Archive for March, 2015

Waco Spinal Cord Injuries: Overview
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A mast cell (also known as a mastocyte or a labrocyte[1]) is derived from the myeloid stem cell and a part of the immune system that contains many granules rich in histamine and heparin. Although best known for their role in allergy and anaphylaxis, mast cells play an important protective role as well, being intimately involved in wound healing and defense against pathogens.[2]

The mast cell is very similar in both appearance and function to the basophil, another type of white blood cell. They differ in that mast cells are tissue resident, e.g., in mucosal tissues, while basophils are found in the blood.[3]

Mast cells were first described by Paul Ehrlich in his 1878 doctoral thesis on the basis of their unique staining characteristics and large granules. These granules also led him to the incorrect belief that they existed to nourish the surrounding tissue, so he named them Mastzellen (from German Mast, meaning "fattening", as of animals).[4][5] They are now considered to be part of the immune system.

Mast cells are very similar to basophil granulocytes (a class of white blood cells) in blood. Both are granulated cells that contain histamine and heparin, an anticoagulant. Both cells also release histamine upon binding to immunoglobulin E.[6] These similarities have led many to speculate that mast cells are basophils that have "homed in" on tissues. Furthermore they share a common precursor in bone marrow expressing the CD34 molecule. Basophils leave the bone marrow already mature, whereas the mast cell circulates in an immature form, only maturing once in a tissue site. The site an immature mast cell settles in probably determines its precise characteristics.[2] The first in vitro differentiation and growth of a pure population of mouse mast cells has been carried out using conditioned medium derived from concanavalin A-stimulated splenocytes.[7] Later, it was discovered that T cell-derived interleukin 3 was the component present in the conditioned media that was required for mast cell differentiation and growth.[8]

Mast cells in rodents are classically divided into two subtypes: connective tissue-type mast cells and mucosal mast cells. The activities of the latter are dependent on T-cells.[9]

Mast cells are present in most tissues characteristically surrounding blood vessels and nerves, and are especially prominent near the boundaries between the outside world and the internal milieu, such as the skin, mucosa of the lungs, and digestive tract, as well as the mouth, conjunctiva, and nose.[2]

Mast cells play a key role in the inflammatory process. When activated, a mast cell rapidly releases its characteristic granules and various hormonal mediators into the interstitium. Mast cells can be stimulated to degranulate by direct injury (e.g., physical or chemical [such as opioids, alcohols, and certain antibiotics such as polymyxins]), cross-linking of immunoglobulin E (IgE) receptors, or complement proteins.[2]

Mast cells express a high-affinity receptor (FcRI) for the Fc region of IgE, the least-abundant member of the antibodies. This receptor is of such high affinity that binding of IgE molecules is in essence irreversible. As a result, mast cells are coated with IgE, which is produced by plasma cells (the antibody-producing cells of the immune system). IgE molecules, like all antibodies, are specific to one particular antigen.

In allergic reactions, mast cells remain inactive until an allergen binds to IgE already in association with the cell (see above). Other membrane activation events can either prime mast cells for subsequent degranulation or act in synergy with FcRI signal transduction.[10] In general, allergens are proteins or polysaccharides. The allergen binds to the antigen-binding sites, which are situated on the variable regions of the IgE molecules bound to the mast cell surface. It appears that binding of two or more IgE molecules (cross-linking) is required to activate the mast cell. The clustering of the intracellular domains of the cell-bound Fc receptors, which are associated with the cross-linked IgE molecules, causes a complex sequence of reactions inside the mast cell that lead to its activation. Although this reaction is most well-understood in terms of allergy, it appears to have evolved as a defense system against intestinal worm infestations (tapeworms, etc.)[citation needed].

The molecules released into the extracellular environment include:[2]

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Mast cell - Wikipedia, the free encyclopedia

(March 5, 2015) - Gender equality has not yet been achieved in science, medicine, and engineering, but The New York Stem Cell Foundation (NYSCF), through its Initiative on Women in Science and Engineering, is committed to making sure progress is made. NYSCF convened the Inaugural Meeting of its Initiative on Women in Science and Engineering (IWISE) Working Group in February 2014, where the group put forward seven actionable strategies for advancing women in science, medicine, and engineering, and reconvened in February 2015 to further develop the strategies.

NYSCF began this initiative after an analysis of its own programs. "We found that the ratio of men and women in our own programs was OK but it could certainly be improved," said Susan L. Solomon, CEO and Co-Founder, of NYSCF. "We wanted to take action and actually make tangible progress, so we brought together many of the leading men and women who have already committed time, energy, and resources towards this problem."

Today, the recommendations were published in Cell Stem Cell. They were divided into three categories: direct financial support strategies, psychological and cultural strategies, and major collaborative and international initiatives. The group chose to highlight the most high-impact and implementable strategies from a larger list developed during the meeting. They also sought to promote promising, long-term initiatives that will require significant collaboration among multiple stakeholders with the aim of connecting potential partners.

"Advancing women in science and medicine is of critical importance to the academic and research enterprise in our country," said Dr. Marc Tessier-Lavigne, President of Rockefeller University. "This paper is important as it not only brings attention to this key issue but also outlines creative strategies that can help break down barriers to gender equality in science."

Changing financing structures, embedded cultural norms, and tying funding to gender balance to enact real change are the pillars underlying the seven strategies recommended by the Working Group.

"The brain power provided by women in science is essential to sustaining a thriving US society and economy. It is time to move beyond just lamenting its loss and embrace the actions called for in this timely report," Dr. Claire Pomeroy, President, the Lasker Foundation and a member of the IWISE Working Group.

The seven strategies include:

1) Implement flexible family care spending 2) Provide "extra hands" awards 3) Recruit gender-balanced external review committees and speaker selection committees 4) Incorporate implicit bias statements 5) Focus on education as a tool 6) Create an institutional report card for gender equality 7) Partner to expand upon existing searchable databases of women in science, medicine, and engineering

The IWISE Working Group reconvened in February 2015 to continue to work on the Institutional Report Card for Gender Equality. The paper published today includes the proposed Phase 1 Institutional Report Card, and the group plans to release the Phase 2 report card once finalized.

###

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Achieving gender equality in science, engineering and medicine

Despite the progress made by women in science, engineering, and medicine, a glance at most university directories or pharmaceutical executive committees tells the more complex story. Women in science can succeed, but they are succeeding in fields that may not even be conscious of the gender imbalances. These imbalances manifest themselves in the number of women that are invited to speak at conferences, the percentage of grants awarded to women scientists, and the higher rates of attrition of women at every stage of the career ladder compared to those of men.

In the March 5 issue of the journal Cell Stem Cell, the Initiative on Women in Science and Engineering Working Group, a collection of more than 30 academic and business leaders organized by the New York Stem Cell Foundation, present seven strategies to advance women in science, engineering, and medicine in this modern landscape.

"We wanted to think about broad ways to elevate the entire field, because when we looked at diversity programs across our organizations we thought that the results were okay, but they really could be better," said Susan L. Solomon, co-founder and CEO of the New York Stem Cell Foundation and a member of the working group. "We've identified some very straightforward things to do that are inexpensive and could be implemented pretty much immediately."

The working group's seven strategies are broken into three categories: the first two are direct financial support strategies, the next three are psychological and cultural strategies, and the final two are major collaborative and international initiatives.

1. Implement flexible family care spending

Make grants gender neutral by permitting grantees to use a certain percentage of grant award funds to pay for childcare, eldercare, or family-related expenses. This provides more freedom for grantees to focus on professional development and participate in the scientific community.

2. Provide "extra hands" awards

Dedicate funds for newly independent young investigators who are also primary caregivers to hire technicians, administrative assistants, or postdoctoral fellows.

3. Recruit gender-balanced review and speaker selection committees

Adopt policies that ensure that peer review committees are conscious of gender and are made up of a sufficient number of women.

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Seven strategies to advance women in science

Published February 10, 2015

A British biotech company founded by a Nobel prize winner has raised what it says is a record 691,000 pounds ($1 million) via crowdfunding to help launch a stem cell-based regenerative medicine for use following heart trauma.

Cell Therapy, based in the Welsh capital Cardiff, says the medicine has the potential to reduce scarring of the heart muscle caused by a heart attack or failure.

Chief Executive Ajan Reginald, previously at Roche, said crowd funding was a quick way to raise money for final stage trials or commercial launches.

"It was very fast and very efficient," he told Reuters on Monday. "We have spent 5 percent of our time on fundraising, which enables me to spend 95 percent of my time on the business."

The company, whose founder Martin Evans shared the 2007 Nobel Prize for medicine for groundbreaking stem cell research, used website Crowdcube to raise nearly three times its original target from more than 300 investors.

Reginald said the backers included investment bankers, hedge fund employees and scientists.

"Crowd funding allows investors to look in detail at a company in their own time," he said, adding that some 10,000 investors had seen the pitch.

The company would publish data from clinical trials of the drug, called Heartcel, next month, before final stage trials with a view to a launch in 2016.

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British biotech firm sets crowdfunding record with heart drug

Under normal conditions, many of the different types of tissue-specific adult stem cells, including hematopoietic stem cells, exist in a state or dormancy where they rarely divide and have very low energy demands. "Our theory was that this state of dormancy protected hematopoietic stem cells from DNA damage and therefore protects them from premature aging," says Dr. Michael Milsom, leader of the study.

However, under conditions of stress, such as during chronic blood loss or infection, hematopoietic stem cells are driven into a state of rapid cell division in order to produce new blood cells and repair the damaged tissue. "It's like forcing you out of your bed in the middle of the night and then putting you into a sports car and asking you to drive as fast as you can around a race circuit while you are still half asleep," explains Milsom. "The stem cells go from a state of rest to very high activity within a short space of time, requiring them to rapidly increase their metabolic rate, synthesize new DNA and coordinate cell division. Suddenly having to simultaneously execute these complicated functions dramatically increases the likelihood that something will go wrong."

Indeed, experiments described in the study show that the increased energy demands of the stem cells during stress result in elevated production of reactive metabolites that can directly damage DNA. If this happens at the same time that the cell is trying to replicate its DNA, then this can cause either the death of the stem cell, or potentially the acquisition of mutations that may cause cancer.

Normal stem cells can repair the majority of this stress-induced DNA damage, but the more times you are exposed to stress, the more likely it is that a given stem cell will inefficiently repair the damage and then die or become mutated and act as a seed in the development of leukemia. "We believe that this model perfectly explains the gradual accumulation of DNA damage in stem cells with age and the associated reduction in the ability of a tissue to maintain and repair itself as you get older," Milsom adds.

In addition, the study goes on to examine how this stress response impacts on a mouse model of a rare inherited premature aging disorder that is caused by a defect in DNA repair. Patients with Fanconi anemia suffer a collapse of their blood system and have an extremely high risk of developing cancer. Mouse models of Fanconi anemia have exactly the same DNA repair defect as found in human patients but the mice never spontaneously develop the bone marrow failure observed in nearly all patients.

"We felt that stress induced DNA damage was the missing ingredient that was required to cause hematopoietic stem cell depletion in these mice," says Milsom. When Fanconi anemia mice were exposed to stimulation mimicking a prolonged viral infection, they were unable to efficiently repair the resulting DNA damage and their stem cells failed. In the same space of time that normal mice showed a gradual decline in hematopoietic stem cell numbers, the stem cells in Fanconi anemia mice were almost completely depleted, resulting in bone marrow failure and an inadequate production of blood cells to sustain life.

"This perfectly recapitulates what happens to Fanconi anemia patients and now gives us an opportunity to understand how this disease works and how we might better treat it," commented Milsom.

Prof. Dr. Andreas Trumpp, director of HI-STEM and head of the Division of Stem Cells and Cancer at the DKFZ believes that this work is a big step towards understanding a range of age-related diseases. "The novel link between physiologic stress, mutations in stem cells and aging is very exciting," says Trumpp, a co-author of the study. "By understanding the mechanism via which stem cells age, we can start to think about strategies to prevent or at least reduce the risk of damaged stem cells which are the cause of aging and the seed of cancer."

###

Dagmar Walter, Amelie Lier, Anja Geiselhart, Frederic B. Thalheimer, Sina Huntscha, Mirko C. Sobotta, Bettina Moehrle, David Brocks, Irem Bayindir, Paul Kaschutnig, Katja Muedder, Corinna Klein, Anna Jauch, Timm Schroeder, Hartmut Geiger, Tobias P. Dick, Tim Holland-Letz, Peter Schmezer, Steven W. Lane, Michael A. Rieger, Marieke A. G. Essers, David A. Williams, Andreas Trumpp und Michael D. Milsom: Exit from dormancy provokes DNA damage-induced attrition in haematopoietic stem cells. Nature 2015, DOI: 10.1038/nature14131

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WATERTOWN, Conn. (AP) A year ago, Nancy Demers, 71, was diagnosed with myelodysplastic syndrome, a deficiency in the bone marrow. The disease can eventually become leukemia.

Its treated as if it were cancer but there is no cure for it, said her son, Scott Demers.

Now Nancy Demers has a new chance at life, thanks to advances in bone marrow stem cell transplants.

If I didnt do this, once I went out of remission its not if, its when I would go into acute leukemia and there will be nothing there to help me, Nancy Demers said. This will save my life and give me time.

Demers is one of a rapidly growing number of people looking to depend on strangers to donate marrow since she doesnt have a match within her family.

The rising number of patients seeking bone marrow has created new demands on registries that seek to match patient needs with willing donors.

Each sibling has a 25 percent chance of being a transplant match, according to Dr. Joseph Antin, chief and program director of the adult stem cell transplantation program at Dana Farber Brigham and Womens Hospital in Boston.

In the United States, about 30 percent of patients find a donor within their family, according to Be the Match. Those who dont must turn to international registries to find an unrelated donor.

Around 15 years ago, doctors couldnt do a transplant on anyone over the age of 50, according to Dr. Leslie Lehmann, clinical director of the Stem Cell Transplant Center at Dana Farber.

Its a big stress on the body, Lehmann said.

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Registries seek to match donors with rising marrow demand

Platelet Rich Plasma - PRP and Adult Stem Cell Therapy
DPM Debra Weinstock discusses #prp and #stemcell injections that may help you avoid surgery and alleviate your foot and ankle pain! #CrossBayFCC is located i...

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Alternative Treatments For COPD - FAT STEM CELL THERAPY in Dallas, Texas
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How does genetic engineering affect us?
Snow day lesson on GE.

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Science: Genetic Engineering
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Labster - Animal Genetics Virtual Lab Simulation
Get free trial: https://www.labster.com/courses/LabsterX/AnimalGenetics/2014/about About the lab Labster Animal Genetics Lab The Animal Genetics lab guides t...

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Rheumatiod Arthritis and Genetics
Adam Mccoy reports on a mother and daughter who both have rheumatoid arthritis.

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1. Introduction

This chapter provides an overview of the main current applications of gene therapy for chronic pain in what concerns animal studies and putative clinical applications. The value of gene therapy in unravelling neuronal brain circuits involved in pain modulation is also analysed. After alerting to the huge socioeconomic impact of chronic pain in modern societies and justifying the need to develop new avenues in pain management, we review the most common animal studies using gene therapy, which consisted on deliveries of replication-defective viral vectors at the periphery with the aim to block nociceptive transmission at the spinal cord. Departing from the data of these animal studies, we present the latest results of clinical trials using gene therapy for pain management in cancer patients. The animal studies dealing with gene delivery in pain control centres of the brain are analysed in what concerns their complexity and interest in unravelling the neurobiological mechanisms of descending pain modulation. The chapter will finish by analysing possible futures of gene therapy for chronic pain management based on the development of vectors which are safer and more specific for the different types of chronic pain.

Pain is not easy to define since it is a highly subjective experience. The more consensual definition of pain was provided by the International Association for the Study of Pain (IASP) and states that Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage [1]. Acute pain is important as an alert signal to potentially threaten situations (internal or external to the organism) and it is important for survival. Acute pain may progress to chronic pain which, according to IASP, is the pain that lasts more than 3 months and persists beyond the normal tissue healing time [2].

Chronic pain may be divided into "nociceptive" and "neuropathic" [3]. Nociceptive pain is caused by activation of nociceptors, the thin nerve fibers which convey nociceptive input from the periphery to the spinal cord. Neuropathic pain is caused by malfunction or damage of the nervous system. Neuropathic pain is frequently difficult to treat being associated to spontaneous pain, exaggerated responses to nociceptive stimuli (hyperalgesia) and nociceptive responses to stimuli which are usually non-nociceptive (allodynia).

The number of people affected by chronic pain is increasing due to multifactorial causes such as increasing aging of the population. In Europe, about 20% of people suffer from moderate to severe chronic pain [4]. In the United States the prevalence of chronic pain ranges from 2% to 40%, with a median of 15% [5], which cost the country 560 to 635 million dollars [6]. People suffering from chronic pain are less able to walk, sleep normally, perform social activities, exercise or have sexual relations. Chronic pain strongly affects the productivity. About 60% of chronic pain patients are unable or less able to work, 19% lost their jobs and 13% change jobs due to their pain [6]. Chronic pain is associated to several co-morbidities, namely depression and anxiety [6]. Besides all of these indirect costs, chronic pain is a burden due to direct costs of pain management. Despite major investments in basic and clinical pain research, the available analgesics remain considerably unchanged during the last decades. Opioids are useful to manage several pain types but they have a modest efficacy in several pain conditions (e.g. neuropathic pain). Furthermore, long term treatments with opioids frequently induce severe off-target effects, like nausea, constipation and addiction [7]. Intractable pain remains a clinical problem and a drama for the patients and their families [8]. During the last decade, pain clinicians and pain researchers were challenged to search for alternatives to conventional pain treatment, which should be more specific and sustained than conventional analgesics. Gene therapy outstands as a powerful technique to overcome some current problems of chronic pain treatments.

Neurobiological research in the pain field provided solid information regarding the transmission and modulation of nociceptive information from the periphery to the brain, where a pain sensation is produced (Fig. 1). Nociceptive signals are conveyed by primary afferent fibers from peripheral organs, like the bladder or muscles, to the spinal cord. This is the first relay station involved in the modulation of nociceptive information namely by local inhibitory interneurons that use opioid peptides or aminoacids (-amminobutiric acid-GABA- and glycine). Nociceptive information is then transmitted supraspinally, namely to the thalamus, and to several brainstem areas, where additional modulation of the nociceptive signal occurs. The thalamo-cortical pathway ensures that the nociceptive information reaches the somatosensory and prefrontal cortices, where the nociceptive signal is finally perceived as a pain sensation [9, 10]. Some brain areas which directly or indirectly receive nociceptive information from the spinal cord are also involved in descending pain modulation. Both inhibition and facilitation may occur and chronic pain may derive from a reduction of the former and enhancement of the latter [9, 11]. This neurobiological knowledge has been used to design gene therapy studies for chronic pain, namely to choose the somatosensory system areas and neurotransmitters/receptors to be targeted in order to block nociceptive transmission.

Schematic diagram of pain pathways involved in pain transmission and modulation. Nociceptive information is transmitted from the periphery to the spinal dorsal horn by primary sensory neurons. At the spinal level, these neurons transmit nociceptive information to second order neurons (Ascending pathways) through the release of neurotransmitters like the excitatory amino acids (EAA) glutamate and aspartate, calcitonin gene-related peptide (CGRP), substance P (SP) galanin (Gal) and neuropeptide Y (NPY). In the brain, the nociceptive information is then perceived as a pain sensation. The transmission of nociceptive information at the spinal level is modulated by interneurons (mainly inhibitory) through the release of opioid pepides and GABA and also by supraspinal descending neurons (Descending pathways) through the release of serotonin (5-HT) and noradrenaline (NA). Descending pathways may inhibit or enhance nociceptive transmission from the spinal cord.

Gene therapy is an especially versatile tool for chronic pain management since it is based in a triad of controllable parameters: the vector, the transgene and the promoter. By knowing the neurobiological features of each chronic pain type, namely the neurotransmitters and receptors affected, it is possible to design gene therapy strategies based on the best combination of vectors, transgenes and promoters. As to vectors, gene therapy for pain uses mainly vehicles which have a certified experience in infecting neurons, namely replication-defective forms of viruses. Non-viral vectors have seldom been used in gene therapy studies for pain but their transduction efficiency and specificity are much lower than those of viral vectors. Some of these vectors have the ability to migrate retrogradely (i.e., contrary to the direction of nerve impulse) which is very useful to target neurons that are located in structures of difficult surgical access. A good example is the application of replication-defective forms of Herpes Simplex Virus type 1 (HSV-1) at the periphery (e.g. the skin) to transduce neurons at the spinal ganglia (dorsal root ganglia-DRGs), which are difficult to access due to their bone protection. Regarding the transgenes to include in the vectors for gene therapy of pain, it is possible to increase the expression of neurotransmitters and receptors involved in nociceptive inhibition (e.g. opioids), neurotrophic factors or substances with anti-inflammatory properties. Finally, and in what concerns the promoters, it is possible to choose those that restrict transgene expression to a cell type, such as a neuron or a glial cell, or even target selective neurochemical neuronal populations. Examples of neuron-specific promoters are synapsin I, calcium/calmodulin-dependent protein kinase II, tubulin alpha I and neuron-specific enolase [12]. Some possibilities of controlling the vectors, transgenes and promoters will be discussed in the next two sections using gene therapy in animal models.

One of the main advantages of experimental gene therapy studies is that they can be performed using several pain models. This is important since each pain type may induce specific changes in neuronal circuits devoted to the transmission and modulation of nociceptive transmission [13]. Studies of gene therapy for pain have used clinically relevant models of inflammatory [14-22] and neuropathic pain [23-34]. In a much lower incidence, models of acute [35-38], post-operative pain [39] and cancer [40] pain have been used in experimental gene therapy studies. The large majority of studies were performed in pain models affecting the limbs or the trunk, in the latter case being of visceral origin [22, 37]. Two studies used gene therapy to block nociceptive transmission coming from the head/face in pain models that reproduces some types of craniofacial pain, like trigeminal neuralgia [41] or temporomandibular joint disorders [42].

Gene therapy studies for pain in animal models may be divided in studies targeting the spinal cord (Table 1) and studies directed to pain control centres located in the brain (Table 2). Studies directed to the spinal cord mainly aim to manipulate the expression of transgenes in order to block the transmission of nociceptive input at the spinal dorsal horn (Table 1). Most of the spinal cord studies using gene therapy for pain elected HSV-1 as the most suitable vector, due to its natural affinity to the neuron and its ability for retrograde transport [43]. HSV-1 has the additional advantage over other vectors of carrying multiple transgenes or large transgenes and not integrating in the host genome, which reduces the possibility of mutagenic events [44, 45]. After application of replication-defective forms of HSV-1 at the periphery in order to transduce DRG neurons (or trigeminal ganglion neurons), delivery of the transgene product by the spinal branch of transduced neurons at the spinal dorsal horn induced analgesia in several rodent models of pain (Table 1). Gene therapy in animal models of craniofacial pain [41, 42] aimed to release the transgene products at the level of the spinal trigeminal nucleus and this structure is homolog of the spinal cord, which prompted to include these studies in the section devoted to spinal cord studies.

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Gene Therapy for Chronic Pain Management | InTechOpen

Obamas State of the Union Address Personalized Medicine
DNA testing Personalized medicine MedXPrime Safe drugs.

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College Station Spinal Cord Injury

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Houston Spinal Cord Injury

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Tucson Spinal Cord Injury

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BioLogic Stem Cell Therapy Cream
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World Over - 2015-02-26 - Vatican latest, ISIS, stem cell therapy, Ray Flynn with Raymond Arroyo
RAY FLYNN, former Mayor of Boston and former US Ambassador to the Vatican on the latest papal news from Rome and his efforts to work with the medical communi...

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World Over - 2015-02-26 - Vatican latest, ISIS, stem cell therapy, Ray Flynn with Raymond Arroyo - Video

Stem Cell-Enhanced Anterior Collateral Ligament (ACL) Reconstruction
Dr. McKenna discusses how using a patient #39;s own bone marrow stem cells augmented with AlphaGEMS amniotic tissue product can reduce recovery time from ACL sur...

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Regenerative Medicine | Graziella Pellegrini
http://www.weforum.org/ Graziella Pellegrini, from the University of Modena and Reggio Emilia, Italy, showcases personalised, regenerative medicine that uses stem cell therapy to help restore sight.

By: World Economic Forum

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Abstract

Stem cells represent natural units of embryonic development and tissue regeneration. Embryonic stem (ES) cells, in particular, possess a nearly unlimited self-renewal capacity and developmental potential to differentiate into virtually any cell type of an organism. Mouse ES cells, which are established as permanent cell lines from early embryos, can be regarded as a versatile biological system that has led to major advances in cell and developmental biology. Human ES cell lines, which have recently been derived, may additionally serve as an unlimited source of cells for regenerative medicine. Before therapeutic applications can be realized, important problems must be resolved. Ethical issues surround the derivation of human ES cells from in vitro fertilized blastocysts. Current techniques for directed differentiation into somatic cell populations remain inefficient and yield heterogeneous cell populations. Transplanted ES cell progeny may not function normally in organs, might retain tumorigenic potential, and could be rejected immunologically. The number of human ES cell lines available for research may also be insufficient to adequately determine their therapeutic potential. Recent molecular and cellular advances with mouse ES cells, however, portend the successful use of these cells in therapeutics. This review therefore focuses both on mouse and human ES cells with respect to in vitro propagation and differentiation as well as their use in basic cell and developmental biology and toxicology and presents prospects for human ES cells in tissue regeneration and transplantation.

Several seminal discoveries during the past 25 years can be regarded not only as major breakthroughs for cell and developmental biology, but also as pivotal events that have substantially influenced our view of life: 1) the establishment of embryonic stem (ES) cell lines derived from mouse (108, 221) and human (362) embryos, 2) the creation of genetic mouse models of disease through homologous recombination in ES cells (360), 3) the reprogramming of somatic cells after nuclear transfer into enucleated eggs (392), and 4) the demonstration of germ-line development of ES cells in vitro (136, 164, 365). Because of these breakthroughs, cell therapies based on an unlimited, renewable source of cells have become an attractive concept of regenerative medicine.

Many of these advances are based on developmental studies of mouse embryogenesis. The first entity of life, the fertilized egg, has the ability to generate an entire organism. This capacity, defined as totipotency, is retained by early progeny of the zygote up to the eight-cell stage of the morula. Subsequently, cell differentiation results in the formation of a blastocyst composed of outer trophoblast cells and undifferentiated inner cells, commonly referred to as the inner cell mass (ICM). Cells of the ICM are no longer totipotent but retain the ability to develop into all cell types of the embryo proper (pluripotency; Fig. 1). The embryonic origin of mouse and human ES cells is the major reason that research in this field is a topic of great scientific interest and vigorous public debate, influenced by both ethical and legal positions.

Stem cell hierarchy. Zygote and early cell division stages (blastomeres) to the morula stage are defined as totipotent, because they can generate a complex organism. At the blastocyst stage, only the cells of the inner cell mass (ICM) retain the capacity to build up all three primary germ layers, the endoderm, mesoderm, and ectoderm as well as the primordial germ cells (PGC), the founder cells of male and female gametes. In adult tissues, multipotent stem and progenitor cells exist in tissues and organs to replace lost or injured cells. At present, it is not known to what extent adult stem cells may also develop (transdifferentiate) into cells of other lineages or what factors could enhance their differentiation capability (dashed lines). Embryonic stem (ES) cells, derived from the ICM, have the developmental capacity to differentiate in vitro into cells of all somatic cell lineages as well as into male and female germ cells.

ES cell research dates back to the early 1970s, when embryonic carcinoma (EC) cells, the stem cells of germ line tumors called teratocarcinomas (344), were established as cell lines (135, 173, 180; see Fig. 2). After transplantation to extrauterine sites of appropriate mouse strains, these funny little tumors produced benign teratomas or malignant teratocarcinomas (107, 345). Clonally isolated EC cells retained the capacity for differentiation and could produce derivatives of all three primary germ layers: ectoderm, mesoderm, and endoderm. More importantly, EC cells demonstrated an ability to participate in embryonic development, when introduced into the ICM of early embryos to generate chimeric mice (232). EC cells, however, showed chromosomal aberrations (261), lost their ability to differentiate (29), or differentiated in vitro only under specialized conditions (248) and with chemical inducers (224). Maintenance of the undifferentiated state relied on cultivation with feeder cells (222), and after transfer into early blastocysts, EC cells only sporadically colonized the germ line (232). These data suggested that the EC cells did not retain the pluripotent capacities of early embryonic cells and had undergone cellular changes during the transient tumorigenic state in vivo (for review, see Ref. 7).

Developmental origin of pluripotent embryonic stem cell lines of the mouse. The scheme demonstrates the derivation of embryonic stem cells (ESC), embryonic carcinoma cells (ECC), and embryonic germ cells (EGC) from different embryonic stages of the mouse. ECC are derived from malignant teratocarcinomas that originate from embryos (blastocysts or egg cylinder stages) transplanted to extrauterine sites. EGC are cultured from primordial germ cells (PGC) isolated from the genital ridges between embryonic day 9 to 12.5. Bar = 100 m. [From Boheler et al. (40).]

To avoid potential alterations connected with the growth of teratocarcinomas, a logical step was the direct in vitro culture of embryonic cells of the mouse. In 1981, two groups succeeded in cultivating pluripotent cell lines from mouse blastocysts. Evans and Kaufman employed a feeder layer of mouse embryonic fibroblasts (108), while Martin used EC cell-conditioned medium (221). These cell lines, termed ES cells, originate from the ICM or epiblast and could be maintained in vitro (Fig. 2) without any apparent loss of differentiation potential. The pluripotency of these cells was demonstrated in vivo by the introduction of ES cells into blastocysts. The resulting mouse chimeras demonstrated that ES cells could contribute to all cell lineages including the germ line (46). In vitro, mouse ES cells showed the capacity to reproduce the various somatic cell types (98, 108, 396) and, only recently, were found to develop into cells of the germ line (136, 164, 365). The establishment of human ES cell lines from in vitro fertilized embryos (362) (Fig. 3) and the demonstration of their developmental potential in vitro (322, 362) have evoked widespread discussions concerning future applications of human ES cells in regenerative medicine.

Human pluripotent embryonic stem (ES) and embryonic germ (EG) cells have been derived from in vitro cultured ICM cells of blastocysts (after in vitro fertilization) and from primordial germ cells (PGC) isolated from aborted fetuses, respectively.

Primordial germ (PG) cells, which form normally within the developing genital ridges, represent a third embryonic cell type with pluripotent capabilities. Isolation and cultivation of mouse PG cells on feeder cells led to the establishment of mouse embryonic germ (EG) cell lines (198, 291, 347; Fig. 2). In most respects, these cells are indistinguishable from blastocyst-derived ES cells and are characterized by high proliferative and differentiation capacities in vitro (310), and the presence of stem cell markers typical of other embryonic stem cell lines (see sect. ii). Once transferred into blastocysts, EG cells can contribute to somatic and germ cell lineages in chimeric animals (197, 223, 347); however, EG cells, unlike ES cells, retain the capacity to erase gene imprints. The in vitro culture of PG cells from 5- to 7-wk-old human fetuses led to the establishment of human EG cell lines (326) (Fig. 3). These cell lines showed multilineage development in vitro but have a limited proliferation capacity, and currently can only be propagated as embryoid body (EB) derivatives (325). Following transplantation into an animal model for neurorepair, human EG cell derivatives, however, show some regenerative capacity, suggesting that these cells could be useful therapeutically (190). Although pluripotent EG and EC cells represent important in vitro models for cell and developmental biology, this review focuses mainly on fundamental properties and potential applications of mouse and human ES cells for stem cell research.

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Embryonic Stem Cells: Prospects for Developmental Biology ...