Stem Cell Clinic

Type 1 diabetes: Reprogramming liver cells may lead to new treatments – Medical News Today

Researchers have discovered a way to reprogram mouse liver cells into precursor pancreatic cells by changing the expression of a single gene. They suggest that the finding is an important step toward showing that reprogramming liver cells might offer a way forward for the treatment of type 1 diabetes in humans.

The team - led by researchers from the Max Delbrck Center for Molecular Medicine in Berlin, Germany - reports the study in the journal Nature Communications.

Diabetes is a chronic disease that develops either when the body cannot make enough insulin, or when it cannot effectively use the insulin that it does make. Insulin is a hormone that regulates blood sugar, or glucose, and it helps to convert glucose from food into energy for cells.

Uncontrolled diabetes leads to high blood sugar, or hyperglycemia, which over time causes serious damage to many parts of the body, including the heart, blood vessels, nerves, eyes, and kidneys.

In the United States, an estimated 29.1 million people have diabetes, including 8.1 million who are undiagnosed.

The most common type of diabetes is type 2, in which the body cannot use insulin effectively. Type 1 diabetes, in which the body does not make enough insulin, accounts for around 5 percent of diabetes cases in adults.

The new study is likely to interest researchers developing treatments for type 1 diabetes. In people with type 1 diabetes, the immune system attacks the insulin-producing beta cells of the pancreas.

Researchers in regenerative medicine are exploring ways to generate new populations of pancreatic beta cells as a possible avenue for the treatment of type 1 diabetes.

Fast facts about type 1 diabetes

Learn more about type 1 diabetes

The new study concerns a method called cell reprogramming, in which it is possible to convert one type of cell into another type of cell, by tweaking genes.

An obvious source of cells for reprogramming into insulin-producing beta cells might be other types of cell in the pancreas.

In their study paper, the researchers mention other research that shows such pancreatic cells display a high degree of the necessary "cellular plasticity."

However, the researchers chose to focus on liver cells because, from a clinical perspective, they offer important advantages over pancreatic cells; for example, they are more accessible and abundant.

They also cite studies that have partially corrected hyperglycemia in diabetic mice by reprogramming liver cells into pancreatic beta cells.

The new study shows how just by changing the expression of a single gene called TGIF2, the team was able to coax mouse liver cells to take on a less specialized state and then stimulate them to develop into cells with pancreatic features.

When the researchers transplanted the modified cells into diabetic mice, the animals' blood sugar levels improved, suggesting the cells were behaving in a way similar to pancreatic beta cells.

The researchers identified TGIF2 (Three-Amino-acid-Loop-Extension homeobox TG-interacting factor 2) by running gene expression profiling tests on immature liver and pancreas cells isolated from mouse embryos as the cells differentiated toward their particular cell fates.

They found that at a particular differentiation branchpoint, the expression of TGIF2 changes in opposite directions as the cells commit to either liver or pancreatic fates.

The authors note that their study shows that "TGIF2 is a developmental regulator of pancreas versus liver fate decision," and when expressed in adult mouse liver cells, it suppresses the transcription program for liver cells and induces a subset of pancreatic genes.

There is still a lot of work to do to investigate whether the results with mice translate to humans. The team has already started working on human liver cells.

"There are differences between mice and humans, which we still have to overcome. But we are well on the path to developing a 'proof of concept' for future therapies."

Senior author Dr. Francesca M. Spagnoli, Max Delbrck Center

Learn how type 1 diabetes kills some insulin-producing cells but not others.

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Type 1 diabetes: Reprogramming liver cells may lead to new treatments - Medical News Today

Area medical clinic offers regenerative cell treatment – RiverBender.com

WOOD RIVER - There is an alternative to using prescription drugs or resorting to joint surgery for pain relief. Dr. Michael Harbison, DC, MCS-P, CCCPC, of iCAN Clinic in Wood River, Illinois, is holding an informational seminar on the use of regenerative cellular medicine for pain relief at 7 p.m. on Tuesday, February 21st, at his clinic located at 203 E. Ferguson Avenue in Wood River.

Harbison, who recently changed the name of his clinic from AlignLife of Wood River to iCAN Clinic, researched regenerative cellular medicine and, based on significant advancements in stem cell research, realized the importance of stem cell injections for treating people suffering from inflammation, reduced mobility, sports injuries, tissue and ligament damage or chronic pain.

Our mission at iCAN Clinic is to help our patients unlock the God given potential of their body. said Harbison. Stem cells are the bodys master cells and can develop into all other cells, so not only is pain relieved, it is possible new cartilage, ligaments and bone can be regenerated. Stem cell therapy gives our patients a choice other than surgery and/or a regimen of possibly addictive narcotics. Harbison went on to say Thats an easy choice to make given that this therapy has been known provide full relief to patients after only one treatment. Generally, the repair process begins immediately and the repair process can continue for up to eight additional months from the date of the initial procedure.

But it wasnt until Dr. Harbison found an ethical source of stem cells that he decided to offer the therapy. Harbison said that the Stem Cell Institute of America provides stem cells that were taken from placentas that were donated by mothers after the birth of their child. There was no destruction of life in the process of obtaining these stem cells.

Harbison is excited about offering the new stem cell therapy because hes seen its results.

Seating for the Tuesday, February 21st, seminar is limited so reservations are required. To reserve a seat for the 7:00 p.m. program, contact iCAN Clinic at 618-254-2273.

Stem Cell Therapy Seminar Tuesday February 21, 7:00 PM

iCAN Clinic

203 E Ferguson Ave.

Wood River, IL 62095

618-254-2273

http://www.iCANClinic.org

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Area medical clinic offers regenerative cell treatment - RiverBender.com

Family Plans To Seek Compensation For Lacks’ Cells – CBS Local

CBS Local

Family Plans To Seek Compensation For Lacks' Cells CBS Local BALTIMORE (WJZ) The family of Henrietta Lacks is suing Johns Hopkins Medicine for using Lacks' blood cells without her permission 66 years ago. For years, Henrietta's oldest son along with his son say they have been turned down by attorneys who ... Henrietta Lacks family members plan to sue Johns Hopkins MedicineFox Baltimore Henrietta Lacks's family wants compensation for her cellsWashington Post all 8 news articles »

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Family Plans To Seek Compensation For Lacks' Cells - CBS Local

Scientists show ‘matchmaker’ role for protein behind SMA – Medical Xpress

February 14, 2017 Credit: axelle b/public domain

A puzzling question has lurked behind SMA (spinal muscular atrophy), the leading genetic cause of death in infants.

The disorder leads to reduced levels of the SMN protein, which is thought to be involved in processing RNA, something that occurs in every cell in the body. So why does interfering with a process that happens everywhere affect motor neurons first?

Scientists at Emory University School of Medicine have been building a case for an answer. It's because motor neurons have long axons. And RNA must be transported to the end of the axons for motor neurons to survive and keep us moving, eating and breathing.

Now the Emory researchers have a detailed picture for what they think the SMN protein is doing, and how its deficiency causes problems in SMA patients' cells. The findings are published in Cell Reports.

"Our model explains the specificitywhy motor neurons are so vulnerable to reductions in SMN," says Wilfried Rossoll, PhD, assistant professor of cell biology at Emory University School of Medicine. "What's new is that we have a mechanism."

Rossoll and his colleagues showed that the SMN protein is acting like a "matchmaker" for messenger RNA that needs partners to transport it into the cell axon.

RNA carries messages from DNA, huddled in the nucleus, to the rest of the cell so that proteins can be produced locally. But RNA can't do that on its own, Rossoll says.

In the paper, the scientists call SMN a "molecular chaperone." That means SMN helps RNA hook up with processing and transport proteins, but doesn't stay attached once the connections are made.

"It loads the truck, but it's not on the truck," Rossoll says.

Using fluorescence inside living cells as well as biochemistry, they showed that SMN promotes an interaction between the 'zipcode' region of a test RNA and a transport protein. Some of the experiments included cells from SMA patients, obtained through a collaboration with Han Phan, MD, a pediatric neurologist at Children's Healthcare of Atlanta, and the Laboratory for Translational Cell Biology at Emory.

The first author of the paper is Paul Donlin-Asp, PhD, a former Biochemistry, Cell and Developmental Biology graduate student, now at the Max Planck Institute in Frankfurt,. Co-senior author is Gary Bassell, PhD, chair of the Department of Cell biology at Emory University School of Medicine.

Scientists have known for 20 years that SMN is necessary in every cell of the body, since disrupting the gene in a mouse causes early embryonic death, before muscle or nerve cells form.

However, humans have two SMN genes, one more than mice, so a mutation in the first gene usually leads to reduced levels of SMN protein but not its elimination.

An antisense-based treatment called nusinersen, which removes a roadblock in the expression of the second SMN gene, was recently approved by the FDA.

Rossoll says his team's research helps to clarify SMN's role in motor neurons and other cells, and insights into its function could be important for optimizing delivery of the newly available treatment or development of additional treatments.

Explore further: Jammed molecular motors may play a role in the development of ALS

More information: Cell Reports, DOI: 10.1016/j.celrep.2017.01.059 , http://www.cell.com/cell-reports/fulltext/S2211-1247(17)30116-X

Journal reference: Cell Reports

Provided by: Emory University

Slowdowns in the transport and delivery of nutrients, proteins and signaling molecules within nerve cells may contribute to the development of the neurodegenerative disorder ALS, according to researchers at the University ...

New research from the Advanced Gene and Cell Therapy Lab at Royal Holloway, University of London has used pioneering stem cell techniques to better understand why certain cells are more at risk of degenerating in spinal muscular ...

Although only 10 percent of amyotrophic lateral sclerosis (ALS) cases are hereditary, a significant number of them are caused by mutations that affect proteins that bind RNA, a type of genetic material. University of California ...

For the first time, scientists found that in spinal muscular atrophy (SMA), the affected nerve cells that control muscle movement, or motor neurons, have defects in their mitochondria, which generate energy used by the cell. ...

Harvard Stem Cell Institute (HSCI) researchers studying spinal muscular atrophy (SMA) have found what they term "surprising similarities" between this childhood disorder that attacks motor neurons and amyotrophic lateral ...

A new study by a team of scientists from the University of Malta and the Institut de Gntique Molculaire de Montpellier (CNRS/Universit de Montpellier) could help develop treatment strategies for a crippling disorder ...

A puzzling question has lurked behind SMA (spinal muscular atrophy), the leading genetic cause of death in infants.

The acid test for a vaccine is: "Does it protect people from infection?" Emory Vaccine Center researchers have analyzed this issue for a leading malaria vaccine called RTS,S, and their results have identified candidate signatures, ...

Patients with inflammatory bowel disease are more likely to see dramatic shifts in the make-up of the community of microbes in their gut than healthy people, according to the results of a study published online Feb. 13 in ...

Walter and Eliza Hall Institute researchers have used advanced cellular, bioinformatics and imaging technology to reveal a long-lived type of stem cell in the breast that is responsible for the growth of the mammary glands ...

Research led by scientists at UC San Francisco and Case Western Reserve University School of Medicine has used brain "organoids"tiny 3-D models of human organs that scientists grow in a dish to study diseaseto identify ...

People with hemophilia require regular infusions of clotting factor to prevent them from experiencing uncontrolled bleeding. But a significant fraction develop antibodies against the clotting factor, essentially experiencing ...

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Scientists show 'matchmaker' role for protein behind SMA - Medical Xpress

Dutch Biopharma launches Phase III trial of Leukemia donor cell therapy – BioPharma-Reporter.com

Amsterdam-based Kiadis Biopharma has received Health Canada approval to initiate a global Phase III trial for an allogenic stem cell therapy for acute leukemia.

Kiadis cell therapy, ATIR101 (Allodepleted T-cell ImmunotheRapeutics) is a modified infusion of a family members donated lymphocytes Kiadis is developing to treat leukemia.

By treating the donor cells, the firm looks to reduce the risk of the patient developing severe Graft-versus-Host-Disease, a life-threatening immune response.

Using the contract research organisation (CRO) CTI Clinical Trial and Consulting Services Inc., the trial will enrol 195 patients across 40-50 clinical sites, including the US and Canada.

Kiadis has since submitted the trial protocol to the US FDA and several European regulators, with anticipated launch of ATIR101 in 2018.

The contract manufacturing organisation PCT LLC has been partnered with Kiadis for producing ATIR101 for the US and Canada since June last year, using PCTs Allendale, New Jersey facility.

For the European supply of the therapy, Kiadis will continue to work with the German Red Cross Blood Donor Service, Baden-Wrttemberg-Hessen e.V.,which provided GMP manufacturing services for the Phase II trial of ATIR101.

Manfred Rdiger, CEO of Kiadis Pharma said We have significant momentum now and the preparation of our MAA submission to EMA is progressing well.

Kiadis declined to comment further.

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Dutch Biopharma launches Phase III trial of Leukemia donor cell therapy - BioPharma-Reporter.com

Clinical cell therapy guidelines for neurorestoration (China version 2016) – Dove Medical Press

Hongyun Huang,1 Lin Chen,2 Qingyan Zou,3 Fabin Han,4 Tiansheng Sun,5 Gengsheng Mao,1 Xijing He6

1Institute of Neurorestoratology, General Hospital of Armed Police Forces, 2Department of Neurosurgery, Yuquan Hospital, Tsinghua University, Beijing, 3Guangdong 999 Brain Hospital, Guangzhou, 4Centre for Stem Cells and Regenerative Medicine, Affiliated Hospital of Taishan Medical University, Liaocheng, Shandong, 5Department of Orthopedics, Beijing Army General Hospital, Beijing, 6Second Department of Orthopedics, The Second Affiliated Hospital of Xian Jiaotong University, Xian, Peoples Republic of China

On behalf of the Chinese Association of Neurorestoratology and Chinese Branch of the International Association of Neurorestoratology

Abstract: Cell therapy has been shown to be a key clinical therapeutic option for central nervous system disease or damage, and >30 types of cells have been identified through preclinical studies as having the capacity for neurorestoration. To standardize the clinical procedures of cell therapy as one of the strategies for treating neurological disorders, the first set of guidelines governing the clinical application of neurorestoration was completed in 2011 by the Chinese Branch of the International Association of Neurorestoratology. Given the rapidly advancing state of the field, the Neurorestoratology Professional Committee of Chinese Medical Doctor Association (Chinese Association of Neurorestoratology) and the Chinese Branch of the International Association of Neurorestoratology have approved the current version known as the Clinical Cell Therapy Guidelines for Neurorestoration (China Version 2016). We hope this guideline will reflect the most recent results demonstrated in preclinical research, transnational studies, and evidence-based clinical studies, as well as guide clinical practice in applying cell therapy for neurorestoration.

Keywords: cell therapy, neurorestoration, China, clinical application

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

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Clinical cell therapy guidelines for neurorestoration (China version 2016) - Dove Medical Press