Sue Decotiis, MD

As we age, even as early as age 30, our internal production of hormones can start to decline. Initially the effects are subtle and vary between individuals. But as we head toward middle age most of us experience adverse symptoms.

Symptoms of low hormones vary with the actual hormone that is low. But many deficiencies overlap, for example weight gain can occur from hypoactive thyroid as well as in menopause and andropause. Men with low testosterone and women with low estrogen may also have low DHEA and need treatment for both.

Common Symptoms of Hormone Deficiency :

We used to accept any or all of the above as normal part of getting older. But if we treat the deficiencies that lead to all of the symptoms touched on above a person can feel their best. He or she can maintain a healthy body weight and have the energy and desire to lead an active life. Plus look great doing it.

Hormone Replacement Doctor is an evidence-based medical practice. In our practice we only prescribe Bioidentical Hormone Therapy.

Why Are Hormones Important to You? Hormones are intrinsic substances that provide a continuum of specific information to nurture and direct specific cells in target organs. Without optimal hormone levels your body function is off balance and you know it. Even after seeing your physician and being told you are okay, something just isnt right. Hormone replacement therapy can make such a difference for these individuals. Most of us are or will become these individuals.

Individual body organs and their systems heart; cardiovascular system, brain; neurological system are not isolated systems. They need communicating hormones to stay vital. Looking back, life expectancy in 1900 was late 40s; so many died before reaching menopause or andropause. Now that we expect to live so many decades more than our grandparents we will have to deal with the effects of low hormone levels.With modern medicine extending life in to the ninth and tenth decade we need to think about the quality of life that hormone replacement treatment produces. Prescription medications and sophisticated treatments are not enough by themselves to produce the level of health and well being that we deserve today.

If you have any questions for the NYC Doctor in regards to Hormone Replacement Therapyor to make a consultation with Sue Decotiis, MD please contact the Doctors NYC office.

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Hormone Replacement Therapy in NYC | NYC Hormone ...

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Having someone elses marrow or stem cells is called a donor transplant, or an allogeneic transplant. This is pronounced al-lo-jen-ay-ik.

The donors bone marrow cells must match your own as closely as possible. The most suitable donor is usually a close relative, such as a brother or sister. It is sometimes possible to find a match in an unrelated donor. Doctors call this a matched unrelated donor (MUD). To find out if there is a suitable donor for you, your doctor will contact The Anthony Nolan Bone Marrow Register and other UK based and international bone marrow registers.

To make sure that your donors cells match, you and the donor will have blood tests. These are to see how many of the proteins on the surface of their blood cells match yours. This is called tissue typing or HLA matching. HLA stands for human leucocyte antigen.

Once you have a donor and are in remission, you have high dose chemotherapy either on its own or with radiotherapy. A week later the donor goes into hospital and their stem cells or marrow are collected. You then have the stem cells or bone marrow as a drip through your central line.

If you've had a transplant from a donor, there is a risk of graft versus host disease (GVHD). This happens because the transplanted stem cells or bone marrow contain cells from your donor's immune system. These cells can sometimes recognise your own tissues as being foreign and attack them. This can be an advantage because the immune cells may also attack any leukaemia cells left after your treatment.

Acute GVHD starts within 100 days of the transplant and can cause

If you develop GVHD after your transplant, your doctor will prescribe medicines to damp down this immune reaction. These are called immunosuppressants.

Chronic GVHD starts more than 100 days after the transplant and you may have

Your doctor is likely to suggest that you stay out of the sun because GVHD skin rashes can often get worse in the sun.

There is detailed information about graft versus host disease in the section about coping physically with cancer.

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Bone marrow or stem cell transplants for AML | Cancer ...

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What Is Arthritis?

Arthritis is inflammation of the joints (the points where bones meet) in one or more areas of the body. There are more than 100 different types of arthritis, all of which have different causes and treatment methods. The symptoms of arthritis usually appear gradually but they may also occur suddenly. Arthritis is most commonly seen in adults over the age of 65 but it can also develop in children and teens. According to the Centers for Disease Control and Prevention, arthritis is more common in women than men and in those that are overweight (CDC).

Cartilage is a flexible, connective tissue in joints that absorbs the pressure and shock created from movement like running and walking. It also protects the joints and allows for smooth movement.

Some forms of arthritis are caused by a reduction in the normal amount of this cartilage tissue. Osteoarthritis, one of the most common forms of arthritis, is caused by normal wear and tear throughout life; this natural breakdown of cartilage tissue can be exacerbated by an infection or injury to the joints.

The risk of developing osteoarthritis may be higher if you have a family history of the disease.

Another common form of arthritis, rheumatoid arthritis, occurs when your bodys immune system attacks the tissues of the body. These attacks affect the synovium, which secretes a fluid that nourishes the cartilage and lubricates the joints. Rheumatoid arthritis can eventually lead to the destruction of both bone and cartilage inside the joint. The exact cause of the immune systems attacks has not yet been discovered, but scientists have discovered genetic markers that increase your risk of developing rheumatoid arthritis tenfold.

The most common symptoms of arthritis involve the joints. Joint pain and stiffness, mostly in the morning, are typical signs, along with swelling of the joints. You may also experience a decrease in range of motion of your joints or redness of the skin around the joint.

In the case of rheumatoid arthritis you may feel tired or experience a loss of appetite because of the inflammation caused by your bodys attacking immune system. You may also become anemic (experience decreased red blood cells) or have a slight fever. Severe rheumatoid arthritis can cause joint deformity if left untreated.

Diagnosis of arthritis will start with your physician performing a physical exam, during which he or she will check for limited range of motion in the joint, the feeling of fluid around joints, or warm or red joints. Extraction and analysis of your bodily fluids like blood and joint fluid can help your doctor determine what kind of arthritis you have by checking for inflammation levels. Imaging scans such as X-ray, MRI, and CT scans are commonly used to produce an image of your bones and cartilage so your doctor can better determine whether something like a bone spur is the cause of your symptoms.

The main goal of treatment is to reduce the amount of pain youre experiencing and prevent any additional damage to the joints. Improving your joint function is also important, and you may be prescribed a combination of treatment methods to achieve the best results.

Read this article:
Arthritis : Causes, Signs & Diagnosis - Healthline

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Charles A. Goldthwaite, Jr., PhD.

Data from 2007 suggest that approximately 1.4 million men and women in the U.S. population are likely to be diagnosed with cancer, and approximately 566,000 American adults are likely to die from cancer in 2008.1 Data collected between 1996 and 2004 indicate that the overall 5-year survival rate for cancers from all sites, relative to the expected survival from a comparable set of people without cancer, is 65.3%.1 However, survival and recurrence rates following diagnosis vary greatly as a function of cancer type and the stage of development at diagnosis. For example, in 2000, the relative survival rate five years following diagnosis of melanoma (skin cancer) was greater than 90%; that of cancers of the brain and nervous system was 35%. Once a cancer has metastasized (or spread to secondary sites via the blood or lymph system), however, the survival rate usually declines dramatically. For example, when melanoma is diagnosed at the localized stage, 99% of people will survive more than five years, compared to 65% of those diagnosed with melanoma that has metastasized regionally and 15% of those whose melanoma has spread to distant sites.2

The term cancer describes a group of diseases that are characterized by uncontrolled cellular growth, cellular invasion into adjacent tissues, and the potential to metastasize if not treated at a sufficiently early stage. These cellular aberrations arise from accumulated genetic modifications, either via changes in the underlying genetic sequence or from epigenetic alterations (e.g., modifications to gene activation- or DNA-related proteins that do not affect the genetic sequence itself).3,4 Cancers may form tumors in solid organs, such as the lung, brain, or liver, or be present as malignancies in tissues such as the blood or lymph. Tumors and other structures that result from aberrant cell growth, contain heterogeneous cell populations with diverse biological characteristics and potentials. As such, a researcher sequencing all of the genes from tumor specimens of two individuals diagnosed with the same type of lung cancer will identify some consistencies along with many differences. In fact, cancerous tissues are sufficiently heterogeneous that the researcher will likely identify differences in the genetic profiles between several tissue samples from the same specimen. While some groupings of genes allow scientists to classify organ-or tissue-specific cancers into subcategories that may ultimately inform treatment and provide predictive information, the remarkable complexity of cancer biology continues to confound treatment efforts.

Once a cancer has been diagnosed, treatments vary according to cancer type and severity. Surgery, radiation therapy, and systemic treatments such as chemotherapy or hormonal therapy represent traditional approaches designed to remove or kill rapidly-dividing cancer cells. These methods have limitations in clinical use. For example, cancer surgeons may be unable to remove all of the tumor tissue due to its location or extent of spreading. Radiation and chemotherapy, on the other hand, are non-specific strategieswhile targeting rapidly-dividing cells, these treatments often destroy healthy tissue as well. Recently, several agents that target specific proteins implicated in cancer-associated molecular pathways have been developed for clinical use. These include trastuzumab, a monoclonal antibody that targets the protein HER2 in breast cancer,5 gefitinib and erlotnib, which target epidermal growth factor receptor (EGFR) in lung cancer,6 imatinib, which targets the BCR-ABL tyrosine kinase in chronic myelogenous leukemia,7 the monoclonal antibodies bevacizumab, which targets vascular endothelial growth factor in colorectal and lung cancer,8 and cetuximab and panitumumab, which target EGFR in colorectal cancer.8 These agents have shown that a targeted approach can be successful, although they are effective only in patients who feature select subclasses of these respective cancers.

All of these treatments are most successful when a cancer is localized; most fail in the metastatic setting.911 This article will discuss the CSC hypothesis and its supporting evidence and provide some perspectives on how CSCs could impact the development of future cancer therapy.

A consensus panel convened by the American Association of Cancer Research has defined a CSC as a cell within a tumor that possesses the capacity to self-renew and to cause the heterogeneous lineages of cancer cells that comprise the tumor.12 It should be noted that this definition does not indicate the source of these cellsthese tumor-forming cells could hypothetically originate from stem, progenitor, or differentiated cells.13 As such, the terms tumor-initiating cell or cancer-initiating cell are sometimes used instead of cancer stem cell to avoid confusion. Tumors originate from the transformation of normal cells through the accumulation of genetic modifications, but it has not been established unequivocally that stem cells are the origin of all CSCs. The CSC hypothesis therefore does not imply that cancer is always caused by stem cells or that the potential application of stem cells to treat conditions such as heart disease or diabetes, as discussed in other chapters of this report, will result in tumor formation. Rather, tumor-initiating cells possess stem-like characteristics to a degree sufficient to warrant the comparison with stem cells; the observed experimental and clinical behaviors of metastatic cancer cells are highly reminiscent of the classical properties of stem cells.9

The CSC hypothesis suggests that the malignancies associated with cancer originate from a small population of stem-like, tumor-initiating cells. Although cancer researchers first isolated CSCs in 1994,14 the concept dates to the mid-19th century. In 1855, German pathologist Rudolf Virchow proposed that cancers arise from the activation of dormant, embryonic-like cells present in mature tissue.15 Virchow argued that cancer does not simply appear spontaneously; rather, cancerous cells, like their non-cancerous counterparts, must originate from other living cells. One hundred and fifty years after Virchows observation, Lapidot and colleagues provided the first solid evidence to support the CSC hypothesis when they used cell-surface protein markers to identify a relatively rare population of stemlike cells in acute myeloid leukemia (AML).14 Present in the peripheral blood of persons with leukemia at approximately 1:250,000 cells, these cells could initiate human AML when transplanted into mice with compromised immune systems. Subsequent analysis of populations of leukemia-initiating cells from various AML subtypes indicated that the cells were relatively immature in terms of differentiation.16 In other words, the cells were stem-likemore closely related to primitive blood-forming (hematopoietic) stem cells than to more mature, committed blood cells.

The identification of leukemia-inducing cells has fostered an intense effort to isolate and characterize CSCs in solid tumors. Stem cell-like populations have since been characterized using cell-surface protein markers in tumors of the breast,17 colon,18 brain,19 pancreas,20,21 and prostate.22,23 However, identifying markers that unequivocally characterize a population of CSCs remains challenging, even when there is evidence that putative CSCs exist in a given solid tumor type. For example, in hepatocellular carcinoma, cellular analysis suggests the presence of stem-like cells.24 Definitive markers have yet to be identified to characterize these putative CSCs, although several potential candidates have been proposed recently.25,26 In other cancers in which CSCs have yet to be identified, researchers are beginning to link established stem-cell markers with malignant cancer cells. For instance, the proteins Nanog, nucleostemin, and musashi1, which are highly expressed in embryonic stem cells and are critical to maintaining those cells pluripotency, are also highly expressed in malignant cervical epithelial cells.27 While this finding does not indicate the existence of cervical cancer CSCs, it suggests that these proteins may play roles in cervical carcinogenesis and progression.

Given the similarities between tumor-initiating cells and stem cells, researchers have sought to determine whether CSCs arise from stem cells, progenitor cells, or differentiated cells present in adult tissue. Of course, different malignancies may present different answers to this question. The issue is currently under debate,9,12 and this section will review several theories about the cellular precursors of cancer cells (see Fig. 9.1).

See original here: Are Stem Cells Involved in Cancer? [Stem Cell Information]

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Stem Cells Therapy

Recommendation and review posted by Bethany Smith

With more than 50 years of experience studying blood-forming stem cells called hematopoietic stem cells, scientists have developed sufficient understanding to actually use them as a therapy. Currently, no other type of stem cell, adult, fetal or embryonic, has attained such status. Hematopoietic stem cell transplants are now routinely used to treat patients with cancers and other disorders of the blood and immune systems. Recently, researchers have observed in animal studies that hematopoietic stem cells appear to be able to form other kinds of cells, such as muscle, blood vessels, and bone. If this can be applied to human cells, it may eventually be possible to use hematopoietic stem cells to replace a wider array of cells and tissues than once thought.

Despite the vast experience with hematopoietic stem cells, scientists face major roadblocks in expanding their use beyond the replacement of blood and immune cells. First, hematopoietic stem cells are unable to proliferate (replicate themselves) and differentiate (become specialized to other cell types) in vitro (in the test tube or culture dish). Second, scientists do not yet have an accurate method to distinguish stem cells from other cells recovered from the blood or bone marrow. Until scientists overcome these technical barriers, they believe it is unlikely that hematopoietic stem cells will be applied as cell replacement therapy in diseases such as diabetes, Parkinson's Disease, spinal cord injury, and many others.

Blood cells are responsible for constant maintenance and immune protection of every cell type of the body. This relentless and brutal work requires that blood cells, along with skin cells, have the greatest powers of self-renewal of any adult tissue.

The stem cells that form blood and immune cells are known as hematopoietic stem cells (HSCs). They are ultimately responsible for the constant renewal of bloodthe production of billions of new blood cells each day. Physicians and basic researchers have known and capitalized on this fact for more than 50 years in treating many diseases. The first evidence and definition of blood-forming stem cells came from studies of people exposed to lethal doses of radiation in 1945.

Basic research soon followed. After duplicating radiation sickness in mice, scientists found they could rescue the mice from death with bone marrow transplants from healthy donor animals. In the early 1960s, Till and McCulloch began analyzing the bone marrow to find out which components were responsible for regenerating blood [56]. They defined what remain the two hallmarks of an HSC: it can renew itself and it can produce cells that give rise to all the different types of blood cells (see Chapter 4. The Adult Stem Cell).

A hematopoietic stem cell is a cell isolated from the blood or bone marrow that can renew itself, can differentiate to a variety of specialized cells, can mobilize out of the bone marrow into circulating blood, and can undergo programmed cell death, called apoptosisa process by which cells that are detrimental or unneeded self-destruct.

A major thrust of basic HSC research since the 1960s has been identifying and characterizing these stem cells. Because HSCs look and behave in culture like ordinary white blood cells, this has been a difficult challenge and this makes them difficult to identify by morphology (size and shape). Even today, scientists must rely on cell surface proteins, which serve, only roughly, as markers of white blood cells.

Identifying and characterizing properties of HSCs began with studies in mice, which laid the groundwork for human studies. The challenge is formidable as about 1 in every 10,000 to 15,000 bone marrow cells is thought to be a stem cell. In the blood stream the proportion falls to 1 in 100,000 blood cells. To this end, scientists began to develop tests for proving the self-renewal and the plasticity of HSCs.

The "gold standard" for proving that a cell derived from mouse bone marrow is indeed an HSC is still based on the same proof described above and used in mice many years ago. That is, the cells are injected into a mouse that has received a dose of irradiation sufficient to kill its own blood-producing cells. If the mouse recovers and all types of blood cells reappear (bearing a genetic marker from the donor animal), the transplanted cells are deemed to have included stem cells.

These studies have revealed that there appear to be two kinds of HSCs. If bone marrow cells from the transplanted mouse can, in turn, be transplanted to another lethally irradiated mouse and restore its hematopoietic system over some months, they are considered to be long-term stem cells that are capable of self-renewal. Other cells from bone marrow can immediately regenerate all the different types of blood cells, but under normal circumstances cannot renew themselves over the long term, and these are referred to as short-term progenitor or precursor cells. Progenitor or precursor cells are relatively immature cells that are precursors to a fully differentiated cell of the same tissue type. They are capable of proliferating, but they have a limited capacity to differentiate into more than one cell type as HSCs do. For example, a blood progenitor cell may only be able to make a red blood cell (see Figure 5.1. Hematopoietic and Stromal Stem Cell Differentiation).

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5. Hematopoietic Stem Cells [Stem Cell Information]

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SAN DIEGO(BUSINESS WIRE)Cytori Therapeutics, Inc. (NASDAQ: CYTX) today confirmed that two Japanese regenerative medicine laws, which went into effect on November 25, 2014, remove regulatory uncertainties and provide a clear path for the Company to commercialize and market Cytori Cell Therapy and its Celution System under the Companys existing and planned regulatory approvals.

Japans new regenerative medicine laws substantially clarify regulatory ambiguities of pre-existing guidelines and this news represents a significant event for Cytori, said Dr. Marc Hedrick, President & CEO of Cytori. We have a decade of operating experience in Japan and Cytori is nicely positioned to see an impact both on existing commercial efforts and on our longer-term efforts to obtain therapeutic claims and reimbursement for our products.

Under the two new laws, Cytori believes its Celution System and autologous adipose-derived regenerative cells (ADRCs) can be provided by physicians under current Class I device regulations and used under the lowest risk category (Tier 3) for many procedures with only the approval by accredited regenerative medicine committees and local agencies of the Ministry of Health, Labour and Welfare (MHLW). This regulatory framework is expected to streamline the approval and regulatory process and increase clinical use of Cytori Cell Therapy and the Celution System over the former regulations.

Before these new laws were enacted, the regulatory pathway for clinical use of regenerative cell therapy was one-size-fits-all, irrespective of the risk posed by certain cell types and approaches, said Dr. Hedrick. Now, Cytoris point-of-care Celution System can be transparently integrated into clinical use by providers under our Class I device status and the streamlined approval process granted to cell therapies that pose the lowest risk. Our technology is unique in that respect.

Cytoris Celution System Is in Lowest of Three Risk Categories

The Act on the Safety of Regenerative Medicines and an amendment of the 2013 Pharmaceutical Affairs Act (the PMD Act), collectively termed the Regenerative Medicine Laws, replace the Human Stem Cell Guidelines. Under the new laws, the cell types used in cell therapy and regenerative medicine are classified based on risk. Cell therapies using cells derived from embryonic, induced pluripotent, cultured, genetically altered, animal and allogeneic cells are considered higher risk (Tiers 1 and 2) and will undergo an approval pathway with greater and more stringent oversight due to the presumed higher risk to patients. Cytoris Celution System, which uses the patients own cells at the point-of-care, will be considered in the lowest risk category (Tier 3) for most cases, and will be considered in Tier 2 if used as a non-homologous therapy.

Streamlined Regulatory Approval for Certain Medical Devices

In the near future, Cytori intends to pursue disease-specific or therapeutic claims and reimbursement for Cytoris Celution System and the Company would, at that point, sponsor a clinical trial to obtain Class III device-based approval and reimbursement. The new laws include changes to streamline regulation of Class II and some Class III devices, which will now require the approval of certification bodies rather than the PMDA, similar to the European notified body model. To date, certification bodies have only been used for some Class II devices.

Conditional Regulatory Approval and Reimbursement Potential

As a supplementary benefit to Cytori, the Company may also choose to take advantage of the new conditional approval opportunities granted under the new laws. Once clinical safety and an indication of efficacy are shown, sponsors may apply for their cell product to receive conditional approval for up to seven years and may be eligible for reimbursement under Japans national insurance coverage. Under the conditional approval, the sponsor can then generate post-marketing data to demonstrate further efficacy and cost effectiveness.

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japanese | StemCell Therapy MD

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Regenerative medicine is a branch of translational research[1] in tissue engineering and molecular biology which deals with the "process of replacing, engineering or regenerating human cells, tissues or organs to restore or establish normal function".[2] This field holds the promise of engineering damaged tissues and organs via stimulating the body's own repair mechanisms to functionally heal previously irreparable tissues or organs.[3]

Regenerative medicine also includes the possibility of growing tissues and organs in the laboratory and safely implanting them when the body cannot heal itself. If a regenerated organ's cells would be derived from the patient's own tissue or cells, this would potentially solve the problem of the shortage of organs available for donation, and the problem of organ transplant rejection.[4][5][6]

Attributed to William Haseltine (founder of Human Genome Sciences),[7] the term "regenerative medicine" was first found in a 1992 article on hospital administration by Leland Kaiser. Kaisers paper closes with a series of short paragraphs on future technologies that will impact hospitals. One paragraph had Regenerative Medicine as a bold print title and stated, A new branch of medicine will develop that attempts to change the course of chronic disease and in many instances will regenerate tired and failing organ systems.[8][9]

Regenerative medicine refers to a group of biomedical approaches to clinical therapies that may involve the use of stem cells.[10] Examples include the injection of stem cells or progenitor cells obtained through Directed differentiation (cell therapies); the induction of regeneration by biologically active molecules administered alone or as a secretion by infused cells (immunomodulation therapy); and transplantation of in vitro grown organs and tissues (tissue engineering).[11][12]

From 1995 to 1998 Michael D. West, PhD, organized and managed the research between Geron Corporation and its academic collaborators James Thomson at the University of Wisconsin-Madison and John Gearhart of Johns Hopkins University that led to the first isolation of human embryonic stem and human embryonic germ cells.[13]

Dr. Stephen Badylak, a Research Professor in the Department of Surgery and director of Tissue Engineering at the McGowan Institute for Regenerative Medicine at the University of Pittsburgh, developed a process for scraping cells from the lining of a pig's bladder, decellularizing (removing cells to leave a clean extracellular structure) the tissue and then drying it to become a sheet or a powder. This extracellular matrix powder was used to regrow the finger of Lee Spievak, who had severed half an inch of his finger after getting it caught in a propeller of a model plane.[14][15][16][dubious discuss] As of 2011, this new technology is being employed by the military on U.S. war veterans in Texas, as well as for some civilian patients. Nicknamed "pixie-dust," the powdered extracellular matrix is being used to successfully regenerate tissue lost and damaged due to traumatic injuries.[17]

In June 2008, at the Hospital Clnic de Barcelona, Professor Paolo Macchiarini and his team, of the University of Barcelona, performed the first tissue engineered trachea (wind pipe) transplantation. Adult stem cells were extracted from the patient's bone marrow, grown into a large population, and matured into cartilage cells, or chondrocytes, using an adaptive method originally devised for treating osteoarthritis. The team then seeded the newly grown chondrocytes, as well as epithileal cells, into a decellularised (free of donor cells) tracheal segment that was donated from a 51 year old transplant donor who had died of cerebral hemorrhage. After four days of seeding, the graft was used to replace the patient's left main bronchus. After one month, a biopsy elicited local bleeding, indicating that the blood vessels had already grown back successfully.[18][19]

In 2009 the SENS Foundation was launched, with its stated aim as "the application of regenerative medicine defined to include the repair of living cells and extracellular material in situ to the diseases and disabilities of ageing." [20]

In 2012, Professor Paolo Macchiarini and his team improved upon the 2008 implant by transplanting a laboratory-made trachea seeded with the patient's own cells.[21]

On Sep 12, 2014, surgeons at the Institute of Biomedical Research and Innovation Hospital in Kobe, Japan, transplanted a 1.3 by 3.0 millimeter sheet of retinal pigment epithelium cells, which were differentiated from iPS cells through Directed differentiation, into an eye of an elderly woman, who suffers from age-related macular degeneration.[22]

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Regenerative medicine - Wikipedia, the free encyclopedia

Recommendation and review posted by sam

A new study from the Forsyth Institute is helping to shed light on latent tuberculosis and the bacteria's ability to hide in stem cells. Some bone marrow stem cells reside in low oxygen (hypoxia) zones. These specialized zones are secured as immune cells and toxic chemicals cannot reach this zone. Hypoxia- activated cell signaling pathways may also protect the stem cells from dying or ageing. A new study led by Forsyth Scientist Dr. Bikul Das has found that Mycobacterium tuberculosis (Mtb) hijack this protective hypoxic zone to hide intracellular to a special stem cell type. The study was published online on June 8th in the American Journal of Pathology.

Mtb, the causative organism of tuberculosis, infects nearly 2.2 billion people worldwide and causes 1.7 million annual deaths. This is largely attributed to the bacteria's ability to stay dormant in the human body and later resurface as active disease. Earlier research at Forsyth revealed that Mtb hides inside a specific stem cell population in bone marrow, the CD271+ mesenchymal stem cells. However, the exact location of the Mtb harboring stem cells was not known.

"From our previous research, we learned that cancer stem cells reside in the hypoxic zones to maintain self-renewal property, and escape from the immune system" said Bikul Das, MBBS, PhD, Associate Research Investigator at the Forsyth Institute, and the honorary director of the KaviKrishna laboratory, Guwahati, India. "So, we hypothesized that Mtb, like cancer, may also have figured out the advantage of hiding in the hypoxic area."

To test this hypothesis, Dr. Das and his collaborators at Jawarharlal Nehru Univeristy (JNU), New Delhi, and KaviKrishna Laboratory, Indian Institute of Technology, Guwahati, utilized a well-known mouse model of Mtb infection, where months after drug treatment, Mtb remain dormant for future reactivation. Using this mouse model of dormancy, scientists isolated the special bone marrow stem cell type, the CD271+ mesenchymal stem cells, from the drug treated mice. Prior to isolation of the stem cells, mice were injected with pimonidazole, a chemical that binds specifically to hypoxic cells. Pimonidazole binding of these cells was visualized under confocal microscope and via flow cytometry. The scientists found that despite months of drug treatment, Mtb could be recovered from the CD271+ stem cells. Most importantly, these stem cells exhibit strong binding to pimonidazole, indicating the hypoxic localization of the stem cells. Experiments also confirmed that these stem cells express a hypoxia activated gene, the hypoxia inducible factor 1 alpha (HIF-1 alpha).

To confirm the findings in clinical subjects, the research team, in collaboration with KaviKrishna Laboratory, the team isolated the CD271+ stem cell type from the bone marrow of TB infected human subjects who had undergone extensive treatment for the disease. They found that not only did the stem cell type contain viable Mtb, but also exhibit strong expression of HIF-1alpha. To their surprise, the CD271+ stem cell population expressed several fold higher expression of HIF-1alpha than the stem cell type obtained from the healthy individuals.

"These findings now explain why it is difficult to develop vaccines against tuberculosis," said Dr. Das. "The immune cells activated by the vaccine agent may not be able to reach the hypoxic site of bone marrow to target these "wolfs-in-stem-cell-clothing".

The success of this international collaborative study is now encouraging the team to develop a Forsyth Institute/KaviKrishna Laboratory global health research initiative to advance stem cell research and its application to global health issues including TB, HIV and oral cancer, all critical problems in the area where KaviKrishna Laboratory is located.

###

Das is the co-senior and co-corresponding author of the study, Rakesh Bhatnagar, PhD, professor of biotechnology, JNU, New Delhi, is the co-senior author of the study. Ms. Jaishree Garhain, a PhD student of Dr. Das and Dr. Bhatnagar, is the first author of the study. Other members of the team are Ms. Seema Bhuyan, Dr. Deepjyoti Kalita, and Dr. Ista Pulu. The research was funded by the KaviKrishna Foundation (Sualkuchi, India), the Laurel Foundation (Pasadena, California), and Department of Biotechnology, India.

About The Forsyth Institute

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Tuberculosis bacteria hide in the low oxygen niches of ...

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Personalization is threaded into the social fabric of America. Innovation is rooted in customizing and personalizing even the smallest parts of our lives, stemming from technology and retail to travel, media and wellness. The future continues to promise even smarter applications where personalization fits, but what about our health? Enter, precision medicine -- this new era of personalized medicine has arrived to healthcare and the possibilities in treating cancer unimaginable just a few years ago, are closer than ever. Imagine a world where your treatment was tailored to you, taking into consideration every cell and gene throughout your individual genetic profile, using that data to specifically design a treatment to fight the exact cancer you have? Sound too good to be true? Think again. The future is here, and the healthcare industry is preparing for massive disruption but for once disruption couldn't have come at a better time.

The Road to Personalized Medicine for Cancer Treatment

For decades, physicians had the same approach for all patients with the same type of cancer, be it breast, lung, liver or prostate cancer, the same way, even through they were aware drug treatments may work on some and fail in others. This is not to say all cancers are treated the same, but the basic approach and process is used when it comes to diagnosing, staging, and recurrence. As significant advances in research progressed over the course of the last 30 years, the medical community created standards of care and treatment when it came to diseases like diabetes, heart disease, and even cancer. However, treating cancer cannot be classified with a standard approach. What we're learning more and more comes down to the individual. Each person is as unique on the inside as they are on the outside. Therefore, why wouldn't we treat their cancer using an individual approach?

For the last 20 years, cancer cells have outsmarted us by protecting themselves, building a wall, not allowing the immune system to identify and kill them. Current treatments are not aimed at stopping cells from spreading and have almost no selective capacity to distinguish between cancer cells and healthy cells. We've basically poisoned the body to kill cancer using chemotherapy and even radiation. But advancements in research has led to a number of potential targeted therapies designed to fight cancer, among them one approach is gaining more and more support -- immunotherapy. This type of targeted therapy teaches our own immune system to fight cancer cells and spare healthy ones. By injecting bacteria inside cancer cells and putting them back into the body, the immune system can learn to recognize and kill them. Think of your T cells as guided missiles aimed at killing the bad cancer cells versus a bomb that kills every cell in its path such as chemotherapy. But an approach we could've never foreseen 10 years ago is right around the corner, leading a transition not just from the diagnosis and treatment of these cancers but much more emphasis on prediction and prevention.

Welcome to the world of precision medicine also deemed "personalized medicine," where each patient is treated individually based on their genetic makeup and the specific genetic mutations present in their body. The National Institutes of Health defines precision medicine as an emerging approach for disease treatment and prevention that integrates an individual's variability in genes, environment and lifestyle. To take it even further, precision health may be the new approach to medicine, rooted in prevention and prediction of various diseases while also maintaining overall health and quality of life.

In my field, which is prostate cancer, we talk a lot about an individual patient's risk factors such as family history, which is a huge proponent of the disease and how aggressive it is. While oftentimes surgery is the first line of defense, the right way to treat prostate cancer and any cancer is through individualized care. Recently at the 110th Annual Scientific Meeting of the American Urological Association, a significant study was presented which showed a combined assessment of genetic bio markers and the genetic profile for a patient would lead to better methods for diagnosing, treating and measuring the likelihood of the disease recurring. The breakthrough here is the role genetic testing plays in cancer, throughout the entire process, from diagnosis to recurrence. We can gather more information about the patient at each step of the way.

Precision Medicine Meets Individualized Care

I've always spoken about the importance of individualized care, especially when it comes to diagnosing and treating cancer. Innovations in genomic testing are leading this emerging era of cancer therapy -- analyzing a group of genes and their activity, which can influence how a cancerous tumor is likely to grow and respond to treatment. This type of diagnostic testing analyzes and detects very specific abnormalities in the tumor cells in a patient's individual cancer. Unlocking the mysteries of genetics holds the promise of finding more customized cures with drugs that attack genetic mutations or repair genetic defects based on the individual patient. Advances in genetic sequencing has increased the likelihood of detecting mutations driving tumor growth and even specific cells inside the tumor. This is the future of treating and diagnosing cancer, integrated with the promise of precision medicine.

Is this revolutionizing everything we know about cancer, from prevention and diagnosis to treatment and recurrence? I would say yes. We've always identified cancer based on the organ it originates in such as the prostate, colon or liver, grouping these together as if they grow the same. What we know now is just because it's deemed "prostate cancer" doesn't mean all prostate cancers develop or progress in the same way. Testing the genetics of an individual patient has opened up an entire new conversation in oncology leading us to define within the cancer what actually drives its development and progression.

The Precision Medicine Initiative

Link:
Conquering Cancer: Personalized Medicine Is the Future ...

Recommendation and review posted by sam

Cardiac stem cells, which have the ability to differentiate (specialize) into mature heart cells and therefore could be used to repair damaged or diseased heart tissue, have garnered significant interest in the development of treatments for heart disease and cardiac defects. Cardiac stem cells can be derived from mature cardiomyocytes through the process of dedifferentiation, in which mature heart cells are stimulated to revert to a stem cell state. The stem cells can then be stimulated to redifferentiate into myocytes or endothelial cells. This approach enables millions of cardiac stem cells to be produced in the laboratory.

In 2009 a team of doctors at Cedars-Sinai Heart Institute in Los Angeles, California, reported the first attempted use of cardiac stem cell transplantation to repair damaged heart tissue. The team removed a small section of tissue from the heart of a patient who had suffered a heart attack, and the tissue was cultured in a laboratory. Cells that had been stimulated to dedifferentiate were then used to produce millions of cardiac stem cells, which were later reinfused directly into the heart of the patient through a catheter in a coronary artery. A similar approach was used in a subsequent clinical trial reported in 2011; this trial involved 14 patients suffering from heart failure who were scheduled to undergo cardiac bypass surgery. More than three months after treatment, there was slight but detectable improvement over cardiac bypass surgery alone in left ventricle ejection fraction (the percentage of the left ventricular volume of blood that is ejected from the heart with each ventricular contraction).

Stem cells derived from bone marrow, the collection of which is considerably less invasive than heart surgery, are also of interest in the development of regenerative heart therapies. The collection and reinfusion into the heart of bone marrow-derived stem cells within hours of a heart attack may limit the amount of damage incurred by the muscle.

There are many types of arterial diseases. Some are generalized and affect arteries throughout the body, though often there is variation in the degree they are affected. Others are localized. These diseases are frequently divided into those that result in arterial occlusion (blockage) and those that are nonocclusive in their manifestations.

Atherosclerosis, the most common form of arteriosclerosis, is a disease found in large and medium-sized arteries. It is characterized by the deposition of fatty substances, such as cholesterol, in the innermost layer of the artery (the intima). As the fat deposits become larger, inflammatory white blood cells called macrophages try to remove the lipid deposition from the wall of the artery. However, lipid-filled macrophages, called foam cells, grow increasingly inefficient at lipid removal and undergo cell death, accumulating at the site of lipid deposition. As these focal lipid deposits grow larger, they become known as atherosclerotic plaques and may be of variable distribution and thickness. Under most conditions the incorporation of cholesterol-rich lipoproteins is the predominant factor in determining whether or not plaques progressively develop. The endothelial injury that results (or that may occur independently) leads to the involvement of two cell types that circulate in the bloodplatelets and monocytes (a type of white blood cell). Platelets adhere to areas of endothelial injury and to themselves. They trap fibrinogen, a plasma protein, leading to the development of platelet-fibrinogen thrombi. Platelets deposit pro-inflammatory factors, called chemokines, on the vessel walls. Observations of infants and young children suggest that atherosclerosis can begin at an early age as streaks of fat deposition (fatty streaks).

Atherosclerotic lesions are frequently found in the aorta and in large aortic branches. They are also prevalent in the coronary arteries, where they cause coronary artery disease. The distribution of lesions is concentrated in points where arterial flow gives rise to abnormal shear stress or turbulence, such as at branch points in vessels. In general the distribution in most arteries tends to be closer to the origin of the vessel, with lesions found less frequently in more distal sites. Hemodynamic forces are particularly important in the system of coronary arteries, where there are unique pressure relationships. The flow of blood through the coronary system into the heart muscle takes place during the phase of ventricular relaxation (diastole) and virtually not at all during the phase of ventricular contraction (systole). During systole the external pressure on coronary arterioles is such that blood cannot flow forward. The external pressure exerted by the contracting myocardium on coronary arteries also influences the distribution of atheromatous obstructive lesions.

Excerpt from:
cardiovascular disease :: Cardiac stem cells | Britannica.com

Recommendation and review posted by Bethany Smith

Cardiac stem cells, which have the ability to differentiate (specialize) into mature heart cells and therefore could be used to repair damaged or diseased heart tissue, have garnered significant interest in the development of treatments for heart disease and cardiac defects. Cardiac stem cells can be derived from mature cardiomyocytes through the process of dedifferentiation, in which mature heart cells are stimulated to revert to a stem cell state. The stem cells can then be stimulated to redifferentiate into myocytes or endothelial cells. This approach enables millions of cardiac stem cells to be produced in the laboratory.

In 2009 a team of doctors at Cedars-Sinai Heart Institute in Los Angeles, California, reported the first attempted use of cardiac stem cell transplantation to repair damaged heart tissue. The team removed a small section of tissue from the heart of a patient who had suffered a heart attack, and the tissue was cultured in a laboratory. Cells that had been stimulated to dedifferentiate were then used to produce millions of cardiac stem cells, which were later reinfused directly into the heart of the patient through a catheter in a coronary artery. A similar approach was used in a subsequent clinical trial reported in 2011; this trial involved 14 patients suffering from heart failure who were scheduled to undergo cardiac bypass surgery. More than three months after treatment, there was slight but detectable improvement over cardiac bypass surgery alone in left ventricle ejection fraction (the percentage of the left ventricular volume of blood that is ejected from the heart with each ventricular contraction).

Stem cells derived from bone marrow, the collection of which is considerably less invasive than heart surgery, are also of interest in the development of regenerative heart therapies. The collection and reinfusion into the heart of bone marrow-derived stem cells within hours of a heart attack may limit the amount of damage incurred by the muscle.

There are many types of arterial diseases. Some are generalized and affect arteries throughout the body, though often there is variation in the degree they are affected. Others are localized. These diseases are frequently divided into those that result in arterial occlusion (blockage) and those that are nonocclusive in their manifestations.

Atherosclerosis, the most common form of arteriosclerosis, is a disease found in large and medium-sized arteries. It is characterized by the deposition of fatty substances, such as cholesterol, in the innermost layer of the artery (the intima). As the fat deposits become larger, inflammatory white blood cells called macrophages try to remove the lipid deposition from the wall of the artery. However, lipid-filled macrophages, called foam cells, grow increasingly inefficient at lipid removal and undergo cell death, accumulating at the site of lipid deposition. As these focal lipid deposits grow larger, they become known as atherosclerotic plaques and may be of variable distribution and thickness. Under most conditions the incorporation of cholesterol-rich lipoproteins is the predominant factor in determining whether or not plaques progressively develop. The endothelial injury that results (or that may occur independently) leads to the involvement of two cell types that circulate in the bloodplatelets and monocytes (a type of white blood cell). Platelets adhere to areas of endothelial injury and to themselves. They trap fibrinogen, a plasma protein, leading to the development of platelet-fibrinogen thrombi. Platelets deposit pro-inflammatory factors, called chemokines, on the vessel walls. Observations of infants and young children suggest that atherosclerosis can begin at an early age as streaks of fat deposition (fatty streaks).

Atherosclerotic lesions are frequently found in the aorta and in large aortic branches. They are also prevalent in the coronary arteries, where they cause coronary artery disease. The distribution of lesions is concentrated in points where arterial flow gives rise to abnormal shear stress or turbulence, such as at branch points in vessels. In general the distribution in most arteries tends to be closer to the origin of the vessel, with lesions found less frequently in more distal sites. Hemodynamic forces are particularly important in the system of coronary arteries, where there are unique pressure relationships. The flow of blood through the coronary system into the heart muscle takes place during the phase of ventricular relaxation (diastole) and virtually not at all during the phase of ventricular contraction (systole). During systole the external pressure on coronary arterioles is such that blood cannot flow forward. The external pressure exerted by the contracting myocardium on coronary arteries also influences the distribution of atheromatous obstructive lesions.

See the original post here:
cardiovascular disease :: Cardiac stem cells | Britannica.com

Recommendation and review posted by sam

By the time Bill Beatty made it to the Emergency Department in Howard County, he was already several hours into a major heart attack. His physicians performed a series of emergency treatments that included an intra-aortic balloon pump, but the 57-year-old engineers blood pressure remained dangerously low. The cardiologist called for a helicopter to transfer him to Johns Hopkins.

It was fortuitous timing: Beatty was an ideal candidate for a clinical trial and soon received an infusion of stem cells derived from his own heart tissue, making him the second patient in the world to undergo the procedure.

Of all the attempts to harness the promise of stem cell therapy, few have garnered more hope than the bid to repair damaged hearts. Previous trials with other stem cells have shown conflicting results. But this new trial, conducted jointly with cardiologist Eduardo Marbn at Cedars-Sinai Medical Center in Los Angeles, is the first time stem cells come from the patients own heart.

Cardiologist Jeffrey Brinker, M.D., a member of the Hopkins team, thinks the new protocol could be a game-changer. That's based partly on recent animal studies in which scientists at both institutions isolated stem cells from the injured animals hearts and infused them back into the hearts of those same animals. The stem cells formed new heart muscle and blood vessel cells. In fact, says Brinker, the new cells have a pre-determined cardiac fate. Even in the culture dish, he says, theyre a beating mass of cells.

Whats more, according to Gary Gerstenblith, M.D., J.D., the animals in these studies showed a significant decrease in relative infarct size, shrinking by about 25 percent. Based on those and earlier findings, investigators were cleared by the FDA and Hopkins Institutional Review Board to move forward with a human trial.

In Beattys case, Hopkins heart failure chief Stuart Russell, M.D., extracted a small sample of heart tissue and shipped it to Cedars Sinai, where stem cells were isolated, cultured and expanded to large numbers. Hopkins cardiologist Peter Johnston, M.D., says cardiac tissue is robust in its ability to generate stem cells, typically yielding several million transplantable cells within two months.

When ready, the cells were returned to Baltimore and infused back into Beatty through a balloon catheter placed in his damaged artery, ensuring target-specific delivery. Then the watching and waiting began. For the Hopkins team, Beattys infarct size will be tracked by imaging chief Joao Lima, M.D., M.B.A.,and his associates using MRI scans.

Now back home and still struggling with episodes of compromised stamina and shortness of breath, Beatty says his Hopkins cardiologists were fairly cautious in their prognosis, but hell be happy for any improvement.

Nurse coordinator Elayne Breton says Beatty is scheduled for follow-up visits at six months and 12 months, when they hope to find an improvement in his hearts function. But at least one member of the Hopkins team was willing acknowledge a certain optimism. The excitement here, says Brinker, is huge.

The trial is expected to be completed within one to two years.

Originally posted here:
Stem Cell Research at Johns Hopkins Medicine: Repairing ...

Recommendation and review posted by sam

In men 45 and older, most cases of hypogonadism or Low-T often go overlooked due to the fact that the symptoms may be more general in nature and slower in onset. Many men simply attribute their symptoms to aging and often dismiss them because they don't think that there is anything that they can do about them. This is largely because the symptoms of hypogonadism are nearly identical to those experienced by men going through andropause (the male menopause): low libido, fatigue, depression, memory loss, difficulty concentrating and irritability. The difference between andropause and hypogonadism is simple. Andropause is a natural part of a man's life where his hormones begin to decline right around the age of 35 and continue to decrease until they plateau in his late 60's. Hypogonadism is a condition where testosterone is not being produced due to a physical abnormality of the testes or brain. It can also be due to an outside factor such as stress, poor diet or pre-existing health conditions. Both Hypogonadism and andropause however can be treated and corrected under the care of experienced hormonal specialists.

There are two basic forms of hypogonadism found in men. Primary hypogonadism is also known as ?testicular failure? and stems from a complication in the testicles. Some common causes of primary hypogonadism are:

The other type of hypogonadism is called secondary hypogonadism, and it describes a condition where the testicles are normal on a physiological level, but still don't function properly due to a problem stemming from the pituitary gland or the hypothalamus. This creates a problem with the signal from the brain to the testicle. Although the testicles function well, they can't get the information from the brain that testosterone needs to be produced. Some common causes of secondary hypogonadism are:

The most effective ways to treat hypogonadism are to enhance the body's ability to make its own testosterone or to supplement the testosterone that your body would produce normally, using natural bioidentical testosterone replacement therapy. It is critical to combine bioidentical hormone therapy with appropriate diet, exercise, lifestyle and stress management. Although there are many different causes for the condition, hypogonadism always leads to hormonal imbalance and can lead to a wide range of symptoms and chronic health issues. Fortunately, under the proper care of a highly trained BodyLogicMD affiliated physician, the condition can be corrected.

Through comprehensive testing, your BodyLogicMD affiliated physician will determine your hormone levels to uncover potential hormone deficiencies. Based on cutting edge diagnostic technologies, BodyLogicMD affiliated physicians pinpoint the source of underlying hormonal imbalances and use all natural bioidentical hormone replacement therapy (BHRT) interlaced with customized nutrition and fitness regimens to help men find relief symptoms of hormonal imbalance. BodyLogicMD affiliated physicians have helped thousands of men get their edge back and overcome testosterone deficiencies such as andropause and hypogonadism.

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Low Testosterone in Men | Hypogonadism

Recommendation and review posted by Bethany Smith

SAN DIEGO(BUSINESS WIRE)Cytori Therapeutics, Inc. (NASDAQ: CYTX) today confirmed that two Japanese regenerative medicine laws, which went into effect on November 25, 2014, remove regulatory uncertainties and provide a clear path for the Company to commercialize and market Cytori Cell Therapy and its Celution System under the Companys existing and planned regulatory approvals.

Japans new regenerative medicine laws substantially clarify regulatory ambiguities of pre-existing guidelines and this news represents a significant event for Cytori, said Dr. Marc Hedrick, President & CEO of Cytori. We have a decade of operating experience in Japan and Cytori is nicely positioned to see an impact both on existing commercial efforts and on our longer-term efforts to obtain therapeutic claims and reimbursement for our products.

Under the two new laws, Cytori believes its Celution System and autologous adipose-derived regenerative cells (ADRCs) can be provided by physicians under current Class I device regulations and used under the lowest risk category (Tier 3) for many procedures with only the approval by accredited regenerative medicine committees and local agencies of the Ministry of Health, Labour and Welfare (MHLW). This regulatory framework is expected to streamline the approval and regulatory process and increase clinical use of Cytori Cell Therapy and the Celution System over the former regulations.

Before these new laws were enacted, the regulatory pathway for clinical use of regenerative cell therapy was one-size-fits-all, irrespective of the risk posed by certain cell types and approaches, said Dr. Hedrick. Now, Cytoris point-of-care Celution System can be transparently integrated into clinical use by providers under our Class I device status and the streamlined approval process granted to cell therapies that pose the lowest risk. Our technology is unique in that respect.

Cytoris Celution System Is in Lowest of Three Risk Categories

The Act on the Safety of Regenerative Medicines and an amendment of the 2013 Pharmaceutical Affairs Act (the PMD Act), collectively termed the Regenerative Medicine Laws, replace the Human Stem Cell Guidelines. Under the new laws, the cell types used in cell therapy and regenerative medicine are classified based on risk. Cell therapies using cells derived from embryonic, induced pluripotent, cultured, genetically altered, animal and allogeneic cells are considered higher risk (Tiers 1 and 2) and will undergo an approval pathway with greater and more stringent oversight due to the presumed higher risk to patients. Cytoris Celution System, which uses the patients own cells at the point-of-care, will be considered in the lowest risk category (Tier 3) for most cases, and will be considered in Tier 2 if used as a non-homologous therapy.

Streamlined Regulatory Approval for Certain Medical Devices

In the near future, Cytori intends to pursue disease-specific or therapeutic claims and reimbursement for Cytoris Celution System and the Company would, at that point, sponsor a clinical trial to obtain Class III device-based approval and reimbursement. The new laws include changes to streamline regulation of Class II and some Class III devices, which will now require the approval of certification bodies rather than the PMDA, similar to the European notified body model. To date, certification bodies have only been used for some Class II devices.

Conditional Regulatory Approval and Reimbursement Potential

As a supplementary benefit to Cytori, the Company may also choose to take advantage of the new conditional approval opportunities granted under the new laws. Once clinical safety and an indication of efficacy are shown, sponsors may apply for their cell product to receive conditional approval for up to seven years and may be eligible for reimbursement under Japans national insurance coverage. Under the conditional approval, the sponsor can then generate post-marketing data to demonstrate further efficacy and cost effectiveness.

Read more:
japanese | StemCell Therapy MD

Recommendation and review posted by Bethany Smith

During development from stem to fully differentiated, cells in the body alternately divide (mitosis) and "appear" to be resting (interphase). This sequence of activities exhibited by cells is called the cell cycle. Follow the events in the entire cell cycle with the following animation.

Interphase: Interphase, which appears to the eye to be a resting stage between cell divisions, is actually a period of diverse activities. Those interphase activities are indispensible in making the next mitosis possible. Interphase generally lasts at least 12 to 24 hours in mammalian tissue. During this period, the cell is constantly synthesizing RNA, producing protein and growing in size. By studying molecular events in cells, scientists have determined that interphase can be divided into 4 steps: Gap 0 (G0), Gap 1 (G1), S (synthesis) phase, Gap 2 (G2).

Gap 0(G0): There are times when a cell will leave the cycle and quit dividing. This may be a temporary resting period or more permanent. An example of the latter is a cell that has reached an end stage of development and will no longer divide (e.g. neuron).

Gap 1(G1): Cells increase in size in Gap 1, produce RNA and synthesize protein. An important cell cycle control mechanism activated during this period (G1 Checkpoint) ensures that everything is ready for DNA synthesis. (Click on the Checkpoints animation, above.)

S Phase: To produce two similar daughter cells, the complete DNA instructions in the cell must be duplicated. DNA replication occurs during this S (synthesis) phase.

Gap 2(G2): During the gap between DNA synthesis and mitosis, the cell will continue to grow and produce new proteins. At the end of this gap is another control checkpoint (G2 Checkpoint) to determine if the cell can now proceed to enter M (mitosis) and divide.

MitosisorM Phase:Cell growth and protein production stop at this stage in the cell cycle. All of the cell's energy is focused on the complex and orderly division into two similar daughter cells. Mitosis is much shorter than interphase, lasting perhaps only one to two hours. As in both G1 and G2, there is a Checkpoint in the middle of mitosis (Metaphase Checkpoint) that ensures the cell is ready to complete cell division. Actual stages of mitosis can be viewed atAnimal Cell Mitosis.

Cancer cells reproduce relatively quickly in culture. In theCancer Cell CAMcompare the length of time these cells spend in interphase to that formitosisto occur.

Excerpt from:
The Cell Cycle - CELLS alive

Recommendation and review posted by Bethany Smith

Please ensure you have JavaScript enabled in your browser. If you leave JavaScript disabled, you will only access a portion of the content we are providing. Here's how. A genetic counselor could... Key Facts & Information Source: O*Net and LifeWorks Training, Other Qualifications

The majority of genetic counselors practicing today are board certified. Board certification to become a Certified Genetic Counselor (CGC) is available through the American Board of Genetic Counseling (ABGC). Requirements include documentation of the following: a graduate degree in genetic counseling from an accredited program; clinical experience in an ABGC-approved training site or sites; a log book of 50 supervised cases; and successful completion of both the general and specialty certification examination.

Students interested in genetic counseling careers should be sure to take all the high school biology, chemistry, and math courses available to them. Good written and communication skills are also important and can be gained in English, foreign languages, and sociology classes.

In college, students should continue to study biology, chemistry, statistics, psychology, sociology, and anthropology.

Students interested in pursuing this career should also seek ways to gain experience in counseling. This can be done in a number of ways, including applying for peer-counseling positions, or volunteering with a crisis center or hotline.

Genetic counselors need to complete a master's degree in genetic counseling. Coursework typically includes clinical genetics, population genetics, cytogenetics, and molecular genetics, coupled with psychosocial theory, ethics, and counseling techniques. Clinical placement in approved medical genetics centers is an integral part of the degree requirement.

Genetic counselors need to have strong analytical reasoning skills in order to evaluate the genetic risks of their patients. Counselors also require robust interpersonal communication skills to help them effectively explain the genetic risks to their patients and then counsel them about their options. Inductive reasoning, active listening, oral communication, and writing skills are all critical to a genetic counselor's career. Genetic counselors also need to be socially perceptive, staying aware of others' reactions and understanding why they react the way they do.

In clinical settings, genetic counselors provide information and support to individuals who have or are at risk of having birth defects or genetic conditions, as well as to their families. They analyze family history information, interpret information about specific disorders, discuss the inheritance patterns, assess the risk to individuals, and review available options for testing or management with families. In addition to informative counseling, genetic counselors also provide supportive counseling to help individuals and families cope with and adapt to their altered circumstances.

Some genetic counselors also work in research settings, where they use the same diagnostic skills to discover how disorders are inherited and evaluate what can be done to treat them.

Genetic counselors often have teaching roles, in addition to their clinical or research work. They are involved in educating medical residents, medical students, genetic counseling students, physicians, other health care providers, and the general public, about human genetics.

See original here:
Genetic Counselor - Science Buddies

Recommendation and review posted by sam

CHERRY HILL, N.J., June 9, 2015 /PRNewswire/ --My MS Manager, the first-of-its kind mobile phone app... This observational study investigates the associations between multiple sclerosis disability and disease type with lower thoracic cord gray matter and white matter areas using phase sensitive inversion recovery magnetic resonance imaging at 3T, as well as compares these relationships with those... A team to address both the physical and emotional outcomes of MS relapse is essential to high quality care. Step closer to understanding why men are better protected from MS than womenAn innocent mistake made by a graduate student in a Northwestern Medicine lab (she... Read about how Opexa Therapeutic's Tcelna is truly a personalized therapy for patients with multiple sclerosis. We mobilize people and resources to drive research for a cure and to address the challenges of everyone affected by MS. Falls Church resident Lisa Emrich was diagnosed with multiple sclerosis, an autoimmune disorder that affects the central nervous system, nearly ten years ago.But the first time she experienced what can be one of the more extreme symptoms of the disorder, temporary blindness, was in 2000. That bout of optic neuritis Background Fingolimod efficiently reduces multiple sclerosis (MS) relapse by inhibiting lymphocyte egress from lymph nodes through down-modulation of sphingosine 1-phosphate (S1P) receptors. We aimed to clarify the alterations in peripheral blood T cell subsets associated with MS relapse on fingolimod. Methods/Principal Findings Blood samples successively collected from 23 relapsing-remitting MS patients before and during fingolimod therapy (0.5 mg/day) for 12 months and 18 healthy Via Krishan Maggon New findings published in the journal Molecular Psychiatry have researchers uncovering the cause of "brain fog." The U.S. Food and Drug Administration today approved the first generic version of Copaxone (glatiramer acetate injection), used to treat patients with relapsing forms of multiple sclerosis (MS). Another study suggests that a telehealth system could help objectively monitor dose adherence. A combination of physical, occupational, hand, speech, cognitive, and behavioral therapy improves outcomes. Insurance coverage can be the determining factor on whether a patient receives DMT or not. Read about the upcoming International Multiple Sclerosis Conference to take place in Rome that will focus on the patients' experience to treat the disease. Multiple sclerosis (MS) is an immune-mediated, neuro-inflammatory, demyelinating and neurodegenerative disease of the central nervous system (CNS) with a heterogeneous clinical presentation and course. There is a remarkable phenotypic heterogeneity in MS, and the molecular mechanisms underlying it remain unknown. We aimed to investigate further the etiopathogenesis related molecular pathways in subclinical types of MS using proteomic and bioinformatics approaches in cerebrospinal fluids of pati Via Krishan Maggon Intracerebral infection of susceptible mouse strains with Theilers murine encephalomyelitis virus (TMEV) results in chronic demyelinating disease with progressive axonal loss and neurologic dysfunction similar to progressive forms of multiple sclerosis (MS). We previously showed that as the disease progresses, a marked decrease in brainstem N-acetyl aspartate (NAA; metabolite associated with neuronal integrity) concentrations, reflecting axon health, is measured. We also demonstrated stimulation of neurite outgrowth by a neuron-binding natural human antibody, IgM12. Treatment with either the serum-derived or recombinant human immunoglobulin M 12 (HIgM12) preserved functional motor activity in the TMEV model. In this study, we examined IgM-mediated changes in brainstem NAA concentrations and central nervous system (CNS) pathology. The myth that African Americans do not get MS is just that a myth. African Americans do get MS. In fact, studies suggest that MS can be especially active. David Lyons doesn't let his battle against multiple sclerosis knock him off his feet. He's fought back, continuing his bodybuilding training while assisting others by creating the MS Fitness Challenge.

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Multiple Sclerosis Research: natalizumab has a ...

Recommendation and review posted by simmons

It started in 2009, lump in throat feeling did barium swallow test whihc was notmal, and had blood test which was normal except ESR slightly high, aske d to take Valprim 2mg and symptoms disappeared after a week or so, Again Sept 2011 felt like I had something in throat, went to doctors, gave me did an gastrocscopy, came clear, also did ultrasound for thyroid right side was in the upper limit s of normal, left was normal, also had some pain in stomach around that time did bariumtest and contrast for MRI to which I was anaphalactic, and had to give a cortizone, also sent me to ENT, during that time I had this white pimple,( have had them previously which ws not often but since 2011 they were there quite often), looking things on right side of tonsil no pain just botherend me making me feel like I need to gag, and sometimes when I coughed it came out other times I had to press on it to get the darn thing out, they were like white heads only two in the same spot all the time, ENT and doctor said food particles believe me they were not I thingk they were tonsil stones, found out through, med help. ENT Dec 2011 ,sent camera through nose said have a drip, I have alleries to hayfever andasthma asked to do a scan , did not do it immediately, until end of March when I woke up and felt that my vison was double digits, was worried as there is glucoma in family, and my previous eye pressure in FEb 2011,check was 19, Since March before I got the blurry vion hadnt been sleeping well, also notedfor getting a lot, putting things in wrong place, sometimes forget what I was looking for as well, had astammer at one time, which I never had but now not often only sometimes, if I am stressed trying to think of words maybe due to lack of slee. Ayway went to emergency did normal test to make sure not a stroke due to double vion and was asked to go toemergency ENT next day, Had terrible headache and went eye pressure was done igt was in 20 and 21, as I was also vomiting, did not have headace when I had the blurry vision, just . They asked if I get sius problems said yes, so they checked it with camera and said may have polyps and do a scan tomake sure hospital put me on antibiotics which had some acid in it made breathing a bit hard felt like something was stuck in chest and itchiness here and there, did scan said have polyps.Went back to GP put me on doxy for 3 weeks while on doxy got me to do a scan of the thyroid and said that it came out normal also did another blood test that came out normal. While on doxy noted the pimples in right side cleared up, but there is a flesh coloured slighly raisedlump on that side, so put finger in there to check it was a small lump size of pea doesnot hurt, but noticed after the doxy was over that it had enlarged , was worried showed it to doctor who said dont worry, been in an oout of doctors, who says my glands are swollen, everytime mentioned it to him but not worried, checked mouth with popsicle stick and light, mentioned to him that it has grown but docotor is not concerned, went back to entwith the report of scan mentioned to him he too said may be due to nasal drip, nasal drip, is back of throat this is in front of the arch where the pimples were,Tthe throat scan for thyroidsdid not show or mention, anything about this lump, as I was on antibiotics at the time, Feel neck is heavy, tightness, so went to chiro who took Xrays of the back top to bottom while on antibiotics, chiro said had a small bend but nothing to worry about, feel a lot of tension in neck area and sometimes a uncomfortable feeling, On the weekend was on bed on the computer, felt the pressure on both side of the neck as if I was going to get choked, have had this dry coughcough too that has started, for some times now but havent taken notice of it as I do have asthma, but it not asthmatic, had breakfast in bed and then got up was in the kitchen felt vision going blurry , as my neck felt tightening on both sides, went and put my feet up for some time took some time for the feeling to leave 20 -30 mts or more. Went back to Dr and mentioned about this, also noted that I had a slightloss of bladder control and did not know until I felt something wet, but was too shy to tell the doctor I am forgetting alotnot sure because of the stress of the lump, my sinus feels fine sometimes get the drip and stuffed nose but not all the time, could it be the lump inside throat that is causing but it is only on the right not left but the compression was on both sides,took a nurofen, yesterday, I am stressed oiut about the lump pressure was fine but my hear rate was 81 and should have been 66 or below, I checkd my poulse when I felt thistightening and it was 99, but when I went to the doctorit was normal, All I want is to get this lump out of my throat so I dont stress anymore, I want to do the polyps but they said they will have to straighten themiddleof nose too, and read that polyps can comeback if you dont know what is causing it so want to get allergy test done, as well as want the doctor to take this lump out at the same time how can I make him do it he is only concentraing on the sinus., will I need my doctor to ask him to remove it too, as it is causing me to stress, sinus not too bad but the vison thing together with the back of neck discomfort, and the side s of throat tightness, is frightening me. when I move the neck around I can hear this funny sound like a crunch noise.do you thing if I go to the dentist will she might be able to help me with this lump on the inside of the neck, I am not sure what to do if anyone can let me know if they have the same problem, I too thought it might be the arteries on the side of neck that is causing this, the doctor said if I get the blur vion next time she will get a scan done, note not sinus when I had the second blured vision. ENT asked me to take prednosoloan, and an antibiotic, not sure for what is if it is for the drip or the lump, as I was sneezing a lot the day I went for the second ENT Please help

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Inflammation of Carotid artery and neck pain - Undiagnosed ...

Recommendation and review posted by Bethany Smith

Overview

Omega-3 fatty acids are considered essential fatty acids: They are necessary for human health but the body cant make them -- you have to get them through food. Omega-3 fatty acids can be found in fish, such as salmon, tuna, and halibut, other seafood including algae and krill, some plants, and nut oils. Also known as polyunsaturated fatty acids (PUFAs), omega-3 fatty acids play a crucial role in brain function, as well as normal growth and development. They have also become popular because they may reduce the risk of heart disease. The American Heart Association recommends eating fish (particularly fatty fish such as mackerel, lake trout, herring, sardines, albacore tuna, and salmon) at least 2 times a week.

Research shows that omega-3 fatty acids reduce inflammation and may help lower risk of chronic diseases such as heart disease, cancer, and arthritis. Omega-3 fatty acids are highly concentrated in the brain and appear to be important for cognitive (brain memory and performance) and behavioral function. In fact, infants who do not get enough omega-3 fatty acids from their mothers during pregnancy are at risk for developing vision and nerve problems. Symptoms of omega-3 fatty acid deficiency include fatigue, poor memory, dry skin, heart problems, mood swings or depression, and poor circulation.

It is important to have the proper ratio of omega-3 and omega-6 (another essential fatty acid) in the diet. Omega-3 fatty acids help reduce inflammation, and most omega-6 fatty acids tend to promote inflammation. The typical American diet tends to contain 14 - 25 times more omega-6 fatty acids than omega-3 fatty acids, which many nutritionally oriented physicians consider to be way too high on the omega-6 side.

The Mediterranean diet, on the other hand, has a healthier balance between omega-3 and omega-6 fatty acids. Many studies have shown that people who follow this diet are less likely to develop heart disease. The Mediterranean diet emphasizes foods rich in omega-3 fatty acids, including whole grains, fresh fruits and vegetables, fish, olive oil, garlic, as well as moderate wine consumption.

Clinical evidence is strongest for heart disease and problems that contribute to heart disease, but omega-3 fatty acids may also be used for:

High cholesterol

People who follow a Mediterranean style diet tend to have higher HDL or good cholesterol levels, which help promote heart health. Inuit Eskimos, who get high amounts of omega-3 fatty acids from eating fatty fish, also tend to have increased HDL cholesterol and decreased triglycerides (fats in the blood). Several studies have shown that fish oil supplements reduce triglyceride levels. Finally, walnuts (which are rich in alpha linolenic acid or ANA, which converts to omega-3s in the body) have been reported to lower total cholesterol and triglycerides in people with high cholesterol levels.

High blood pressure

Several clinical studies suggest that diets rich in omega-3 fatty acids lower blood pressure in people with hypertension. An analysis of 17 clinical studies using fish oil supplements found that taking 3 or more grams of fish oil daily may reduce blood pressure in people with untreated hypertension. Doses this high, however, should only be taken under the direction of a physician.

More here:
Omega-3 fatty acids | University of Maryland Medical Center

Recommendation and review posted by Bethany Smith

An Interesting Finding

Susceptible strains of rodents fed high-fat diets overeat, gain fat and become profoundly insulin resistant. Dr. Jianping Ye's group recently published a paper showing that the harmful metabolic effects of a high-fat diet (lard and soybean oil) on mice can be prevented, and even reversed, using a short-chain saturated fatty acid called butyric acid (hereafter, butyrate). Here's a graph of the percent body fat over time of the two groups:

The butyrate-fed mice remained lean and avoided metabolic problems. Butyrate increased their energy expenditure by increasing body heat production and modestly increasing physical activity. It also massively increased the function of their mitochondria, the tiny power plants of the cell.

Butyrate lowered their blood cholesterol by approximately 25 percent, and their triglycerides by nearly 50 percent. It lowered their fasting insulin by nearly 50 percent, and increased their insulin sensitivity by nearly 300 percent*. The investigators concluded:

I found this study thought-provoking, so I looked into butyrate further.

Butyrate Suppresses Inflammation in the Gut and Other Tissues

In most animals, the highest concentration of butyrate is found in the gut. That's because it's produced by intestinal bacteria from carbohydrate that the host cannot digest, such as cellulose and pectin. Indigestible carbohydrate is the main form of dietary fiber.

It turns out, butyrate has been around in the mammalian gut for so long that the lining of our large intestine has evolved to use it as its primary source of energy. It does more than just feed the bowel, however. It also has potent anti-inflammatory and anti-cancer effects. So much so, that investigators are using oral butyrate supplements and butyrate enemas to treat inflammatory bowel diseases such as Crohn's and ulcerative colitis. Some investigators are also suggesting that inflammatory bowel disorders may be caused or exacerbated by a deficiency of butyrate in the first place.

Butyrate, and other short-chain fatty acids produced by gut bacteria**, has a remarkable effect on intestinal permeability. In tissue culture and live rats, short-chain fatty acids cause a large and rapid decrease in intestinal permeability. Butyrate, or dietary fiber, prevents the loss of intestinal permeability in rat models of ulcerative colitis. This shows that short-chain fatty acids, including butyrate, play an important role in the maintenance of gut barrier integrity. Impaired gut barrier integrity is associated with many diseases, including fatty liver, heart failure and autoimmune diseases (thanks to Pedro Bastos for this information-- I'll be covering the topic in more detail later).

Butyrate's role doesn't end in the gut. It's absorbed into the circulation, and may exert effects on the rest of the body as well. In human blood immune cells, butyrate is potently anti-inflammatory***.

View original post here:
Butyric Acid: An Ancient Controller of Metabolism ...

Recommendation and review posted by Bethany Smith

Rheumatoid arthritis (RA) causes premature mortality, disability and compromised quality of life in the industrialized and developing world (1). Rheumatoid arthritis is a systemic inflammatory disease which manifests itself in multiple joints of the body. The inflammatory process primarily affects the lining of the joints (synovial membrane), but can also affect other organs. The inflamed synovium leads to erosions of the cartilage and bone and sometimes joint deformity. Pain, swelling, and redness are common joint manifestations. Although the causes are unknown, RA is believed to be the result of a faulty immune response. RA can begin at any age and is associated with fatigue and prolonged stiffness after rest. There is no cure for RA, but new effective drugs are increasingly available to treat the disease and prevent deformed joints. In addition to medications and surgery, good self-management, including exercise, are known to reduce pain and disability.

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The etiology, or cause, of RA is unknown. Many cases are believed to result from an interaction between genetic factors and environmental exposures.

Socio-demographics: The incidence of RA is typically two to three times higher in women than men. The onset of RA, in both women and men, is highest among those in their sixties(2)

Genetics: There is longstanding evidence that specific HLA class II genotypes are associated with increased risk. Most attention has been given to the DR4 and DRB1 molecules of the major histocompatability complex HLA class II genes. The strongest associations have been found between RA and the DRB1*0401 and DRB1*0404 alleles (12). More recent investigations indicate that of the more than 30 genes studied, the strongest candidate gene is PTPN22, a gene that has been linked to several autoimmune conditions(12).

Modifiable: Several modifiable risk factors have been studied in association with RA including reproductive hormonal exposures, tobacco use, dietary factors, and microbial exposures.

Smoking Among these risk factors, the strongest and most consistent evidence is for an association between smoking and RA. A history of smoking is associated with a modest to moderate (1.3 to 2.4 times) increased risk of RA onset (2). This relationship between smoking and RA is strongest among people who are ACPA-positive (anti-citrullinated protein/peptide antibodies), a marker of auto-immune activity (12).

Reproductive and breastfeeding history Hormones related to reproduction have been studied extensively as potential risk factors for RA:

Read more:
CDC - Arthritis - Basics - Definition - Rheumatoid Arthritis

Recommendation and review posted by simmons

What is multiple sclerosis (MS)?

MS is a disease where patches of inflammation occur in parts of the brain and/or spinal cord. This can cause damage to parts of the brain and lead to various symptoms (described below).

Many thousands of nerve fibres transmit tiny electrical impulses (messages) between different parts of the brain and spinal cord. Each nerve fibre in the brain and spinal cord is surrounded by a protective sheath made from a substance called myelin. The myelin sheath acts like the insulation around an electrical wire, and is needed for the electrical impulses to travel correctly along the nerve fibre.

Nerves are made up from many nerve fibres. Nerves come out of the brain and spinal cord and take messages to and from muscles, the skin, body organs and tissues.

MS is thought to be an autoimmune disease. This means that cells of the immune system, which normally attack germs (bacteria, viruses, etc), attack part of the body. When the disease is active, parts of the immune system, mainly cells called T cells, attack the myelin sheath which surrounds the nerve fibres in the brain and spinal cord. This leads to small patches of inflammation.

Something may trigger the immune system to act in this way. One theory is that a virus, or another factor in the environment, triggers the immune system in some people with a certain genetic makeup.

The inflammation around the myelin sheath stops the affected nerve fibres from working properly, and symptoms develop. When the inflammation clears, the myelin sheath may heal and repair, and nerve fibres start to work again. However, the inflammation, or repeated bouts of inflammation, can leave a small scar (sclerosis) which can permanently damage nerve fibres. In a typical person with MS, many (multiple) small areas of scarring develop in the brain and spinal cord. These scars may also be called plaques.

Once the disease is triggered, it tends to follow one of the following four patterns.

Nearly 9 in 10 people with MS have the common relapsing-remitting form of the disease. A relapse is when an attack (episode) of symptoms occurs. During a relapse, symptoms develop (described below) and may last for days, but usually last for 2-6 weeks. They sometimes last for several months. Symptoms then ease or go away (remit). You are said to be in remission when symptoms have eased or gone away. Further relapses then occur from time to time.

The type and number of symptoms that occur during a relapse vary from person to person, depending on where myelin damage occurs. The frequency of relapses also varies. One or two relapses every two years is fairly typical. However, relapses can occur more or less often than this. When a relapse occurs, previous symptoms may return, or new ones may appear.

Here is the original post:
Multiple Sclerosis. Medical information about MS | Patient

Recommendation and review posted by simmons

Your Expert in Male Fertility & Sexual Health

High technology approaches to fertility, including ICSI, are really a two edged sword: they allow us to treat severe male infertility, but they may alter natural selection in that decisions regarding sperm and eggs are made in the laboratory and not by nature.

Dr. Paul Turek

Among the 15% of couples who experience infertility, about 40% of the time the infertility is due to male factors. About half of male infertility cases are due to defined reasons, including varicocele, infection, hormone imbalances, exposures such as drugs or medications, x-rays, tobacco use and hot tubs, blockage of the reproductive tract ducts, and previous surgery that has left scarring. Another cause of male infertility that has been underestimated in the past, but is now gaining in importance is genetic infertility. The reason for its increased importance is that our knowledge about genetics is growing so quickly. Men who may have had unexplained infertility in the past may now be diagnosed with genetic causes of infertility through recently available testing. In fact, this field is progressing so quickly that genetic infertility has already become one of the most commonly diagnosed reasons for male infertility.

Developed in the early 1990s, assisted reproduction in the form of IVF and ICSI (intracytoplasmic sperm injection) is a revolutionary laboratory technique in which a single sperm is placed directly inside an egg for fertilization. This technique has opened the door to fertility for men who formerly had few available treatment options, as it allows men who were previously considered severely infertile or sterile the possibility of fatherhood. However, with ICSI sperm are chosen by laboratory technicians and not by nature and because of this, it is not clear what barriers to natural selection are altered. Thus, along with this technology comes the possibility of passing on to a child certain genetic issues that may have caused the fathers infertility, or even more severe conditions. Another reason to know whether male

Infertility is genetic or not is because classic treatments such as varicocele repair or medications given to improve male infertility. In fact, Dr Turek was one of the first to publish on this issue, showing that varicocele repair was not effective in improving fertility in men with genetic infertility. Because he recognized these issues early on, Dr. Turek, while at UCSF in 1997, founded the first formal genetic counseling and testing program for infertility in the U.S. Called the Program in the Genetics of Infertility (PROGENI), Dr. Tureks program has helped over 2000 patients at risk for genetic infertility to navigate the decision-making waters that surround this condition.

Men with infertility should be seen by a urologist for a thorough medical history, physical examination, and appropriate medical testing. If genetic infertility is a possibility, then a genetic counselor can help couples understand the possible reasons, offer appropriate genetic testing, and discuss the complex emotional and medical implications of the test results. The approach taken early on by Dr. Turek is outlined in Figure 1. Just like the medical diagnosis from a urologist or fertility specialist, information about family history plays a critical role in genetic risk assessment. This approach to genetic evaluation, termed non-prescriptive, has been the corner- stone of Dr. Tureks critically acclaimed clinical program that now has over a dozen publications contributing to our current knowledge in the field. It is important to note that a lack of family history of infertility or other medical problems does not eliminate or reduce the risk of genetic infertility. In fact, a family history review will often be unremarkable. However, family history can provide crucial supporting in- formation toward making a genetic diagnosis (such as a family history of recurrent miscarriages or babies born with problems). Dr. Turek has published that having a genetic counselor obtain family history information is much more accurate than simply giving patients a written questionnaire to fill out and bring to their visit. A genetic counselor can also discuss appropriate genetic testing options and review the test results in patients in a meaningful way.

When speaking to Dr. Tureks genetic counselor about genetic testing, keep in mind that he or she will not tell you what to do. Genetic counselors are trained to provide information, address questions and concerns, and support you in the decision making process. A genetic counselor does not assume which decisions are most appropriate for you.

Read the original post:
The Genetics of Male Infertility - The Turek Clinic

Recommendation and review posted by Bethany Smith

Anxiety is known as a psychological/mental health disorder, and at its core, it is. But scientists now know that your genetics and current physical health can play a very significant role in both the development of anxiety and how it manifests. For example, it's known that low levels of serotonin - a common neurotransmitter - may lead to anxiety and depression, which is why drugs that improve the flow of serotonin are prescribed for anxiety.

Hormones also appear to play a significant role in anxiety development. Those that feel as though their anxieties appeared over time despite effective coping strategies and a high overall quality of life may be suffering from hormonal anxiety, caused by any number of problems with hormone balance.

When the body causes anxiety, treatment may seem more difficult. But powerful anxiety cures can stop anxiety forever. Want to learn more about your anxiety and how to cure it forever?

Take my free 7 minute anxiety test now.

The truth is that it's almost impossible to know the exact cause of your anxiety. Your hormonal imbalance may have caused your anxiety, but your anxiety may also have caused your hormonal imbalance, and in some cases the imbalance may have no effect on anxiety whatsoever.

That's why it's best to start at the symptoms and move forward from there. If you haven't yet, click here to take my free anxiety symptoms questionnaire.

Anxiety hormone imbalance has the potential to cause anxiety, because anxiety is often caused by those whose bodies are under stress trying to operate efficiently. It's the reason that those that don't exercise and those that eat an unhealthy diet often have anxiety as well - without exercise or nutrition, your body struggles to function. In addition, hormones are the messengers to the brain. Without hormones, your body may not produce the right amount of neurotransmitters, and anxiety may be the result.

That said, some examples of hormones that may contribute to anxiety include:

Again, nearly any type of hormonal dysfunction can contribute to anxiety, because the body often responds to poorly functioning hormones with stress. But the three examples above tend to be the most common hormones that cause anxiety.

What is perhaps most interesting about anxiety, however, is that even if your anxiety is caused by a change in hormones, it rarely requires any hormonal therapy. Those in natural medicine often talk about the mind/body connection, and many of those that support research-based treatments laugh at the idea that the mind can genuinely affect the body, and vice versa.

Read more:
How Are Hormones And Anxiety Related? - Calm Clinic

Recommendation and review posted by Bethany Smith

Directory: Characters Villains DBZ villains Bio-Androids

Perfect Cell Super Perfect Cell Android 21 Artifical Human no. 21 The Ultimate Fighter Mr. Cell The Perfect Being Future Cell Super (Albanian dub) The Perfect Warrior Celula (Spanish dub) Komrczak (Polish dub) Selas (Lithuanian dub) Artificial Human Cell

Cell () is a major supervillain who comes from a future timeline in the Dragon Ball manga and the Dragon Ball Z anime, also making an appearance in Dragon Ball GT. He is the ultimate creation of Dr. Gero, designed to possess all the abilities of the greatest fighters to have ever inhabited or visited Earth; the result is a "perfect warrior", possessing numerous favorable genetic traits and special abilities. Cell is one of the few Red Ribbon Androids not directly completed by Dr. Gero; the others are Android 15, Android 14, Android 13, and possibly Android 8. Cell, Android 13, Android 14, and Android 15's completions involve Dr. Gero's Super Computer.

Cell was named after the English word for "cell" because he absorbs humans and transforms.[8]Insects served as the model for Cell's design. Besides his design, the way in which he hatches from an egg and sheds his skin as he grows was also based on insects.[8] Thus Cell very much resembles an insect in both in appearances and in the way he goes through different stages of metamorphosis.

"You fool! Don't you realize yet you're up against the perfect weapon?!" "Save the World"

Cell has as an original personality with various other characters' personalities added in; Gero's computer redesigned the weak parts of the original personality, adding in the personalities of various different characters to make him the perfect weapon.[8] Throughout the Androids Arc, Cell's personality changes drastically with each transformation. At first, Cell's desire to complete his evolution by absorbing both Android 17 and Android 18 is what fuels him in his imperfect form. Upon reaching his final form, his eagerness to test the limits of his newfound power is what defines his character. Cell is unique among most villains of the series in that he is quite sophisticated. Because of his genetic composition from other warriors, he is able to psychologically manipulate those warriors and exploit their weaknesses to his advantage. He also found the Dragon Balls' reviving ability to be a nuisance, as evidenced by his relief when he learned that the Dragon Balls were rendered inert due to Piccolo and Kami's fusion.

Some initial sketches of Cell (Daizenshuu 4)

Initially, Cell is completely single-minded in pursuit of his goals and is very cautious, sneaky, cunning and calculating in achieving his main goal of perfection. Upon reaching his first transformation, he becomes far more brash and impulsive in his actions, relying less on strategy and more on brute force, often becoming clouded and not thinking rationally when things do not go his way. Upon reaching perfection, Cell displays a number of traits shared by those whose cells he possesses; Piccolo's cunning, Vegeta's pride, Goku's laid-back disposition, Frieza's smugness, and the Saiyan lust for battle. He is also shown to be calm and genuinely polite in this Perfect form. Perhaps Cell's most distinguishable trait in this form is his uninhibited vanity, which he shamelessly puts on display by launching the Cell Games, a tournament organized for the sole purpose of showing off his newfound power. It can also be seen during Cell's confrontation with Gohan when he affirms his true purpose: the annihilation of anything he considers imperfect, a category in which he places everyone and everything but himself.

In the English manga, Cell is referred to as "it", while in the anime (and the Japanese versions of both), he is referred to as "he." He is likely described that way in the English manga to emphasize the fact that he is an artificial being.

First colored image of Cell, made for the anime staff ("Ginger Town Showdown")

Continue reading here:
Cell - Dragon Ball Wiki

Recommendation and review posted by Bethany Smith