Archive for August, 2015
Skin Stem Cells: Benefits, Types, Medical Applications and …
Our skin has the amazing capability to renew itself throughout our adult life. Also, our hair follicle goes through a cycle of growth and degeneration. This happens all the time in our skin even though we are not aware of it. However, even though skin renews itself we still have to help it a little bit to get better results. Stem cells play an important role in this process of skin renewal or hair growth and the purpose of this article is to discuss and provide additional information about these tiny cells that play a big part in our life.
Skin stem cell is defined as multipotent adult skin cells which are able to self-renew or differentiate into various cell lineages of the skin. These cells are active throughout our life via skin renewal process or during skin repair after injuries. These cells reside in the epidermis and hair follicle and one of their purposes is to ensure the maintenance of adult skin and hair regeneration.
The truth is, without these little cells, our skin wouldnt be able to cope with various environmental influences. Our skin is exposed to different influences 24/7, for example, washing your face with soap, going out during summer or cold winter days etc. All these factors have a big impact on our skin and it constantly has to renew itself to stay in a good condition. This is where skin stem cells step in. They make sure your skin survives the influence of constant stress, heat, cold, even makeup, soap, etc.
Our skin is quite sensitive and due to its constant exposure to different influences throughout the day, it can get easily damage. Damage to skin cells can be caused by pretty much everything, from soap to cigarette smoke. One of the most frequent skin cell damages are the result of:
Skin stem cells are still subjected to scientific projects where researchers are trying to discover as much as possible about them. So far, they have identified several types of these cells, and they are:
Also, some scientists suggest that there is another type of stem cells mesenchymal stem cells which can be found in dermis (layer situated below the epidermis) and hypodermis (innermost and the thickest layer of the skin). However, this claim has been branded controversial and is a subject of many arguments and disputes between scientists. It is needed to conduct more experiments to find out whether this statement really is true.
Stem cells are found in many organs and tissues, besides skin. For example, scientists have discovered stem sells in brain, heart, bone marrow, peripheral blood, skeletal muscle, teeth, liver, gut etc. Stem cells reside in a specific area of each tissue or organ and that area is called stem cell niche. The same case is with the skin as well.
The ability of stem cells to regenerate and form almost any cell type in the body inspired scientists to work on various skin products that contain stem cells. Also, they decided to investigate the effect of plant stem cells on human skin. They discovered that plant stem cells are, actually, very similar to human skin stem cells and they function in a similar way as well. This discovery made scientists turn to plants as the source of stem cells and are trying to include them into the skin products due to their effectiveness in supporting skins cellular turnover. Another similarity between plant stem cells and human skin stem cells is their ability to develop according to their environment.
Fun Fact: The inspiration to use plant stem cells in skin care came from an unusual place almost extinct apple tree from Switzerland.
The benefits of plant stem cells on human skin are versatile. They offer possibility to treat some skin conditions, heal wounds, and repair the skin after some injury faster than it would usually take. Also, they bring back elasticity to the skin, reduce the appearance of wrinkles and slow down the aging process.
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Research Specialist, Gene Therapy Job
Jobing Description
Who we are:
Calico is a research and development company whose mission is to harness advanced technologies to increase our understanding of the biology that controls lifespan. We will use that knowledge to devise interventions that enable people to lead longer and healthier lives. Executing on this mission will require an unprecedented level of interdisciplinary effort and a long-term focus for which funding is already in place.
Position description:
Calico is recruiting biologists to work as part of a cutting-edge research team focused on studying and experimentally altering age-related physiological dysfunction in preclinical models. We are particularly excited about candidates with experience in gene therapy, vector-based delivery of genetic material in vivo, cell-based therapeutic strategies, and physiological endpoints in preclinical models. Experience with genome-editing technologies and pluripotent cell culture is a plus. The successful candidate will develop gene therapy tools to regulate biological networks in a temporal and tissue-specific manner, and to use those tools to alter age-related physiological dysfunction in a manner relevant to future clinical therapy.
Position requirements:
A Ph.D. in biology, cell biology, molecular biology, genetics, or biochemistry with a completed postdoc or 3+ years of additional, relevant experience, with a strong track record of research productivity as evidenced by high-quality, impactful publications. You need to be an enthusiastic team player, thrive on attention to detail, have excellent verbal/written communication skills, and be excited about studying aging!
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Research Specialist, Gene Therapy Job
Effects of Tanshinone IIA on osteogenic differentiation of …
Date: 01 Aug 2015
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Tanshinone IIA (TSA) is a lipophilic diterpene purified from the Chinese herb Danshen, which exhibits potent antioxidant and anti-inflammatory properties. Effect of TSA remains largely uninvestigated on the osteogenic differentiation of bone marrow mesenchymal stem cells (BM-MSCs), which are widely used in cell-based therapy of bone diseases. In the present study, both ALP activity at day 7 and calcium content at day 24 were upregulated during the osteogenesis of mouse BM-MSCs treated with TSA (1 and 5M), demonstrating that it promoted the osteogenesis at both early and late stages. We found that TSA promoted osteogenesis and inhibited osteoclastogenesis, evident by RT-PCR analysis of osteogenic marker gene expressions. However, osteogenesis was inhibited by TSA at 20M. We further revealed that TSA (1 and 5M) upregulated BMP and Wnt signaling. Co-treatment with Wnt inhibitor DKK-1 or BMP inhibitor noggin significantly decreased the TSA-promoted osteogenesis, indicating that upregulation of BMP and Wnt signaling plays a significant role and contributes to the TSA-promoted osteogenesis. Of clinical interest, our study suggests TSA as a promising therapeutic strategy during implantation of BM-MSCs for a more effective treatment of bone diseases.
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Effects of Tanshinone IIA on osteogenic differentiation of ...
Pharmacogenomic Testing Services | Personalized Medicine …
Welcome to DNA Stat. We specialize in personalized medicine services, specifically in the pain management and pharmacogenomics arena. We take pride in both our research and unsurpassed customer service, providing clients with genetic & pharmacogenomics testing which is the fastest growing field in the medical industry today.
Pain management and pharmacogenomics is vitally important as we progress into the 21st century as it is a realization and acknowledgement that one size does not fit all when it comes to medications. What might work for one individual flawlessly could mean an adverse reaction and a trip to the emergency room for another. Genetic Testing is the tool used to determine the difference before the medication is ingested. In this way, we are spearheading and defining personalized medicine services and enabling people to recover and maintain their illnesses and conditions worry-free. By eliminating the guess work, patients can recover more fully and quicker than ever before.
We know that the medical industry can be daunting to most people. Fortunately, the genetic & pharmacogenomics testing at DNA Stat comes down to a simple Buccal swab of the cheek. No needles involved, no fear, no blood no problem. Within three weeks, the patients doctor will have in his or her hands a Pharm D Report which is the roadmap to prescribing better medications and better treatments for their patient. DNA Stat, the leader in genetic& pharmacogenomics testing, is changing the way the world sees medicine one patient at a time.
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Multiple Sclerosis Market in the US 2015-2019 – Research …
FEATURED COMPANIES AB Science Artielle Biogen GlaxoSmithKline medDay Pharmaceuticals Novartis AG MORE
About Multiple Sclerosis Multiple sclerosis is a chronic, inflammatory medical condition, which results in demyelination, axonal transection, and neurodegeneration of the nerve cells of the brain and spinal cord. The immune system of the body targets the neurons within the CNS and damages the myelin sheath. It is a potentially debilitating disease, causing disruption in the communication and coordination functions of the body. The symptoms of multiple sclerosis differ widely, subject to the extent of damage and the number of neurons affected. Some of the symptoms observed are fatigue, numbness, spasticity, bladder dysfunction, cognitive changes, emotional changes, and depression. An individual with severe form of the disease can experience speech and movement problems. Multiple sclerosis can be broadly classified into four types: RRMS, SPMS, PPMS, and PRMS.
The analysts forecast the multiple sclerosis market in the US to grow at a CAGR of 3.8% over the period 2014-2019.
Covered in this Report
This report covers the present scenario and the growth prospects of the multiple sclerosis market in the US for the period 2015-2019. To calculate the market size, the report considers revenue generated from sales of various drugs used in the treatment of multiple sclerosis.
On the basis of route of administration of the drugs, the market is grouped into the following categories: - Oral - Parenteral
On the basis of type of molecule of the drugs, the market is grouped into the following categories: - Small Molecules - Biologics
The report also presents the vendor landscape and a corresponding detailed analysis of the top vendors and competitive performances of their product portfolios in the market. In addition, it discusses the major drivers that influence the growth of the market. It also outlines the challenges faced by vendors and the market at large, as well as the key trends that are emerging in the market.
The report, the multiple sclerosis market in the US 2015-2019, has been prepared based on an in-depth market analysis with inputs from industry experts. The report covers the multiple sclerosis market in US market landscape and its growth prospects in the coming years. The report also includes a discussion of the key vendors operating in this market.
Key Vendors - Bayer AG - Biogen - Merck Serono - Novartis AG - Teva Pharmaceutical Industries Ltd.
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Multiple Sclerosis Market in the US 2015-2019 - Research ...
Male-pattern hair loss – Wikipedia, the free encyclopedia
Male-pattern hair loss, also known as androgenic alopecia and male pattern baldness (MPB), is hair loss that occurs due to an underlying susceptibility of hair follicles to androgenic miniaturization. It is the most common cause of hair loss and will affect up to 70% of men and 40% of women at some point in their lifetimes. Men typically present with hairline recession at the temples and vertex balding, while women normally thin diffusely over the top of their scalps.[1][2][3] Both genetic and environmental factors play a role, and many etiologies remain unknown.
Classic androgenic hair loss in males begins above the temples and vertex, or 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.[4] The Hamilton-Norwood scale has been developed to grade androgenic alopecia in males.
Female androgenic alopecia is known colloquially as "female pattern baldness", although its characteristics can also occur in males. It more often causes diffuse thinning without hairline recession; and, like its male counterpart, rarely leads to total hair loss.[5] The Ludwig scale grades severity of androgenic alopecia in females.
Animal models of androgenic alopecia occur naturally and have been developed in transgenic mice;[6]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.[7][8]
Androgenic alopecia is typically experienced as a "moderately stressful condition that diminishes body image satisfaction".[9] However, although most men regard baldness as an unwanted and distressing experience, they usually are able to cope and retain integrity of personality.[10]
Research indicates that the initial programming of pilosebaceous units begins in utero.[11] The physiology is primarily androgenic, with dihydrotestosterone (DHT) the major contributor at the dermal papillae. Below-normal values of sex hormone-binding globulin, follicle-stimulating hormone, testosterone, and epitestosterone are present in men with premature androgenic alopecia compared to normal controls.[12] Although follicles were previously thought permanently gone in areas of complete hair loss, they are more likely dormant, as recent studies have shown the scalp contains the stem cell progenitors from which the follicles arose.[13]
Transgenic studies have shown that growth and dormancy of hair follicles are related to the activity of insulin-like growth factor at the dermal papillae, which is affected by DHT.[14]Androgens are important in male sexual development around birth and at puberty. They regulate sebaceous glands, apocrine hair growth, and libido. With increasing age,[15] androgens stimulate hair growth on the face, but suppress it at the temples and scalp vertex, a condition that has been referred to as the 'androgen paradox'.[16]
These observations have led to study at the level of the mesenchymal dermal papillae.[17][18]Types 1 and 2 5 reductase enzymes are present at pilosebaceous units in papillae of individual hair follicles.[19] They catalyze formation of the androgens testosterone and DHT, which in turn regulate hair growth.[16] Androgens have different effects at different follicles: they stimulate IGF-1 at facial hair, leading to growth, but stimulate TGF 1, TGF 2, dickkopf1, and IL-6 at the scalp, leading to catagenic miniaturization.[16] Hair follicles in anaphase express four different caspases. Tumor necrosis factor inhibits elongation of hair follicles in vitro with abnormal morphology and cell death in the bulb matrix.[20]
Studies of serum levels of IGF-1 show it to be increased with vertex balding.[21][22] Earlier work looking at in vitro administration of IGF had no effect on hair follicles when insulin was present, but when absent, caused follicle growth. The effects on hair of IGF-I were found to be greater than IGF-II.[23] Later work also showed IGF-1 signalling controls the hair growth cycle and differentiation of hair shafts,[14] possibly having an anti-apoptotic effect during the catagen phase.[24]In situ hybridization in adult human skin has shown morphogenic and mitogenic actions of IGF-1.[25] Mutations of the gene encoding IGF-1 result in shortened and morphologically bizarre hair growth and alopecia.[26] IGF-1 is modulated by IGF binding protein, which is produced in the dermal papilla.[27]
DHT inhibits IGF-1 at the dermal papillae.[28] Extracellular histones inhibit hair shaft elongation and promote regression of hair follicles by decreasing IGF and alkaline phosphatase in transgenic mice.[29] Silencing P-cadherin, a hair follicle protein at adherens junctions, decreases IGF-1, and increases TGF beta 2, although neutralizing TGF decreased catagenesis caused by loss of cadherin, suggesting additional molecular targets for therapy. P-cadherin mutants have short, sparse hair.[30]
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Male-pattern hair loss - Wikipedia, the free encyclopedia
Male Hormone Replacement – Testosterone – The Turek Clinic
The average age of men in the US is projected to rise significantly over the next 25 years, with the greatest increase occurring in men > 65 years old.
As this happens, there will be a dramatic increase in age-related health problems too, including cancer, strokes, heart disease and hormone deficiency. Although the health risks associated with age-related hormonal decline in women, termed menopause, have been thoroughly addressed, it has now been shown that hormonal changes in the aging male are associated with significant health problems.
Specialty board certified Dr. Paul Turek at The Turek Clinic, a Best Doctors in America choice for 7 years running, has expertise and interest in helping patients understand all of the issues, good and bad, that surround testosterone replacement therapy in men of all ages.
To learn more about male hormone replacement, please select one of the following topics. If you are ready to schedule a consultation with Dr. Turek, please request a consultation here.
There is a progressive decline in testosterone production in men with age. These changes can be dramatic, such that 50% of men >60 years old have low levels of testosterone. Although the rate of decline varies widely, a general rule of thumb is that testosterone levels decrease about 1% yearly after age 50. Despite the fact that it is not as rapid a drop in hormones as women get with menopause, it certainly is just as real. This has been termed male menopause, male climacteric, andropause, or more appropriately, partial androgen deficiency in the aging male (PADAM). Serum testosterone levels in men fall progressively from the third decade to the end of life, mainly due to a decline in the cells in the testis that make the hormone (Leydig cells). This decline may also be due to changes in hormones (GnRH, LH) and proteins (SHBG, albumin) that regulate testosterone production.
One issue with testosterone that complicates matters is the fact that it exists in several different forms in the blood, and each form has different hormonal activity (Figure 1). Free or unbound testosterone is a fully active hormone, but protein-bound testosterone are only partly active, or sometimes completely inactive. What is usually measured in a blood draw is the total testosterone, which is a combination of the free and protein-bound forms. An analogy to explain this is to think of the total testosterone as all of the cars in a parking lot.
Importantly, though, only the cars that can start or drive are useful or active. Free testosterone comprises all of the cars that can start and be driven away, but the protein-bound testosterone are those cars that may or may not start, and those that may or may not be able to be driven away. So, aging is associated with 1) lower total testosterone production (fewer cars in the lot) and 2) higher levels of certain proteins that bind testosterone (sex hormone-binding globulin, SHBG), such that even fewer cars can start and run, and it is this combination of events that leads to declining testosterone activity with age. Thus, the complex physiology of testosterone balance often clouds the interpretation of age-related declining levels of the hormone.
Testosterone affects the function of many organs in the body (Table 1). In the brain, it influences libido or sex drive, male aggression, mood and thinking. Testosterone can improve verbal memory and visual-spatial skills. It as also been shown to decrease fatigue and depression in men with low levels. It is responsible for muscle strength and growth, and stimulates stem cells and blood cells in bones and kidneys. Penile growth, erections, sperm production, and prostatic growth and function all depend on testosterone. It also causes body hair growth, balding, and drives beard growth. Thus, testosterone makes us who we are, and influences how we look.
In men with low testosterone levels, testosterone can improve bone mineral density and reduce bone fractures, an effect similar to that found in postmenopausal women on estrogen replacement. Importantly, hip fractures are 2-3 times as likely to kill an older man as a woman of the same age, and 40% of older male patients with hip fractures die within 1 year of the injury.
Testosterone results in increases in lean body mass, possibly strength and can decrease fat mass. By stimulating erythropoietin, testosterone increases blood counts. It appears to improve lipid profiles and dilates blood vessels in the heart but no data has yet shown that it reduces heart attacks or strokes. It appears not to alter LDL or total cholesterol levels. In recent work, it has been shown that men with chronically low testosterone levels have 2-3 fold higher risk of developing metabolic syndrome and have up to a 40% greater risk of death than men with normal testosterone levels.
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Male Hormone Replacement - Testosterone - The Turek Clinic
Hypergonadotropic hypogonadism – Wikipedia, the free …
Hypergonadotropic hypogonadism (HH), also known as primary or peripheral/gonadal hypogonadism, is a condition which is characterized by hypogonadism due to an impaired response of the gonads to the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), and in turn a lack of sex steroid production and elevated gonadotropin levels (as an attempt of compensation by the body). HH may present as either congenital or acquired, but the majority of cases are of the former nature.[1][2]
There are a multitude of different etiologies of HH. Congenital causes include the following:[1][3][4]
Acquired causes (due to damage to or dysfunction of the gonads) include gonadal torsion, vanishing/anorchia, orchitis, premature ovarian failure, ovarian resistance syndrome, trauma, surgery, autoimmunity, chemotherapy, radiation, infections (e.g., sexually-transmitted diseases), toxins (e.g., endocrine disruptors), and drugs (e.g., antiandrogens, opioids, alcohol).[1][3][4]
Examples of symptoms of hypogonadism include delayed, reduced, or absent puberty, low libido, and infertility.
Treatment of HH is usually with hormone replacement therapy, consisting of androgen and estrogen administration in males and females, respectively.[3]
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