaccinate that small percentage of children who have been missed.

The vaccine itself isn't the biggest expense in a vaccination. It's the distribution of the vaccine --- transportation and staffing, for example --- that costs so much. In January, a grant from Rotary covered the costs of an Afghanistan vaccination campaign that involved more than 57,000 vaccinators, 3,100 vehicles, and 3,400 social mobilizers. In Niger, funds covered the cost of using 17 boats, 1,150 carts, 1,071 vehicles, and 1,530 motorbikes.

Funds also went to initiatives in Somalia to cover the cost of more than 400 micro-planning workshops, 13,800 vaccinator and announcer trainings, and the use of more than 1,700 vehicles.

"I think sometimes people don't realize the scale of what these immunization campaigns are actually like," McGovern says. "Rotary and its partners have administered 15 billion doses since 2000. We've immunized 2.5 billion kids. Repeatedly reaching the kids to raise their immunization levels is very personnel-intensive."

A vaccination campaign is almost mind-bogglingly complex. Rotarians' contributions pay for planning by technical experts, large-scale communication efforts to make people aware of the benefits of vaccinations and the dates of the campaign, and support for volunteers to go door-to-door in large cities as well as in remote areas that may not appear on any map.

It sometimes includes overcoming local distrust of government or outsiders and negotiating complicated religious doctrine. And it means trying to understand the movements of nomadic populations or people pushed out of their homes because of unrest.

Regardless of how they live their lives, each of these children must be vaccinated.

Even if the last case of polio is identified this year, a huge amount of work will remain to ensure that it stays gone, which means vaccinating children for at least three more years.

And the vaccine itself will have to change.

Today's oral vaccines contain a weakened live version of the virus, which is much more effective at protecting communities from outbreaks and is less expensive to manufacture and distribute.

The live-virus vaccine, which has reduced polio by more than 99.9 percent, can, rarely, mutate back to a virulent form.

So once the virus has been certified eradicated, all of the live-virus vaccine around the world will be destroyed and replaced with an injectable vaccine that does not contain the live virus. And polio vaccinations will become a part of routine immunization programs around the world.

Once the final case of polio is recorded, it will take at least three years to ensure that the last case is, in fact, the final one. All of the eradication activities will continue to need funding and volunteers through at least 2020.

"We are so close," says John Sever, vice chair of Rotary's International PolioPlus Committee, who has been part of the eradication effort since the beginning. "We've got a 99.9 percent reduction in polio. But we're not there yet. Rotarians and others have to keep working. People will naturally say, 'Well, it seems to be basically gone so let's move on to other things,' but the fact is it isn't gone, and if we move on and don't complete the job, we set ourselves up for having the disease come right back."

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Why Rotary is investing in zero and beyond - World - ReliefWeb

She's the oldest snake documented in a zoo, and now the Saint Louis Zoo says this ball python just laid eggs, despite not being with a male companion in 15 years

ST. LOUIS A snake at the Saint Louis Zoo pulled off what seems like an impossible feat. She laid eggs this summer despite not being with a male companion in more than a decade.

On Tuesday, the zoo announced a ball python laid eggs back on July 23 at the Charles H. Hoessle Herpetarium.

This snake is more than 50 years old and is the oldest snake documented in a zoo, the Saint Louis Zoo reported. Plus, she hasnt been with a male in more than 15 years.

The zoo explained this isnt unheard of. Plus, theres not just one way it could have happened but actually two.

Keepers at the zoo explained ball pythons can reproduce sexually and asexually, which means the snake wouldnt need a partner to produce the eggs. On top of that, snakes are known to store sperm to fertilize eggs at a later time.

Now the question is, which of the two explanations is the reason for the eggs? the Saint Louis Zoo asked on social media. Zoo staff members plan to find out.

Without genetic testing, Zoo staff won't know if this ball python reproduced sexually or asexually, but they intend to find out. As the keepers continue to incubate the eggs, they will be sending off samples for genetic testing, the zoo explained.

The Saint Louis Zoo shared a video of the ball python featuring photos of her wrapped around her eggs and staff members carefully examining them.

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50-year-old snake that hasn't been with a partner in 15 years just laid eggs - 11Alive.com WXIA

Global Newborn Genetic Testing Market 20202026: Industry Analysis, Growth Analysis, Price Analysis, And Trends

The comprehensive research report on theNewborn Genetic TestingMarketinfluences iterative and comprehensive research methodology to offer insights of the existing market scenario over the forecast timeframe. The report also delivers in-depth details about the growth and development trends that will have a major impact on the behavior of theNewborn Genetic Testingmarket in the approaching years. Furthermore, the report touches upon other key pointers such as the regional aspects and policies overriding the industry. Apart from this, the study highlights the COVID-19 pandemics effect on the revenue share and yearly growth rate of the market.

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The Newborn Genetic Testing market report has comprehensively provided information regarding the driving forces that have a huge impact on the market size. In addition, the dynamics of the industry are defined by studying the current and future trends of this industry vertical. Along with the competitive terrain even the regional landscape of the Newborn Genetic Testing market is provided. The vast research can be clearly seen through the market analysis that provides data associated with advantages and disadvantages of the products developed by the manufacturersSequenom, Agilent Technologies, Bio-Rad Laboratories, Illumina. Additionally, the entire evolution of the market dynamics along with the supply and demand chain of the product is presented in the research report. Furthermore, the market segmentation that is included in the report is{Techniques, Polymerase Chain Reaction (PCR), Fluorescence In-Situ Hybridization (FISH), Array-Comparative Genomic Hybridization (aCGH)}; {Clinics, Hospitals, Laboratories, Other}.

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Global Newborn Genetic Testing Market Forecast Revised in a New Market Research Store Report as COVID-19 Projected to Hold a Massive Impact on Sales...

New research shows that the novel coronavirus can essentially dice the muscle fibers of the human heart into pieces, sparking concerns about the potential for heart failure among Covid-19 survivors, Elizabeth Cooney reports for STAT News.

Resources to support your CV telehealth strategy

For the study, which was published preprint on bioRxiv and has not yet been peer reviewed, researchers added the new coronavirus, SARS-CoV-2, to three types of human heart cellscardiomyocytes, cardiac fibroblasts, and endothelial cellsthat were grown in lab dishes from stem cells.

Only the cardiomyocytes, which are muscle cells, showed indication of viral infection that spread to other muscle cells, the researchers said. However, what they found in the infected cells was remarkable: The sarcomeres, which are the long muscle fibers that keep the heart beating, had been sliced into small bits. According to the researchers, the fibers looked as if they had been surgically sliced.

The researchers also found black holes where DNA was supposed to be in the nucleus of the infected cells. The researchers said they found similar, but not identical, changes when they observed autopsy specimens from patients with Covid-19, the disease caused by the novel coronavirus.

It's unclear whether the heart is able to reassemble the sarcomeres after they're severed, but that might be possible after the coronavirus infection clears, the researchers said. However, the researchers said they felt an urgency to share their results as quickly as possible, because their findings may help to further scientists' understanding of how the coronavirus causes heart damagesand possibly how to prevent or treat the injuries.

"When we saw this disruption in those microfibers that was when we made the decision to pull the trigger and put out this preprint," Todd McDevitt, a senior investigator at Gladstone Institutes and a co-author of the study, said. "I'm not a scientist who likes to stoke these things [but] I did not sleep, honestly, while we were finishing this paper and putting it out there."

Bruce Conklin, also a senior investigator at Gladstone and a co-author of the study, said the virus caused "carnage in the human cells" unlike anything seen with other diseases. "Nothing that we see in the published literature is like this in terms of this exact cutting and precise dicing," he explained.

Conklin said the findings should alter the way providers and scientists think about the novel coronavirus and Covid-19. "We should think about this as not only a pulmonary disease, but also potentially a cardiac one."

Gregg Fonarow, interim chief of the UCLA Division of Cardiology and director of the Ahmanson-UCLA Cardiomyopathy Center, said the study is "really important and elegant work, helping to define the potential mechanisms by which SARS-CoV-2 is leading to the observed heart damage and clinical manifestations."

Sahil Parikh, an interventional cardiologist at Columbia University Irving Medical Center, called findings "provocative," but added, "[t]he challenge here is that this paper has not been peer-reviewed by people who are experts in cardiology, who have not had a chance to tear it apart." She said, "I am reluctant to make a lot out of a pre-publication manuscript, no matter how provocative the finding."

The researchers who worked on the study agreed that their work should be reviewed, and they've submitted the study to a leading scientific journal (Cooney, STAT News, 9/4).

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How the coronavirus causes 'carnage' in the heart - The Daily Briefing

Concerning heart failure (HF), the current COVID-19 pandemic is having a dramatic effect on the daily life of each individual, ranging from social distancing measures applied in most countries to getting severely diseased due to the virus. Cardiovascular Disease (CVD) is among the most common conditions in people that die of the infection. The burden of CVD accounts for over 60 million people in the EU alone, therefore, it is the leading cause of death in the world.

Although COVID-19 shows us the direct impact of a potential treatment for peoples health, CVD is a stealthy pandemic killer. HF is a chronic disease condition in which the heart is not able to fill properly or efficiently pump blood throughout your body, caused by different stress conditions including myocardial infarction, atherosclerosis, diabetes and high blood pressure. Several measures are commonly used to treat heart disease, such as lifestyle changes and medications like beta-blockers and ACE inhibitors, yet these typically only slow down the progression of the disease.

Biomedical research is exploring new avenues by combining scientific insights with new technologies to overcome chronic diseases like HF. Among the most appealing and promising technologies are the use of cardiac tissue engineering and extracellular vesicles-mediated repair strategies.

Upon an initial cell loss post-infarction, it is appealing to replace this massive loss in contractile cells for new cells and thereby not treating patients symptoms, but repairing the cause of the disease. Cardiac cell therapy has been pursued for many years with variable results in small initial trials upon injection into patients. Different cell types have been used to help the myocardium in need, but the most promising approaches aim to use induced pluripotent cells (iPS) from reprogrammed cells from the patient themselves that can be directed towards contractile myocardial cells. These cells in combination with natural materials, in which the cells are embedded in the heart, can be used for tissue engineering strategies (1). Together with different international partners, Sluijters team are trying to develop strategies to use these iPS-derived contractile cells for myocardial repair via direct myocardial injection (H2020-Technobeat-66724) or to make a scaffold that can be used as a personalised biological ventricular assist device (H2020-BRAV-874827). A combination of engineering and biology to mimic the native myocardium aims to replace the chronically ill tissue for healthy and well-coupled heart tissue that can enhance the contractile performance of the heart.

Recently, a Dutch national programme started, called RegMedXB, in which the reparative treatment of the heart is aimed to be performed outside the patients body. During the time the heart is outside the body; the patient is connected to the heart-lung machine, and after restoring function, it will be re-implanted. The so-called Cardiovascular Moonshot aims to create a therapy that best suits the individual patient, by having their heart beating in a bioreactor, outside the body. Although it sounds very futuristic, many small lessons will be learned to feet novel therapeutic insights.

The initial injection of stem cells did result in a nice improvement of myocardial performance. We have now learned that rather than these delivered cells helping the heart themselves, the release of small lipid carriers called extracellular vesicles (EVs) (2) from these cells occur. These EVs carry different biological molecules, including nucleotides, proteins and lipids, and are considered to be the bodies nanosized messengers for communication. The use of stem cell-derived EVs are now being explored as a powerful means to change the course of the disease. Via these small messengers, natural biologics are delivered to diseased cells and thereby help them to overcome the stressful circumstances. EVs carry reparative signals that can be transferred to the diseased heart and thereby change the course of heart disease in some patients.

Within the EVICARE program (3) (H2020-ERC-725229), Sluijters team are using stem cell-derived EVs to change the response of the heart to injury. Also, to understand which heart cells and processes are being affected, they use materials to facilitate a slow release of biomaterials over an extended period rather than a single dose, which is probably essential for a chronic disease like HF. For now, improved blood flow is the main aim but the team have seen other effects as well, such as cardiovascular cell proliferation (4) by which the heart cells themselves start to repair the organ.

The use of EVs basically aims to enhance the endogenous repair mechanisms of the heart. These natural carriers can be mimicked with synthetic materials, or used as a hybrid of the two, thereby creating an engineered nanoparticle, that is superior in the intracellular delivery of genetic materials. The possibility of loading different biological materials allows a further tuning of its effectiveness and use in different disease conditions, creating a new off-the-shelf delivery system for nanomedicine to treat cancer and CVD (H2020-Expert-825828).

As is true of the current COVID-19 pandemic, HF is also a growing chronic disease that affects millions of people worldwide. The chronic damaged myocardium needs reparative strategies in the future to lower the social burden for patients, but also to keep the economic consequences affordable. New scientific insights with cutting edge technological developments will help to address these needs of CVD patients and their families.

References

(1) Madonna R, Van Laake LW, Botker HE, Davidson SM, De Caterina R, Engel FB, Eschenhagen T, Fernandez-Aviles F, Hausenloy DJ, Hulot JS, Lecour S, Leor J, Menasch P, Pesce M, Perrino C, Prunier F, Van Linthout S, Ytrehus K, Zimmermann WH, Ferdinandy P, Sluijter JPG. ESC Working Group on Cellular Biology of the Heart: position paper for Cardiovascular Research: tissue engineering strategies combined with cell therapies for cardiac repair in ischaemic heart disease and heart failure. Cardiovasc Res. 2019 Mar 1;115(3):488-500.

(2) Sluijter JPG, Davidson SM, Boulanger, CM, Buzs EI, de Kleijn DPV, Engel FB, Giricz Z, Hausenloy DJ, Kishore R, Lecour S, Leor J, Madonna R, Perrino C, Prunier F, Sahoo S, Schiffelers RM, Schulz R, Van Laake LW, Ytrehus K, Ferdinandy P. Extracellular vesicles in diagnostics and therapy of the ischaemic heart: Position Paper from the Working Group on Cellular Biology of the Heart of the European Society of Cardiology. Cardiovasc Res. 2018 Jan 1;114(1):19-34.

(3) https://www.sluijterlab.com/extracellular-vesicle-inspired-ther

(4) Maring JA, Lodder K, Mol E, Verhage V, Wiesmeijer KC, Dingenouts CKE, Moerkamp AT, Deddens JC, Vader P, Smits, AM, Sluijter JPG, Goumans MJ. Cardiac Progenitor Cell-Derived Extracellular Vesicles Reduce Infarct Size and Associate with Increased Cardiovascular Cell Proliferation. J Cardiovasc Transl Res. 2019 Feb;12(1):5-17.

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Innovative treatments for heart failure - Open Access Government

A proficient data and brilliant forecasting techniques used in this Autologous Stem Cell and Non-Stem Cell Based Therapies Market report are synonymous with accurateness and correctness. The document is a meticulous analysis of existing scenario of the market, which covers several market dynamics. This market research report endows with the plentiful insights and business solutions that will support to stay ahead of the competition. The most precise way to forecast what future holds is to understand the trend today and hence Autologous Stem Cell and Non-Stem Cell Based Therapies Marketing report has been structured by chewing over numerous fragments of the present and upcoming market scenario.

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This Autologous Stem Cell and Non-Stem Cell Based Therapies Market report is the consequence of incessant efforts lead by clued-up forecasters, innovative analysts and bright researchers who indulge in detailed and attentive research on different markets, trends and emerging opportunities in the consecutive direction for the business needs. Company snapshot, geographical presence, product portfolio, and recent developments are taken into account for studying the company profiles that are part of this report. Quality and transparency has been strictly maintained while carrying out research studies to offer an exceptional market research report for a niche. A thoughtful knowledge of industrial unanimity, market trends and incredible techniques via this Autologous Stem Cell and Non-Stem Cell Based Therapies Market report gives an upper hand in the market.

TheGlobalAutologous Stem Cell and Non-Stem Cell Based Therapies Marketis expected to reach USD113.04 billion by 2025, from USD 87.59 billion in 2017 growing at a CAGR of 3.7% during the forecast period of 2018 to 2025. The upcoming market report contains data for historic years 2015 & 2016, the base year of calculation is 2017 and the forecast period is 2018 to 2025.

Some of the major players operating in the globalautologous stem cell and non-stem cell based therapies marketareAntria (Cro), Bioheart, Brainstorm Cell Therapeutics, Cytori, Dendreon Corporation, Fibrocell, Genesis Biopharma, Georgia Health Sciences University, Neostem, Opexa Therapeutics, Orgenesis, Regenexx, Regeneus, Tengion, Tigenix, Virxsys and many more.

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Market Definition:Global Autologous Stem Cell and Non-Stem Cell Based Therapies Market

In autologous stem-cell transplantation persons own undifferentiated cells or stem cells are collected and transplanted back to the person after intensive therapy. These therapies are performed by means of hematopoietic stem cells, in some of the cases cardiac cells are used to fix the damages caused due to heart attacks. The autologous stem cell and non-stem cell based therapies are used in the treatment of various diseases such as neurodegenerative diseases, cardiovascular diseases, cancer and autoimmune diseases, infectious disease.

According to World Health Organization (WHO), cardiovascular disease (CVD) causes more than half of all deaths across the European Region. The disease leads to death or frequently it is caused by AIDS, tuberculosis and malaria combined in Europe. With the prevalence of cancer and diabetes in all age groups globally the need of steam cell based therapies is increasing, according to article published by the US National Library of Medicine National Institutes of Health, it was reported that around 382 million people had diabetes in 2013 and the number is growing at alarming rate which has increased the need to improve treatment and therapies regarding the diseases.

Market Segmentation:Global Autologous Stem Cell and Non-Stem Cell Based Therapies Market

Major Autologous Stem Cell and Non-Stem Cell Based Therapies Market Drivers and Restraints:

Introduction of novel autologous stem cell based therapies in regenerative medicine

Reduction in transplant associated risks

Prevalence of cancer and diabetes in all age groups

High cost of autologous cellular therapies

Lack of skilled professionals

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Autologous Stem Cell and Non-Stem Cell Based Therapies Market Scope And Price Analysis 2020 | Major Giants Fibrocell, Genesis Biopharma, Georgia...

Abstract

Fibrosis, characterized by aberrant tissue scarring from activated myofibroblasts, is often untreatable. Although the extracellular matrix becomes increasingly stiff and fibrous during disease progression, how these physical cues affect myofibroblast differentiation in 3D is poorly understood. Here, we describe a multicomponent hydrogel that recapitulates the 3D fibrous structure of interstitial tissue regions where idiopathic pulmonary fibrosis (IPF) initiates. In contrast to findings on 2D hydrogels, myofibroblast differentiation in 3D was inversely correlated with hydrogel stiffness but positively correlated with matrix fibers. Using a multistep bioinformatics analysis of IPF patient transcriptomes and in vitro pharmacologic screening, we identify matrix metalloproteinase activity to be essential for 3D but not 2D myofibroblast differentiation. Given our observation that compliant degradable 3D matrices amply support fibrogenesis, these studies demonstrate a departure from the established relationship between stiffness and myofibroblast differentiation in 2D, and provide a new 3D model for studying fibrosis and identifying antifibrotic therapeutics.

Fibrosis is implicated in nearly 45% of all deaths in the developed world and plays a role in numerous pathologies, including pulmonary fibrosis, cardiac disease, atherosclerosis, and cancer (1). In particular, interstitial lung diseases, such as idiopathic pulmonary fibrosis (IPF), are fatal and incurable with a median survival of only 2 to 5 years (2). Often described as dysregulated or incessant wound healing, fibrosis involves persistent cycles of tissue injury and deposition of extracellular matrix (ECM) by myofibroblasts (MFs). These critical cellular mediators of fibrogenesis are primarily derived from tissue-resident fibroblasts (1). MFs drive eventual organ failure through excessive fibrous ECM deposition, force generation and tissue contraction, and eventual disruption of parenchymal tissue function (1). As organ transplantation remains the only curative option for late-stage disease, effective antifibrotic therapeutics that slow MF expansion or even reverse fibrosed tissue remain a major unmet clinical need. Undoubtedly, the limited efficacy of antifibrotic drugs at present underscores limitations of existing models for identifying therapeutics, the complexity of the disease, and an incomplete understanding of MF biology.

A strong correlation between lung tissue stiffening and worse patient outcomes suggests an important role for matrix mechanosensing in fibrotic disease progression (3). Preclinical models of fibrosis in mice have supported the link between tissue stiffening and disease progression. However, a precise understanding of how physical cues from the microenvironment influence MF differentiation in vivo is confounded by concurrent structural (e.g., collagen density and laminin/elastin degradation) and biochemical (e.g., matrix composition and inflammatory) changes to the microenvironment (4). Consequently, natural and synthetic in vitro tissue models have provided great utility for the study of MF mechanobiology. Seminal studies using natural type I collagen gels have elucidated the role of profibrotic soluble cues [e.g., transforming growth factor1 (TGF-1)] in promoting cell contractility, ECM compaction, and MF differentiation, and more recently, precision-cut lung slices, have emerged as a powerful tool to study the complexity of the pulmonary microenvironment in IPF (4, 5). However, their utility in identifying physical microenvironmental determinants of MF differentiation suffers from an intrinsic coupling of multiple biochemical and mechanical material properties (6). Rapid degradation kinetics (1 to 3 days) and resulting issues with material stability (1 to 2 weeks) further impede the use of natural materials for studying fibrogenic events and drug responses, which occur over weeks to months in in vivo models or years in patients (7, 8).

Synthetic hydrogels that are more resistant to cell-mediated degradation have provided a better controlled setting for long-term studies of disease-related processes (9). For example, synthetic hydrogel-based cell culture substrates with tunable stiffness have helped establish a paradigm for mechanosensing during MF differentiation in two-dimensions (2D), where compliant matrices maintain fibroblast quiescence in contrast to stiffer matrices that promote MF differentiation (10, 11). Extensive findings in 2D suggest a causal role for matrix mechanics (e.g., stiffness) during MF differentiation in vitro and potentially in human disease, but these models lack the 3D nature of interstitial spaces where fibrosis originates (12). The interstitium surrounding alveoli is structurally composed of two key components: networks of fibrous ECM proteins (namely, type I collagen fibers) and interpenetrating ground substance, an amorphous hydrogel network rich in glycosaminoglycans such as heparan sulfate proteoglycan. Mechanical cues from fibrotic ECM that promote MF differentiation may arise from changes to the collagen fiber architecture or the gel-like ground substance; whether matrix stiffness is a prerequisite for MF differentiation in 3D fibrous interstitial spaces remains unclear (13). Furthermore, the limited efficacy of antifibrotic therapies identified in preclinical and in vitro models of IPF motivates the development of 3D tissue-engineered systems with improved structural and mechanical biomimicry, relevant pharmacokinetics, and the potential to incorporate patient cells (9). Furthermore, recapitulating key features of the fibrotic progression in an in vitro setting that better approximates interstitial tissues could (i) improve our current understanding of MF mechanobiology and (ii) serve as a more suitable test bed for potential antifibrotic therapeutics.

Accordingly, here, we describe a microengineered pulmonary interstitial matrix that recapitulates mechanical and structural features of fibrotic tissue as well as key biological events observed during IPF progression. Design parameters of these engineered microenvironments were informed by mechanical and structural characterization of fibrotic lung tissue from a bleomycin mouse model. We then investigated the influence of dimensionality, matrix cross-linking/stiffness, and fiber density on TGF-1induced MF differentiation in our pulmonary interstitial matrices. Increased hydrogel cross-linking/stiffness substantially hindered MF differentiation in 3D in contrast to findings in 2D, while fibrotic matrix architecture (i.e., high fiber density) potently promoted fibroblast proliferation and differentiation into MFs. Long-term (21 days) culture of hydrogels with a fibrotic architecture engendered tissue stiffening, collagen deposition, and secretion of profibrotic cytokines, implicating fiber density as a potent fibrogenic cue in 3D microenvironments. Pharmacologic screening in fibrotic pulmonary interstitial matrices revealed matrix metalloproteinase (MMP) activity and hydrogel remodeling as a key step during 3D fibrogenesis, but not in traditional 2D settings. To explore the clinical relevance of our findings, we leveraged a multistep bioinformatics analysis of transcriptional profiles from 231 patients, highlighting increased MMP gene expression and enriched signaling domains associated with matrix degradation in patients with IPF. Together, these results highlight the utility of studying fibrogenesis in a physiologically relevant 3D hydrogel model, underscore the requirement of matrix remodeling in IPF, and establish a new platform for screening antifibrotic therapies.

To inform key design criteria for our pulmonary interstitial matrices, we began by characterizing mechanical properties of fibrotic interstitial tissue in a bleomycin-induced lung injury model in mouse. Nave C57BL/6 mice were intratracheally challenged with bleomycin to induce lung injury and subsequent fibro-proliferative repair, with saline-treated animals maintained as a control group. After 2 weeks, animals were sacrificed and lung tissue was dissected out, sectioned and stained, and then mechanically tested by atomic force microscopy (AFM) nanoindentation to map the stiffness of interstitial tissue surrounding alveoli. While single-dose bleomycin administration does not recapitulate human IPF, the fibro-proliferative response is well characterized and leads to MF differentiation, collagen deposition, and lung stiffening events that are reminiscent of what occurs in human disease over longer time scales. As previously documented (14), bleomycin treatment corresponded to an increase in the thickness of interstitial tissue regions surrounding alveoli, a structural change that occurred alongside matrix stiffening (Fig. 1, A and B); bleomycin-treated lungs had elastic moduli nearly fivefold greater than healthy control tissues. To generate synthetic hydrogels with elastic moduli tunable over this range, we functionalized a biocompatible and protein-resistant polysaccharide, dextran, with pendant vinyl sulfone groups amenable to peptide conjugation (termed DexVS; Fig. 1C). To permit cell-mediated proteolytic hydrogel degradation and thus spreading of encapsulated cells, we cross-linked DexVS with a bifunctional peptide (GCVPMSMRGGCG, abbreviated VPMS) primarily sensitive to MMP9 and MMP14, two MMPs implicated in fibrosis-associated matrix remodeling (15, 16). Tuning input VPMS cross-linker concentration yielded stable hydrogels spanning the full range of elastic moduli we measured by AFM nanoindentation of lung tissue (Fig. 1D). Additional functionalization with cell-adhesive moieties (CGRGDS, abbreviated RGD) facilitated adhesion of primary normal human lung fibroblasts (NHLFs) (Fig. 1E).

(A) Histological preparations of healthy control and bleomycin-treated murine lung tissue (n = 3 mice per group) stained for collagen by picrosirius red (scale bar, 100 m). (B) Youngs modulus of mouse lung tissue as measured by AFM nanoindentation, with data fit to the Hertz contact model to determine Youngs modulus (n = 3 mice per group, n = 50 indentations per group on n = 9 tissue sections). (C) Schematic of proteolytically sensitive, cell-adhesive DexVS-VPMS bulk hydrogels. (D) Youngs modulus determined by AFM nanoindentation of DexVS-VPMS hydrogels formed with different concentrations of VPMS cross-linker (n = 4 samples per group, n = 20 total indentations per group). (E and F) Representative images of F-actin (cyan), nuclei (yellow), and -SMA (magenta); image-based quantification of -SMA expression (left axis, magenta bars, day 9) and nuclear Ki67 (right axis, gray bars, day 5) in 2D and 3D (n = 4 samples per group, n = 10 fields of view per group, n > 50 cells per field of view; scale bars, 200 m). All data presented are means SDs with superimposed data points; asterisk denotes significance with P < 0.05 determined by one-way analysis of variance (ANOVA). AU, arbitrary units.

To confirm the role of matrix mechanics on cell proliferation and MF differentiation, we seeded patient-derived NHLFs on 2D DexVS protease-sensitive hydrogel surfaces varying in VPMS cross-linker density and resulting stiffness and stimulated cultures with TGF-1 to promote MF differentiation. In accordance with previous literature, we observed a stiffness-dependent stepwise increase in cell proliferation (day 5) and MF differentiation (day 9) as measured by Ki67 and -smooth muscle actin (-SMA) immunofluorescence, respectively (Fig. 1E) (11). As the influence of matrix elasticity on MF differentiation in 3D synthetic matrices has not previously been documented, we also encapsulated NHLFs in 3D within identical DexVS hydrogels. The opposing trend with respect to stiffness was noted for cells encapsulated in 3D; compliant (E = 560 Pa) hydrogels that limited -SMA expression in 2D plated cells instead exhibited the highest levels of MF differentiation in 3D (Fig. 1F). Decreasing proliferation and cell-cell contact formation as a function of increasing hydrogel stiffness were also noted in 3D matrices and may be one reason why rigid hydrogels limit differentiation in 3D. Similar findings have been reported for mesenchymal stem cells encapsulated in hyaluronic acid matrices, where compliant gels promoted stem cell proliferation and yes-associated protein (YAP) activity in 3D, yet inhibited YAP activity and proliferation in 2D (17). These results suggest that while stiff, cross-linked 2D surfaces promote cell spreading, proliferation, and MF differentiation, an equivalent relationship does not directly translate to 3D settings. High cross-linking and stiffness (E = 6.1 kPa) in 3D matrices sterically hinder cell spreading, proliferation, and the formation of cell-cell contacts, all well-established promoters of MF differentiation (18).

Cell-degradable synthetic hydrogels with elastic moduli approximating that of fibrotic tissue proved nonpermissive to MF differentiation in 3D. Although matrix cross-linking and densification of ground substance has previously been implicated in fibrotic tissue stiffening, remodeled collagenous architecture can also engender changes in tissue mechanics and may modulate MF development in IPF independently. To characterize the fibrous matrix architecture within healthy and fibrotic lung interstitium, we used second-harmonic generation (SHG) microscopy to visualize collagen microstructure in saline- and bleomycin-treated lungs, respectively. Per previous literature, saline-treated lungs contained limited numbers of micrometer-scale (~1-m-diameter) collagen fibers, primarily localized to the interstitial spaces supporting the alveoli (Fig. 2A) (19). In contrast, bleomycin-treated lungs had, on average, fourfold higher overall SHG intensity, with collagen fibers localized to both an expanded interstitial region and in disrupted alveolar networks. While no difference in fiber diameter was noted with bleomycin treatment, we did observe thick (~2- to 5-m) collagen bundles containing numerous individual fibers in fibrotic lungs, potentially arising from physical remodeling by resident fibroblasts (Fig. 2A and fig. S1). Given that typical synthetic hydrogels amenable to cell encapsulation (as in Fig. 1) lack fibrous architecture, we leveraged a previously established methodology for generating fiber-reinforced hydrogel composites (20). Electrospun DexVS fibers approximating the diameter of collagen fibers characterized by SHG imaging (fig. S1) were co-encapsulated alongside NHLFs in DexVS-VPMS hydrogel matrices, yielding a 3D interpenetrating network of DexVS fibers ensconced within proteolytically cleavable DexVS hydrogel (Fig. 2B). To recapitulate the adhesive nature of collagen and fibronectin fibers within interstitial tissues, we functionalized DexVS fibers with RGD to support integrin engagement and 3D cell spreading. While increasing the weight % of type I collagen matrices increases collagen fiber density and simultaneously increases hydrogel stiffness (fig. S2), our synthetic matrix platform enables changes to fiber density (0.0 to 5.0%) without altering mechanical properties assessed by AFM nanoindentation (Fig. 2C), likely due to the constant weight percentage of DexVS and VPMS cross-linker within the bulk hydrogel.

(A) SHG imaging of collagen microstructure within healthy and bleomycin-treated lungs on day 14, with quantification of average signal intensity (arrows indicate interstitial tissue regions adjacent to alveoli; n = 3 mice per group, n = 10 fields of view per group; scale bar, 100 m). (B) Schematic depicting polymer cross-linking and functionalization for generating fibrous DexVS hydrogel composites to model changes in fiber density within lung interstitial tissue ECM. (C) Images and intensity quantification of fluorophore-labeled fibers within composites varying in fiber density (n = 4 samples per group, n = 10 fields of view per group; scale bar, 100 m). Youngs modulus determined by AFM nanoindentation of fibrous composites formed with different concentrations of VPMS cross-linker (n = 4 samples per group, n = 20 measurements per group). (D) Representative high-resolution images of NHLFs on day 1 in fibrous composites formed with bulk hydrogels (12.5 mM VPMS) functionalized with integrin ligand arginylglycylaspartic acid (RGD) or heparin-binding peptide (HBP) [F-actin (cyan), nuclei (yellow), and DexVS fibers (magenta); scale bar, 50 m]. Quantification of fiber recruitment as measured by contact between cells and DexVS fibers (n = 10 fields of view per group, n > 25 cells analyzed). (E) Representative high-resolution images of NHLF on day 1 fibrous composites formed with bulk hydrogels functionalized with integrin ligand RGD or HBP [F-actin (cyan), fibronectin (yellow), and DexVS fibers (magenta); scale bar, 5 m]. Quantification of fibronectin deposition into tshe hydrogel matrix as measured by immunostain intensity (n = 10 fields of view per group, n > 25 cells analyzed). All data presented are means SDs with superimposed data points; asterisk denotes significance with P < 0.05 determined by one-way ANOVA or Students t test, where appropriate; NS denotes nonsignificant comparison.

Beyond recapitulating the multiphase structural composition of interstitial ECM, we also sought to mimic the adhesive ligand presentation and protein sequestration functions of native interstitial tissue. More specifically, the gel-like ground substance within fibrotic tissue intrinsically lacks integrin-binding moieties and is increasingly rich in heparan sulfate proteoglycans, primarily serving as a local reservoir for nascent ECM proteins, growth factors, and profibrotic cytokines. In contrast, synthetic hydrogels are often intentionally designed to have minimal interactions with secreted proteins and require uniform functionalization with a cell-adhesive ligand to support cell attachment and mechanosensing. We hypothesized that RGD-presenting fibers alone would support cell spreading (20), enabling the use of a nonadhesive bulk DexVS hydrogel functionalized with heparin-binding peptide (HBP; CGFAKLAARLYRKAG) (21). While both RGD- and HBP-functionalized bulk DexVS gels supported cell spreading upon incorporation of RGD-presenting fibers, HBP-functionalized hydrogels encouraged matrix remodeling in the form of cell-mediated fiber recruitment (Fig. 2D) and enhanced the deposition of fibronectin fibrils into the adjacent matrix (Fig. 2E). Given the multiphase structure of lung interstitium, changes in collagen fiber density noted with fibrotic progression, and the importance of physical and biochemical matrix remodeling to fibrogenesis, we used HBP-tethered 560-Pa DexVS-VPMS bulk hydrogels with tunable density of RGD-presenting fibers in all subsequent studies.

We next investigated whether changes in fiber density reflecting fibrosis-associated alterations to matrix architecture could influence MF differentiation in our 3D model. NHLFs were encapsulated in compliant DexVS-VPMS hydrogels ranging in fiber density (E = 560 Pa, 0.0 to 5.0 volume % fibers). Examining cell morphology after 3 days of culture, we noted increased cell spreading (Fig. 3, A and B) and evident F-actin stress fibers (fig. S3) in fibrous conditions compared to nonfibrous controls. Increased frequency of direct cell-cell interactions was also observed as a function of fiber density, as evidenced by higher area:perimeter ratios and the number of fibroblasts per contiguous multicellular cluster (Fig. 3A and fig. S3). As evidenced by changes in the ratio of nuclear to cytosolic YAP localization, we detected changes in mechanosensing as a function of fiber density, with the highest nuclear ratio measured in samples containing the highest fiber density examined. Given that nuclear YAP activity (a transcriptional coactivator required for downstream mechanotransduction) has been implicated as a promoter of MF differentiation (22), we also assayed other markers associated with fibroblast activation. With increases in fiber density, we found significant increases in cell proliferation and local fibronectin deposition (Fig. 3, A and B). Luminex quantification of cytokine secretion at this time point revealed elevated secretion of inflammatory and profibrotic cytokines (Fig. 3C), suggesting that matrix fibers may modulate the soluble milieu known to regulate the response to tissue damage and repair in vivo (2325). While no -SMA expression or collagen deposition was observed at this early time point, F-actin stress fibers, YAP activity, and fibronectin expression have been previously established as proto-MF markers in vivo (26), suggesting that physical interactions with matrix fibers prime fibroblasts for activation into MFs. Supplying the profibrotic soluble factor TGF-1 prompted increases in the expression of various profibrotic YAP-target genes (ACTA2, COL1A1, FN1, CD11, and CTGF) relative to nonfibrous (FD 0.0%) controls at day 5 (Fig. 3D). Together, these data suggest that heightened fiber density promotes a fibrotic phenotype (Fig. 3, A to C) and gene expression (Fig. 3D), despite the absence of a stiff surrounding hydrogel.

(A) Immunofluorescence images of NHLFs in hydrogel composites over a range of fiber densities after 3 days of culture [F-actin (cyan), fibronectin (FN, yellow), YAP (magenta), Ki67 (white), and nuclei (blue); scale bars, 100 m (F-actin), 20 m (FN), 20 m (YAP), and 100 m (Ki67/nuclei)]. (B) Corresponding image-based quantification of cell area, deposited FN, YAP nuclear to cytosolic ratio, and % of proliferating cells (n = 4 samples per group; for cell spread area analysis, n > 50 cells per group; for FN, YAP, and Ki67 analyses, n = 10 fields of view per group and n > 25 cells per field of view). (C) Cytokine secretion into culture medium on day 3 (all data were normalized to background levels in control medium, n = 4 samples per condition). (D) Expression of MF-related genes in NHLFs stimulated with TGF-1 on day 3, in either highly fibrous (FD 5.0%) or nonfibrous (FD 0.0%) hydrogels (data presented are GAPDH-normalized fold changes relative to NHLFs within an FD 0% hydrogel lacking TGF-1 supplementation). All data presented are means SDs with superimposed data points; asterisk denotes significance with P < 0.05 determined by one-way ANOVA or Students t test where appropriate.

To explore whether fibrotic matrix cues in the form of heightened fiber density could promote 3D MF differentiation over longer-term culture, NHLFs were encapsulated within hydrogels varying in fiber density and maintained in medium supplemented with TGF-1 beginning on day 1. Immunofluorescent imaging and cytokine quantification were performed on days 3, 5, 7, and 9 to capture dynamic changes in cellular phenotype and secretion, respectively. No -SMApositive stress fibers or changes in total cytokine secretion were observed on day 3 or 5. On day 7, we noted the sparse appearance of -SMApositive cells alongside increased total cytokine secretion (Fig. 4D) in FD 5.0% conditions containing TGF-1, indicating the beginning of a potential phenotypic shift. Extensive MF differentiation (designated by -SMApositive cells) and a sixfold increase in total cytokine secretion occurred rapidly between days 7 and 9 (Fig. 4, B, D, and E) in the highest fiber density (FD 5.0%) condition. Despite the high proliferation within high fiber density hydrogels (Fig. 4C), -SMApositive cells were not evident in samples lacking exogenous TGF-1 supplementation. Moreover, -SMApositive cells were also absent in TGF-1 supplemented conditions that lacked fibrous architecture, indicating a requirement for both soluble and physical fibrogenic cues in 3D. Furthermore, inhibiting integrin engagement by incorporating fibers lacking RGD also abrogated MF differentiation and proliferation despite the presence of TGF-1 (Fig. 4, A and B), suggesting that a fibrotic matrix architecture drives -SMA expression primarily through integrin engagement and downstream mechanosensing pathways. These results were replicated with primary human dermal fibroblasts and mammary fibroblasts, where similar trends with -SMA expression as a function of fiber density were observed (fig. S4). While high fiber density promoted proliferation in dermal fibroblasts, mammary fibroblasts underwent MF differentiation in the absence of higher proliferation rates, demonstrating intrinsic differences between cell populations originating from different tissues. Nevertheless, these results suggest that fibrotic matrix architecture may be promoting MF differentiation in other pathologies, namely, dermal scarring in systemic sclerosis and desmoplasia in breast cancer.

(A) Representative immunofluorescence images of NHLFs in microenvironmental conditions leading to low (top row) or high (bottom row) MF differentiation after 9 days in culture [-SMA (magenta) and nuclei (cyan); n = 4 samples per group, n = 10 fields of view per group, and n > 50 cells per field of view; scale bar, 200 m], with corresponding image-based quantification in (B) and (C). Insets depict representative fiber densities. (D) Measurement of total cytokine secretion over time as a function of fiber density (n = 4 samples per condition; * indicates significant differences between FD 5.0% and all other groups at a given time point; NS denotes nonsignificant comparison). (E) Secretion of specific cytokines and chemoattractants as a function of fiber density on day 9 (n = 4 samples per condition). (F) Representative images and quantification of tissue contraction within day 14 fibroblast-laden hydrogels of varying fiber density (n = 4 samples per group, dashed line indicates initial diameter of 5 mm). Photo credit: Daniel Matera, University of Michigan. (G) AFM measurements of day 14 fibroblast-laden hydrogels of varying fiber density (n = 20 measurements from n = 4 samples per group). Dashed line indicates original hydrogel stiffness. (H) SHG images of fibrous collagen within fibroblast-laden hydrogels after 21 days of culture in medium supplemented with ascorbic acid (scale bar, 100 m). (I) Measurement of total collagen content within digested DexVS hydrogels at day 21 as measured by biochemical assay (n = 4 samples per group). All data presented are means SDs with superimposed data points; asterisk denotes significance with P < 0.05 determined by one-way ANOVA; NS denotes nonsignificant comparison.

While proliferation and -SMA expression are accepted markers of activated fibroblasts, fibrotic lesions contribute to patient mortality through airway inflammation, collagen secretion, tissue contraction, and lung stiffeningpathogenic events that hinder the physical process of respiration (27). Luminex screening of 41 cytokines and chemokines within hydrogel supernatant revealed elevated total cytokine secretion as a function of fiber density over time (Fig. 4D), many of which were soluble mediators known to regulate airway inflammation (Fig. 4E) (23). Numerous other cytokines were additionally secreted at day 9 but did not change as a function of fiber density despite differences in cell number at this time point (fig. S5), suggesting that cell number alone cannot account for the increased cytokine secretion in high fiber density conditions. By generating free-floating hydrogels that allow contraction over time, we also examined macroscale changes in tissue geometry. Consistent with the influence of fiber density on -SMA expression, hydrogels containing high fiber densities underwent greater hydrogel contraction compared to nonfibrous or low fiber density conditions (Fig. 4F). Day 14 fibrotic hydrogels (FD 5.0%) were also fourfold stiffer (2.0 versus 0.5 kPa) as measured by AFM nanoindentation (Fig. 4G) compared to conditions that yielded low rates of MF differentiation in shorter-term studies (i.e., FD 0.0 or FD 0.5% in Fig. 4, A and B). When medium was supplemented with ascorbic acid to permit procollagen hydroxylation, collagen deposition into the surrounding matrix was evident by SHG microscopy by day 21 in high fiber density hydrogels (Fig. 4H) as compared to nonfibrous controls. Further biochemical analysis of hydrogel collagen content confirmed a stepwise increase in collagen production as a function of fiber density (Fig. 4I). Together, these findings demonstrate a clear influence of fiber density on MF differentiation and phenotype in 3D and furthermore suggest that this in vitro model recapitulates key pathogenic events associated with the progression of fibrosis in vivo.

Having established microenvironmental cues that promote robust 3D MF differentiation, we next evaluated the potential of our fibrous hydrogel model for use as an antifibrotic drug screening platform. Nintedanib, a broad-spectrum receptor tyrosine kinase inhibitor, and pirfenidone, an inhibitor of the mitogen-activated protein kinase (MAPK)/nuclear factor B (NF-B) pathway, were selected due to their recent Food and Drug Administration approval for use in patients with IPF (28). We also included dimethyl fumarate, an inhibitor of the YAP/TAZ pathway clinically approved for treatment of systemic sclerosis, and marimastat, a broad-spectrum MMP inhibitor that has shown efficacy in murine preclinical models of fibrosis (29, 30). We generated fibrotic matrices (560-Pa DexVS-VPMS-HBP bulk hydrogels containing 5.0 volume % DexVS-RGD fibers) that elicited the highest levels of MF differentiation, matrix contraction, and collagen secretion in our previous studies (Fig. 4). As a comparison to the current standard for high-throughput compound screening, we also seeded identical numbers of NHLFs on 2D tissue culture plastic in parallel. Cultures were stimulated with TGF-1 on day 1, and pharmacologic treatments were added on day 3, following extensive fibroblast spreading, cell-cell junction formation, and proliferation (Fig. 3A).

As in our earlier studies, TGF-1 supplementation promoted proliferation and -SMA expression within 3D constructs as well as on rigid tissue culture plastic (Fig. 5A). Nintedanib and pirfenidone had differential effects on NHLFs depending on culture format; NHLFs on 2D tissue culture plastic were resistant to pirfenidone/nintedanib treatment with no difference in proliferation or -SMA expression relative to vehicle controls, whereas modest but significant decreases in -SMA expression (pirfenidone and nintedanib) and proliferation (nintedanib) were detected in 3D (Fig. 5, A to E). Combined treatment with pirfenidone and nintedanib provided an antifibrotic effect only in fibrotic matrices, supporting ongoing clinical studies exploring their use as a combinatorial therapy (ClinicalTrials.gov identifier NCT03939520). Dimethyl fumarate abrogated cell proliferation and -SMA expression across all conditions, suggesting that inhibition of downstream mechanosensing inhibits MF differentiation in both 2D and 3D contexts in support of the general requirement for mechanosensing during MF differentiation independent of culture substrate (11). Inhibition of YAP activity in vivo has been shown to mitigate fibrosis and may be an advantageous therapeutic target (22). Blockade of MMP activity via marimastat treatment proved ineffectual in reducing -SMA expression or proliferation on 2D tissue culture plastic, but surprisingly fully abrogated the proliferation and differentiation response in 3D fibrotic matrices (Fig. 5, A to E). Given the role of protease activity in tissue remodeling in vivo (30) and in cellular outgrowth within 3D hydrogels (17, 31), our data suggest that degradative matrix remodeling is a requirement for MF differentiation in 3D, but not in more simplified 2D settings. To summarize, multiple antifibrotic agents (pirfenidone, nintedanib, dimethyl fumarate, and marimastat) demonstrating efficacy in clinical literature elicited an antifibrotic effect in our engineered fibrotic pulmonary interstitial matrices, but not in the 2D tissue culture plastic contexts traditionally used for compound screening.

(A) Representative confocal images stained for -SMA (magenta), F-actin (cyan), and nuclei (yellow) of NHLFs after 9 days of culture on tissue culture plastic (TCP) (top row) or 3D fibrotic matrices (bottom row) with pharmacologic treatment indicated from days 3 to 9 (scale bar, 100 m). Imaged regions were selected to maximize the number of -SMA+ cells per field of view within each sample. (B) Quantification of -SMA and (C) total cell count within 2D NHLF cultures. (D) Quantification of -SMA and (E) total cell count within 3D fibrotic matrices (n = 4 samples per group, n = 10 fields of view per group, and n > 50 cells per field of view). All data presented are means SDs with superimposed data points; asterisk denotes significance with P < 0.05 determined by one-way ANOVA; NS denotes nonsignificant comparison.

As the protease inhibitor marimastat fully ablated TGF-1induced -SMA expression and proliferation in our 3D fibrotic matrices, we leveraged bioinformatics methodologies to investigate the role of matrix proteases in patients with IPF on a network (Reactome) and protein (STRING) basis. Differential expression analysis of microarray data within the National Center for Biotechnology Information (NCBI) Gene Expression Omnibus (GEO) (dataset #GSE47460) was used to generate an uncurated/unbiased dataset composed of the top 1000 differentially regulated genes in IPF, revealing MMP1 as the most up-regulated gene in patients with IPF, with other matrix proteases (MMP1, MMP3, MMP7, MMP9, MMP10, MMP11, and MMP12) and matrix remodeling proteins (COL1A2, LOX, ACAN, DCN, and HS6ST2) similarly up-regulated (Fig. 6B, table S1, and data file S1). To focus on genes associated with MF differentiation for subsequent analyses, we performed Gene Ontology (GO) term enrichment (via GEO2R) to compile a curated dataset containing 188 key genes associated with MF differentiation (data file S1) and used Reactome and STRING analyses to investigate network signaling within both the uncurated and curated datasets. Analyses revealed 103 (uncurated) and 89 (curated) enriched signaling pathways in IPF (data file S1). The top 3/5 (uncurated) and 5/5 (curated) significantly enriched pathways in IPF involved matrix degradation and remodeling (Fig. 6C). Subsequent STRING protein-protein interaction analysis of datasets revealed that top signaling nodes were MMPs (uncurated: MMP1 and MMP3; Fig. 6D), fibrous collagens (uncurated: COL1A2 and COL3A1), or cytokines (curated: IL6, VEGFA, IL1B, and IGF1; Fig. 6D) known to increase MMP expression in fibroblasts (3235). These results emphasize the interdependence between MMP activity and systems-level pathogenic signaling in IPF and, in combination with our 3D drug screening results, highlight fibroblast-specific protease activity as a potential therapeutic target. Furthermore, given that protease inhibition had no effect on MF differentiation in 2D culture, these data also support the growing sentiment that simplified 2D screening models may be masking the identification of potentially viable antifibrotics.

(A) Schematic representation of bioinformatics workflow: Whole-genome transcriptomes from 91 healthy and 140 patients with lung fibrosis were fetched from the NCBI GEO. Differential expression analysis was used to assemble an uncurated list of the top 1000 differentially expressed genes. GO enrichment of choice biological pathways was used to assemble a curated list of genes associated with MF differentiation. Datasets were fed through a previous knowledgebased analysis pipeline to identify enriched signaling pathways (Reactome) and key protein signaling nodes (STRING) within patients with IPF. (B) Heatmaps of the top 20 differentially expressed genes within specified GO categories, which were manually selected for curated analysis. CN values indicate a high degree of interaction between proteins selected for curated analysis. Colors are based on differential expression values that were not log-normalized. (C) Summary of the top 5 significantly enriched pathways in the curated and uncurated gene set. (D) Representative STRING diagram depicting protein interactions within the curated dataset, with summary of the top 5 signaling nodes in the uncurated and curated gene set. Blue nodes and edges represent interactions within the top 5 signaling nodes for the curated dataset.

Despite fibrosis widely contributing to mortality worldwide, inadequate understanding of fibrotic disease pathogenesis has limited the development of efficacious therapies (12). Preclinical studies in vivo, while indispensable, often fail to translate to clinical settings as evidenced by the failure of ~90% of drugs identified in animal studies (36). In addition, limitations in current technologies (e.g., the embryonic lethality of many genetic ECM knockouts and the limited resolution/imaging depth of intravital microscopy) have hindered the application of preclinical in vivo models for the study of cell-ECM interactions that underlie fibrogenesis (37). In contrast, existing in vitro models use patient-derived cells that are affordable, scalable, and amenable to microscopy, but often fail to recapitulate the complex 3D matrix structure of the interstitial tissue regions where fibrotic diseases such as IPF originate. We leveraged electrospinning and bio-orthogonal chemistries to engineer novel pulmonary interstitial matrices that are 3D and have fibrous architecture with biomimetic ligand presentation. In the presence of profibrotic soluble factors, these settings reproduce hallmarks of fibrosis at cellular and tissue levels (Figs. 2 to 4). Examining the influence of physical microenvironmental cues (cross-linking/stiffness and fiber density) on MF differentiation, we find that cross-linking/stiffness has opposing effects on MF differentiation in 2D versus 3D (Fig. 1) and that incorporation of a fibrous architecture in 3D is a prerequisite to MF differentiation (Fig. 4). Furthermore, supported by the importance of protease signaling in IPF (Fig. 6), we performed proof-of-concept pharmacologic screening within our 3D fibrotic matrices (Fig. 5) and highlighted enhanced biomimicry as compared to traditional 2D drug screening substrates where matrix remodeling appears to be dispensable for MF differentiation.

While tunable synthetic hydrogels have identified mechanosensing pathways critical to MF differentiation in 2D, these observations have yet to be translated to 3D fibrous settings relevant to the interstitial spaces where fibrosis originates. Given that late-stage IPF progresses in the absence of external tissue damage, current dogma implicates fibrotic matrix stiffness as the continual driver of MF differentiation in vivo (10, 11, 38). While we cannot disregard this hypothesis, our work elucidates a contrasting MMP-dependent mechanism at play in 3D, whereby a compliant, degradable, and fibrous matrix architecture supports MF differentiation, with matrix contraction and stiffening occurring downstream of -SMA expression, nearly a week later. Given numerous 2D studies indicating matrix stiffness as a driver of MF differentiation, the finding that a compliant matrix promotes MF differentiation may appear counterintuitive (10, 11). However, MF accumulation has been documented before tissue stiffening in human disease (3), and a recent phase 2 clinical trial (ClinicalTrials.gov Identifier: NCT01769196) targeting the LOX pathway (the family of enzymes responsible for matrix stiffening in vivo) failed to prevent disease progression in patients with IPF and was terminated due to lack of efficacy (39). Furthermore, compelling recent work by Fiore et al. (3) combined immunohistochemistry with high-resolution AFM to characterize human IPF tissue mechanics and found that regions of active fibrogenesis were highly fibrous but had a similar Youngs modulus as healthy tissue. In concert with our in vitro data, these findings suggest that MF differentiation is possible within soft provisional ECM in vivo and that the initiation of fibrogenesis may not be dependent on heightened tissue stiffness so long as matrix fibers and appropriate soluble cues (e.g., TGF-1) are present.

Consequently, understanding the source of profibrotic soluble cues in vivo is of critical importance when identifying therapeutic targets for IPF. Luminex screening of supernatant from 3D fibrotic matrices revealed sixfold increases in cytokine secretion during fibrogenesis, most of which were potent inflammatory factors [e.g., granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-6 (IL-6), IL-8, and vascular endothelial growth factor A (VEGF-A)] and chemoattractants (e.g., CCL2, CCL7, CCL11, and CXCL1) (Fig. 4E). Furthermore, IL-6 and VEGF-A were found to be major signaling nodes in patients with IPF (Fig. 6D). While not typically regarded as an immunomodulatory cell population, these findings suggest that MFs may maintain localized inflammation to support continual fibrogenesis. Mitogens such as IL-6 and IL-8 promote endothelial- and epithelial-to-mesenchymal transition, a process that gives rise to matrix-producing MF-like cells in IPF (40). CCR2 (CCL2 and CCL7) and CXCR1 (CXCL1 and IL-8) ligation facilitates macrophage chemotaxis, potentially leading to a sustained influx of TGF-1producing cells in IPF, and glycoproteins such as GM-CSF inhibit caspase activity in mononuclear cells, potentially preventing apoptotic events required for the resolution of wound repair and return to homeostasis (23, 41). In addition, secretion of nearly all cytokines was increased as a function of fiber density, highlighting a potential feed-forward loop distinct from canonical TGF-1 signaling. Further model development (e.g., coculture platforms) will be required to examine these hypotheses and the role of MF-derived cytokines in persistent inflammation and fibrosis.

In addition to documenting the role of fibrotic matrix architecture in 3D fibrogenesis, we demonstrate proof-of-concept pharmacologic screening within our synthetic pulmonary interstitial matrices and highlight their improved relevance to human disease. Previous work in vitro has documented profound reductions in MF differentiation after treatment with clinically approved antifibrotics (pirfenidone and nintedanib), whereas in the clinic, pirfenidone and nintedanib impede disease progression but are far from curative (4, 28, 42, 43). Pirfenidone or nintedanib had insignificant effects in 2D settings in our hands and only modest effects in 3D (Fig. 5). One reason for this discrepancy may be the use of supraphysiologic pirfenidone and nintedanib concentrations in previous in vitro studies, whereas we selected dosages based on plasma concentrations in patients with IPF (44). Differences in pharmacokinetics, nutrient/growth factor diffusion, and cell metabolism between 2D and 3D tissue constructs likely also play a role. Furthermore, as evidenced by the preventative effect of the protease inhibitor marimastat in 3D hydrogels but not 2D settings (Fig. 5), pharmacologics that influence matrix degradation and remodeling are likely to have a minimized effect in 2D settings due to the less dynamic nature of tissue culture plastic and flat hydrogels (45). Nintedanib and pirfenidone have been shown to influence protease activity and matrix remodeling in vivo (16), and may be mediating their effects within fibrotic matrices through modulation of ECM remodeling. Given the identification of numerous potential antifibrotic agents (microRNA, TGF-1 inhibitors, IL-4, IL-13 neutralizing antibodies, and integrin blockers) in preclinical models, application of the system described here could elucidate how choice pharmacologics affect MF differentiation and matrix remodeling processes that are difficult to recapitulate in 2D culture. Further development of our interstitial matrices as an arrayed platform, as has been elegantly implemented with collagen matrices (42), is a critical next step to moving this technology toward high-throughput screening applications.

It is important to note that this work has several potential limitations. Our material approach allows facile control of initial microenvironmental conditions (e.g., dimensionality, fiber density, ligand density, and elastic modulus), and of note, composites of RGD-bearing nondegradable fibers and degradable bulk hydrogel decouple degradation-induced changes in matrix mechanics and ligand availability. However, we have no experimental control over subsequent dynamic cell-driven remodeling events (e.g., MMP-mediated hydrogel softening, fibronectin and collagen deposition, and hydrogel contraction/stiffening from resident cells) that likely affect local matrix mechanics, cellular mechanosensing, and MF differentiation. Exciting recent technologies such as 3D traction force microscopy (TFM) and magnetic bead microrheology could enable future examination of how these dynamic changes in cell-scale mechanics potentiate MF differentiation in 3D. Along similar lines, although our study suggests a requirement for initial adhesion to the surrounding matrix, how the dynamics of ligand presentation due to matrix remodeling regulates mechanosensing was not explored here. We present this platform as a reductionist approach to modeling the activation of fibroblasts within the 3D fibrous interstitia associated with fibrosis, a pathology that develops over years in vivo and involves multiple cell types. Human pulmonary tissue and fibrotic foci, in particular, also have viscoelastic and nonlinear mechanical behaviors (3, 46) that were not explored in our AFM measurements of murine lung or hydrogel composites. Given the important role such mechanical features can play in ECM mechanosensing, incorporating new synthetic material strategies in combination with cell-scale mechanical measurements will be essential to modeling physiologic complexity. Given that the development of lung organoids is still in its infancy, decellularized precision-cut lung slices currently represent the best culture platform to capture the full complexity of the lung microenvironment (5).

In summary, we designed a tunable 3D and fibrous hydrogel model that recapitulates dynamic physical (e.g., stiffening and contraction) and biochemical (e.g., secretion of fibronectin, collagen, and cytokines) alterations to the microenvironment observed during the progression of IPF. Implementation of our model allowed us to establish a developing mechanism for MF differentiation in 3D compliant environments, whereby cell spreading upon matrix fibers drives YAP activity, cytokine release, and proteolysis-dependent MF differentiation. Furthermore, we leveraged bioinformatics techniques to explore protease signaling in clinical IPF and, in concert with our therapeutic screening data, establish a strong role for proteases during IPF pathogenesis and in 3D MF differentiation. Whether protease activity promoted MF differentiation directly through modulation of intracellular signaling or indirectly through affects on the local matrix environment has yet to be explored in these settings but will be the focus of future efforts. Consequently, these results highlight critical design parameters (3D degradability and matrix architecture) frequently overlooked in established synthetic models of MF differentiation. Future work incorporating macrophages, endothelial cells, and epithelial cells may expand current understanding of how developing MF populations influence otherwise homeostatic cells and how matrix remodeling influences paracrine signaling networks and corresponding drug response. Given the low translation rate of drugs identified in high-throughput screening assays, we show that the application and development of engineered biomimetics, in combination with preclinical models, can improve drug discovery and pathophysiological understanding.

All reagents were purchased from Sigma-Aldrich and used as received, unless otherwise stated.

Dextran vinyl sulfone. A previously described protocol for vinyl sulfonating polysaccharides was adapted for use with linear highmolecular weight (MW) dextran (MW 86,000 Da; MP Biomedicals, Santa Ana, CA) (20). Briefly, pure divinyl sulfone (12.5 ml; Thermo Fisher Scientific, Hampton, NH) was added to a sodium hydroxide solution (0.1 M, 250 ml) containing dextran (5 g). This reaction was carried out at 1500 rpm for 3.5 min, after which the reaction was terminated by adjusting the pH to 5.0 via the addition of hydrochloric acid. A lower functionalization of DexVS was used for hydrogels, where the volume of divinyl sulfone reagent was reduced to 3.875 ml. All reaction products were dialyzed for 5 days against Milli-Q ultrapure water, with two water exchanges daily, and then lyophilized for 3 days to obtain the pure product. Functionalization of DexVS was characterized by 1H nuclear magnetic resonance (NMR) spectroscopy in D2O and was calculated as the ratio of the proton integral [6.91 parts per million (ppm)] and the anomeric proton of the glucopyranosyl ring (5.166 and 4.923 ppm); here, vinyl sulfone/dextran repeat unit ratios of 0.376 and 0.156 were determined for electrospinning and hydrogel DexVS polymers, respectively.

DexVS was dissolved at 0.6 g ml1 in a 1:1 mixture of Milli-Q ultrapure water and dimethylformamide with 0.015% Irgacure 2959 photoinitiator. Methacrylated rhodamine (0.5 mM; Polysciences Inc., Warrington, PA) was incorporated into the electrospinning solution to fluorescently visualize fibers under 555 laser. This polymer solution was used for electrospinning within an environment-controlled glovebox held at 21C and 30% relative humidity. Electrospinning was performed at a flow rate of 0.3 ml hour1, gap distance of 5 cm, and voltage of 10.0 kV onto a grounded collecting surface attached to a linear actuator. Fiber layers were collected on glass slabs and primary cross-linked under ultraviolet light (100 mW cm2) and then secondary cross-linked (100 mW cm2) in an Irgacure 2959 solution (1 mg ml1). After polymerization, fiber segments were resuspended in a known volume of phosphate-buffered saline (PBS) (typically 3 ml). The total volume of fibers was then calculated via a conservation of volume equation: total resulting solution volume = volume of fibers + volume of PBS (3 ml). After calculating total fiber volume, solutions were re-centrifuged, supernatant was removed, and fiber pellets were resuspended to create a 10 volume % fiber solution, which were then aliquoted and stored at 4C. To support cell adhesion, 2.0 mM RGD was coupled to vinyl sulfone groups along the DexVS backbone via Michael-type addition chemistry for 30 min, followed by quenching of excess VS groups in a 300 mM cysteine solution for 30 min.

DexVS gels were formed via a thiol-ene click reaction at 3.3% (w/v) (pH 7.4, 37C, 45 min) with VPMS cross-linker (12.5, 20, and 27.5 mM) (GCRDVPMSMRGGDRCG, GenScript, George Town, KY) in the presence of varying amounts of arginylglycylaspartic acid (RGD, CGRGDS, 2.0 mM; GenScript, George Town, KY), HBP (GCGAFAKLAARLYRKA, 1.0 mM; GenScript, George Town, KY), and fiber segments (0.0 to 5.0%, v/v). For experiments comparing hydrogels of varying ligand type (1 mM HBP versus 2 mM RGD), cysteine was added to precursor solutions to maintain a final vinyl sulfone concentration of 60 mM. All hydrogel and peptide precursor solutions were made in PBS containing 50 mM Hepes. To create fibrous hydrogels, a defined stock solution (10% v/v) of suspended fibers in PBS/Hepes was mixed into hydrogel precursor solutions before gelation. By controlling the dilution of the fiber suspension, fiber density was readily tuned within the hydrogel at a constant hydrogel weight percentage. For gel contraction experiments, DexVS was polymerized within a 5-mm-diameter polydimethylsiloxane (PDMS) gasket to ensure consistent hydrogel area on day 0.

NHLFs (University of Michigan Central Biorepository), normal human dermal fibroblasts (Lonza, Basel, Switzerland), and normal human mammary fibroblasts (Sciencal, Carlsbad, CA) were cultured in Dulbeccos modified Eagles medium containing 1% penicillin/streptomycin, l-glutamine, and 10% fetal bovine serum (Atlanta Biologicals, Flowery Branch, GA). NHLFs derived from three separate donors were used for experiments. Cells were passaged upon achieving 90% confluency at a 1:4 ratio and used for studies until passage 7. For all hydrogel studies, cells were trypsinized, counted and either encapsulated into or seeded onto 25-l hydrogels at a density of 1,000,000 cells ml1 of hydrogel, and subsequently cultured at 37C and 5% CO2 in serum-containing medium. For studies comparing 3D hydrogels to tissue culture plastic, the number of cells seeded into 2D conditions was analogous to the total cell number within hydrogel matrices. Medium was refreshed the day after encapsulation and every 2 days after. In selected experiments, recombinant human TGF-1 (5 ng/ml; PeproTech, Rocky Hill, NJ) was supplemented into the medium at 5 ng ml1. For pharmacological studies, nintedanib (50 nM; Thermo Fisher Scientific, Hampton, NH), pirfenidone (100 M; Thermo Fisher Scientific, Hampton, NH), marimastat (1.0 M), and dimethyl fumarate (100 nM) were supplemented in serum-containing medium and refreshed every 2 days.

Cultures were fixed with 4% paraformaldehyde for 30 min at room temperature. To stain the actin cytoskeleton and nuclei, samples were permeabilized in PBS solution containing Triton X-100 (5%, v/v), sucrose (10%, w/v), and magnesium chloride (0.6%, w/v); blocked in 1% bovine serum albumin (BSA); and stained simultaneously with phalloidin and 4,6-diamidino-2-phenylindole (DAPI). For immunostaining, samples were permeabilized, blocked for 8 hours in 1% (w/v) BSA, and incubated with mouse monoclonal anti-YAP antibody (1:1000; Santa Cruz Biotechnology, SC-101199), mouse monoclonal anti-fibronectin antibody (FN, 1:2000; Sigma-Aldrich, #F6140), rabbit monoclonal anti-Ki67 (1:500; Sigma-Aldrich #PIMA514520), or mouse monoclonal anti-SMA (1:2000; Sigma-Aldrich, #A2547) followed by secondary antibody for 6 hours each at room temperature with 3 PBS washes in between. High-resolution images of YAP, FN, and actin morphology were acquired with a 40 objective. Unless otherwise specified, images are presented as maximum intensity projections of 100-m Z-stacks. Hydrogel samples were imaged on a Zeiss LSM 800 laser scanning confocal microscope. SHG imaging of lung tissue was conducted on a Leica SPX8 laser scanning confocal microscope with an excitation wavelength of 820 nm and a collection window of 400 to 440 nm. Single-cell morphometric analyses (cell spread area) were performed using custom Matlab scripts with sample sizes >50 cells per group, while YAP, -SMA, Ki67, and FN immunostains were quantified on an image basis with a total of 10 frames of view. MFs were denoted as nucleated, F-actin+, -SMA+ cells. For cell density (number of nuclei) calculations, DAPI-stained cell nuclei were thresholded and counted in six separate 600 m 600 m 200 m image volumes, allowing us to calculate a total number of cells per mm3 of gel. Fiber recruitment analysis was conducted via a custom Matlab script; briefly, cell outlines were created via actin masking and total fiber fluorescence was quantified under each actin mask on a per-cell basis. A similar analysis method using Matlab was used for cell-cell junction analysis as published previously, with higher area:perimeter ratios and clusters/cell indicative as more pronounced network formation (47).

For all experiments, additional hydrogel replicates were finely minced and degraded in dextranase solution (4 IU/ml; Sigma-Aldrich) for 20 min and homogenized in buffer RLT (Qiagen, Venlo, The Netherlands), and RNA was isolated according to the manufacturers protocols. Complementary DNA (cDNA) was generated from deoxyribonuclease (DNase)free RNA and amplified, and gene expression was normalized to the housekeeping gene glyceraldehyde-3-phosphate dehydrogenase (GAPDH). Experiments were run with technical triplicates across three individual biological experiments. For a complete list of primers, see table S2.

To determine the elastic modulus of lung tissue and DexVS hydrogels, indentation tests were used with a Nanosurf FlexBio AFM (Nanosurf, Liestal, Switzerland). Samples were indented via a 5-m bead at a depth of 10 m and an indentation rate of 0.333 m/s. Resulting force-displacement curves were fit to a spherical Hertz model using AtomicJ. Poissons ratios of 0.5 and 0.4 were used for hydrogels and lung tissue, respectively.

All animal studies were approved by the Animal Care and Use Committee at the University of Michigan. Bleomycin (0.025 U; Sigma-Aldrich) was instilled intratracheally in C57BL6 mice (8 weeks of age; The Jackson Laboratory, Bar Harbor, ME, USA) on day 0. Briefly, mice were anesthetized with sodium pentobarbital, the trachea was exposed and entered with a 30-gauge needle under direct visualization, and a single 30-l injection containing 0.025 U of bleomycin (Sigma-Aldrich) diluted in normal saline was injected. Lungs were collected on day 14 for mechanical and histological analysis. For histology samples, lungs were perfused with saline and inflated with 4% paraformaldehyde, sectioned, and stained with picrosirius red. For mechanical characterization via AFM, lungs were perfused with saline, infused with OCT (optimal cutting temperature) compound (Thermo Fisher Scientific), and flash-frozen in a slurry of dry ice and ethanol. Sections were mechanically tested via AFM nanoindentation immediately upon thawing.

To characterize the inflammatory secretome associated with various DexVS-VPMS environments, medium was collected from NHLF cultures 3, 5, 7, and 9 days after encapsulation. A Luminex FlexMAP 3D (Luminex Corporation, Austin, TX) systems technology was used to measure 41 cytokines/chemokines (HCTYMAG-60 K-PX41, Milliplex, EMD Millipore Corporation) in the medium samples according to the manufacturers instructions. Total secretion was reported as the sum of all 41 analytes measured for each respective condition. Cell-secreted collagen was measured using the established colorimetric Sircol assay in hydrogels cultured with serum-free medium in the presence of ascorbic acid (25 g ml1).

The NCBI GEO database was consulted [dataset GSE47460 (GP14550)] to fetch gene expression data from 91 healthy patients and 140 patients with IPF; patients with chronic obstructive pulmonary disease and nonidiopathic fibrotic lung diseases were excluded from the analysis (48). GEO2R (www.ncbi.nlm.nih.gov/geo/geo2r/) software was used for GO term enrichment, with keywords ECM, MMP, integrin, cytoskeleton, cytokine, chemokine, and MAPK used as search terms for dataset curation (48). Noncurated datasets were composed of the top 1000 differentially expressed genes between healthy and interstitial lung disease (ILD) conditions. Differential expression was calculated on the basis of subtracting normalized expression values between diseased and healthy patients. All genes were normalized before analysis with GEO2R via a pairwise cyclic losses approach. For pathway and protein-protein enrichment analyses, a curated pathway database [Reactome (49)] and Search Tool for Retrieval of Interacting Genes/Proteins [STRING (50)] methodology were consulted, respectively. For STRING analyses, up-regulated genes within the druggable genome were focused upon. A tabulated list of top genes, pathways, and nodes can be seen in data file S1.

Statistical significance was determined by one-way analysis of variance (ANOVA) or Students t test where appropriate, with significance indicated by P < 0.05. All data are presented as means SD.

Acknowledgments: We thank E. S. White (University of Michigan) for providing patient-derived lung fibroblasts used in these studies. Funding: This work was supported, in part, by the NIH (HL124322, R35HL144481). D.L.M. and C.D.D. acknowledge financial support from the NSF Graduate Research Fellowship Program (DGE1256260). Author contributions: D.L.M. and B.M.B. conceived and supervised the project. D.L.M. designed and performed the experiments. K.M.D. and K.B.A. performed and aided in analysis of the Luminex experiments. M.R.S. and C.D.D. helped with data analysis. R.P. and M.S. aided in polymer syntheses and microfiber fabrication. I.M.L. provided equipment for and assisted in polymerase chain reaction experiments. C.A.W. and B.B.M. helped perform the animal experiments for the bleomycin-induced lung fibrosis model. All authors edited and approved the manuscript. Competing interests: The authors declare that they have no competing interests. Data and materials availability: All data needed to evaluate the conclusions in the paper are present in the paper and/or the Supplementary Materials. Additional data related to this paper may be requested from the authors.

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Microengineered 3D pulmonary interstitial mimetics highlight a critical role for matrix degradation in myofibroblast differentiation - Science...

There is no silver bullet at the moment, and there might never be, said World Health Organization Director-General Tedros Adhanom at a virtual press conference at the beginning of August. While it was this bleak sound bite that made the headlines, Tedros also had words of praise for the progress made towards identifying treatments that aid the recovery of COVID-19 patients with the most serious forms of the disease.Research towards treatments for COVID-19 has been developing at a phenomenal speed, even though it feels as though solutions cant come soon enough; the widespread transmission of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has had significant health, economic and social impacts across the globe, and as of September 8th more than 27 million cases and 890,000 deaths have been recorded in 188 countries.

Research groups across the world have set about identifying drugs for the treatment of COVID-19, by screening both novel and existing drugs for their ability to alleviate symptoms and stem viral replication. Here, we provide an update on ongoing global efforts to develop and test drugs for the treatment of COVID-19 and explore the range of strategies being employed.

COVID-19 is a disease which can leave you with anything between a mild sniffle to an unpleasant combination of high fever, heavy fatigue, and lung inflammation and damage. The drivers of clinical symptoms can be roughly divided into two categories: the virus itself and the hyperinflammatory response to the virus that occurs in the most severely ill people. Consequently, efforts to identify appropriate treatments are often focused on one category, and sometimes, a particular patient group or stage of disease. Given the nature of COVID-19, it is highly likely that a combination of drugs (drug cocktail) will be needed to both neutralize the virus and suppress the symptoms of COVID-19. Antiviral treatments may target viral components directly, or other cellular processes involved in viral infection or replication. To date, interventional studies for COVID-19 have attempted to achieve a wide range of goals, including:

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Meet the scientists on the frontline with coronavirus. Video credit: Sanford Burnham Prebys Medical Discovery Institute

Of the ~12,000 compounds screened, 100 inhibited SARS-CoV-2 replication in mammalian cells, 21 of which did so in a dose-response fashion. Achieving a sufficiently high dose concentration to elicit antiviral effects in vivo was predicted to be practical and possible for 13 of these compounds based on EC50 values in various cell lines. The most potent of these were evaluated for antiviral activity in human induced pluripotent stems cell (iPSC)-derived pneumocyte-like cells (five candidates) and in an ex vivo lung culture system (one candidate). The latter candidate is called apilimod, a small molecule inhibitor of an enzyme (phosphoinositide 5-kinase or PIKfyve, an endosomal lipid kinase) important to the endocytic pathway in which SARS-CoV-2 travels along during its journey through the cell. Encouragingly, apilimod potently antagonized viral replication in these tissues, and the findings are in agreement with those of another research group. This month, Kang et al. published an article in PNAS, describing the potent inhibition of SARS-CoV-2 by apilimod, providing further evidence to suggest PIKfyve-inhibition as a potential strategy that could limit infection and disease pathogenesis. The authors also noted that apilimod has passed safety tests in previous clinical trials for nonviral indications.

Chanda highlights the incredible pace at which this work was produced. Typically, a project like this would take years, rather than months. He points out that by wanting to do something quickly, there were sacrifices (and not just weekends). For example, they ran with the assay and the cell lines that allowed them to produce results quickly. This is the reason we put the entire dataset out there not one/three/20 molecules, we put all 100 molecules out there. These are the ones we found because of our experimental system, but please keep testing the others because youll probably find other things that work, said Chanda.

To design multiple peptide sequences that can competitively bind to the SARS-CoV-2 receptor binding domain, the University of Michigan research group used a protein design system called EvoDesign.EvoDesign is the first de novo protein design protocol developed in our lab; it performs design simulation by combining the evolution-based information collected from protein databases and an accurate physics- and knowledge-based energy function, namely EvoEF2, for computing atomic interactions such as van der Waals forces, electrostatics, hydrogen bonding, and desolvation energies, said Huang.

Overall, these sophisticated computational tools represent a promising new avenue for the de novo development of drug discovery studies.

Michele Wilson is a freelance science writer for Choice Science Writing.

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COVID-19 Drug Discovery and Development Why Diverse Strategies Are Critical - Technology Networks

A piercing smile that beams out of his photos is not the only legacy left behind by much-loved Joe Brown.

At just 29, his life was cut short, but not before he made a decision that would save the lives of three other people.

Prior to his untimely death, the avid gamer signed up to donate all his organs to help those waiting for a life-saving transplant.

For his mother and siblings, nothing could prepare them for losing "kind and generous" Joe so suddenly, but they have found solace in knowing part of him lives on.

Big sister, Louise Edwards, told Black Country Live: "He had opted to donate all his organs. Initially, my mum struggled with this decision but its what he wanted.

"He saved two 29-year-old men who had been waiting nearly two years for a life-saving transplant and he also helped a lady in her 50s.

Joes liver and kidneys were donated shortly after his death at Walsall Manor Hospital on July 23 this year.

Louise said: "My brother was a caring person and, even on his deathbed, he wanted to help. He chose to do it so we had to support it. He agreed to have his stem cells taken to help children. Although he is no longer here, he is still helping people.

"Its comforting to know he saved the lives of three people and his legacy lives on."

According to figures released by the NHS blood and transplant service, there are currently around 6,000 people on the UK transplant waiting list.

Last year, more than 350 people died while waiting for a transplant. Just eight per cent of organs donated were from those of African, Caribbean or Asian heritage.

While his final gesture represented the gift of life, Joe was hiding a silent battle with mental health.

An inquest hearing held at Black Country Coroners Court decided he had tragically taken his own life.

Louise said: "He didnt talk about his struggles with mental health, he always said he didnt want to be a burden. He had stopped talking to us, we only got him back two weeks before his death."

During the inquest, it was revealed that, in the weeks before Joe's death, he had tried to contact the emergency mental health crisis team but was denied a face-to-face appointment because of the COVID-19 outbreak.

"He only used to confide in his friends on the Xbox, he talked about his past, his troubles in his relationship and previous suicide attempts, his sister continued.

She added: "He was a family person, he was a kind and generous person, thats the legacy that he left behind. More than 200 people came to pay their respects at his funeral, he didnt know how loved he was.

"To those struggling with mental health, speak out. It doesnt make you weak to speak out. If he had told us how he was feeling we could have helped to get him the help he needed.

Samaritans (116 123) samaritans.org operates a 24-hour service available every day of the year. If you prefer to write down how youre feeling, or if youre worried about being overheard on the phone, you can email Samaritans at jo@samaritans.org , write to Freepost RSRB-KKBY-CYJK, PO Box 9090, STIRLING, FK8 2SA and visit http://www.samaritans.org/branches to find your nearest branch.

CALM (0800 58 58 58) thecalmzone.net has a helpline is for men who are down or have hit a wall for any reason, who need to talk or find information and support. They're open 5pm to midnight, 365 days a year.

Childline (0800 1111 ) runs a helpline for children and young people in the UK. Calls are free and the number wont show up on your phone bill. PAPYRUS (0800 068 41 41) is a voluntary organisation supporting teenagers and young adults who are feeling suicidal.

Depression Alliance is a charity for people with depression. It doesnt have a helpline, but offers a wide range of useful resources and links to other relevant information depressionalliance.org Students Against Depression is a website for students who are depressed, have a low mood or are having suicidal thoughts. Bullying UK is a website for both children and adults affected by bullying studentsagainstdepression.org The Sanctuary (0300 003 7029 ) helps people who are struggling to cope - experiencing depression, anxiety, panic attacks or in crisis. You can call them between 8pm and 6am every night.There are other depression charities.

"The family are distraught, my kids and the younger siblings dont understand why Joe isnt here. Im the oldest and I never thought he would be gone before me."

At the hearing, coroner, Joanne Lees, told the court that Joe had been found unresponsive in his room by his ex-girlfriend on July 20, 2020.

Paramedics were able to resuscitate him and he was rushed to Walsall Manor Hospital but, due to a cardiac arrest, he suffered a brain injury which led to his death.

Fondly recalling her sons warm character, Vicky Spriggs told the court: "He was a happy go lucky person who didnt believe in mental health, he would always say, 'suck it up' or 'man up'.

"He was bubbly and outgoing. Joe was always smiling and joking around.

Ms Lees recorded a verdict of suicide and offered her condolences to the family.

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Much-loved son Joe Brown saved three lives after tragic death at just 29 - Birmingham Live

WASHINGTON, Sept. 4, 2020 /PRNewswire/ -- During the COVID-19 pandemic, many stem cell transplant centers including guidance from the National Marrow Donor Program (NMDP) recommend that stem cell products be frozen for preservation. However, a new study in Blood Advances suggests that the freezing process can decrease the quality of stem cells, particularly if they were manipulated before being preserved, if they had high white blood cell content, or if they were stored for a long period of time.

Stem cells can develop into many different types of cells, so they are often used in treatment to replace or repair damaged organs or tissues. Allogeneic stem cell transplantation, which involves transferring stem cells from a healthy donor to a patient, can treat a variety of diseases, including leukemia, lymphoma, myeloma, thalassemia, and sickle cell disease.

Before the coronavirus outbreak, it was not common to freeze allogeneic donor stem cells prior to infusion. However, due to COVID-19's effects on donor and hospital availability, as well as new travel and transportation restrictions, more transplant centers including the NMDP are recommending cryopreservation.

"Prior to COVID-19, the donor and transplant systems were well coordinated and effective. Now, with irregular flights and closed borders, travel and transportation are not assured," said lead study author Duncan Purtill, MD, of Fiona Stanley Hospital in Western Australia. "Five to seven days before stem cell transplant, the recipient usually starts chemotherapy to remove all their bone marrow cells. Without a healthy transplant to replace the cells on the same day, they would be left with no functioning bone marrow, which would of course be very high risk and carry a poor prognosis. Life literally depends on the safe arrival and immediate infusion of stem cells."

Dr. Purtill and his team analyzed 305 samples of allogeneic stem cell products that were cryopreserved at participating Australian cell processing labs between 2015 and 2019. They found that, on average, the recovery of the stem cell products was 74%. This is considered an acceptable, viable recovery, enabling the cells to be used in transplantation. However, some products did not recover to that level: around 15% of the surveyed products had a cell recovery of less than 50%. In fact, the study found that quality recovery could range as low as just 6%. Such a significant cell loss after thawing may mean that the remaining cells may be too few, or too damaged, to achieve timely bone marrow recovery in the patient after infusion.

"It seems that there is variability in recovery and more work needs to be done to determine why," said Dr. Purtill. "When we freeze stem cells and then thaw them afterwards, we sometimes get unexpected results. In this study we identified some possible factors influencing that variability."

The research team pointed to three possible reasons for the loss of quality in some of the stem cells products they analyzed. First, they noted that prolonged transportation and storage time prior to cryopreservation was associated with a loss of quality. They also found that higher white cell concentration of the product affected its quality. It was thought that the presence of other white cells could adversely affect the stem cells, either by releasing damaging enzymes or chemicals, or else by consuming nutritional elements within the product and resulting in less healthy stem cells. And finally, they pointed out that a small proportion of cells which underwent complex manipulation before being frozen also suffered quality loss for instance, when the cell processing lab removed lymphocytes or washed the product to remove plasma and other noncellular components.

Dr. Purtill and his collaborators expressed hope that their findings could serve to inform and improve stem cell transplantation, collection, and processing procedures. "Our findings could be a note of caution for transplant centers to not take for granted that the frozen product they have received will show perfect recovery once thawed," said Dr. Purtill. "I hope centers will insist on receiving a pilot vial which has been frozen and transported in the same way. They can assess the pilot vial to determine its viability before they use the full product and start chemotherapy for the patient."

Blood Advancesis a peer-reviewed, online only, open access journal of the American Society of Hematology (ASH), the world's largest professional society concerned with the causes and treatment of blood disorders.

Blood Advances is a registered trademark of the American Society of Hematology.

SOURCE Blood Advances

http://www.bloodadvances.org

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Study: Cryopreservation Associated with Loss of Quality in Donor Stem Cell Products - PRNewswire