Pet Stem Cell Therapy

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Regenerative Therapies Market 2018 By Emerging Trends, Industry Share, Regional Overview and SWOT Analysis till 2026 - Digital Journal

Regenerative Therapies Market

The use of certain kinds of cells or cell products for sick organs or tissues is known as regenerative therapy. This procedure might eventually aid in the restoration of function of tissues and organs. It also includes the prospect of developing tissues and organs in the lab and then implanting them securely when the body is unable to mend itself. The lack of treatment requirements is the primary growth factor for the global regenerative therapies market. The formulation and acceptance of supporting legislation and policy measures are likely to boost government assistance for the treatment of numerous diseases across the world. It also comprises significant expenditures in regenerative medicines, such as commercialization centers, the establishment of research networks, centers of excellence and manufacturing infrastructure.

In addition to that, rising demand for stem cell and tissue-cell research methods, as well as the items developed using them is likely to propel the global regenerative therapies market forward in the years to come. These products are utilized to treat a wide variety of chronic diseases that do not have permanent cure. Nevertheless, a trend in the market has been seen in which corporations are shifting away from making synthetic pharmaceuticals and toward exploring potential for producing medications from an individuals own stem cells and tissues. The global regenerative therapies market, which is still in its early stages of commercialization, offers attractive investment possibilities provided by the private firms, regional governing bodies, and government bodies.

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Global Regenerative Therapies Market: Overview

The demand for regenerative therapies is growing markedly as regenerative medicines are considered promising to treat complex degenerative diseases. Growing government support to provide better and effective treatment for chronic disorders has also created growth opportunities for this market. Moreover, growing investment by private and government organizations that support research and development of stem cell and regenerative medicine, thus, fueling the markets growth. In addition, rising investment in research networks, manufacturing infrastructure, building commercialization centers, and centers for excellence are means indirectly supporting the growth of the regenerative therapies market at the global level.

The global regenerative therapies market is categorized on the basis of type of tissue, application, and end user. Based on end-user, the global market could be segmented into ambulatory surgical centers, educational institutes, and hospitals.

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The report elaborates on the key factors that are responsible for the growth of the regenerative therapies market. These factors include drivers, restraints, trends, and opportunities. Moreover, it provides an in-depth analysis of geography and on the key segments that are derived through factual knowledge.

Global Regenerative Therapies Market: Trends and Opportunities

The demand for regenerative therapies is expected to increase in the near future due to long-term effectiveness and safer results provided by it. Globally, people nowadays want fast treatment has also triggered the demand for regenerative therapies. The recent trend prevalent is by producing medicines with the help of tissues and stem cells derived from human body, this is expected to provide a fillip to the market. Moreover, growing investment from governments and private firms is likely to open new avenues for growth for manufacturers. Adding to it, manufacturers are shifting from synthetic drugs manufacturing to regenerative therapy drugs. Furthermore, the regenerative therapies are also used in treating ocular, neurological, autoimmune, orthopedic, rare and cardiovascular disorders.

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Global Regenerative Therapies Market: Geographic Analysis

The global regenerative therapies market is expected to find North America taking the drivers seat in terms of growth in the forthcoming years. Favorable government policies for regenerative therapies in Canada and in the United States is supporting the growth in this market. In addition to that, development of new clinical infrastructure and high penetration of tissue banks could likely increase the demand in the regenerative therapies market in the near future.

Asia Pacific is offering lucrative growth opportunities and is expected to rise at a healthy CAGR over the forecast tenure. Growing investment in healthcare research in the emerging economies is observed as a crucial driver for this market. On the other hand, the Middle East and Africa are expected to witness sluggish growth due to lack of suitable regulations in the region.

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Global Regenerative Therapies Market: Competitive Landscape

The vendor landscape presented in the report gives a complete information about the various players operating in the regenerative therapies market at the global level. To mention some of the prominent players in the market are Astellas Pharma U.S., Organovo Holdings Inc., Inc., Nuo Therapeutics, Inc., Acelity L.P. Inc., and Mesoblast Ltd. to meet the demand for unmet clinical needs these players are focusing on developing innovative novel therapies. They are also investing heavily in mergers and acquisitions to expand their geographical reach. This will further aid the companies to get a stronghold in the global market.

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Dad with ‘tennis ball’ sized lump finds out he has two cancers – Liverpool Echo

A dad who found a "tennis ball sized lump" on his neck found out he had two life-threatening cancers at the same time.

In 2019, Jason Wilcox, 46, went for tests at Southport Hospital following a large lump that appeared on his neck. He was soon given the diagnosis of Non-Hodgkin Lymphoma, a rare cancer that develops in the lymphatic system.

But as he was being treated for that, three years later in May 2022, a routine PET scan discovered he had a rare neuroendocrine tumour, the Manchester Evening News reports. Following treatment at the Christie, the Assistant Manager at Howdens Joinery is now in remission for the Non-Hodgkin Lymphoma, but is continuing treatment for the neuroendocrine tumour.

READ MORE: Ryanair air hostess fighting for life after being hit by car

Jason started chemotherapy at Southport and Ormskirk Hospital but was soon referred to The Christie Hospital in January 2021 for a highly specialist treatment called CAR-T therapy, where he remained as an inpatient for five-weeks. This treatment involves removing immune cells called T-cells through a sample of the patient's blood and reprogrammed.

In September that year, the dad battling two cancers joined a clinical trial for the drug epcoritamab. He is now hoping to have a stem cell transplant, which was delayed when Jason developed a cough after having covid in July.

The Southport dad said: "I have always felt like the staff all really care about me. Everyone is friendly and approachable, during the good times and bad. It is good to know that Im in the best place with all the resources under the same roof. The doctors and nurses are some of the best in the world and I couldnt ask for more."

Since July 2022, Jason has also been having hormone therapy injections once a month to hopefully prevent his neuroendocrine tumour from getting bigger or spreading. The plan is to have this tumour surgically removed once he has recovered from the stem cell transplant.

But the family, including wife Jen, and their two children Ella, 12, and Harry, nine, will be taking on a 10k walk to raise funds for the Manchester cancer treatment centre at Tatton Park n September 17. More information about the The Walk of Hope and how to get involved can be found here.

Wife of 13-years Jen added: "Jason has spent the last 20 months receiving the very best care and support from The Christie. His team have been a tremendous support and we have felt so well looked after.

"The overwhelming feeling you get is they care, and they want to do their best for every single patient. But unless you have seen that up close you dont realise how much The Christie does for people with cancer and how much they rely on the fundraising that The Christie charity does.

"We like to get out and about as much as possible as a family and have a dog who keeps us active, however, Jason isnt able to walk as far as he used to due to all the treatment hes had.

"After everything that has been done for us, we wanted to do something as a family to support The Christie and The Walk of Hope seemed like an ideal opportunity. Its family-friendly and sounds like itll be a wonderful evening whilst raising money for a very worthy cause. Its unlikely that Jason will be able to complete the walk, however, he will be there to cheer us on."

Abbie Wicks Sporting Events Officer from The Christie charity said: "We are very grateful to Jason, Jen, Ella and Harry for signing up to the Walk of Hope this year and for the fundraising they have already done to support our cancer patients. The Walk of Hope is one of our most emotional and inspirational events each year with so many people walking in memory, walking in support or walking in hope.

"Before the walk begins, we have lantern decorating, face painting and live entertainment. This is followed by a peaceful dove release to start the walk. After taking in the stunning scenery of Tatton Park, the evening will finish with a chorus of live music."

Scientists use stem cells to create synthetic mouse embryos

Scientists have created synthetic mouse embryos from stem cells without a dads sperm or a moms egg or womb.

The lab-created embryos mirror a natural mouse embryo up to 8 days after fertilization, containing the same structures, including one like a beating heart.

In the near term, researchers hope to use these so-called embryoids to better understand early stages of development and study mechanisms behind disease without the need for as many lab animals. The feat could also lay the foundation for creating synthetic human embryos for research in the future.

We are undoubtedly facing a new technological revolution, still very inefficient but with enormous potential, said Llus Montoliu, a research professor at the National Biotechnology Centre in Spain who is not part of the research. It is reminiscent of such spectacular scientific advances as the birth of Dolly the sheep and others.

A study published Thursday in thejournal Nature, by Magdalena Zernicka-Goetz at the California Institute of Technology and her colleagues, was the latest to describe the synthetic mouse embryos. A similar study, by Jacob Hanna at the Weizmann Institute of Science in Israel and his colleagues, waspublished earlier this monthin the journal Cell. Hanna was also a coauthor on the Nature paper.

Zernicka-Goetz, an expert in stem cell biology, said one reason to study the early stages of development is to get more insight into why the majority of human pregnancies are lost at an early stage and embryos created for in vitro fertilization fail to implant and develop in up to 70% of cases. Studying natural development is difficult for many reasons, she said, including the fact that very few human embryos are donated for research and scientists face ethical constraints.

Building embryo models is an alternative way to study these issues.

To create the synthetic embryos, or embryoids, described in the Nature paper, scientists combined embryonic stem cells and two other types of stem cells all from mice. They did this in the lab, using a particular type of dish that allowed the three types of cells to come together. While the embryoids they created werent all perfect, Zernicka-Goetz said, the best ones were indistinguishable from natural mouse embryos. Besides the heart-like structure, they also develop head-like structures.

This is really the first model that allows you to study brain development in the context of the whole developing mouse embryo, she said.

The roots of this work go back decades, and both Zernicka-Goetz and Hanna said their groups were working on this line of research for many years. Zernicka-Goetz said her group submitted its study to Nature in November.

Scientists said next steps include trying to coax the synthetic mouse embryos to develop past 8 days with the eventual goal of getting them to term, which is 20 days for a mouse.

At this point, they struggle to go past the 8 1/2-day mark, said Gianluca Amadei, a coauthor on the Nature paper based at the University of Cambridge. We think that we will be able to get them over the hump, so to speak, so they can continue developing.

The scientists expect that after about 11 days of development the embryo will fail without a placenta, but they hope researchers can someday also find a way to create a synthetic placenta. At this point, they dont know if they will be able to get the synthetic embryos all the way to term without a mouse womb.

Researchers said they dont see creating human versions of these synthetic embryos soon but do see it happening in time. Hanna called it the next obvious thing.

Other scientists have already used human stem cells tocreate a blastoid, a structure mimicking a pre-embryo, that can serve as a research alternative to a real one.

Such work is subject to ethical concerns. For decades, a 14-day rule on growing embryos in the lab growing human embryos in the lab has guided researchers. Last year, the International Society for Stem Cell Research recommended relaxing the rule under limited circumstances.

Scientists stress that growing a baby from a synthetic human embryo is neither possible nor under consideration.

Perspective on this report is important since, without it, the headline that a mammalian embryo has been built in vitro can lead to the thought that the same can be done with humans soon, said developmental biologist Alfonso Martinez Arias of the Universitat Pompeu Fabra in Spain, whose group has developed alternative stem cell based models of animal development.

In the future, similar experiments will be done with human cells and that, at some point, will yield similar results, he said. This should encourage considerations of the ethics and societal impact of these experiments before they happen.

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Scientists use stem cells to create synthetic mouse embryos

Scientists Create Synthetic Mouse Embryos Using Stem Cells

Scientists have created synthetic mouse embryos from stem cells without a dads sperm or a moms egg or womb.

The lab-created embryos mirror a natural mouse embryo up to 8 days after fertilization, containing the same structures, including one like a beating heart.

A study published Thursday in the journal Nature, by Magdalena Zernicka-Goetz at the California Institute of Technology and her colleagues, was the latest to describe the synthetic mouse embryos. A similar study, by Jacob Hanna at the Weizmann Institute of Science in Israel and his colleagues, was published earlier this month in the journal Cell. Hanna was also a coauthor on the Nature paper.

Building embryo models is an alternative way to study these issues.

This is really the first model that allows you to study brain development in the context of the whole developing mouse embryo, she said.

Scientists said next steps include trying to coax the synthetic mouse embryos to develop past 8 days with the eventual goal of getting them to term, which is 20 days for a mouse.

Researchers said they dont see creating human versions of these synthetic embryos soon but do see it happening in time. Hanna called it the next obvious thing.

Other scientists have already used human stem cells to create a blastoid, a structure mimicking a pre-embryo, that can serve as a research alternative to a real one.

Such work is subject to ethical concerns. For decades, a 14-day rule on growing human embryos in the lab has guided researchers. Last year, the International Society for Stem Cell Research recommended relaxing the rule under limited circumstances.

Scientists stress that growing a baby from a synthetic human embryo is neither possible nor under consideration.

The Associated Press Health and Science Department receives support from the Howard Hughes Medical Institutes Department of Science Education. The AP is solely responsible for all content.

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Scientists Create Synthetic Mouse Embryos Using Stem Cells

Red Blood Cells of Dogs – Dog Owners – MSD Veterinary Manual

The main function of red blood cells (also called erythrocytes) is to carry oxygen to the tissues, where it is required for cellular metabolism. Oxygen molecules attach themselves to carrier molecules, called hemoglobin, which are the iron-containing proteins in red blood cells that give the cells their red color. Oxygen is carried from the lungs and delivered to all body tissues by the hemoglobin within red blood cells. Oxygen is used by cells to produce energy that the body needs. Carbon dioxide is left behind as a waste product during this process. The red blood cells then carry that carbon dioxide away from the tissues and back to the lungs, where it is exhaled. When the number of red blood cells is too low, this is called anemia. Having too few red blood cells means the blood carries less oxygen, resulting in fatigue and weakness. When the number of red blood cells is too high, which is called polycythemia, blood can become too thick, impairing the ability of the heart to deliver oxygen throughout the body. An animals metabolism is geared to protect both the red blood cells and the hemoglobin from damage. Interference with the formation or release of hemoglobin, the production or survival of red blood cells, or their metabolism causes disease.

The total number of red cells, and thus the oxygen-carrying capacity, remains constant over time in healthy animals. Mature red blood cells have a limited life span; their production and destruction must be carefully balanced, or disease develops.

Production of red blood cells begins with stem cells in the bone marrow and ends with the release of mature red blood cells into the bodys circulation. Within the bone marrow, all blood cells begin from a single cell type called a stem cell. The stem cell divides to form immature forms of red blood cells, white blood cells, or a platelet-producing cell. Those immature cells then divide again, mature even more, and ultimately become red blood cells, white blood cells, or platelets.

The rate of blood cell production is determined by the bodys needs. Erythropoietin, a hormone produced by the kidneys, stimulates development of red blood cells in the bone marrow. Erythropoietin increases if the body lacks oxygen (a condition called hypoxia). In most species, the kidney is both the sensor organ that determines how much oxygen the bodys tissues are receiving and the major site of erythropoietin production; so chronic kidney failure leads to anemia. Erythropoietin plays a major role in determining whether to increase the number of stem cells entering red blood cell production, to shorten maturation time of the red blood cells, or to cause early release of red blood cells. Other factors that affect red blood cell production are the supply of nutrients (such as iron and vitamins) and cell-cell interactions between compounds that aid in their production. Some disorders are the direct result of abnormal red blood cell metabolism. For example, an inherited enzyme deficiency reduces the life span of red blood cells and a condition known as hemolytic anemia Anemia in Dogs Anemia occurs when there is a decrease in the number of red blood cells, which can be measured by red blood cell count or hemoglobin concentration. It can develop from loss, destruction, or... read more .

It is important to remember that a decrease in the total number of red blood cells in the body (anemia) is a sign of disease, not a specific diagnosis. Anemia may be caused by blood loss, destruction of red blood cells (hemolysis), or decreased production. In severe blood loss anemia, red blood cells are lost, but death usually results from the loss of total blood volume, rather than from the lack of oxygen caused by loss of red blood cells. Hemolysis may be caused by toxins, infections, abnormalities present at birth, drugs, or antibodies that attack the red blood cells. In dogs the most common cause of serious hemolysis is an antibody directed against that dogs own red blood cells (immune-mediated hemolytic anemia).

Factors that may prevent red blood cell production include bone marrow failure or malignancy, loss of erythropoietin secondary to kidney failure, certain drugs or toxins, longterm debilitating diseases, or antibodies targeted at developing red blood cells. The outlook and treatment depend on the underlying cause of the anemia.

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Red Blood Cells of Dogs - Dog Owners - MSD Veterinary Manual

Science is Getting Closer To a World Without Animal Testing – Slashdot

Academics and pharmaceutical companies hope that technology based on human cells will help them phase mice and monkeys out of their labs. From a report: The umbrella term for the new field is microphysiological systems or MPS, which includes tumoroids, organoids and organs-on-a-chip. Organoids are grown from stem cells to create 3D tissue in a dish resembling miniature human organs; heart organoids beat like the real thing, for example. Organs-on-a-chip are plastic blocks lined with stem cells and a circuit that stimulates the mechanics of an organ. "We need to move away from animals in a systematic way," says Salim Abdool Karim, South Africa's leading infectious disease expert. "That...involves regulators being given the data to show that non-animal biological systems will give us compatible, if not better, information." Nathalie Brandenburg co-founded Swiss start-up Sun Bioscience in 2016 to create standard versions of organoids, which makes it easier to trust that results are comparable, and convince scientists and regulators to use them. "When we started we had to tell people what organoids were," she says, referring to the early stage of her research journey.

In the past two years, and particularly as scientists emerged from lockdowns -- when many had time to read up on the technology -- demand from large pharmaceutical companies for Sun's products has soared, she says. Companies are becoming more interested in reducing their reliance on animals for ethical reasons, says Arron Tolley, chief executive of Aptamer Group, which creates artificial antibodies for use in diagnostics and drugs. "People are becoming more responsible now, from a corporate governance point of view, and looking to remove animal testing when necessary," he says. Using larger animals, such as monkeys, is particularly problematic, Tolley adds. "The bigger and cuter they get, the more people are aware of the impact." Rare diseases are especially fertile ground for models based on human tissues, says James Hickman, chief scientist at Hesperos, an organ-on-a-chip company based in Florida. "There are 7,000 rare diseases and only 400 are being actively researched because there are no animal models," Hickman says. "We're not just talking about replacing animals or reducing animals, these systems fill a void where animal models don't exist."

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Science is Getting Closer To a World Without Animal Testing - Slashdot

At Oxford Recovery Center, autism treatment on the fringes of science – Crain’s Detroit Business

The walls of the hyperbaric chamber room are lined with under-the-sea wallpaper, providing an aquarium-like sensory experience to the children, and televisions hang above as a distraction if needed.

As Peterson discussed the benefits of hyperbaric oxygen therapy (HBOT) removes bacteria, increases stem cell generation her elderly parents were placed in nearby chambers for their daily dives.

HBOT involves breathing pure oxygen in a pressurized chamber, pumping 350 liters of oxygen per minute inside to create double the air pressure from outside. Its been a well-established treatment for decompression sickness, more commonly known as the bends, that occurs when a scuba diver ascends too quickly. Other major uses include treatment for wounds that won't heal, anemia, radiation burns and vision or hearing loss.

On its various social media channels, Oxford advertises HBOT can be used to reverse aging, improve general wellness and even to potentially treat individuals with long-haul COVID-19 symptoms.

Andrew Kistner, marketing director for Oxford, moved his family from Toledo in June 2021 to be close to the center. His daughter, Grace, has cerebral palsy and the family was desperate for a treatment.

We had tried everything, Kistner said, whose daughter had been in therapybetween nine months and a year old."She was making some progress but it was so slow. We didnt have anything to lose. Wed rather lose a little bit of money and time than later say we should have done it.

Kistners daughter did four sets of 40-round dives in the chamber and said positive results started early on.

We noticed cognitive improvements pretty quickly, along with improvement in problem solving, Kistner said.

His daughter was later diagnosed with an autism spectrum disorder and she continues the therapy today. Oxford even hired his wife as a nurse and later Kistner as its marketing director.

The center told Crain's in early August that about three-quarters of the roughly80 pediatric patients at Oxford Recovery receive HBOT therapy. After this story was published, the center said that figure was inaccurateand it has eight pediatric patients now. Peterson first discovered HBOT after her daughter JeAnnah was diagnosed with viral encephalitis at 9 years old, leaving her unable to speak and nearly blind. Through her own research, Peterson sought out HBOT for her daughter, who eventually recovered from the brain infection.

All the doctors said it wouldnt work, Peterson said. I had to have a $72,000 down payment to get that treatment. They only treated her after a foreign doctor said they used HBOT back home. We dont treat neurological disorders like we should in the U.S.

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At Oxford Recovery Center, autism treatment on the fringes of science - Crain's Detroit Business

Patient Profile 1: A 63-Year-Old Female with Relapsed Multiple Myeloma – OncLive

Brea Lipe, MD: Hello and welcome to this OncLive My Treatment Approach program titled, "Recent Advances in the Treatment of Multiple Myeloma at First Relapse." I am Brea Lipe, and I'm the associate professor at the department of medicine at the University of Rochester in New York, and the director of the multiple myeloma program. I am joined today by my colleague, Dr Peter Forsberg, and I would like to welcome him to introduce himself.

Peter Forsberg, MD: Hi, Dr Lipe. I'm Peter Forsberg, I'm associate professor at the University of Colorado and the director of our myeloma program. So happy to participate in the conversation today. So welcome and thanks for joining us. And today we're going to discuss recent updates in the treatment of relapse/refractory multiple myeloma, and its impact on clinical practice. So, we'll be doing that by presenting two hypothetical patient cases, and then discussing our treatment approach to illustrate how we incorporate recent data in our clinical practice. So, let's go ahead and get started. So as Dr. Lipe said, our- the name of our presentation today is my treatment approach, recent advances in the treatment of multiple myeloma and early relapse specifically. And this is a patient profile to start with. So, this is a patient who was diagnosis, a 63-year-old female. This was in January 2017 when she presented with anemia, hypercalcemia, and after being evaluated by her primary care physician was found to have acute onset severe rib pain. And then radiographs had evidence of non-displaced rib fractures, bilaterally. Workup showed an IgG kappa multiple myeloma, and subsequent bone marrow biopsy demonstrated 35% clonal plasma cells. And cytogenetics included FISH, which showed a gain of chromosome 1q. So, she underwent a PET CT, which confirmed lytic disease throughout the spine and multiple rib lesions, and was treated initially with RVD, or lenalidomide, revlimid, bortezomib, Velcade, and dexamethasone starting in February 2017. Completed five cycles, achieved a very good partial response and then proceeded with autologous stem cell transplant with melphalan 200 milligrams meter squared conditioning, and after recovery was started on lenalidomide maintenance. So unfortunately, at follow up, on four years follow up state reevaluation was found to have progressive disease and at that time was started on isatuximab, carfilzomib, dexamethasone as second line therapy in May of 2021. So as of last follow up, the patient continues on the isatuximab, carfilzomib and dexamethasone in a very good partial response and is tolerating therapy well without issue. So, I believe, I think that brings us into discussion. In terms of my initial impressions of this case, I think it's a pretty standard consideration. A patient in 2017 diagnosed with new myeloma in their early to mid-60s. Treated with RVD induction, has long been a standard of care initial combination. And then followed by an autologous stem cell transplant and lenalidomide maintenance. And we know that based on recent data that patients with this combination of induction followed by transplant, followed by maintenance can have really stable long-lasting remissions potentially. So, patient experiencing relapse several years in- following the initiation of their induction, is pretty common. So, I think this is a pretty common scenario for us to be dealing with. And I think that the main consideration that's sort of become more prominent in the last couple of years is, do we start still with RVD or would we think about using a four-drug combination in this patient for initial induction, incorporating a CD38 monoclonal antibody like daratumumab plus RVD. So, I think that's probably the biggest practice change that might inform how we treat this patient that'd be a little different than what we might have been doing in 2017. Certainly, something that's does not uniform necessarily across myeloma providers, but is appropriate consideration, I think. And I- but otherwise I think still considering stem cell transplant and often lenalidomide based maintenance remains our kind of primary standard of care. I guess, I'd ask you if you had any additional thoughts. And then, I know the question of defining relapse, how we identify a progressive event. Defining with biochemical versus clinical relapse and sort of characteristics and standard criteria that define those. Maybe sort of delineating how you define progressive disease for [myeloma] in your practice.

Brea Lipe, MD: So, I always think it's fun to kind of look back and we see these patients in our practice, and they were started on therapy in 2017 or whenever that might have been, and to think about how our practice has changed. And I would agree that quads are something that I use a lot more frequently now, pretty much uniformly for induction in patients who are able. The only other thing that I thought was different about this case, that I might have done something different about even back in 2017 was the gain of 1q and that portending some higher risk features. And I often even back then used a more combination maintenance approach for those patients with higher risk cytogenetics. But regardless the patient did really well after transplant with just lenalidomide maintenance, which is great. And so, I think that it does come to this interesting question of what biochemical versus clinical relapse is and how those are defined. And so, the goal in my practice is to always have biochemical relapses because by the time we have clinical relapses, that's really defined by those CRAB criteria or symptomatic myeloma. So, my goal is to avoid symptoms because those can be compounding over time and can increase the toxicities of our therapy. So, my goal is always to catch it before it gets to the point where the patients are beginning to have suffering and side effects. And what we know is that biochemical relapse, so that's defined by the International Myeloma Working Group, the relapse criteria, and it's a biochemical relapse when we don't have those classic myeloma symptoms. And that's pretty much the standard IMWG relapse criteria, which includes changes of 25% to the paraprotein, as long as it's at least a rise of 0.5 and changes to the involved versus uninvolved light chains of at least 10. And so, there are pretty standard criteria for that, that you can follow over time for patients who achieve a CR, which this patient might not have. But anytime you start to see the reemergence of a paraprotein that's also a biochemical relapse. And so, I think that it's important to keep close track of our patients. I like to follow my patients in their labs, even when they're several years out closely, just so that I know that when they're starting to have these biochemical relapses, so I can intervene before they get a clinical relapse. We know that on average patients with biochemical relapses will have symptomatic development of myeloma defining events within about five months. So, I think that just highlights the need to identify those biochemical relapses. When you intervene on that is- can be up for debate but constitutes a biochemical relapse it's relevant for treatment versus those patients who will just kind of slowly progress biochemically and might be- might not progress within five months symptomatically. So, I think it's just important to keep an idea on.

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Patient Profile 1: A 63-Year-Old Female with Relapsed Multiple Myeloma - OncLive

Melanocyte – Wikipedia

August 13, 2022 admin Pet Stem Cell Therapy

Melanin-producing cells of the skin

Melanocytes are melanin-producing neural crest-derived[3] cells located in the bottom layer (the stratum basale) of the skin's epidermis, the middle layer of the eye (the uvea),[4] the inner ear,[5] vaginal epithelium,[6] meninges,[7] bones,[8] and heart.[9] Melanin is a dark pigment primarily responsible for skin color. Once synthesized, melanin is contained in special organelles called melanosomes which can be transported to nearby keratinocytes to induce pigmentation. Thus darker skin tones have more melanosomes present than lighter skin tones. Functionally, melanin serves as protection against UV radiation. Melanocytes also have a role in the immune system.

Through a process called melanogenesis, melanocytes produce melanin, which is a pigment found in the skin, eyes, hair, nasal cavity, and inner ear. This melanogenesis leads to a long-lasting pigmentation, which is in contrast to the pigmentation that originates from oxidation of already-existing melanin.

There are both basal and activated levels of melanogenesis; in general, lighter-skinned people have low basal levels of melanogenesis. Exposure to UV-B radiation causes increased melanogenesis. The purpose of melanogenesis is to protect the hypodermis, the layer under the skin, from damage by UV radiation. The color of the melanin is black, allowing it to absorb a majority of the UV light and block it from passing through the epidermis.[10]

Since the action spectrum of sunburn and melanogenesis are virtually identical, they are assumed to be induced by the same mechanism.[11] The agreement of the action spectrum with the absorption spectrum of DNA points towards the formation of cyclobutane pyrimidine dimers (CPDs) - direct DNA damage.

Typically, between 1000 and 2000 melanocytes are found per square millimeter of skin or approximately 5% to 10% of the cells in the basal layer of epidermis. Although their size can vary, melanocytes are typically 7 m in length.

The difference in skin color between lightly and darkly pigmented individuals is due not to the number (quantity) of melanocytes in their skin, but to the melanocytes' level of activity (quantity and relative amounts of eumelanin and pheomelanin). This process is under hormonal control, including the MSH and ACTH peptides that are produced from the precursor proopiomelanocortin.

Vitiligo is a skin disease where people lack melanin in certain areas in the skin.

People with oculocutaneous albinism typically have a very low level of melanin production. Albinism is often but not always related to the TYR gene coding the tyrosinase enzyme. Tyrosinase is required for melanocytes to produce melanin from the amino acid tyrosine.[12] Albinism may be caused by a number of other genes as well, like OCA2,[13] SLC45A2,[14] TYRP1,[15] and HPS1[16] to name some. In all, already 17 types of oculocutaneous albinism have been recognized.[17]Each gene is related to different protein having a role in pigment production.

People with ChdiakHigashi syndrome have a buildup of melanin granules due to abnormal function of microtubules.

In addition to their role as UV radical scavengers, melanocytes are also part of the immune system, and are considered to be immune cells.[18] Although the full role of melanocytes in immune response is not fully understood, melanocytes share many characteristics with dendritic cells: branched morphology; phagocytic capabilities; presentation of antigens to T-cells; and production and release of cytokines.[18][19][20] Although melanocytes are dendritic in form and share many characteristics with dendritic cells, they are derived from two different cell lineages. Dendritic cells are derived from hematopoietic stem cells in the bone marrow. Melanocytes on the other hand originate from neural crest cells. As such, although morphologically and functionally similar, melanocytes and dendritic cells are not the same.

Melanocytes are capable of expressing MHC Class II,[19] a type of MHC expressed only by certain antigen presenting cells of the immune system, when stimulated by interactions with antigen or cytokines. All cells in any given vertebrate express MHC, but most cells only express MHC class I. The other class of MHC, Class II, is found only on "professional" antigen presenting cells such as dendritic cells, macrophages, B cells, and melanocytes. Importantly, melanocytes stimulated by cytokines express surface proteins such as CD40 and ICAM1 in addition to MHC class II, allowing for co-stimulation of T cells.[18]

In addition to presenting antigen, one of the roles of melanocytes in the immune response is cytokine production.[21] Melanocytes express many proinflammatory cytokines including IL-1, IL-3, IL-6, IL-8, TNF-, and TGF-.[18][19] Like other immune cells, melanocytes secrete these cytokines in response to activation of Pattern Recognition Receptors (PRRs) such as Toll Like Receptor 4 (TLR4) which recognize MAMPs. MAMPs, also known as PAMPs, are microbial associated molecular patterns, small molecular elements such as proteins, carbohydrates, and lipids present on or in a given pathogen. In addition, cytokine production by melanocytes can be triggered by cytokines secreted by other nearby immune cells.[18]

Melanocytes are ideally positioned in the epidermis to be sentinels against harmful pathogens. Melanocytes reside in the stratum basale,[21] the lowest layer of the epidermis, but they use their dendrites to interact with cells in other layers,[22] and to capture pathogens that enter the epidermis.[19] Melanocytes likely work in concert with both keratinocytes and Langerhans cells,[18][19] both of which are also actively phagocytic,[21] to contribute to the immune response.

Tyrosine is the non-essential amino acid precursor of melanin. Tyrosine is converted to dihydroxyphenylalanine (DOPA) via the enzyme tyrosinase. Then DOPA is polymerized into melanin. The copper-ion based enzyme-catalyzed oxidative transformation of catechol derivative dopa to light absorbingdopaquinone to indole-5,6-qionone is clearly seen following the polymerization to melanin, the color of the pigment ranges from red to dark brown.

Numerous stimuli are able to alter melanogenesis, or the production of melanin by cultured melanocytes, although the method by which it works is not fully understood. Certain melanocortins have been shown in laboratory testing to have effect on appetite and sexual activity in mice.[23] Eicosanoids, retinoids, oestrogens, melanocyte-stimulating hormone, endothelins, psoralens, hydantoin, forskolin, cholera toxin, isobutylmethylxanthine, diacylglycerol analogues, and UV irradiation all trigger melanogenesis and, in turn, pigmentation.[24] Increased melanin production is seen in conditions where adrenocorticotropic hormone (ACTH) is elevated, such as Addison's and Cushing's disease. This is mainly a consequence of alpha-MSH being secreted along with the hormone associated with reproductive tendencies in primates. Alpha-MSH is a cleavage product of ACTH that has an equal affinity for the MC1 receptor on melanocytes as ACTH.[25]

Melanosomes are vesicles that package the chemical inside a plasma membrane. The melanosomes are organized as a cap protecting the nucleus of the keratinocyte.When ultraviolet rays penetrate the skin and damage DNA, thymidine dinucleotide (pTpT) fragments from damaged DNA will trigger melanogenesis[26] and cause the melanocyte to produce melanosomes, which are then transferred by dendrites to the top layer of keratinocytes.

The precursor of the melanocyte is the melanoblast. In adults, stem cells are contained in the bulge area of the outer root sheath of hair follicles. When a hair is lost and the hair follicle regenerates, the stem cells are activated. These stem cells develop into both keratinocyte precursors and melanoblasts - and these melanoblasts supply both hair and skin (moving into the basal layer of the epidermis). There is additionally evidence that melanocyte stem cells are present in cutaneous nerves, with nerve signals causing these cells to differentiate into melanocytes for the skin.[27]

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PVM to Play Role in Research on New Patent-pending Method to Mass-produce Antitumor Cells to Treat Blood Diseases and Cancer – Purdue University

August 13, 2022 admin Pet Stem Cell Therapy

Friday, August 12, 2022

A Purdue University chemical engineer has improved upon traditional methods to produce off-the-shelf human immune cells that show strong antitumor activity, according to a paper published in the peer-reviewed journal Cell Reports. And future research plans include clinical trials involving the Purdue University College of Veterinary Medicine.

Dr. Xiaoping Bao, a Purdue University assistant professor in the Davidson School of Chemical Engineering, said CAR-neutrophils, or chimeric antigen receptor neutrophils, and engraftable HSCs, or hematopoietic stem cells, are effective types of therapies for blood diseases and cancer. Neutrophils are the most abundant white cell blood type and effectively cross physiological barriers to infiltrate solid tumors. HSCs are specific progenitor cells that will replenish all blood lineages, including neutrophils, throughout life.

These cells are not readily available for broad clinical or research use because of the difficulty to expand ex vivo to a sufficient number required for infusion after isolation from donors, Dr. Bao said. Primary neutrophils especially are resistant to genetic modification and have a short half-life.

Dr. Bao has developed a patent-pending method to mass-produce CAR-neutrophils from human pluripotent stem cells (hPSCs), that is, cells that self-renew and are able to become any type of human cell. The chimeric antigen receptor constructs were engineered to express on the surface of the hPSCs, which were directed into functional CAR-neutrophils through a novel, chemically defined protocol.

The method was created in collaboration with Dr. Qing Deng in Purdues Department of Biological Sciences; Dr. Hal E. Broxmeyer, now deceased, at the Indiana University School of Medicine; and Dr. Xiaojun Lian at Pennsylvania State University.

We developed a robust protocol for massive production of de novo neutrophils from human pluripotent stem cells, Dr. Bao said. These hPSC-derived neutrophils displayed superior and specific antitumor activities against glioblastoma after engineering with chimeric antigen receptors.

Dr. Bao disclosed the innovation to the Purdue Research Foundation Office of Technology Commercialization, which has applied for an international patent under the Patent Cooperation Treaty system of the World Intellectual Property Organization. The innovation has been optioned to an Indiana-headquartered life sciences company.

We will also work with Dr. Timothy Bentley and his team at the Purdue College of Veterinary Medicine to run clinical trials in pet dogs with spontaneous glioma, Dr. Bao explained. Dr. Bentley is professor of neurology and neurosurgery in the College of Veterinary Medicines Department of Veterinary Clinical Sciences.

This research project was partially supported by the Davidson School of Chemical Engineering and College of Engineering Startup Funds, Purdue Center for Cancer Research, Showalter Research Trust and federal grants from the National Science Foundation and National Institute of General Medical Sciences.

Click here to view a complete news release.

Writer(s): Steve Martin | pvmnews@purdue.edu