Archive for December, 2022

Since 2017, Cell & Gene Therapy World Asia haswitnessed huge success in bringing over 300industry pioneers from both cell & gene therapyindustry. With the mission to facilitate the research& development and manufacturing of high qualitycell & gene therapy treatments and regenerativemedicines in Asia, Cell & Gene Therapy World Asia isgoing to continue its legacy.

In addition, this year, speakers will be exploringinnovations in cell & gene therapy in Asia region,best practices on cell & gene therapymanufacturing and process development, scale outstrategies, cost optimization, next generation onCART, advances in CART manufacturing,preparation for commercialization, regulation casestudies and more.

Join the conference to interact with key andupcoming entities from Asia cell & gene therapycompanies including BeiGene, GracellBiotechnologies, Fosun Kite Biotechnology, TessaTherapeutics, CARSgen, Senlang Bio, KangstemBiotech, Medigen Biotechnology Corp, ShangaiUniCAR Therapy among others.

Catch the latest cell & gene therapy development inAsia. From current best R&D practices to advancingtowards manufacturing and commercializationfrom most-exclusive case studies to industry's keyneeds. All this and more under 1 roof.

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Cell and Gene Therapy World Asia Event - IMAPAC

Parkinsons disease is a neurological disorder with symptoms that become more severe over time. It affects about 1% of people ages 60 years and older in industrialized nations. The exact cause of the disease isnt known, but experts believe that both genetic and environmental factors play a role.

Parkinsons disease causes neurons to die in certain parts of your brain, leading to a decrease of dopamine. Dopamine is a neurotransmitter. Cells in your brain release dopamine as a way of sending signals to other nearby cells.

When you have Parkinsons, a decrease in dopamine activity can lead to such symptoms as:

Theres no cure for Parkinsons disease. But over the past few decades, researchers have been studying stem cell therapy to provide better treatment options.

Read on to learn more about current and future developments in using stem cell therapy to treat Parkinsons disease.

Stem cells are special because theyre undifferentiated, meaning they have the potential to become many types of specialized cells.

You might think of stem cells as natural resources for your body. When your body needs a specific type of cell from bone cells to brain cells an undifferentiated stem cell can transform to fit the need.

There are three main types of stem cells:

Stem cell therapy is the use of stem cells usually from a donor, but sometimes from your own body to treat a disorder.

Because Parkinsons disease leads to the death of brain cells, researchers are trying to use stem cells to replace brain cells in the affected areas. This could help treat the symptoms of Parkinsons disease.

Researchers are exploring various approaches to use stem cells to treat Parkinsons disease.

The current idea is to introduce stem cells directly into the affected areas of your brain where they can transform into brain cells. These new brain cells could then help regulate dopamine levels, which should improve the symptoms of the disease.

Its important to note that experts believe this would only be a treatment for Parkinsons disease and not a cure.

While stem cell therapy has the potential to replace the brain cells destroyed by Parkinsons disease, the disease would still be present. Parkinsons disease would likely destroy the implanted stem cells eventually.

Its unclear right now whether stem cell therapy could be used multiple times to continue to reduce symptoms of Parkinsons disease or if the effect would be the same after multiple procedures.

Until the discovery of the process of creating iPSCs, the only stem cell therapies for Parkinsons disease required the use of embryonic stem cells. This came with ethical and practical challenges, making research more difficult.

After iPSCs became available, stem cells have been used in clinical trials for many conditions involving neural damage with overall mixed results.

The first clinical trial using iPSCs to treat Parkinsons disease was in 2018 in Japan. It was a very small trial with only seven participants. Other trials have been completed using animal models.

So far, trials have shown improvement to symptoms affecting movement as well as nonmotor symptoms such as bladder control.

Some challenges do arise from the source of the stem cells.

Stem cell therapy can be thought of as being similar to an organ transplant. If the iPSCs are derived from a donor, you may need to use immunosuppressant drugs to prevent your body from rejecting the cells.

If the iPSCs are derived from your own cells, your body might be less likely to reject them. But experts believe that this will delay stem cell therapy while the iPSCs are made in a lab. This will probably be more costly than using an established line of tested iPSCs from a donor.

There are many symptoms of Parkinsons disease. Theyre often rated using the Unified Parkinsons Disease Rating Scale (UPDRS) or the Movement Disorder Societys updated revision of that scale, the MDS-UPDRS.

Clinical trials today are generally looking to significantly improve UPDRS or MDS-UPDRS scores for people with Parkinsons disease.

Some trials are testing new delivery methods, such as intravenous infusion or topical applications. Others are looking to determine the safest number of effective doses. And other trials are measuring overall safety while using new medical devices in stem cell therapy.

This is an active area of research. Future trials will help narrow down the most safe and effective approach to stem cell therapy for Parkinsons disease.

Clinical trials are usually conducted in three phases. Each phase adds more participants, with the first phase usually limited to a few dozen people and several thousand in the third phase. The purpose is to test the treatments safety and effectiveness.

Clinical trials testing stem cell therapy for Parkinsons disease are still in the early phases. If the current trials are successful, it will likely still be 4 to 8 years before this treatment is widely available.

The goal of stem cell therapy for Parkinsons disease is to replace destroyed brain cells with healthy, undifferentiated stem cells. These stem cells can then transform into brain cells and help regulate your dopamine levels. Experts believe this can relieve many of the symptoms of Parkinsons disease.

This therapy is still in the early stages of clinical testing. Many trials are either proposed, currently recruiting, or already active. The results of these trials will determine how soon stem cell therapy might become widely available as a treatment for Parkinsons disease.

At the moment, its not believed that stem cell therapy will cure Parkinsons disease. But it might be an alternative to existing treatments such as drug therapies and deep brain stimulation.

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Stem Cell Therapy for Parkinson's: Current Developments - Healthline

Heart failure is a life-threatening disorder worldwide and many papers reported about myocardial regeneration through surgical method induced by LVAD, cellular cardiomyoplasty (cell injection), tissue cardiomyoplasty (bioengineered cardiac graft implantation), in situ engineering (scaffold implantation), and LV restrictive devices. Some of these innovated technologies have been introduced to clinical settings. Especially, cell sheet technology has been developed and has already been introduced to clinical situation. As the first step in development of cell sheet, neonatal cardiomyocyte sheets were established and these sheets showed electrical and histological homogeneous heart-like tissue with contractile ability in vitro and worked as functional heart muscle which has electrical communication with recipient myocardium in small animal heart failure model. Next, as a preclinical study, noncontractile myoblast sheets have been established and these sheets have proved to secrete multiple cytokines such as HGF or VEGF in vitro study. Moreover, in vivo studies using large and small animal heart failure model have been done and myoblast sheets could improve diastolic and systolic performance by cytokine paracrine effect such as angiogenesis, antifibrosis, and stem cell migration. Recently evidenced by these preclinical results, clinical trials using autologous myoblast sheets have been started in ICM and DCM patients and some patients showed LV reverse remodelling, improved symptoms, and exercise tolerance. Recent works demonstrated that iPS cell-derived cardiomyocyte sheet were developed and showed electrical and microstructural homogeneity of heart tissue in vitro, leading to the establishment of proof of concept in small and large animal heart failure model.

Therapeutic treatments using cells or cell-based tissues have been developed to regenerate the damaged myocardium associated with ischemic heart disease. This technique has already been evaluated in the clinical setting, using myoblasts [1] or bone marrow mononuclear cells (BM-MNCs) [2]. Although these studies demonstrated the feasibility and safety of this approach, the efficacy associated with this technology was generally insufficient to repair severe myocardial damage. Thus, a second generation of myocardial regenerative therapy, tissue-engineered cardiomyoplasty, is currently being developed. A large number of achievements concerning basic, preclinical, and clinical works about cell sheet technology have been done and this review summarizes recent advances in myocardial regeneration emerging from the development of cell sheet technology.

Cell-sheet techniques have been applied to several diseased organs, such as the heart [3], eye [4], and kidney [5], in the laboratory and the clinic. Cell sheets can be prepared on special dishes that are coated with a temperature-responsive polymer, poly(N-isopropylacrylamide) (PIPAAm), that changes from being hydrophobic to hydrophilic when the temperature is lowered. This change allows cells to be removed without EDTA or enzymatic treatment and without destroying the cell-cell or cell-extracellular matrix (ECM) interactions within the cell sheet.

Shimizu et al. used such temperature-sensitive culture dishes to develop a contractile chick cardiomyocyte sheet that exhibited a recognizable heart tissue-like structure and showed electrical pulsatile amplitude [6]. Next, they layered single-cell sheets to generate bilayer-cell sheets, forming an electrically communicative three-dimensional cardiac construct, which exhibited spontaneous and synchronous pulsation with electrical communication between the cell sheets, mediated by connexin 43. Furthermore, the cell sheets adhered together rapidly, as indicated by the presence of desmosomes and intercalated disks between them [7]. When the pulsatile cardiac tissue was implanted subcutaneously, it was found to assume a heart tissue-like structure and exhibited neovascularization and spontaneous beating for up to one year. The size, conduction velocity, and contractile force of the engrafted sheets increased in proportion to the host growth [8, 9].

Miyagawa et al. demonstrated that a neonatal cardiomyocyte sheet could communicate electrically with the host myocardium, as indicated by the presence of connexin 43, and changes in the QRS wave and action potential amplitude, leading to improved cardiac performance in a rat model of ischemic heart disease [3]. This study clearly showed electrical and morphological coupling between the cell sheet and host myocardium and that the cell sheet could contract synchronously with the beating of the host heart and improve the regional systolic function.

A detailed analysis of the vascularization process following cell sheet implantation was undertaken by Sekiya et al. These authors reported that the cardiomyocyte sheet expresses angiogenesis-associated genes and forms an endothelial cell network. Evidence was also presented suggesting that the vessels arising in the engrafted sheet migrate to connect with the host vasculature [10].

Myocardial tissue grafts engineered with cell sheet technology represent a promising therapy for repairing the damaged myocardium, but there may be some inherent limitations. For example, cellular treatment for heart failure may be not suitable for emergency situations. Another issue is that wide therapeutic use will require improvement in the uniformity in the quality of the cultured cells.

Recently, new medications that imitate the paracrine effects of cytokines in cell sheets have been reported, and the addition of such medications could improve the regenerative treatment for heart failure. It was reported that the direct introduction of a prostacyclin agonist into the damaged myocardium induced significant functional recovery in a canine model of dilated cardiomyopathy, via the upregulation of multiple cytokines, including HGF, VEGF, and SDF-1 [11]. Similarly, the implantation of an atelocollagen sheet containing a prostacyclin analogue induced improved cardiac function and a prolonged survival rate in a mouse model of acute myocardial infarction, accompanied by an enhanced expression of SDF-1 [12]. Recent work has also revealed that prostacyclin may be upregulated in the implanted myoblast sheet in the early phases after implantation in response to ischemic conditions and may in turn stimulate endothelial or smooth muscle cells to secrete multiple cytokines including HGF, VEGF, and SDF-1 (data not shown).

In the clinical setting, cellular cardiomyoplasty is reported to have potential regenerative capability, and a method using skeletal myoblasts has been evaluated in clinical trials and found to be relatively feasible and safe [13]. For tissue cardiomyoplasty, skeletal myoblasts are the cell source closest to being ready for clinical application at this time. Memon et al. demonstrated that the nonligature implantation of a skeletal myoblast sheet into a rat cardiac ligation model regenerated the damaged myocardium and improved global cardiac function, by attenuating cardiac remodeling via hematopoietic stem-cell recruitment and growth-factor release, with better restoration of the implanted cells than that obtained using needle injection [14]. In another study, the application of a skeletal myoblast sheet into a 27-week dilated cardiomyopathy hamster model resulted in the attenuated deterioration of cardiac performance accompanied by the preservation of alpha-sarcoglycan and beta-sarcoglycan expression in the host myocytes, and an inhibition of fibrosis, leading to prolonged survival rates [15]. In addition, the grafting of skeletal myoblast sheets attenuated cardiac remodeling and improved cardiac performance in a pacing-induced canine heart failure model [16]. Studies from our group have shown that myoblast sheets may improve cardiac performance via cytokines such as HGF or VEGF (XX).

The mechanism of recovery in the damaged myocardium has not been completely elucidated and may be very complicated. As mentioned above, cytokine release and hematopoietic stem-cell recruitment are possible mechanisms of regeneration; however, other regenerative mechanisms are likely to be involved as well. Skeletal myoblasts cannot beat synchronously with the host myocardium in vitro [17] or in vivo [18], and, thus, they do not appear to be functionally integrated. However, data from our human and porcine studies suggested that after myoblast sheet implantation, the diastolic dysfunction in the distressed region of the myocardium was significantly recovered compared with controls, leading to improved systolic function in the same region, without contraction of the implanted myoblasts (data not shown). Massive angiogenesis in the implanted region was detected histologically and appeared to be a critical feature associated with the improvement. Thus, we speculate that angiogenesis and the recovery of diastolic function are both major components of the regenerative mechanism in myoblast sheet implantation [19].

On the other hand, immunohistochemical analysis has indicated that the myoblast sheet may only survive for a few months after implantation. We speculate that in the early phases after implantation of the myoblast sheet, the ischemic conditions induce the upregulated expression of several cytokines by the myoblasts that promote their own survival. These cytokines then in turn enhance angiogenesis and the recruitment of stem cells, leading to improved blood perfusion to reactivate the damaged myocardium. The system may continue to be effective in spite of the short-lived myoblast sheet, due to long-term maintenance of the newly developed vasculature.

We recently initiated a clinical evaluation of autologous myoblast sheet implantation. We tested the technology in four patients who were using left ventricular assist devises (LVADs); three of the four patients showed functional recovery, and in two of the patients, the treatment provided a bridge to recovery [20]. Six years later, these two patients have no symptoms of heart failure. We have also implanted myoblast sheets into eight patients with ischemic cardiomyopathy and seven with dilated cardiomyopathy (who were not using LVADs). In that study, some of the patients exhibited left ventricle reverse remodeling and improvements in exercise tolerance and symptoms, with no major adverse cardiac events (MACEs) (data not shown). This clinical research program is ongoing, as we continue to evaluate patients with dilated cardiomyopathy and ischemic cardiomyopathy with and without the use of LVADs.

In addition to cardiomyocytes and myoblasts, other types of cell sheets have been used effectively to improve cardiac performance. The transplantation of a mesenchymal stem cell (MSC) sheet onto the infarcted myocardium of rats resulted in increased anterior wall thickness and new vessel formation, accompanied by a low incidence of differentiation of the implanted cells to cardiomyocytes [21]. While the small number of differentiated cardiomyocytes may not have contributed to the observed improvement in systolic function in this study, the cell sheet exhibited self-propagating properties that promoted the generation of a thick-layered sheet. Although the MSC sheet exhibited a maximum thickness of approximately 600m, which would not be strong enough to correct human end-stage heart failure [22], this method of self-propagation is a potential strategy for creating a thick-layered sheet in vivo, with the potential for cardiac tissue regeneration.

A further development in cell sheet technology is the creation of a cell sheet composed of two types of cocultured cells; this type of cell sheet was developed to enhance angiogenesis [23, 24]. The cocultured cell sheet, which combined fibroblasts and endothelial progenitor cells, enhanced blood vessel formation and led to functional improvement in a rat myocardial infarction model [24]. Cocultured cell sheets combining fibroblasts and human smooth muscle cells were found to accelerate the secretion of angiogenic factors in vitro and to increase blood perfusion in vivo by the formation of new vessels [25]. This enhanced effectiveness attained by coculturing two cell types is supported by another study in which the coimplantation of BMCs and myoblasts showed improved results compared to the transplantation of a single cell type in a canine model of ischemic cardiomyopathy [26].

Cell sheets composed of stem cell antigen-1- (sca-1-) positive, or kit-positive cells may represent additional promising approaches. Matsuura et al. demonstrated that sca-1-positive cell sheets could differentiate into cardiomyocytes in vivo and produce VCAM-1, leading to improved cardiac performance in a mouse model of myocardial infarction [27]. The administration of c-kit-positive stem cells has shown efficacy in animal models of cardiac dysfunction, and this approach is currently being tested in clinical trials in combination with coronary artery bypass grafting, with encouraging preliminary results [28]. In another study, a c-kit-positive cell sheet combined with endothelial progenitor cell injection was found to induce better functional recovery of endocardial scar tissue than that induced by the cell sheet alone, despite the poor transdifferentiation ability of the c-kit-positive cells into cardiomyocytes [29].

Many of the cell sources mentioned above demonstrate regenerative ability based on the paracrine effect of secreted cytokines; however, newly differentiated cardiomyocytes may be the best candidate cells to regenerate the damaged myocardium. In 2006, Takahashi and Yamanaka reported the development of induced pluripotent stem (iPS) cells that can differentiate into various types of cells, such as cardiomyocytes, cartilage, and nerve cells [30]. Since then, there have been many reports showing that cardiomyocytes derived from iPS cells demonstrate electrophysiological, functional, and microstructural similarities to native cardiomyocytes [31]. Cardiomyocyte sheets derived from human or mouse iPS cells that contract synchronously in vitro have been developed, and studies indicate that these cardiomyocyte sheets can contract in vivo as analyzed by X-ray diffraction with synchrotron radiation. The transplantation of these sheets leads to functional recovery with upregulated electrical potential in the scarred areas in large [32] and small animal myocardial infarction models [33].

Although preclinical studies appear promising, the safety of these artificially generated cells must be evaluated thoroughly before they can be used in the clinic. In addition, a potential limitation of iPS cell-derived cardiomyocytes may be the loss of cardiomyocytes due to ischemia after implantation. Recent studies have proposed supplemental strategies to avoid ischemia. In one study, the combination of an iPS-derived cardiomyocyte sheet with omentum, which has a rich vasculature network, resulted in retention of the implanted cardiomyocytes and enhanced functional recovery compared with the cardiomyocyte sheet alone [34]. In another study, the transplantation of a cardiomyocyte sheet containing iPS cell-derived endothelial cells led to enhanced functional recovery in a rat myocardial infarction model and increased survival of the implanted cardiomyocytes [35]. Thus, to successfully treat the severely damaged myocardium using iPS cell-derived cardiomyocyte sheets, additional strategies to increase angiogenesis and reduce ischemia may be required.

Studies on the original myoblast cell therapy, in which cells were directly injected into the myocardium, indicated that the proportion of injected cells surviving to engraft the infarcted myocardium was too low to be effective. This low level of engraftment may have been caused by the injected cells leaking out of the injected region and being carried to other organs, or due to mechanical stress resulting in cellular loss of function. The resulting rapid cell loss [14] limited the usefulness of the original myoblast cell therapy.

To overcome the problems associated with the intramyocardial injection of cells, many investigators have combined cell transplantation with protein or gene therapy [36], or with tissue-engineered techniques [3]. We have also developed a new cell delivery system that uses tissue-engineered myoblast grafts grown as cell sheets and have utilized animal studies to guide clinical trials. These studies showed that the viability of the transplanted cells was higher than that of injected cells, and that the transplanted myoblasts survived for at least 3 months in the cardiac tissue of a porcine model of heart failure treated with autologous myoblast sheets. Using tissue-engineered temperature responsive techniques, we found that the implanted cells could be applied in larger numbers, were viable during transplantation, and were not lost from the applied region. Furthermore, we showed that cell sheets could be engrafted onto the failed myocardium and contribute to the attenuation of cardiac dysfunction and remodeling [14].

In cell therapy for cardiac disease, life-threatening adverse events involving arrhythmogenicity are a potential risk in both animal models and human clinical trials [37]; however, life-threatening arrhythmias have not been observed during the clinical course of patients who have received autologous cell sheet transplants. In any case, arrhythmias can occur during the natural clinical course of severe heart failure, so their cause may not be easily determined. Procedures using needle injection may cause scars in the myocardium that could in turn induce arrhythmias. Our cell delivery techniques using cell sheets prepared on temperature-responsive culture dishes may carry less risk for the induction of arrhythmias. Myoblasts have a weak electrical potential, and it may be possible for these cells to induce arrhythmia if they survive in the myocardium. However, cell sheets may not be able to induce arrhythmia, since they are attached to the epicardium.

Another potential problem is the limited blood perfusion to the implanted cell sheets. Although the survival of implanted cells using the cell sheet technique has already been shown to exceed the cell survival using other delivery routes, the survival rate was still found to be relatively low when the cells were implanted on the epicardium with this technique [38]. Although we have reported that improved cardiac performance depends on the dose of implanted myoblast sheets, the use of too many cell sheets results in a reduced blood supply. Thus, additional strategies, such as combining myoblasts with angiogenic factors [36] or other types of cells [23] to establish a vasculature network, may be needed to solve this problem. One strategy discussed above, is the combination of a myoblast sheet with omentum tissue that has a rich vasculature network. One report recently demonstrated the effectiveness of this approach for retention of the implanted cell sheets [39]. This report also suggested that the implanted myoblast sheet might induce vasculature connections between arteries of the transplanted omentum and the native coronary arteries, suggesting the possibility of biocoronary artery bypass grafting. This method may also be used in conjunction with iPS cell-derived cardiomyocytes to generate an artificial thick cardiac structure with increased vascular connections.

In this review, we surveyed many exciting topics in the area of cell sheet technology for cardiac repair. Owing to these studies, some techniques have already been tested in clinical applications, but the mechanisms by which they improve cardiac function are only partially understood, and much of the technology is still in the early stages of development, both experimentally and in the clinic. Nevertheless, the field of clinical myocardial regenerative therapy holds much promise, and we expect to witness more progress in this innovative technology in the near future.

The authors declare that there is no conflict of interests regarding the publication of this paper.

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Present and Future Perspectives on Cell Sheet-Based ... - Hindawi

Your Health and Hormones Close

We are here to help you understand how hormones work and use that knowledge to manage your health.

We empower high-quality, equitable healthcare for people with hormone health conditions, including diabetes and obesity, infertility, thyroid conditions, osteoporosis, and hormone-related cancers. Together, we promote an environment that helps people of all backgrounds and ethnicities access the medical care they need.

Through our multi-lingual educational materials, and EndoCares program, the Endocrine Society provides opportunities for you to connect with endocrinologists across the globe. For more than two decades, our 18,000 members have leveraged their medical and scientific expertise to provide trusted information to the public.

Endocrinology is the study of medicine that relates to the endocrine system, which is the system that controls hormones. Hormones regulate:

Hormones are produced by glands and sent into the bloodstream to the various tissues in the body. They send signals to those tissues to tell them what they are supposed to do. When the glands do not produce the right amount of hormones, diseases develop that can affect many aspects of life.

Endocrinologists are specially trained physicians, who treat those that suffer from hormonal imbalances. They have thoroughly studied hormonal conditions and know the best treatments and therapies. options. Most general practitioners have the skills necessary to diagnose and treat basic hormonal conditions, but sometimes the help of a specialist is needed.

The Patient Engagement Committee is comprised of Endocrine Society members, clinicians, researchers, educators, with expertise in endocrinology's major therapeutic areas. The committees role is to identify the educational needs of endocrine science for patients and the public, oversee the impact and outcomes of our program, and provide translational knowledge on specific hormone-related conditions.

Are you an Endocrine Society member interested in creating or reviewing content? Let us know you are interested, by filling out the volunteer form here.

DISCLAIMER:WE DO NOT PROVIDE MEDICAL ADVICE -The information, including but not limited to, text, graphics, images and other material contained on this website are for informational and educational purposes only. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition.

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Patient Engagement | Endocrine Society

Anemia: Abnormally low levels of red blood cells in the bloodstream. Most cases are caused by iron deficiency (lack of iron).

Cervix: The lower, narrow end of the uterus at the top of the vagina.

Cesarean Birth: Birth of a fetus from the uterus through an incision made in the womans abdomen.

Computed Tomography (CT): A type of X-ray that shows internal organs and structures in cross section.

Estrogen: A female hormone produced in the ovaries.

Fetus: The stage of human development beyond 8 completed weeks after fertilization.

Fallopian Tubes: Tubes through which an egg travels from the ovary to the uterus.

Gonadotropin-releasing Hormone (GnRH): A hormone made in the brain that tells the pituitary gland when to produce follicle-stimulating hormone (FSH) and luteinizing hormone.

Hysterectomy: Surgery to remove the uterus.

Hysterosalpingography: A special X-ray procedure in which a small amount of fluid is placed in the uterus and fallopian tubes to find abnormal changes or see if the tubes are blocked.

Hysteroscopy: A procedure in which a lighted telescope is inserted into the uterus through the cervix to view the inside of the uterus or perform surgery.

Intrauterine Device (IUD): A small device that is inserted and left inside the uterus to prevent pregnancy.

Laparoscopy: A surgical procedure in which a thin, lighted telescope called a laparoscope is inserted through a small incision (cut) in the abdomen. The laparoscope is used to view the pelvic organs. Other instruments can be used with it to perform surgery.

Laparotomy: A surgical procedure in which an incision is made in the abdomen.

Magnetic Resonance Imaging (MRI): A test to view internal organs and structures by using a strong magnetic field and sound waves.

Menopause: The time when a woman's menstrual periods stop permanently. Menopause is confirmed after 1 year of no periods.

Menstruation: The monthly shedding of blood and tissue from the uterus that happens when a woman is not pregnant.

Osteoporosis: A condition of thin bones that could allow them to break more easily.

Pelvic Exam: A physical examination of a womans pelvic organs.

Progesterone: A female hormone that is made in the ovaries and prepares the lining of the uterus for pregnancy.

Progestin: A synthetic form of progesterone that is similar to the hormone made naturally by the body.

Resectoscope: A slender telescope with an electrical wire loop or roller-ball tip used to remove or destroy tissue.

Sonohysterography: A procedure in which sterile fluid is injected into the uterus through the cervix while ultrasound images are taken of the inside of the uterus.

Tranexamic Acid: A drug to treat or prevent heavy bleeding.

Ultrasound Exam: A test in which sound waves are used to examine inner parts of the body. During pregnancy, ultrasound can be used to check the fetus.

Uterus: A muscular organ in the female pelvis. During pregnancy, this organ holds and nourishes the fetus. Also called the womb.

Uterine Artery Embolization: A procedure to block the blood vessels to the uterus. This procedure is used to stop bleeding after delivery. It is also used to stop other causes of bleeding from the uterus.

Vagina: A tube-like structure surrounded by muscles. The vagina leads from the uterus to the outside of the body.

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Uterine Fibroids | ACOG

New Illinois Laws in 2023 That Focus on the Health, Wellness of State Residents  NBC Chicago

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New Illinois Laws in 2023 That Focus on the Health, Wellness of State Residents - NBC Chicago

Topiramate Weight Loss Reviews: Top 4 Over The Counter Alternative To Topamax For Weight Loss  Outlook India

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Topiramate Weight Loss Reviews: Top 4 Over The Counter Alternative To Topamax For Weight Loss - Outlook India

Milanova next to her award-winning microscopy image named "Making Waves: Delivery for Ageless Skin" ... [+] which was on display in 2017 at the Koch Institute Gallery celebrating extraordinary visuals at MIT

In my previous articles, I covered the wonderful female medical doctors working in longevity medicine, female reproductive longevity and inequality, skincare, and other areas. Here, we continue on this journey and look at the stellar scientist and entrepreneur, Dr. Denitsa Milanova. I heard about Dr. Milanova a few years back when she just joined Harvard, and met her for the first time in person in May 2022 when she told me about her new exciting venture - Marble Therapeutics and her quest to use genetic engineering to target aging.

Denitsa Milanova, PhD, founder and CEO of Marble Therapeutics

Denitsa was born in Bulgaria to a family of engineers. As a child, she excelled at analytical disciplines, and especially in math and physics. She learned at a young age that exceptional results can be achieved with hard work and perseverance. In school, she participated in science competitions routinely winning top places. For college, she moved to Florida, and then continued her graduate studies at Stanford University where she earned her masters and doctorate degrees in mechanical engineering and completed a business degree. Her studies were focused on microfluidics and she pursued research in single-cell sequencing using microfluidic technologies with prominent scientists including Michael Snyder. For her postdoctoral training, she moved to Harvard Medical School and Wyss Institute to work with George Church and soon focused on aging research.

Professor George Church of Harvard Medical School in Boston, MA on November 30, 2012. Church, a ... [+] professor of Genetics with the MAGE Device Multiplex automated Genome Engineering. (Photo by Rick Friedman/rickfriedman.com/Corbis via Getty Images)

Milanova tells me that this is simply the perfect time to build a rejuvenation company with new tools and large amounts of human data. We are doing great things in molecular biology, she says. But from her perspective, scientists are too focused on accumulating experimental evidence - hugely important - but when a field is starting to mature, we need to ask larger questions beyond what is there? but more how can we manipulate it? We need to shift from knowledge-based to inquiry-based frameworks, focusing on the complexities and stabilities of aging systems, and how they evolved to be a certain way.

Milanova and her team spend a lot of time on the why questions. This is the data but why does it look like that? We want to think from first principles, she explains. Drug development is expensive and betting on the wrong targets can be detrimental to companies. Identifying the right drivers amidst a sea of passengers, and spurious events is very hard. We are building algorithms that probe tipping points, thresholds and breakpoints, regime shifts. Going after those genetic perturbations that lead to the largest changes of aging states, she continues.

While Marble is still more or less in stealth mode without a public website, word had gotten around over the last year through top biotechnology and longevity investors that George Churchs lab was cooking up a secretive rejuvenation startup. Now known as Marble, led by his engineer-biotechnologist protg Dr. Milanova, the effort has garnered considerable inbound attention. Denitsa says that her team is developing methods to drive rejuvenation of skin cells with gene therapy and is working on a product that could reverse wrinkles like a genetic Botox.

The magic words in longevity biotech nowadays are platform and pipeline, where the company develops a platform for drug discovery and is using this platform to discover and develop its own therapeutic programs. And Marble is building target discovery and delivery platforms to drive its first pipeline program in the skin. To search for such powerful genes, they use computational methods taken from the study of non-linear dynamics and complex systems. The sort of things which can infer causality in other fields like ecology and finance. And they are attempting to predict the effects of changes in gene expression over time and thereby identifying key driving events and genes of aging.

The Marble team is taking an unbiased approach, agnostic to biological mechanism, and instead search the entire genome for those genes and proteins responsible for large, global shifts in the biology of cells as they transition from young to old. The aging field has leaned too heavily on hypothesis-driven approaches which insist that specific pathways must be involved in longevity and age-associated molecular mechanisms. These things do not necessarily tell us how a cell becomes old, or how to make it young, Milanova points out. The precise details of Marbles approach are being kept a secret, but Milanova has assembled an all-star team led by chairman Matt Rabinowitz (the man behind Natera) and an acclaimed scientific board that includes George Church, Michael Snyder, Carl June, Bob Langer, George Sugihara, Yoav Freund. Rabinowitz says, Aging is the king of all maladies. It remains to be seen how much we can massage our natural mortality, but usually when people place limits on science - and biotech in particular - they are wrong. The approaches Marble is working on to better understand dynamic gene signaling networks and drive those networks with gene therapy are important, would have broad application and are guided by a strong team of scientists.

NEW YORK, NY - MARCH 07: Tony Robbins attends Build series to discuss "UNSHAKEABLE: Your Financial ... [+] Freedom Playbook" at Build Studio on March 7, 2017 in New York City. (Photo by Chance Yeh/FilmMagic)

While building Marble, Milanova sought the advice of a man who would become one of her early backers, Tony Robbins. Robbins, who has coached presidents, elite athletes, and business leaders on the psychology and mechanics of building organizations, became a mentor and advised her on building the most effective team. I met Denitsa when she had just assembled an impressive team of experts prior to any funding into the company. People had signed solely based on the science and mission. What stood out to me was her ability to influence, in a very raw, authentic way. To sell the dream equally well to scientists, and business people, Robbins says. This quality is crucially important and at the core of exceptional leadership. It is truly amazing to see how much Marble has grown in a short period of time and I am excited to be part of it.

As one example of how the company is building competitive advantage, Milanova points to the future collection of proprietary human multi-omics data to fuel rejuvenation target discovery. And the company is well positioned to execute on this goal. Not only are two of its founders Church and Snyder pioneers in multi-omic technologies, they have also worked for decades to develop primary human data collection initiatives. As Church explains, Despite 20 million-fold improvement in the cost of reading human genomes, and trillion dollars per year avoidable by testing, the word is spreading slowly - in part because people feel that they are in the lucky 98% (similar to past denialism for cigarettes and seat belts.) He continues, We need to know our genome but for most of us, it is not actionable. It is different with aging and epigenetics (broadly defined as all -omes). We all age and likely care about aspects of aging (at least most of us).

Dr. Denitsa Milanova at Abundance360 with early supporter and visionary entrepreneur scientist, Dr. ... [+] Peter Diamandis.

This focus on human data is at the core of Marble. Our vision is that aging research will become more human data focused. That is, discovery will start with human data first, not hypotheses based on comparative longevity or mechanistic studies between species. We expect that targets best-suited for rejuvenation of specific cells and tissues may not be one-size-fits-all. And its hard to identify such targets if we are focused solely on highly conserved master regulators, explains Milanova.

Dr. Denitsa Milanova, founder and CEO of Marble Therapeutics

Marble is starting with skin rejuvenation, but they arent trying to be just a skin company. Think of deep-omic profiling of skin, blood, muscle, even reproductive cells with a time stamp on it, Milanova says. Our vision is to have high-quality cross-sectional and longitudinal datasets and all discoveries being data-driven rather than hypothesis-driven, she continues. If you think about those tissues, there are some unique and untapped markets to break into, if you had the right technology, says Milanova. And importantly, they may not have to follow human subjects over years to collect the right data. The cross-sectional data capability is really where our data analytics could shine. We could potentially cut through the noise of human-to-human variation to find deterministic signals, and likely with hundreds of donors. Not like with GWAS where you need tens of thousands.

Longevity Dinner in Boston, 2022. Right to left: Denitsa Milanova, PhD, Marble Therapeutics; Joe ... [+] Betts-LaCroix and Anastasia Shindyapina, PhD, Retro Biosciences; Alex Zhavoronkov, PhD, Insilico Medicine; Vadim Gladyshev, PhD, Brigham and Women's Hospital, Harvard Medical School.

Alex: Denitsa, you have a very impressive resum with multiple graduate degrees from Stanford, postdoctoral training at one of the top labs at Harvard and consulting engagements with a variety of companies. When did you decide to go into aging research?

Denitsa: Thank you, Alex. Id say about five years ago when I started working with George Church. Being new to the field helps with bringing in a fresh perspective. George took a chance on me when I had no background in aging research and taught me how to take risks and pursue groundbreaking science. And this is the best way to tackle big problems, starting with the basic science but also being comfortable for things to take time and even failing before succeeding.

From the beginning I had a vision to do gene therapy for skin rejuvenation, and at the time, everyone thought that was a totally crazy idea. The cost of gene therapy then was as high as $2.8 million, but we have seen huge reductions in the cost of similar modalities like mRNA to as low as $2 per dose, largely driven by the market size. Clinical products in the skin have an enormous market (Botox alone is larger than all of cell and gene therapy combined), and true rejuvenation therapies could reach markets larger even than COVID vaccines.

Alex: This is your first venture. Did you think you would be able to raise funding? Do you have any notable investors in your seed round?

Denitsa: I am a big optimist and even a little bit of a dreamer by nature, but I do get anxious about fundraising. I think some fear of failure and a certain level of anxiety actually helps me, it motivates me to deliver. Yes, we were fortunate to attract prominent investors, and even more so to have them mentor and advise. Success leaves clues and learning from experience saves years. I force myself to maintain a no limitations mindset, both in science and business. What keeps me highly motivated is the certainty that rejuvenation is fundamentally possible, that we have the tools, and is worth doing it is one of the biggest problems of our time.

Alex: When are you planning to get to the preclinical proof of concept (POC) in animals and start IND-enabling studies? And if all goes well, when do you think we will be able to see Marbles products in the clinic? I understand how speculative this is but what is your vision?

Denitsa: It is early to say, we are at the preclinical stage right now. Skin is a very interesting organ clinically and an attractive entry point for newer therapies both in terms of targets and modality. You can test human organ skin grafts in mice to validate function in live human tissue physiology. Clinical trials and endpoints are more defined too because you can have multiple treatment and control locations across the skin, and the accessibility of the skin lets you assess aging phenotypes visually and mechanically to prove effectiveness of your therapy and approach in general.

Alex: What is your long-term vision for the company and for longevity biotechnology in general?

Denitsa: Over the long term we have no shortage of ambition. Skin is the start, because thats where we could get the right data. But I want all tissues. All ages made functionally young. We are starting with single-gene perturbations, but changes in complex cell states are typically polygenic processes. So we have a plan for moving into multi-gene targets using concepts analogous to those which have powered engineering and evolution of antibodies, enzymes, and protein-based drugs, but applied to whole-cell states. That is where I think the future is. We should be evolving cells in the lab to just be very good at being young. Thats not how our cells have evolved naturally, but it is how we can select them to be. Screening, genetic libraries and evolutionary approaches are central to the world of George Churchs lab, and that mindset has definitely rubbed off on me. We will need to intelligently explore genetic space to really ratchet up young-like cell behaviors.

Alex: And another very personal question. You do not need to answer it if it is too sensitive. I know what it takes to run a startup in the longevity space. It does not get intense from time to time - it is a life at full throttle when there is no time to stop and take a breath. How are you planning to maintain the work-life balance?

I have no idea what that [work-life balance] is, she smiles. But really, this isnt work to me. Its not some necessary evil to be balanced. Its a mission, its my life and I love what we are doing, she continued. Of course, I do things to keep sane. I love cryotherapy, another smile.

See more here:
This Harvard Female Scientist Wants To Use Genetics To Reverse The Age ...

Aspect of human growth

Human height or stature is the distance from the bottom of the feet to the top of the head in a human body, standing erect. It is measured using a stadiometer,[1] in centimetres when using the metric system or SI system,[2][3] or feet and inches when using United States customary units or the imperial system.[4][5]

In the early phase of anthropometric research history, questions about height techniques for measuring nutritional status often concerned genetic differences.[6]

Height is also important because it is closely correlated with other health components, such as life expectancy.[6] Studies show that there is a correlation between small stature and a longer life expectancy. Individuals of small stature are also more likely to have lower blood pressure and are less likely to acquire cancer. The University of Hawaii has found that the "longevity gene" FOXO3 that reduces the effects of aging is more commonly found in individuals of small body size.[7] Short stature decreases the risk of venous insufficiency.[8]

When populations share genetic backgrounds and environmental factors, average height is frequently characteristic within the group. Exceptional height variation (around 20% deviation from average) within such a population is sometimes due to gigantism or dwarfism, which are medical conditions caused by specific genes or endocrine abnormalities.[9]

The development of human height can serve as an indicator of two key welfare components, namely nutritional quality and health.[10] In regions of poverty or warfare, environmental factors like chronic malnutrition during childhood or adolescence may result in delayed growth and/or marked reductions in adult stature even without the presence of any of these medical conditions.

A study of 20th-century British natality trends indicated that while tall men tended to reproduce more than short men, women of below-average height had more children than taller women.[11]

The study of height is known as auxology.[12] Growth has long been recognized as a measure of the health of individuals, hence part of the reasoning for the use of growth charts. For individuals, as indicators of health problems, growth trends are tracked for significant deviations, and growth is also monitored for significant deficiency from genetic expectations. Genetics is a major factor in determining the height of individuals, though it is far less influential regarding differences among populations. Average height is relevant to the measurement of the health and wellness (standard of living and quality of life) of populations.[13]

Attributed as a significant reason for the trend of increasing height in parts of Europe are the egalitarian populations where proper medical care and adequate nutrition are relatively equally distributed.[14] The uneven distribution of nutritional resources makes it more plausible for individuals with better access to resources to grow taller, while the other population group who does not have so much of a nutritious food availability height growth is not as promising.[15] Average height in a nation is correlated with protein quality. Nations that consume more protein in the form of meat, dairy, eggs, and fish tend to be taller, while those that obtain more protein from cereals tend to be shorter.[citation needed] Therefore, populations with high cattle per capita and high consumption of dairy live longer and are taller. Historically, this can be seen in the cases of the United States, Argentina, New Zealand and Australia in the beginning of the 19th century.[16] Moreover, when the production and consumption of milk and beef is taken to consideration, it can be seen why the Germanic people who lived outside of the imperium Romanum were taller than those who lived at the heart of the Empire.[17]

Changes in diet (nutrition) and a general rise in quality of health care and standard of living are the cited factors in the Asian populations. Malnutrition including chronic undernutrition and acute malnutrition is known to have caused stunted growth in various populations.[18] This has been seen in North Korea, parts of Africa, certain historical Europe, and other populations.[19] Developing countries such as Guatemala have rates of stunting in children under 5 living as high as 82.2% in Totonicapn, and 49.8% nationwide.[20]

Height measurements are by nature subject to statistical sampling errors even for a single individual. In a clinical situation, height measurements are seldom taken more often than once per office visit, which may mean sampling taking place a week to several months apart. The smooth 50th percentile male and female growth curves illustrated above are aggregate values from thousands of individuals sampled at ages from birth to age 20. In reality, a single individual's growth curve shows large upward and downward spikes, partly due to actual differences in growth velocity, and partly due to small measurement errors.

For example, a typical measurement error of plus or minus 0.5cm (0.20in) may completely nullify 0.5 cm of actual growth resulting in either a "negative" 0.5 cm growth (due to overestimation in the previous visit combined with underestimation in the latter), up to a 1.5cm (0.6in) growth (the first visit underestimating and the second visit overestimating) in the same elapsed period between measurements. Note there is a discontinuity in the growth curves at age 2, which reflects the difference in recumbent length (with the child on his or her back), used in measuring infants and toddlers, and standing height typically measured from age 2 onwards.

Height, like other phenotypic traits, is determined by a combination of genetics and environmental factors. A child's height based on parental heights is subject to regression toward the mean, therefore extremely tall or short parents will likely have correspondingly taller or shorter offspring, but their offspring will also likely be closer to average height than the parents themselves. Genetic potential and several hormones, minus illness, is a basic determinant for height. Other factors include the genetic response to external factors such as diet, exercise, environment, and life circumstances.

Humans grow fastest (other than in the womb) as infants and toddlers, rapidly declining from a maximum at birth to roughly age 2, tapering to a slowly declining rate, and then, during the pubertal growth spurt (with an average girl starting her puberty and pubertal growth spurt at 10 years[21] and an average boy starting his puberty and pubertal growth spurt at 12 years[22][23]), a rapid rise to a second maximum (at around 1112 years for an average female, and 1314 years for an average male), followed by a steady decline to zero. The average female growth speed trails off to zero at about 15 or 16 years, whereas the average male curve continues for approximately 3 more years, going to zero at about 1819. These are also critical periods where stressors such as malnutrition (or even severe child neglect) have the greatest effect.

Moreover, the health of a mother throughout her life, especially during her critical period and pregnancy, has a role. A healthier child and adult develops a body that is better able to provide optimal prenatal conditions.[19] The pregnant mother's health is essential for herself but also the fetus as gestation is itself a critical period for an embryo/fetus, though some problems affecting height during this period are resolved by catch-up growth assuming childhood conditions are good. Thus, there is a cumulative generation effect such that nutrition and health over generations influence the height of descendants to vary degrees.

The age of the mother also has some influence on her child's height. Studies in modern times have observed a gradual increase in height with maternal age, though these early studies suggest that trend is due to various socio-economic situations that select certain demographics as being more likely to have a first birth early in the mother's life.[24][25][26] These same studies show that children born to a young mother are more likely to have below-average educational and behavioural development, again suggesting an ultimate cause of resources and family status rather than a purely biological explanation.[25][26]

It has been observed that first-born males are shorter than later-born males.[27]However, more recently the reverse observation was made.[28] The study authors suggest that the cause may be socio-economic in nature.

The precise relationship between genetics and environment is complex and uncertain. Differences in human height is 6080% heritable, according to several twin studies[29] and has been considered polygenic since the Mendelian-biometrician debate a hundred years ago. A genome-wide association (GWA) study of more than 180,000 individuals has identified hundreds of genetic variants in at least 180 loci associated with adult human height.[30] The number of individuals has since been expanded to 253,288 individuals and the number of genetic variants identified is 697 in 423 genetic loci.[31] In a separate study of body proportion using sitting-height ratio, it reports that these 697 variants can be partitioned into 3 specific classes, (1) variants that primarily determine leg length, (2) variants that primarily determine spine and head length, or (3) variants that affect overall body size. This gives insights into the biological mechanisms underlying how these 697 genetic variants affect overall height.[32] These loci do not only determine height, but other features or characteristics. As an example, 4 of the 7 loci identified for intracranial volume had previously been discovered for human height.[33]

The effect of environment on height is illustrated by studies performed by anthropologist Barry Bogin and coworkers of Guatemala Mayan children living in the United States. In the early 1970s, when Bogin first visited Guatemala, he observed that Mayan Indian men averaged 157.5 centimetres (5ft 2in) in height and the women averaged 142.2 centimetres (4ft 8in). Bogin took another series of measurements after the Guatemalan Civil War, during which up to a million Guatemalans fled to the United States. He discovered that Maya refugees, who ranged from six to twelve years old, were significantly taller than their Guatemalan counterparts.[34] By 2000, the American Maya were 10.24cm (4.03in) taller than the Guatemalan Maya of the same age, largely due to better nutrition and health care.[35] Bogin also noted that American Maya children had relatively longer legs, averaging 7.02cm (2.76in) longer than the Guatemalan Maya (a significantly lower sitting height ratio).[35][36]

The Nilotic peoples of Sudan such as the Shilluk and Dinka have been described as some of the tallest in the world. Dinka Ruweng males investigated by Roberts in 195354 were on average 181.3 centimetres (5ft 11+12in) tall, and Shilluk males averaged 182.6 centimetres (6ft 0in).[37] The Nilotic people are characterized as having long legs, narrow bodies and short trunks, an adaptation to hot weather.[38] However, male Dinka and Shilluk refugees measured in 1995 in Southwestern Ethiopia were on average only 176.4cm (5ft 9+12in) and 172.6cm (5ft 8in) tall, respectively. As the study points out, Nilotic people "may attain greater height if privileged with favourable environmental conditions during early childhood and adolescence, allowing full expression of the genetic material."[39] Before fleeing, these refugees were subject to privation as a consequence of the succession of civil wars in their country from 1955 to the present.

The tallest living married couple are ex-basketball players Yao Ming and Ye Li (both of China) who measure 228.6cm (7ft 6in) and 190.5cm (6ft 3in) respectively, giving a combined height of 419.1cm (13ft 9in). They married in Shanghai, China, on 6 August 2007.[40]

In Tibet, the Khampas are known for their great height. Khampa males are on average 180cm (5ft 11in).[41][42]

Studies show that there is a correlation between small stature and a longer life expectancy. Individuals of small stature are also more likely to have lower blood pressure and are less likely to acquire cancer. The University of Hawaii has found that the longevity gene FOXO3 that reduces the effects of aging is more commonly found in individuals of a small body size.[7] Short stature decreases the risk of venous insufficiency.[8] Certain studies have shown that height is a factor in overall health while some suggest tallness is associated with better cardiovascular health and shortness with longevity.[43] Cancer risk has also been found to grow with height.[44] Moreover, scientists have also observed a protective effect of height on risk for Alzheimer's disease, although this fact could be a result of the genetic overlap between height and intracraneal volume and there are also genetic variants influencing height that could affect biological mechanisms involved in Alzheimer's disease etiology, such as Insulin-like growth factor 1 (IGF-1).[45]

Nonetheless, modern westernized interpretations of the relationship between height and health fail to account for the observed height variations worldwide.[46] Cavalli-Sforza and Cavalli-Sforza note that variations in height worldwide can be partly attributed to evolutionary pressures resulting from differing environments. These evolutionary pressures result in height-related health implications. While tallness is an adaptive benefit in colder climates such as those found in Europe, shortness helps dissipate body heat in warmer climatic regions.[46] Consequently, the relationships between health and height cannot be easily generalized since tallness and shortness can both provide health benefits in different environmental settings.

In the end, being excessively tall can cause various medical problems, including cardiovascular problems, because of the increased load on the heart to supply the body with blood, and problems resulting from the increased time it takes the brain to communicate with the extremities. For example, Robert Wadlow, the tallest man known to verifiable history, developed trouble walking as his height increased throughout his life. In many of the pictures of the latter portion of his life, Wadlow can be seen gripping something for support. Late in his life, although he died at age 22, he had to wear braces on his legs and walk with a cane; and he died after developing an infection in his legs because he was unable to feel the irritation and cutting caused by his leg braces.

Sources are in disagreement about the overall relationship between height and longevity. Samaras and Elrick, in the Western Journal of Medicine, demonstrate an inverse correlation between height and longevity in several mammals including humans.[43]

Women whose height is under 150cm (4ft 11in) may have a small pelvis, resulting in such complications during childbirth as shoulder dystocia.[47]

A study done in Sweden in 2005 has shown that there is a strong inverse correlation between height and suicide among Swedish men.[48]

A large body of human and animal evidence indicates that shorter, smaller bodies age more slowly, and have fewer chronic diseases and greater longevity. For example, a study found eight areas of support for the "smaller lives longer" thesis. These areas of evidence include studies involving longevity, life expectancy, centenarians, male vs. female longevity differences, mortality advantages of shorter people, survival findings, smaller body size due to calorie restriction, and within-species body size differences. They all support the conclusion that smaller individuals live longer in healthy environments and with good nutrition. However, the difference in longevity is modest. Several human studies have found a loss of 0.5 years/centimeter of increased height (1.2 yr/inch). But these findings do not mean that all tall people die young. Many live to advanced ages and some become centenarians.[49][dubious discuss]

In medicine, height is measured to monitor child development, this is a better indicator of growth than weight in the long term.[50]For older people, excessive height loss is a symptom of osteoporosis.[51] Height is also used to compute indicators like body surface area or body mass index.

There is a large body of research in psychology, economics, and human biology that has assessed the relationship between several physical features (e.g., body height) and occupational success.[52] The correlation between height and success was explored decades ago.[53][54] Shorter people are considered to have an advantage in certain sports (e.g., gymnastics, race car driving, etc.), whereas in many other sports taller people have a major advantage. In most occupational fields, body height is not relevant to how well people are able to perform; nonetheless several studies found that success was positively correlated with body height, although there may be other factors such as gender or socioeconomic status that are correlated with height which may account for the difference in success.[52][53][55][56]

A demonstration of the height-success association can be found in the realm of politics. In the United States presidential elections, the taller candidate won 22 out of 25 times in the 20th century.[57] Nevertheless, Ignatius Loyola, founder of the Jesuits, was 150cm (4ft 11in) and several prominent world leaders of the 20th century, such as Vladimir Lenin, Benito Mussolini, Nicolae Ceauescu and Joseph Stalin were of below-average height. These examples, however, were all before modern forms of multi-media, i.e., television, which may further height discrimination in modern society. Further, growing evidence suggests that height may be a proxy for confidence, which is likewise strongly correlated with occupational success.[58]

In the 150 years since the mid-nineteenth century, the average human height in industrialised countries has increased by up to 10 centimetres (3.9in).[59] However, these increases appear to have largely levelled off.[59][60] Before the mid-nineteenth century, there were cycles in height, with periods of increase and decrease;[61] however, apart from the decline associated with the transition to agriculture, examinations of skeletons show no significant differences in height from the neolithic revolution through the early-1800s.[62][63]

In general, there were no significant differences in regional height levels throughout the nineteenth century.[64] The only exceptions of this rather uniform height distribution were people in the Anglo-Saxon settlement regions who were taller than the average and people from Southeast Asia with below-average heights. However, at the end of the nineteenth century and in the middle of the first globalization period, heights between rich and poor countries began to diverge.[65] These differences did not disappear in the deglobalization period of the two World wars. Baten and Blum (2014) [66] find that in the nineteenth century, important determinants of height were the local availability of cattle, meat and milk as well as the local disease environment. In the late twentieth century, however, technologies and trade became more important, decreasing the impact of local availability of agricultural products.

In the eighteenth and nineteenth centuries, people of European descent in North America were far taller than those in Europe and were the tallest in the world.[14] The original indigenous population of Plains Native Americans was also among the tallest populations of the world at the time.[67]

Some studies also suggest that there existed the correlation between the height and the real wage, moreover, the correlation was higher among the less developed countries. The difference in height between children from different social classes was already observed by age two.[68]

In the late nineteenth century, the Netherlands was a land renowned for its short population, but today Dutch people are among the world's tallest with young men averaging 183.8cm (6ft 0.4in) tall.[69]

According to a study by economist John Komlos and Francesco Cinnirella, in the first half of the eighteenth century, the average height of an English male was 165cm (5ft 5in), and the average height of an Irish male was 168cm (5ft 6in). The estimated mean height of English, German, and Scottish soldiers was 163.6cm (5ft 4+12in) 165.9cm (5ft 5+12in) for the period as a whole, while that of Irish was 167.9cm (5ft 6in). The average height of male slaves and convicts in North America was 171cm (5ft 7+12in).[70]

The average height of Americans and Europeans decreased during periods of rapid industrialization, possibly due to rapid population growth and broad decreases in economic status.[71] This has become known as the early-industrial growth puzzle in the U.S. context the Antebellum Puzzle. In England during the early nineteenth century, the difference between the average height of English upper-class youth (students of Sandhurst Military Academy) and English working-class youth (Marine Society boys) reached 22cm (8+12in), the highest that has been observed.[72]

Data derived from burials show that before 1850, the mean stature of males and females in Leiden, The Netherlands was respectively 167.7cm (5ft 6in) and 156.7cm (5ft 1+12in). The average height of 19-year-old Dutch orphans in 1865 was 160cm (5ft 3in).[73]

According to a study by J.W. Drukker and Vincent Tassenaar, the average height of a Dutch person decreased from 1830 to 1857, even while Dutch real GNP per capita was growing at an average rate of more than 0.5% per year. The worst decline was in urban areas that in 1847, the urban height penalty was 2.5cm (0.98in). Urban mortality was also much higher than in rural regions. In 1829, the average urban and rural Dutchman was 164cm (5ft 4+12in). By 1856, the average rural Dutchman was 162cm (5ft 4in) and urban Dutchman was 158.5cm (5ft 2+12in).[74]

A 2004 report citing a 2003 UNICEF study on the effects of malnutrition in North Korea, due to "successive famines," found young adult males to be significantly shorter.[specify] In contrast South Koreans "feasting on an increasingly Western-influenced diet," without famine, were growing taller. The height difference is minimal for Koreans over forty years old, who grew up at a time when economic conditions in the North were roughly comparable to those in the South, while height disparities are most acute for Koreans who grew up in the mid-1990s a demographic in which South Koreans are about 12cm (4.7in) taller than their North Korean counterparts as this was a period during which the North was affected by a harsh famine where hundreds of thousands, if not millions, died of hunger.[75] A study by South Korean anthropologists of North Korean children who had defected to China found that eighteen-year-old males were 13 centimetres (5in) shorter than South Koreans their age due to malnutrition.[76]

The tallest living man is Sultan Ksen of Turkey, at 251cm (8ft 3in). The tallest man in modern history was Robert Pershing Wadlow (19181940), from Illinois, United States, who was 272cm (8ft 11in) at the time of his death. The tallest woman in medical history was Trijntje Keever of Edam, Netherlands, who stood 254cm (8ft 4in) when she died at the age of seventeen. The shortest adult human on record was Chandra Bahadur Dangi of Nepal at 54.6cm (1ft 9+12in).

An anecdotal article titled "Ancient American Giants" from the 14 August 1880 edition of Scientific American notes a case from Brushcreek Township, Ohio, when Dr. J. F. Everhart supervised a team that discovered ancient clay coffins within a mound which were reported to contain skeletons of the following length: 8ft 0in (2.44m) woman with a child 3.5ft 0in (1.07m), a second coffin with a 9ft 0in (2.74m) man and 8ft 0in (2.44m) woman, a third coffin with a 9ft 4in (2.84m) man and 8ft 0in (2.44m) woman, and seven other independent skeletons measuring between 8ft 0in (2.44m) and 10ft 0in (3.05m). An image and stone tablet were found with the giants.[77]

Adult height between populations often differs significantly. For example, the average height of women from the Czech Republic is greater than that of men from Malawi. This may be caused by genetic differences, childhood lifestyle differences (nutrition, sleep patterns, physical labor), or both.

Depending on sex, genetic and environmental factors, shrinkage of stature may begin in middle age in some individuals but tends to be universal in the extremely aged. This decrease in height is due to such factors as decreased height of inter-vertebral discs because of desiccation, atrophy of soft tissues, and postural changes secondary to degenerative disease.

Working on data of Indonesia, the study by Baten, Stegl and van der Eng suggests a positive relationship of economic development and average height. In Indonesia, human height has decreased coincidentally with natural or political shocks.[78]

As with any statistical data, the accuracy of such data may be questionable for various reasons:

Crown-rump length is the measurement of the length of human embryos and fetuses from the top of the head (crown) to the bottom of the buttocks (rump). It is typically determined from ultrasound imagery and can be used to estimate gestational age.

Until two years old, recumbent length is used to measure infants.[92] Length measures the same dimension as height, but height is measured standing up while the length is measured lying down. In developed nations, the average total body length of a newborn is about 50cm (20in), although premature newborns may be much smaller.

Standing height is used to measure children over two years old[93] and adults who can stand without assistance. Measure is done with a stadiometer. In general, standing height is about 0.7cm (0.28in) less than recumbent length.[94]

Surrogate height measurements are used when standing height and recumbent length are impractical. For sample Chumlea equation use knee height as indicator of stature.[95] Other techniques include: arm span, sitting height, ulna length, etc.

Original post:
Human height - Wikipedia

Medical condition

Pattern hair loss (also known as androgenetic alopecia (AGA)[1]) is a hair loss condition that primarily affects the top and front of the scalp.[2][3] In male-pattern hair loss (MPHL), the hair loss typically presents itself as either a receding front hairline, loss of hair on the crown (vertex) of the scalp, or a combination of both. Female-pattern hair loss (FPHL) typically presents as a diffuse thinning of the hair across the entire scalp.[3]

Male pattern hair loss seems to be due to a combination of oxidative stress,[4] the microbiome of the scalp,[5][6] genetics, and circulating androgens; particularly dihydrotestosterone (DHT).[3] Men with early onset androgenic alopecia (before the age of 35) have been deemed as the male phenotypic equivalent for polycystic ovary syndrome (PCOS).[7][8][9][10] As an early clinical expression of insulin resistance and metabolic syndrome, AGA is related to being an increased risk factor for cardiovascular diseases, glucose metabolism disorders,[11] type 2 diabetes,[12][13] and enlargement of the prostate.[14]

The cause in female pattern hair loss remains unclear,[3] androgenetic alopecia for women is associated with an increased risk of polycystic ovary syndrome (PCOS).[15][16][17]

Management may include simply accepting the condition[3] or shaving one's head to improve the aesthetic aspect of the condition.[18] Otherwise, common medical treatments include minoxidil, finasteride, dutasteride, or hair transplant surgery.[3] Use of finasteride and dutasteride in women is not well-studied and may result in birth defects if taken during pregnancy.[3]

Pattern hair loss by the age of 50 affects about half of males and a quarter of females.[3] It is the most common cause of hair loss. Both males aged 4091 [19] and younger male patients of early onset AGA (before the age of 35), had a higher likelihood of metabolic syndrome (MetS) [20][21][22][23] and insulin resistance.[24] With younger males, studies found metabolic syndrome to be at approximately a 4x increased frequency which is clinically deemed as significant.[25][26] Abdominal obesity, hypertension and lowered high density lipoprotein were also significantly higher for younger groups.[27]

Pattern hair loss is classified as a form of non-scarring hair loss.

Male-pattern hair loss begins above the temples and at the vertex (calvaria) of the scalp. As it progresses, a rim of hair at the sides and rear of the head remains. This has been referred to as a "Hippocratic wreath", and rarely progresses to complete baldness.[28]

Female-pattern hair loss more often causes diffuse thinning without hairline recession; similar to its male counterpart, female androgenic alopecia rarely leads to total hair loss.[29] The Ludwig scale grades severity of female-pattern hair loss. These include Grades 1, 2, 3 of balding in women based on their scalp showing in the front due to thinning of hair.[citation needed]

In most cases, receding hairline is the first starting point; the hairline starts moving backwards from the front of the head and the sides.[30][citation needed]

KRT37 is the only keratin that is regulated by androgens.[31] This sensitivity to androgens was acquired by Homo sapiens and is not shared with their great ape cousins. Although Winter et al. found that KRT37 is expressed in all the hair follices of chimpanzees, it was not detected in the head hair of modern humans. As androgens are known to grow hair on the body, but decrease it on the scalp, this lack of scalp KRT37 may help explain the paradoxical nature of Androgenic alopecia as well as the fact that head hair anagen cycles are extremely long.[citation needed]

The initial programming of pilosebaceous units of hair follicles begins in utero.[32] The physiology is primarily androgenic, with dihydrotestosterone (DHT) being the major contributor at the dermal papillae. Men with premature androgenic alopecia tend to have lower than normal values of sex hormone-binding globulin (SHBG), follicle stimulating hormone (FSH), testosterone, and epitestosterone when compared to men without pattern hair loss.[10] Although hair follicles were previously thought to be permanently gone in areas of complete hair loss, they are more likely dormant, as recent studies have shown the scalp contains the stem cell progenitor cells from which the follicles arose.[33][34][non-primary source needed]

Transgenic studies have shown that growth and dormancy of hair follicles are related to the activity of insulin-like growth factor (IGF) at the dermal papillae, which is affected by DHT. Androgens are important in male sexual development around birth and at puberty. They regulate sebaceous glands, apocrine hair growth, and libido. With increasing age, androgens stimulate hair growth on the face, but can suppress it at the temples and scalp vertex, a condition that has been referred to as the 'androgen paradox'.[35]

Men with androgenic alopecia typically have higher 5-reductase, higher total testosterone, higher unbound/free testosterone, and higher free androgens, including DHT.[36] 5-alpha-reductase converts free testosterone into DHT, and is highest in the scalp and prostate gland. DHT is most commonly formed at the tissue level by 5-reduction of testosterone.[37] The genetic corollary that codes for this enzyme has been discovered.[38] Prolactin has also been suggested to have different effects on the hair follicle across gender.[39]

Also, crosstalk occurs between androgens and the Wnt-beta-catenin signaling pathway that leads to hair loss. At the level of the somatic stem cell, androgens promote differentiation of facial hair dermal papillae, but inhibit it at the scalp.[35] Other research suggests the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles as contributive.[40]

These observations have led to study at the level of the mesenchymal dermal papillae.[41] Types 1 and 2 5 reductase enzymes are present at pilosebaceous units in papillae of individual hair follicles.[42] They catalyze formation of the androgens testosterone and DHT, which in turn regulate hair growth.[35] Androgens have different effects at different follicles: they stimulate IGF-1 at facial hair, leading to growth, but can also stimulate TGF 1, TGF 2, dickkopf1, and IL-6 at the scalp, leading to catagenic miniaturization.[35] Hair follicles in anaphase express four different caspases. Significant levels of inflammatory infiltrate have been found in transitional hair follicles.[43] Interleukin 1 is suspected to be a cytokine mediator that promotes hair loss.[44]

The fact that hair loss is cumulative with age while androgen levels fall as well as the fact that finasteride does not reverse advanced stages of androgenetic alopecia remains a mystery, but possible explanations are higher conversion of testosterone to DHT locally with age as higher levels of 5-alpha reductase are noted in balding scalp, and higher levels of DNA damage in the dermal papilla as well as senescence of the dermal papilla due to androgen receptor activation and environmental stress.[45] The mechanism by which the androgen receptor triggers dermal papilla permanent senescence is not known, but may involve IL6, TGFB-1 and oxidative stress. Senescence of the dermal papilla is measured by lack of mobility, different size and shape, lower replication and altered output of molecules and different expression of markers. The dermal papilla is the primary location of androgen action and its migration towards the hair bulge and subsequent signaling and size increase are required to maintain the hair follicle so senescence via the androgen receptor explains much of the physiology.[citation needed]

Male pattern baldness is a complex genetic condition with a "particularly strong signals on the X chromosome".[46]

Multiple cross-sectional studies have found associations between early androgenic alopecia, insulin resistance, and metabolic syndrome,[47][48] with low HDL being the component of metabolic syndrome with highest association.[49] Linolenic and linoleic acids, two major dietary sources of HDL, are 5 alpha reductase inhibitors.[50] Premature androgenic alopecia and insulin resistance may be a clinical constellation that represents the male homologue, or phenotype, of polycystic ovary syndrome.[51] Others have found a higher rate of hyperinsulinemia in family members of women with polycystic ovarian syndrome.[52] With early-onset AGA having an increased risk of metabolic syndrome, poorer metabolic profiles are noticed in those with AGA, including metrics for body mass index, waist circumference, fasting glucose, blood lipids, and blood pressure.[53]

In support of the association, finasteride improves glucose metabolism and decreases glycated hemoglobin HbA1c, a surrogate marker for diabetes mellitus.[54] The low SHBG seen with premature androgenic alopecia is also associated with, and likely contributory to, insulin resistance,[55] and for which it still is used as an assay for pediatric diabetes mellitus.[56]

Obesity leads to upregulation of insulin production and decrease in SHBG. Further reinforcing the relationship, SHBG is downregulated by insulin in vitro, although SHBG levels do not appear to affect insulin production.[57] In vivo, insulin stimulates both testosterone production and SHBG inhibition in normal and obese men.[58] The relationship between SHBG and insulin resistance has been known for some time; decades prior, ratios of SHBG and adiponectin were used before glucose to predict insulin resistance.[59] Patients with Laron syndrome, with resultant deficient IGF, demonstrate varying degrees of alopecia and structural defects in hair follicles when examined microscopically.[60]

Because of its association with metabolic syndrome and altered glucose metabolism, both men and women with early androgenic hair loss should be screened for impaired glucose tolerance and diabetes mellitus II.[10] Measurement of subcutaneous and visceral adipose stores by MRI, demonstrated inverse association between visceral adipose tissue and testosterone/DHT, while subcutaneous adipose correlated negatively with SHBG and positively with estrogen.[61] SHBG association with fasting blood glucose is most dependent on intrahepatic fat, which can be measured by MRI in and out of phase imaging sequences. Serum indices of hepatic function and surrogate markers for diabetes, previously used, show less correlation with SHBG by comparison.[62]

Female patients with mineralocorticoid resistance present with androgenic alopecia.[63]

IGF levels have been found lower in those with metabolic syndrome.[64] Circulating serum levels of IGF-1 are increased with vertex balding, although this study did not look at mRNA expression at the follicle itself.[65] Locally, IGF is mitogenic at the dermal papillae and promotes elongation of hair follicles. The major site of production of IGF is the liver, although local mRNA expression at hair follicles correlates with increase in hair growth. IGF release is stimulated by growth hormone (GH). Methods of increasing IGF include exercise, hypoglycemia, low fatty acids, deep sleep (stage IV REM), estrogens, and consumption of amino acids such as arginine and leucine. Obesity and hyperglycemia inhibit its release. IGF also circulates in the blood bound to a large protein whose production is also dependent on GH. GH release is dependent on normal thyroid hormone. During the sixth decade of life, GH decreases in production. Because growth hormone is pulsatile and peaks during sleep, serum IGF is used as an index of overall growth hormone secretion. The surge of androgens at puberty drives an accompanying surge in growth hormone.[66]

A number of hormonal changes occur with aging:

This decrease in androgens and androgen receptors, and the increase in SHBG are opposite the increase in androgenic alopecia with aging. This is not intuitive, as testosterone and its peripheral metabolite, DHT, accelerate hair loss, and SHBG is thought to be protective. The ratio of T/SHBG, DHT/SHBG decreases by as much as 80% by age 80, in numeric parallel to hair loss, and approximates the pharmacology of antiandrogens such as finasteride.[69]

Free testosterone decreases in men by age 80 to levels double that of a woman at age 20. About 30% of normal male testosterone level, the approximate level in females, is not enough to induce alopecia; 60%, closer to the amount found in elderly men, is sufficient.[70] The testicular secretion of testosterone perhaps "sets the stage" for androgenic alopecia as a multifactorial diathesis stress model, related to hormonal predisposition, environment, and age. Supplementing eunuchs with testosterone during their second decade, for example, causes slow progression of androgenic alopecia over many years, while testosterone late in life causes rapid hair loss within a month.[71]

An example of premature age effect is Werner's syndrome, a condition of accelerated aging from low-fidelity copying of mRNA. Affected children display premature androgenic alopecia.[72]

Permanent hair-loss is a result of reduction of the number of living hair matrixes. Long-term of insufficiency of nutrition is an important cause for the death of hair matrixes. Misrepair-accumulation aging theory [73][74] suggests that dermal fibrosis is associated with the progressive hair-loss and hair-whitening in old people.[75] With age, the dermal layer of the skin has progressive deposition of collagen fibers, and this is a result of accumulation of Misrepairs of derma. Fibrosis makes the derma stiff and makes the tissue have increased resistance to the walls of blood vessels. The tissue resistance to arteries will lead to the reduction of blood supply to the local tissue including the papillas. Dermal fibrosis is progressive; thus the insufficiency of nutrition to papillas is permanent. Senile hair-loss and hair-whitening are partially a consequence of the fibrosis of the skin.

The diagnosis of androgenic alopecia can be usually established based on clinical presentation in men. In women, the diagnosis usually requires more complex diagnostic evaluation. Further evaluation of the differential requires exclusion of other causes of hair loss, and assessing for the typical progressive hair loss pattern of androgenic alopecia.[76] Trichoscopy can be used for further evaluation.[77] Biopsy may be needed to exclude other causes of hair loss,[78] and histology would demonstrate perifollicular fibrosis.[79][80] The HamiltonNorwood scale has been developed to grade androgenic alopecia in males by severity.

Finasteride is a medication of the 5-reductase inhibitors (5-ARIs) class.[81] By inhibiting type II 5-AR, finasteride prevents the conversion of testosterone to dihydrotestosterone in various tissues including the scalp.[81][82] Increased hair on the scalp can be seen within three months of starting finasteride treatment and longer-term studies have demonstrated increased hair on the scalp at 24 and 48 months with continued use.[82] Treatment with finasteride more effectively treats male-pattern hair loss at the crown than male-pattern hair loss at the front of the head and temples.[82]

Dutasteride is a medication in the same class as finasteride but inhibits both type I and type II 5-alpha reductase.[82] Dutasteride is approved for the treatment of male-pattern hair loss in Korea and Japan, but not in the United States.[82] However, it is commonly used off-label to treat male-pattern hair loss.[82]

Minoxidil dilates small blood vessels; it is not clear how this causes hair to grow.[83] Other treatments include tretinoin combined with minoxidil, ketoconazole shampoo, dermarolling (Collagen induction therapy), spironolactone,[84] alfatradiol, topilutamide (fluridil),[81] topical melatonin,[85][86][87] and intradermal and intramuscular botulinum toxin injections to the scalp.[88]

There is evidence supporting the use of minoxidil as a safe and effective treatment for female pattern hair loss, and there is no significant difference in efficiency between 2% and 5% formulations.[89] Finasteride was shown to be no more effective than placebo based on low-quality studies.[89] The effectiveness of laser-based therapies is unclear.[89] Bicalutamide, an antiandrogen, is another option for the treatment of female pattern hair loss.[90][4][91]

More advanced cases may be resistant or unresponsive to medical therapy and require hair transplantation. Naturally occurring units of one to four hairs, called follicular units, are excised and moved to areas of hair restoration.[84] These follicular units are surgically implanted in the scalp in close proximity and in large numbers. The grafts are obtained from either follicular unit transplantation (FUT) or follicular unit extraction (FUE). In the former, a strip of skin with follicular units is extracted and dissected into individual follicular unit grafts, and in the latter individual hairs are extracted manually or robotically. The surgeon then implants the grafts into small incisions, called recipient sites.[92][93] Cosmetic scalp tattoos can also mimic the appearance of a short, buzzed haircut.

Many people use unproven treatments.[94] Regarding female pattern alopecia, there is no evidence for vitamins, minerals, or other dietary supplements.[95] As of 2008, there is little evidence to support the use of lasers to treat male-pattern hair loss.[96] The same applies to special lights.[95] Dietary supplements are not typically recommended.[96] A 2015 review found a growing number of papers in which plant extracts were studied but only one randomized controlled clinical trial, namely a study in 10 people of saw palmetto extract.[97][98]

Androgenic alopecia is typically experienced as a "moderately stressful condition that diminishes body image satisfaction".[99] However, although most men regard baldness as an unwanted and distressing experience, they usually are able to cope and retain integrity of personality.[100]

Although baldness is not as common in women as in men, the psychological effects of hair loss tend to be much greater. Typically, the frontal hairline is preserved, but the density of hair is decreased on all areas of the scalp. Previously, it was believed to be caused by testosterone just as in male baldness, but most women who lose hair have normal testosterone levels.[101]

Female androgenic alopecia has become a growing problem that, according to the American Academy of Dermatology, affects around 30million women in the United States. Although hair loss in females normally occurs after the age of 50 or even later when it does not follow events like pregnancy, chronic illness, crash diets, and stress among others, it is now occurring at earlier ages with reported cases in women as young as 15 or 16.[102]

For male androgenic alopecia, by the age of 50 30-50% of men have it, hereditarily there is an 80% predisposition.[103] Notably, the link between androgenetic alopecia and metabolic syndrome is strongest in non-obese men.[104]

Studies have been inconsistent across cultures regarding how balding men rate on the attraction scale. While a 2001 South Korean study showed that most people rated balding men as less attractive,[105] a 2002 survey of Welsh women found that they rated bald and gray-haired men quite desirable.[106] One of the proposed social theories for male pattern hair loss is that men who embraced complete baldness by shaving their heads subsequently signaled dominance, high social status, and/or longevity.[18]

Biologists have hypothesized the larger sunlight-exposed area would allow more vitamin D to be synthesized, which might have been a "finely tuned mechanism to prevent prostate cancer" as the malignancy itself is also associated with higher levels of DHT.[107]

Many myths exist regarding the possible causes of baldness and its relationship with one's virility, intelligence, ethnicity, job, social class, wealth, and many other characteristics.

Because it increases testosterone levels, many Internet forums[which?] have put forward the idea that weight training and other forms of exercise increase hair loss in predisposed individuals. Although scientific studies do support a correlation between exercise and testosterone, no direct study has found a link between exercise and baldness. However, a few have found a relationship between a sedentary life and baldness, suggesting exercise is causally relevant. The type or quantity of exercise may influence hair loss.[108][109]Testosterone levels are not a good marker of baldness, and many studies actually show paradoxical low testosterone in balding persons, although research on the implications is limited.[citation needed]

Emotional stress has been shown to accelerate baldness in genetically susceptible individuals.[110]Stress due to sleep deprivation in military recruits lowered testosterone levels, but is not noted to have affected SHBG.[111] Thus, stress due to sleep deprivation in fit males is unlikely to elevate DHT, which is one cause of male pattern baldness. Whether sleep deprivation can cause hair loss by some other mechanism is not clear.

Levels of free testosterone are strongly linked to libido and DHT levels, but unless free testosterone is virtually nonexistent, levels have not been shown to affect virility. Men with androgenic alopecia are more likely to have a higher baseline of free androgens. However, sexual activity is multifactoral, and androgenic profile is not the only determining factor in baldness. Additionally, because hair loss is progressive and free testosterone declines with age, a male's hairline may be more indicative of his past than his present disposition.[112][113]

Many misconceptions exist about what can help prevent hair loss, one of these being that lack of sexual activity will automatically prevent hair loss. While a proven direct correlation exists between increased frequency of ejaculation and increased levels of DHT, as shown in a recent study by Harvard Medical School, the study suggests that ejaculation frequency may be a sign, rather than a cause, of higher DHT levels.[114] Another study shows that although sexual arousal and masturbation-induced orgasm increase testosterone concentration around orgasm, they reduce testosterone concentration on average, and because about 5% of testosterone is converted to DHT, ejaculation does not elevate DHT levels.[115]

The only published study to test correlation between ejaculation frequency and baldness was probably large enough to detect an association (1,390 subjects) and found no correlation, although persons with only vertex androgenetic alopecia had fewer female sexual partners than those of other androgenetic alopecia categories (such as frontal or both frontal and vertex). One study may not be enough, especially in baldness, where there is a complex with age.[116]

Animal models of androgenic alopecia occur naturally and have been developed in transgenic mice;[117] chimpanzees (Pan troglodytes); bald uakaris (Cacajao rubicundus); and stump-tailed macaques (Macaca speciosa and M. arctoides). Of these, macaques have demonstrated the greatest incidence and most prominent degrees of hair loss.[118][119]

Baldness is not a trait unique to human beings. One possible case study is about a maneless male lion in the Tsavo area. The Tsavo lion prides are unique in that they frequently have only a single male lion with usually seven or eight adult females, as opposed to four females in other lion prides. Male lions may have heightened levels of testosterone, which could explain their reputation for aggression and dominance, indicating that lack of mane may at one time have had an alpha correlation.[120]

Although primates do not go bald, their hairlines do undergo recession. In infancy the hairline starts at the top of the supraorbital ridge, but slowly recedes after puberty to create the appearance of a small forehead.[citation needed]

Diseases of the skin and appendages by morphology

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Pattern hair loss - Wikipedia

Figure 4.. Terminal differentiation of T EFF cells is dependent upon Pofut1 and associated with

(A) Differentially expressed genes in sgPofut1- compared to sgNTC-transduced P14 cells at day 7.5 post-infection (p.i.). Upregulated (orange) or downregulated (blue) transcripts [false discovery rate (FDR) < 0.05] are highlighted. Selective MP- and TE-associated genes are labelled. (B) Enrichment plots of cell cycle-related signatures. NES, normalized enrichment score. (C) Flow cytometry (left) and quantification (right) of BrdU incorporation. (D) UMAP plot of published scRNA-seq dataset of P14 cells at day 8 p.i. (Chen et al., 2019). Each dot corresponds to an individual cell. The number and frequency of cells in each of the color-coded clusters (clusters 13) are indi cated. (E) Violin plots of Klrg1, Cxcr3 or Il7r expression in clusters 13 from (D). (F) Gating str ategy (left) and quantification (right) of the proportions of TE (KLRG1hiCXCR3loCD127lo), MP (KLRG1loCXCR3hiCD127hi) and TINT (CXCR3hiCD127lo) cells among WT P14 cells. (G) PCA plot of TE, MP and TINT cells [gating strategy in (F)] at day 7.5 p.i., with the percentage of variance shown. (H) Quantification of the relative frequency of BrdU+ cells in MP and TINT cells compared to TE cells. (I) Diagram of the in vivo differentiation assay (left), flow cytometry of KLRG1 versus CXCR3 expression (middle), and quantification of TINT, TE and CXCR3hiCD127hi cells (right). Only representative plots of KLRG1 versus CXCR3 are shown (TE population is largely defined by KLRG1hiCXCR3lo cells, which constitute ~ 95% of TE cells). (J) Quantification of TE, MP and TINT cells in the indicated P14 cells. (K) UMAP plot of Pofut1-dependent signature [downregulated genes as identified in (A)] in published scRNA-seq dataset from (D) (Chen et al., 2019). (L) UMAP plot of scRNA-seq data from sgNTC- (in black, left) and sgPofut1- (in red, right) transduced P14 cells (from dual-color transfer system) at day 7 p.i. Gray shadow indicates location of all cells; the number of analyzed cells in each group is indicated. (M) UMAP plot of the expression of Klrg1 (left), Cxcr3 (middle) and Il7r (right) in scRNA-seq data described in (L). (N) Flow cytometry of KLRG1 versus CXCR3 expression (left) and quantification (right) of TE cells in the in vivo differentiation assay similar as (I), except for the use of both wild-type and Pofut1-null TINT groups as the pretransfer cells. Data are from one (A, B, D, E, G, and KM), representative of two (C, H, and N), or compiled from at least two (I, J, and N) independent experiments, with 4 (A, C, G, H, and I), 17 (F), 11 (J), or 3 (L and N) biological replicates per group. *P < 0.05, **P < 0.01, and ***P < 0.001; NS, not significant; two-tailed paired Students t-test (C), two-tailed unpaired Students t-test (I, J, and N), or one-way analysis of variance (ANOVA) (F and H). Data are presented as mean s.e.m. See also Figures S4S6 and Tables S3S6.

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In vivo CRISPR screening reveals nutrient signaling processes ... - PubMed

A risk factor is anything that affects your chance of getting a disease, such as breast cancer.

But having a risk factor, or even many, does not mean that you are sure to get the disease. Some men with one or more breast cancer risk factors never develop the disease, while most men with breast cancer have no apparent risk factors.

We don't yet completely understand the causes of breast cancer in men, but researchers have found several factors that may increase the risk of getting it. As with female breast cancer, many of these factors are related to your body's sex hormone levels.

Aging is an important risk factor for the development of breast cancer in men. The risk of breast cancer goes up as a man ages. On average, men with breast cancer are about 72 years old when they are diagnosed.

Breast cancer risk is increased if other members of the family (blood relatives) have had breast cancer. About 1 out of 5 men with breast cancer have a close relative, male or female, with the disease.

Men with a mutation (defect) in the BRCA2 gene have an increased risk of breast cancer, with a lifetime risk of about 6 in 100. BRCA1 mutations can also cause breast cancer in men, but the risk is lower, about 1 in 100.

Although mutations in these genes most often are found in members of families with many cases of breast and/or ovarian cancer, they have also been found in men with breast cancer who did not have a strong family history.

Mutations in CHEK2, PTEN and PALB2 genesmight also be responsible for some breast cancers in men.

Klinefelter syndrome is a congenital (present at birth) condition that affects about 1 in 1,000 men. Normally the cells in men's bodies have a single X chromosome along with a Y chromosome, while women's cells have two X chromosomes. Men with Klinefelter syndrome have cells with a Y chromosome plus at least two X chromosomes (but sometimes more).

Men with Klinefelter syndrome also have small testicles and are often infertile because they are unable to produce functioning sperm cells. Compared with other men, they have lower levels of androgens (male hormones) and more estrogens (female hormones). For this reason, they often develop gynecomastia (benign male breast growth).

Men with Klinefelter syndrome are more likely to get breast cancer than other men. Having this condition can increase the risk anywhere between 20 - 60 times the risk of a man in the general population.

A man whose chest area has been treated with radiation (such as for the treatment of a cancer in the chest, like lymphoma) has an increased risk of developing breast cancer.

Heavy drinking (of alcoholic beverages) increases the risk of breast cancer in men. This may be because of its effects on the liver (see next paragraph).

The liver plays an important role in balancing the levels of sex hormones. In cases of severe liver disease, such as cirrhosis, the liver is not working well and the hormone levels are uneven, causinglower levels of androgens and higher levels of estrogen. Men with liver disease can also have a higher chance of developing benign male breast growth (gynecomastia) and also have an higher risk of developing breast cancer.

Estrogen-related drugs were once used in hormonal therapy for men with prostate cancer. This treatment may slightly increase breast cancer risk.

There is concern that transgender/transsexual individuals who take high doses of estrogens as part of sex reassignment could also have a higher breast cancer risk. Still, there havent been any studies of breast cancer risk in transgendered individuals, so it isnt clear what their breast cancer risk is.

Studies have shown that women's breast cancer risk is increased by obesity (being extremely overweight) after menopause. Obesity is also a risk factor for male breast cancer as well. The reason is that fat cells in the body convert male hormones (androgens) into female hormones (estrogens). This means that obese men have higher levels of estrogens in their body.

Certain conditions, such as having an undescended testicle, having mumps as an adult, or having one or both testicles surgically removed (orchiectomy) may increase male breast cancer risk.

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Risk Factors for Breast Cancer in Men - American Cancer Society

A

Adenine

Allele

Amino Acid

Aneuploidy

Animal Model

Anticodon

Antisense

Autism

Autosomal Dominant Disorder

Autosomal Recessive Disorder

Autosome

Base Pair

Bioinformatics

Birth Defect

BRCA1/BRCA2

Cancer

Cancer-Susceptibility Gene

Candidate Gene

Carcinogen

Carrier

Carrier Screening

Copy DNA (cDNA)

Cell-Free DNA Testing

Centimorgan (cM)

Central Dogma

Centromere

Chromatid

Chromatin

Chromosome

Cloning

Codominance

Codon

Complex Disease

Congenital

Contig

Copy Number Variation (CNV)

CRISPR

Crossing Over

Cystic Fibrosis (CF)

Cytogenetics

Cytosine

Data Science

Deletion

Deoxyribonucleic Acid (DNA)

Diploid

DNA Fingerprinting

DNA Replication

DNA Sequencing

Dominant Traits and Alleles

Double Helix

Down Syndrome (Trisomy 21)

Duplication

Electrophoresis

Environmental Factors

Epigenetics

Epistasis

Eugenics

Evolution

Exome

Exon

Family History

Fibroblast

First-Degree Relative

Fluorescence In Situ Hybridization (FISH)

Founder Effect

Fragile X Syndrome

Frameshift Mutation

Fraternal Twins

Gamete

Gender

Gene

Gene Amplification

Gene Expression

Gene Mapping

Gene Pool

Gene Regulation

Gene Therapy

GeneEnvironment Interaction

Genetic Ancestry

Genetic Code

Genetic Counseling

Genetic Discrimination

Genetic Drift

Genetic Engineering

Genetic Epidemiology

Genetic Imprinting

Genetic Information Nondiscrimination Act (GINA)

Genetic Map

Genetic Testing

Genetics

Genome

Genome-Wide Association Study (GWAS)

Genomic Medicine

Genomic Variation

Genomics

Genotype

Germ Line

Gigabase (Gb)

GMO (Genetically Modified Organism)

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Talking Glossary of Genetic Terms | NHGRI - Genome

We have the killers DNA, we just need a name: Genetic game changer offers hope for near-unsolvable Ontario cold cases  Toronto Star

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We have the killers DNA, we just need a name: Genetic game changer offers hope for near-unsolvable Ontario cold cases - Toronto Star

US leukemia patient becomes 1st woman & 3rd person in the world to be cured of HIV  Republic World

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US leukemia patient becomes 1st woman & 3rd person in the world to be cured of HIV - Republic World

Woman, 41, With Bubbles In Her Urine Dismissed By Doctors. Turns Out To Have The Blood Cancer Multiple Myeloma.  SurvivorNet

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Woman, 41, With Bubbles In Her Urine Dismissed By Doctors. Turns Out To Have The Blood Cancer Multiple Myeloma. - SurvivorNet

Given that death is one of the things people fear more than anything, its not surprising that weve been thinking for awhile about how we can thwart it.

Cryonics, which is the attempt to freeze the bodies of the recently deceased in the hope that they can be revived and cured later on, has a long and honestly pretty grim history.

An article published in 1992 detailed some of the more gruesome mistakes, probably in the hopes that future scientists would be able to learn from previous miscalculations.

One of the biggest issues is the freezing process itselfthe ice crystals that for in your cells will eventually destroy them beyond repair.

Basically, you remain a popsicle forever, because no one can revive you if you have no working cells.

Cryonics company Alcor defrosted three corpses in 1984 with the intention of checking what damage had been sustained. First, the bodies were converted to neuropreservation, which means their heads were preserved (ew), and then scientists dug in.

From the outside, the damage didnt look all that bad, resembling the type of cracking observed in deteriorating coatings, such as is seen in paint peeling away from a wall. The skin adjoining the fracture fissure was somewhat raised from the underlying fat and gave the appearance of having peeled away slightly.

Again, ew.

Deeper fractures were discovered, however, as the bodies thawed, and there was also plenty of organ damage to go around.

Examination of the internal organs of patient three revealed fractures present in almost every organ. The spinal cord, aorta, thoracic inferior vena cava, pulmonary artery, myocardium, right lung, liver, pericardium, stomach, ileum, colon, mesentery, spleen, skeletal muscle, and pancreas, were all seriously fractured.

Also? The spinal cord had been snapped in three places.

The team believed that all of the damage could be put down to the thawing process.

As cooling proceeds below the glass transition phase of water (TG), different organs and tissues within the patients body will begin to contract at different rates. However, because the system is now in a solid state, these materials, bonded to each other by ice/cryoprotective agent mixtures, will be unable to contract independently.

And this is what happens when everything goesright during the freezing process.

What happens if, for some reasons, bodies are not kept at the optimal temperature in their chambers?

Unsurprisingly, nothing pretty.

We know that because at least one company, started by Robert Nelson, saw too many storage, venue, and payment issues that resulted in him just eventually allowing the bodies in his care to thaw.

The stench near the crypt is disarming, strips away all defenses, spins the stomach into a thousand dizzying somersaults.

Nelson defended himself, though he likely realized they had not realized the best possible outcome.

I havent done anything criminal, anything wrong other than a lot of bad decisions. It didnt work. It failed. There was no money. Who can guarantee that youre going to be suspended for 10 or 15 years.

When malfunctions happen, families usually opt to bury their loved ones traditionally, though the reality of being the mortician in these cases is less than pleasant.

One detailed that they used a breathing apparatus when the capsule on its side had to be entered to remove the remains which had fallen to the bottom and frozen in place in a plug of body fluids.

Ew. Right?

Now that cryonics has garnered more financial backing and interest from those who are invested in its future, proponents are sure all of those hurdles will be overcome.

Only time will tell.

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The Gross And Horrifying Early Days Of Cryonics TwistedSifter

Slowing or stopping of life without death

Suspended animation is the temporary (short- or long-term) slowing or stopping of biological function so that physiological capabilities are preserved. It may be either hypometabolic or ametabolic in nature. It may be induced by either endogenous, natural or artificial biological, chemical or physical means. In its natural form it may be spontaneously reversible as in the case of species demonstrating hypometabolic states of hibernation or require technologically mediated revival when applied with therapeutic intent in the medical setting as in the case of deep hypothermic circulatory arrest (DHCA).[1][2]

Suspended animation is understood as the pausing of life processes by exogenous or endogenous means without terminating life itself.[3] Breathing, heartbeat and other involuntary functions may still occur, but they can only be detected by artificial means.[4] For this reason, this procedure has been associated with a lethargic state in nature when animals or plants appear, over a period, to be dead but then can wake up or prevail without suffering any harm. This has been termed in different contexts hibernation, dormancy or anabiosis (this last in some aquatic invertebrates and plants in scarcity conditions).

In July 2020, marine biologists reported that aerobic microorganisms (mainly), in "quasi-suspended animation", were found in organically-poor sediments, up to 101.5 million years old, 68.9 metres (226 feet) below the seafloor in the South Pacific Gyre (SPG) ("the deadest spot in the ocean"), and could be the longest-living life forms ever found.[5][6]

This condition of apparent death or interruption of vital signs may be similar to a medical interpretation of suspended animation. It is only possible to recover signs of life if the brain and other vital organs suffer no cell deterioration, necrosis or molecular death principally caused by oxygen deprivation or excess temperature (especially high temperature).[7]

Some examples of people that have returned from this apparent interruption of life lasting over half an hour, two hours, eight hours or more while adhering to these specific conditions for oxygen and temperature have been reported and analysed in depth, but these cases are not considered scientifically valid. The brain begins to die after five minutes without oxygen; nervous tissues die intermediately when a "somatic death" occurs while muscles die over one to two hours following this last condition.[8]

It has been possible to obtain a successful resuscitation and recover life in some instances, including after anaesthesia, heat stroke, electrocution, narcotic poisoning, heart attack or cardiac arrest, shock, newborn infants, cerebral concussion, or cholera.

Supposedly, in suspended animation, a person technically would not die, as long as he or she were able to preserve the minimum conditions in an environment extremely close to death and return to a normal living state. An example of such a case is Anna Bgenholm, a Swedish radiologist who allegedly survived 80 minutes under ice in a frozen lake in a state of cardiac arrest with no brain damage in 1999.[9] [10]

Other cases of hypothermia where people survived without damage are:

It has been suggested that bone lesions provide evidence of hibernation among the early human population whose remains have been retrieved at the Archaeological site of Atapuerca. In a paper published in the journal LAnthropologie, researchers Juan-Luis Arsuaga and Antonis Bartsiokas point out that primitive mammals and primates like bush babies and lorises hibernate, which suggests that the genetic basis and physiology for such a hypometabolism could be preserved in many mammalian species, including humans.[15]

Since the 1970s, induced hypothermia has been performed for some open-heart surgeries as an alternative to heart-lung machines. Hypothermia, however, provides only a limited amount of time in which to operate and there is a risk of tissue and brain damage for prolonged periods.

There are many research projects currently investigating how to achieve "induced hibernation" in humans.[16][17] This ability to hibernate humans would be useful for a number of reasons, such as saving the lives of seriously ill or injured people by temporarily putting them in a state of hibernation until treatment can be given.

The primary focus of research for human hibernation is to reach a state of torpor, defined as a gradual physiological inhibition to reduce oxygen demand and obtain energy conservation by hypometabolic behaviors altering biochemical processes. In previous studies, it was demonstrated that physiological and biochemical events could inhibit endogenous thermoregulation before the onset of hypothermia in a challenging process known as "estivation". This is indispensable to survive harsh environmental conditions, as seen in some amphibians and reptiles.[18]

Lowering the temperature of a substance reduces chemical activity by the Arrhenius equation. This includes life processes such as metabolism. If cryonics are ever perfected, it would then be a form of long-term suspended animation.[19]

Emergency Preservation and Resuscitation (EPR) is a way to slow the bodily processes that would lead to death in cases of severe injury.[20] This involves lowering the body's temperature below 34C (93F), which is the current standard for therapeutic hypothermia.[20]

In June 2005, scientists at the University of Pittsburgh's Safar Center for Resuscitation Research announced they had managed to place dogs in suspended animation and bring them back to life, most of them without brain damage, by draining the blood out of the dogs' bodies and injecting a low temperature solution into their circulatory systems, which in turn keeps the bodies alive in stasis. After three hours of being clinically dead, the dogs' blood was returned to their circulatory systems, and the animals were revived by delivering an electric shock to their hearts. The heart started pumping the blood around the body, and the dogs were brought back to life.[21]

On 20 January 2006, doctors from the Massachusetts General Hospital in Boston announced they had placed pigs in suspended animation with a similar technique. The pigs were anaesthetized and major blood loss was induced, along with simulated - via scalpel - severe injuries (e.g. a punctured aorta as might happen in a car accident or shooting). After the pigs lost about half their blood the remaining blood was replaced with a chilled saline solution. As the body temperature reached 10C (50F) the damaged blood vessels were repaired and the blood was returned.[22] The method was tested 200 times with a 90% success rate.[23]

The laboratory of Mark Roth at the Fred Hutchinson Cancer Research Center and institutes such as Suspended Animation, Inc are trying to implement suspended animation as a medical procedure which involves the therapeutic induction to a complete and temporary systemic ischemia, directed to obtain a state of tolerance for the protection-preservation of the entire organism, this during a circulatory collapse "only by a limited period of one hour". The purpose is to avoid a serious injury, risk of brain damage or death, until the patient reaches specialized attention.[24]

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Suspended animation - Wikipedia

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