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Category Archives: Cell Medicine

Researchers cooperate to find risk factors for B cell non-Hodgkin lymphoma – Medical Xpress

Posted: February 20, 2017 at 4:42 pm

February 20, 2017 by Dov Smith

Non-Hodgkin lymphomas (NHL), tumors which may originate from B or T lymphocytes, account for approximately 3% of the worldwide cancer burden. Most epidemiological studies of NHL have been carried out in North American and European populations, with a few focusing on East Asian populations. Very few epidemiological studies have been conducted on B-cell non-Hodgkin lymphoma (B-NHL) in Middle Eastern populations.

Since Israelis and Palestinians represent genetically and culturally diverse populations living in geographic proximity, research analyzing their risk factors can enrich our understanding of genes and environment in the causation of lymphoma. Despite sharing the same ecosystem, the populations differ in terms of lifestyle, health behaviors and medical systems. Yet both populations report high incidences of NHL, which represents the fifth most common malignancy in Israel and the eighth most common malignancy among West Bank Palestinians. (As of 2012, Israel also ranked first in the world in NHL incidence rates.)

Now, Israeli and Palestinian researchers, led by Prof. Ora Paltiel, Director of the Hebrew University-Hadassah Braun School of Public Health and Community Medicine, and a Senior Physician in Hadassah's Hematology Department, have conducted a large scale epidemiological study examining risk factors for B-NHL and its subtypes in these two populations.

Recruiting from both the Palestinian Arab and Israeli Jewish populations, the researchers looked at medical history, environmental and lifestyle factors among 823 people with B-cell non-Hodgkin lymphoma (B-NHL) and 808 healthy controls. Using data from questionnaires, pathology review, serology and genotyping, they uncovered some risk factors common to both populations and other factors unique to each population.

The data, reported in the peer-reviewed journal PLOS ONE, showed that in both populations, overall B-NHL was associated with recreational sun exposure, black hair-dye use, a history of hospitalization for infection, and having a first-degree relative with a blood cancer. An inverse association was noted with alcohol use. Some exposures, including smoking and greater-than-monthly indoor pesticide use, were associated with specific subtypes of B-NHL.

The data also pointed to differences between the populations. Among Palestinian Arabs only, risk factors included gardening and a history of herpes, mononucleosis, rubella, or blood transfusion, while these factors were not identified in the Israeli Jewish population. In contrast, risk factors that applied to Israeli Jews only included growing fruits and vegetables, and self-reported autoimmune diseases.

The researchers concluded that differences in the observed risk factors by ethnicity could reflect differences in lifestyle, medical systems, and reporting patterns, while variations by lymphoma subtypes infer specific causal factors for different types of the disease. These findings require further investigation as to their mechanisms.

The fact that risk factors operate differently in different ethnic groups raises the possibility of gene-environment interactions, that is, that environmental exposures act differently in individuals of different genetic backgrounds. But this divergence may reflect differences in diet, cultural habits, socioeconomic, environmental and housing conditions, medical services, exposure to infections in early life or other factors.

This study reflects a unique joint scientific effort involving Israeli and Palestinian investigators, and demonstrates the importance of cooperative research even in politically uncertain climates. Cancer epidemiology will be enriched through the broadening of analytic research to include under-studied populations from a variety of ethnicities and geographic regions.

"Apart from the scientific contribution that this research provides in terms of understanding risk factors for NHL, the study entails an important research cooperation among many institutions. The study provided opportunities for training Palestinian and Israeli researchers, and will provide for intellectual interaction for years to come. The data collected will also provide a research platform for the future study of lymphoma. Epidemiologic research has the potential to improve and preserve human health, and it can also serve as a bridge to dialogue among nations," said Prof. Ora Paltiel, Director of the Hebrew University-Hadassah Braun School of Public Health and Community Medicine, and a Senior Physician in Hadassah's Hematology Department.

Explore further: Israeli lifestyle and environment may pose exceptional risks for Hodgkin's lymphoma

More information: Geffen Kleinstern et al. Ethnic variation in medical and lifestyle risk factors for B cell non-Hodgkin lymphoma: A case-control study among Israelis and Palestinians, PLOS ONE (2017). DOI: 10.1371/journal.pone.0171709

Hodgkin's Lymphoma (HL) is a common malignancy in early adulthood, accounting for approximately 30 percent of all lymphomas (cancers of the lymph system). The incidence of HL in Israel is among the highest in the world: based ...

A new analysis indicates that higher body weight and taller stature during adolescence increase the risk of developing Non-Hodgkin's Lymphoma (NHL), a type of cancer of the lymphatic system. The findings are published early ...

In 2001, Christine Skibola, Ph.D., now a professor of epidemiology at the University of Alabama at Birmingham School of Public Health, joined forces with a small group seeking a large goal discovery of genetic and environmental ...

In HIV-infected patients receiving antiretroviral therapy (ART), chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) coinfection is associated with an increased risk for non-Hodgkin's lymphoma. The findings are published ...

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Researchers cooperate to find risk factors for B cell non-Hodgkin lymphoma - Medical Xpress

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Henrietta Lacks family calls for inquiry into Johns Hopkins’ use of her cells – Baltimore Sun

Posted: February 18, 2017 at 3:41 am

The eldest son of Henrietta Lacks doubled down Friday on his efforts to reclaim his mother's legacy, calling for a congressional inquiry into Johns Hopkins Medicine's unauthorized use of her cells and the suspension of nearly $2 billion in National Institutes of Health funding.

Lawrence Lacks, the executor of his mother's estate, said the years of research using his mother's cells helped the medical institution build its reputation and led to scores of studies and medical breakthroughs. All of this in turn contributed to the funding Johns Hopkins received and continues to get, Lacks and other family members said.

In a statement, Lacks said he wanted a congressional inquiry into the money the medical institution made from Henrietta Lacks' cells, known as the HeLa cells, and called for the NIH to suspend $1.89 billion in research funding allocated to Johns Hopkins for 2017 during any investigation.

The cells, collected from the 31-year-old Turners Station woman during a diagnostic procedure before she died of an aggressive form of cervical cancer in 1951, were the first to live outside the body in a glass tube. They have become the most widely used human cells that exist today in scientific research.

Vaccines, cancer treatments and in vitro fertilization are among the many medical techniques derived from her cells.

Lawrence Lacks, 82, was not available for a phone interview Friday, but his son, Ron Lacks, and nephew Alfred Lacks Carter spoke on his behalf.

"The HeLa cells put Johns Hopkins at the top of the research chain worldwide," Ron Lacks said. "And we're thinking that we need Congress to step in and stop Johns Hopkins until we find out what is going on."

Lawrence Lacks asserted Monday that the family wanted compensation from Johns Hopkins for its use of his mother's cells. His statements come as an HBO movie about his mother's life starring Oprah Winfrey is scheduled for release in April. Lacks' story garnered national attention after Rebecca Skloot wrote a best-selling book, "The Immortal Life of Henrietta Lacks."

Hopkins declined to comment Friday, referring to a statement it released Monday that said it had not made money from the cells.

"Johns Hopkins never patented HeLa cells, and therefore does not own the rights to the HeLa cell line," the statement said. "Johns Hopkins also did not sell or profit from the discovery or distribution of HeLa cells." It also said there was no established practice for informing or obtaining consent from cell or tissue donors when the cells were taken, nor were there any regulations on the use of cells in research.

NIH spokesman John Burklow disagreed with Lacks' belief that NIH funding is based on research of the HeLa cells.

"The assertion that NIH funding to Hopkins is given in large part due to the HeLa cell discovery is not correct," Burklow said in a written statement. "NIH provides funding support to Hopkins and other research institutions for a broad array of projects that are peer reviewed for scientific merit, public health needs, and scientific opportunity, among many other considerations."

Lawrence Lacks also criticized an agreement NIH reached with other family members in 2013 that required scientists to get permission from the government agency to use her genetic blueprint. The agreement also required researchers who get NIH funding to use a database of Lacks' genome that they can only access by applying through the federal agency. Two family members were appointed to a working group to help make the decisions.

While NIH officials said they would ask biomedical researchers not funded by the agency to abide by the agreement, they acknowledged at the time that the new restrictions were limited and scientists could create a map of her genome using already available data on HeLa cells.

Lawrence Lacks said that as executor of her estate he never signed off on that agreement and told NIH he didn't want the database created. He said the relatives on the board were not legally allowed to make decision on behalf of his mother's estate. Jerri Lacks, one of the family members on the board, said earlier this week that she did not agree with many of Lawrence Lacks' assertions, but she and other family members declined to comment further.

Ron Lacks said his father would like to see that agreement renegotiated.

Burklow said in his statement that the NIH was trying to help the family have more control over use of the HeLa cells.

"Without those discussions, initiated by NIH and facilitated by Rebecca Skloot and Dan Ford, the HeLa sequence would have been available without restriction to anyone," Burklow said. "Our desire was to respect the family's interest in confidentiality and privacy, and to recognize the contributions of Henrietta Lacks and her descendants."

Lawrence Lacks said Skloot represented the family before the NIH without his permission and also raised questions about a foundation she created to help the family. He and other family members also said she didn't accurately portray the family in the book.

Skloot could not be reached for comment Friday.

Crown Publishing Group, which published the book, said Skloot provided the manuscript to members of the Lacks family for comment and corrections that were put into the book. The statement didn't specify which members saw the book, but said that Lawrence Lacks participated in meetings and interviews with Skloot. Lawrence Lack's son Ron said Skloot spent only an hour with his father and late mother.

"The veracity of the book, which has brought heightened awareness to the important contributions of HeLa cells to medicine and modern science, has not been challenged in the seven years since its initial publication in February 2010," the Crown Publishing statement said. "In the subsequent years, numerous members of the Lacks family have participated in interviews and public events in support of the book and of the need to tell the story of Henrietta Lacks."

Members of the Lacks family said they would like compensation for the use of Henrietta Lacks' cells. Two of her sons have debilitating illnesses and can't afford proper care, said Alfred Lacks Carter, Henrietta Lacks' grandson and Lawrence Lacks' nephew. They would like to set up a foundation to start a school for kids who want to study science and math.

They don't want to disrupt research, they said, but they want more say in it as well as compensation for Henrietta Lacks' contributions.

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Henrietta Lacks family calls for inquiry into Johns Hopkins' use of her cells - Baltimore Sun

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Team tracks rare T cells in blood to better understand annual flu vaccine – Medical Xpress

Posted: February 18, 2017 at 3:41 am

February 17, 2017 The expansion and formation of T memory cells over time after infection or vaccination. Credit: The lab of John Wherry, PhD, Perelman School of Medicine, University of Pennsylvania

For most vaccines to work the body needs two cell types - B cells and T helper cells - to make antibodies. B cells are the antibody factories and the T helper cells refine the strength and accuracy of antibodies to home and attack their targets. A technique that identifies these helper immune cells could inform future vaccine design, especially for vulnerable populations.

Flu vaccines work by priming the immune system with purified proteins from the outer layer of killed flu viruses. An antibody is a protein that recognizes a unique pathogen molecule called an antigen that is specific for a particular strain. Antibodies bind to their targets with precision in the best of circumstances. In doing so, the antibody blocks a harmful microbe from replicating or marks it to be killed by other immune cells.

The level of antibodies in the blood tells immunologists how well a vaccine is working, specifically, how many antibodies are made and how strongly they disable microbes. The relatively scarce circulating T follicular helper cells, or cTfh for short, are key to antibody strength. Without Tfh, effective antibodies cannot be made, yet very little is known about cTfh cells in humans after vaccination.

Now, a team led by researchers from the Perelman School of Medicine at the University of Pennsylvania has found a way to identify the small population of cTfh present in the blood after an annual flu vaccine to monitor their contribution to antibody strength. They published their findings in Science Immunology this week. The studies, led by Ramin Herati, MD, an instructor of Infectious Disease, used high dimensional immune-cell profiling and specific genomic tests to identify and track these rare cells over time.

"The poor understanding of cTfh function is, in part, because these cells spend most of their time waiting in lymph nodes for the next infection, and not circulating in the blood," said senior author E. John Wherry, PhD, a professor of Microbiology and director of the Institute of Immunology at Penn. "To get a handle on how well these cells are doing their job following vaccination, we have needed a way to measure their responses without gaining direct access to lymph nodes. Because of the central role of circulating T follicular helper cells in antibody development, new vaccine development strategies will benefit from a better understanding of the properties of these essential cells in the immune response."

Molecular Bar Codes

Every T cell has a unique receptor on its outer surface. After receiving a vaccine, the result is one T cell with this unique bar code of sorts that replicates, making thousands of clones with identical copies of the same bar code. After vaccination this expansion of T cells dies down and a few clones remain behind. These memory cells wait it out in lymph nodes and other organs for the next time the infection or vaccine enters the body. These clones can then be called into action to protect the individual or help boost the vaccine immunity.

In the current study, the team was able to track circulating helper T cells because the unique bar code they possessed is specific to the strains used in an annual flu vaccine. Wherry and colleagues traced antibody production in 12 healthy subjects, aged 20 to 45 for three years from 2013 to 2105. The circulating subset of helper follicular T cells expressed different transcription factors and cytokinesBcl-6, c-Maf, and IL-21 - compared to other T-cell subpopulations in the blood. The number of the cTfh cells sharply increased at seven days after a subject received a flu shot.

Repeated vaccination of the study participants brought back genetically identical clones of cTfh cells in successive years, indicating robust cTfh memory to the flu vaccine. These responses are a proxy for specific antibodies to the flu vaccine each year. In addition, these results measure the dynamics of vaccine-induced cTfh memory and recall over time, allowing investigators to monitor the key human-vaccine-induced cTfh responses and gain insights into why responses to flu vaccines are suboptimal in many people.

The ability to track these cTfh responses in the blood, instead of accessing lymph nodes in humans, allows for real-time monitoring of key cellular mechanisms involved in vaccination. Such knowledge should allow further optimization of vaccines for hard-to-treat diseases like the flu, but also HIV, and other infections in which inducing potent vaccines has been a challenge.

"These cTfh are a missing piece of being able to truly monitor and predict their ability to induce the desired magnitude and quality of immune memory, and therefore protection by vaccines," Wherry said. The team next intends to look at elderly populations in which vaccines are not as effective and ask what role cTfh cell populations play in that part of the human population.

Explore further: Reservoir divers: Select antiviral cells can access HIV's hideouts

More information: "Successive annual influenza vaccination induces a recurrent oligoclonotypic memory response in circulating T follicular helper cells," Science Immunology, immunology.sciencemag.org/lookup/doi/10.1126/sciimmunol.aag2152

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Mayo researcher Abba Zubair is sending stem cells for study on the International Space Station – Florida Times-Union

Posted: February 17, 2017 at 9:45 am

As a boy growing up in Nigeria, Abba Zubair dreamed of becoming an astronaut.

But as he prepared to apply to college, an advisor told him to find a different path.

He said it may be a long time before Nigeria sends rockets and astronauts into space, so I should consider something more practical, Zubair saud.

He decided to become a physician, and is currently the medical and scientific director of the Cell Therapy Laboratory at the Mayo Clinic in Jacksonville. And while hell almost certainly never get to make a journey outside the Earths atmosphere himself, if the weather stays good Saturday hell be sending a payload into space.

A SpaceX Falcon 9 rocket is scheduled to launch at 10:01 a.m. Saturday from the Kennedy Space Center on a cargo delivery mission to the International Space Station. Among the cargo it will be carrying are several samples of donated adult stem cells from Zubairs research lab.

Zubair believes adult stem cells, extracted from bone marrow, are the future of regenerative medicine. Currently at the Mayo Clinic in Jacksonville they are being used in clinical trials to treat knee injuries and transplanted lungs.

But a big problem with using stem cells to treat illnesses is that it may require up to 200 million cells to treat a human being and the cells take a long time to reproduce. Based on studies using simulators on Earth, Zubair believes that the stem cells will more quickly mass produce in microgravity.

Thats the hypothesis hell be testing as the stem cells from his lab spend a month aboard the space station. Astronauts will conduct experiments measuring changes in the cells. They will then be returned on an unmanned rocket and Zubair will continue to study them in his lab.

We want to undersrand the process by which stem cells divide so we can grow them at a faster rate and also so we can suppress them when treating cancer, he said.

Zubair became interested in the idea of sending stem cells into space four years ago, when he learned of a request for proposals that involved medicine and outer space. Hes been trying to arrange to send stem cells into space for three years.

In May 2015, he sent stem cells to the edge of space as a hot-air balloon carried a capsule filled with cells from his lab to about 100,000 feet then dropped the capsule. The idea was to test how the cells handled re-entry into the Earths atmosphere.

It turned out well, he said. The cells were alive and functioning.

Zubair was supported in that effort as he is being supported in sending cells to the space station by the Center for Applied Science Technology. Its chief executive is Lee Harvey, a retired Navy pilot and former astronaut candidate who lives in Orange Park.

While stem cells have myriad potential medical applications, one that particularly interests Zubair is the use of them in treating stroke patients. Its a personal cause to Zubair, whose mother died of a stroke in 1997.

Weve shown that an infusion of stem cells at the site of stroke improves the inflammation and also secretes factors for the regeneration of neurons and blood vessels, he said.

Zubair hasnt entirely given up on his old dream of being an astronaut. Hes applied for the civilian astronaut program. But he doesnt expect that to happen.

Im not sure I made a cut, he said. I just wanted to apply.

And he realizes what a long, strange trip hes made.

I have come so far from Africa to here, he said, and now Im sending stem cells into space.

Charlie Patton: (904) 359-4413

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This startup preserves your cells for the future, to capitalize on … – GeekWire

Posted: February 17, 2017 at 9:45 am

Silene Biotech co-founders Alex Jiao, left, and Jenna Strully. (Silene Biotech Photo)

Silene Biotech wants to help you grow a new heart or liver, in case those organs fail when you get older. The ambitious Seattle startup founded two years ago and a member of the 2017 TechStars Seattle class today is launching a new service that freezes and stores your white blood cells so they can be used decades later when troubling ailments set in.

The big idea? You could preserve the cells from your 23-year-old body for use when you are 65, and possibly facing life-threatening diseases.

Founded by four Seattleites, including two former University of Washington researchers, Silene is on the cutting-edge of a new field of regenerative medicine, which rebuilds parts of the body.

While growing a new heart with your own cells may be decades off, two of Silenes co-founders, Alex Jiao and Jenna Strully, believe preparing for those medical breakthroughs now could be a huge advantage.

Jiao and Strully came up with the idea for Silene after meeting in a science business class at the University of Washington, where Jiao was studying bioengineering and Strully, who is also a medical doctor, was in the MBA program.

They competed in the UWs business plan competition and won some initial funding during the process. The startup has raised $450,000 in total from UW grants and awards, angel investments, the founders own cash and funds from TechStars.

Jiao, who is just28 years old, said he hopes the startup will educate and raise awareness and provide a service, along with pushing the needle towards personalized medicine, a kind of medicine that tailors treatments to specific individuals.

The company was originally named miPS Labs, a nod to its focus on induced pluripotent stem (iPS)cell technology. Unlike most stem cells, which naturally occur in the body, these cells are engineered from an average adults white blood cells and could be used in regenerative medicine to grow extra tissue or even entire organs.

The first applications of this regenerative medicine technology are starting to hit clinical trials, Jiao said.

But the older we get, the less effectively the process works, he said. Silene Biotech is collecting and storing cells now, so customers can use them years or decades down the line.

Part of their plan is a newly-developed collection system. Instead of collecting urine samples, which the startup did in their beta trial, it is now partnering with Bloodworks Northwest to collect samples of customers blood.

Starting Thursday, customers can sign up to have blood drawn at Bloodworks Northwests downtown Seattle location.Jiao said they will soon also be taking samples at other Bloodworks locations throughout the Northwest.

The sample will then be processed by the company and stored in a facility in Indianapolis, far from Seattles threat of disruptive earthquakes. The service costs $299 for the initial processing and first year of storage, and $50 per year after that.

Customers can access their cells at any time, retrieving them to be used in medical procedures. The cells areanonymized during processing to protect patient confidentiality, and customers also retain the right to have the cells destroyed at any time.

Theres no way to know exactly what these cells could be used for in the future, but early possibilities includegrowing tissue to repair organs, using lab-grown tissue to test patients for drug resistance, and even growing entire organs for patients who need transplants.

To explain the possible uses of these specialized cells, Jiao cited the first clinical trial in which they were studied. In the trial, researchers took skin cells from a patient with vision loss and converted them into lab-grown stem cells. The cells were then grown into retinal cells and implanted in the patients eye, and halted her vision loss.

Maybe a decade or so off is when well really start seeing the fruits of this research turn into viable therapies that can treat and cure diseases, and maybe a couple more decades until we can regrow entire organs, Jiao said. Were not going to grow a heart tomorrow, he said, but trials are about to begin that aim to growing parts of a heart.

While iPS cells are the area of Jiaos expertise, he said the company changed its namebecause itrealized there were many more applications to its service than just iPS cells. Stored white blood cells are being studied as a treatment for Leukemia, for example.

But the switch was also inspired by a remarkable story.

In 2007, in the Northern reaches of Siberia, Russian scientists dug up a cache of seeds hidden by a squirrel. The seeds were estimated to be 32,000 years old.

A few years later, scientists were able togerminate one of the seeds and grow it into an adult plant: the silene stenophylla. That seed is officially the oldest living organism to survive being frozen.

Jiao said he hopes Silene Biotech will do a better job than squirrels did 32,000 years ago.

We caught up with Silenes founders for this Startup Spotlight, a regular GeekWire feature. Keep reading for a Q&A with Jiaoand Strully, and check out all our Startup Spotlights here.

Explain what you do so our parents can understand it:We store your younger cells today so you can use them in personalized therapies and diagnostics in the future.

Inspiration hit us when: Alex (Jiao) worked on deriving patient stem cells and turning them into heart cells and he realized he could be doing this easily for himself.

VC, Angel or Bootstrap: Bootstrap and angels. Need a fair amount of capital to start a lab, now trying to prove the market.

Our secret sauce is: Our passion, backgrounds, and our partnerships with UW and BloodworksNW

The smartest move weve made so far: Switching to blood and partnering with BloodworksNW

The biggest mistake weve made so far: Not moving faster

Would you rather have Gates, Zuckerberg or Bezos in your corner: Zuckerberg. Goals are more in line regarding biotech, pretty audacious (Chan + Zuckerberg initiative).

Our favorite team-building activity is: Grabbing snacks or meals (team loves food).

The biggest thing we look for when hiring is: Chemistry

Whats the one piece of advice youd give to other entrepreneurs just starting out: Meet and talk to everyone and keep an open mind.

Company Site: http://www.silenebiotech.com

Twitter: http://www.twitter.com/silenebiotech

LinkedIN: https://www.linkedin.com/in/silenebiotech

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Seattle company allows blood donors to deep freeze cells for future … – KOMO News

Posted: February 16, 2017 at 7:42 am

SEATTLE - Melissa Wasserman is used to getting stuck. Shes a regular donor of blood but, this trip to Bloodworks Northwest is not intend to save the life of another, but quite possibly her own in the future.

My cells are not getting any younger, so collecting them now is kind of insurance, said Wasserman.

Wasserman is one of the first official customers for Silene Biotech, a pharmaceutical-grade cell preservation service with a relatively simple idea. The intent is a long-term freezing of a customers blood, with the hope that scientists will develop cures to what ails us and the cells could then be thawed and used to heal ourselves.

The older we get, our cells just get damaged and mutilated, said Dr. Alex Jiao, co-founder and CEO of Silene Biotech. We are looking right now to regenerate peoples bodies using stems cells and thats incredible."

Work by scientists at the University of Washington to regenerate portions of the human heart is already showing some success.

Customers of Silene Biotech are banking their blood on the hope the stem cells can be used to regenerate portions of their own faulty organs or joints when the technology become available.

While technology for regenerating people's body's and treating your diseases are still being developed we can preserve their cells today. said Jiao That way they will have a better opportunity to use their own cells for regenerative medicine or personalize therapies."

The process involves a low-volume blood draw. Silene Biotech then processes the blood then isolates the cells and freezes them in their Seattle lab. The blood is then sent to a long-term medical storage facility in Indianapolis, Ind.

The customer retains full ownership of their own cells and can retrieve or destroy them at any time. Customers can also opt in to have the cells used anonymously for scientific purposes.

Jiao said all personal information is kept confidential with Silene Biotech. Theres even a provision in case the company goes out of business.

We prepay a lot of the storage costs, but if we go out of business and [the customers] storage is up, they have the ability to pay for the storage themselves, said Jiao.

Wendy Riedy was one of the companys early beta testers after she saw KOMO Newss initial story on Jiaos idea more than a year ago.

I thought why not, it cant hurt and Im not getting any younger, said Riedy.

In the future, a persons own stem cells could be used to reverse macular degeneration, which runs in Wendys family.

My mother had both knees replaced, said Riedy. If I could not do that using my own stem cells, why would I not want to do that."

The younger the donor, the better shape the stem cells could be and likely free from pre-cancer factors said Jiao. So, Wendy convinced her daughter to bank her blood just in case.

Id like to have that option to utilize my own cells and helping my body heal itself, said Riedys daughter, Chandler Batiste.

The company currently offers two payment options. There is a $50 annual payment plan with a one-time processing fee of $299. Or theres one-time lifetime payment of $999.

Core blood storage via freezing is not a new concept. Its been done for years for diagnostic reasons and large qualities can be frozen for future surgeries.

But, Jiao believes their niche will be smaller, affordable blood storage for future stem cell harvesting.

The ethics come into play when you over-promise and you say theres something today and its not, said Jiao. We definitely dont do that."

Who better to help yourself in the future than yourself.

I do hope that my own self will make me less miserable, said Wasserman.

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Seattle company allows blood donors to deep freeze cells for future ... - KOMO News

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Cancer: New method tags elusive tumors for targeted therapy … – Medical News Today

Posted: February 16, 2017 at 7:42 am

Researchers have discovered a way to tag cancer cells of tumors that are difficult to target because they lack suitable receptors. They suggest that their approach, which they tested in mice, could lead to new targeted therapies for cancers that do not respond to those currently available, such as triple-negative breast cancer.

The team - including scientists from the University of Illinois at Urbana-Champaign and research centers in China - reports the findings in the journal Nature Chemical Biology.

The method uses small-molecule sugars to produce unique, artificial cell surface receptors on cancer cells.

Study leader Jianjun Cheng, a professor in materials science and engineering at Illinois, explains that there is a lack of targeted therapies for certain cancers because they do not have any of the receptors that available treatments normally target.

One such cancer is triple-negative breast cancer - an aggressive cancer with a low survival rate.

Prof. Cheng says that this got them thinking that perhaps they could create an artificial receptor.

Targeted cancer therapies are treatments that target specific molecules involved in the growth, progression, and spread of cancer. They belong to a relatively new field called precision medicine.

There are several differences between targeted cancer therapy and conventional chemotherapy, the main one being that most chemotherapy treatments target all rapidly dividing cells, including healthy ones.

Targeted cancer therapy aims to single out only cancer cells and leave healthy cells intact. In order to do this, researchers must find features that distinguish the tumor cells of a particular cancer from healthy cells, so that the treatment can target those features specifically.

One feature that can differentiate cancer cells from healthy cells is the cell surface receptor, a type of molecule that protrudes on the outside of the cell and acts as a conduit for signals between the cell and its environment.

Scientists can devise antibodies that seek out the receptors that are specific to cancer cells in order to deliver targeted drugs or imaging agents.

However, some cancers are notoriously difficult to distinguish in this way because they lack suitable surface receptors.

One such cancer is triple-negative breast cancer. Tumor cells of this type of cancer lack the three most common types of receptor known to drive most breast cancer growth: estrogen receptors, progesterone receptors, and human epidermal growth factor receptor 2 (HER2).

Prof. Cheng and colleagues found a way to insert unique molecules into cancer cells that the cells metabolize into cell surface receptors, without the molecules affecting healthy cells.

The molecules belong to a class of small-molecule sugars called azides. The cancer cell metabolizes the molecules and expresses them on their cell surfaces, where they can be uniquely targeted by another molecule called DBCO, as Prof. Cheng explains:

"It's very much like a key in a lock. They are very specific to each other. DBCO and azide react with each other with high specificity. We call it click chemistry. The key question is, how do you put azide just on the tumor?"

To ensure that the azide would only be expressed by the cancer cells, the team attached a chemical group to the azide that only enzymes in the cancer cell can remove.

The modified azide just passes through healthy tissue. In tumor cells, however, the enzymes digest the attached group and express the azide as a cell surface receptor that binds uniquely to DBCO, which can be used to deliver cancer drugs or imaging agents.

After showing that the method works in cells cultured in the laboratory, the team tested it in mice with triple-negative breast cancer, colon cancer, and metastatic breast cancer tumors, and they found that the tumors expressed very strong signals compared with other types of tissue.

"For the first time, we labeled and targeted tumors with small molecule sugars in vivo, and we used the cancer cell's own internal mechanisms to do it."

Prof. Jianjun Cheng

Learn how a prolactin receptor screen may lead to new treatments for triple-negative breast cancer.

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Calcium imbalance within brain cells may trigger Alzheimer’s disease – Medical News Today

Posted: February 15, 2017 at 8:46 am

New research investigates the role of calcium production in Alzheimer's disease. The neurodegenerative process may be caused by a calcium imbalance within the brain cell.

Mitochondria - sometimes referred to as the "powerhouse of the cell" - are small structures that transform energy from food into cell "fuel."

In the mitochondria of a brain cell, calcium ions control how much energy is produced for the brain to function. Previous research has shown that an excessive production of calcium can cause neurons to die, therefore linking a calcium imbalance with the neurodegenerative process involved in Alzheimer's disease.

Until now, however, the exact mechanism that links Alzheimer's-related neurodegeneration and mitochondrial calcium imbalance was unknown. The new research - led by Pooja Jadiya, a postdoctoral fellow at Temple University in Philadelphia, PA - sheds light on this association.

The study was carried out by researchers from the Center for Translational Medicine at Temple University, and the findings were presented at the 61st Meeting of the Biophysical Society in New Orleans, LA.

Jadiya and colleagues studied brain samples from Alzheimer's patients, a mouse model genetically modified to replicate Alzheimer's-like symptoms, and a mutant Alzheimer's-affected cell line.

They examined the mitochondrial alterations in calcium processing, together with reactive oxygen species (ROS) generation, the metabolism of the active amyloid precursor protein, membrane potential, and cell death. They also looked at the activation of the mitochondrial permeability transition pores and oxidative phosphorylation.

In a healthy brain, calcium ions leave a neuron's mitochondria to prevent an excessive buildup. A transporter protein - called the mitochondrial sodium-calcium exchanger - enables this process.

In Alzheimer's-affected tissue, Jadiya and team found that the sodium-calcium exchanger levels were extremely low. In fact, the protein was so low that it was difficult to detect.

The researchers hypothesized that this would cause an overproduction of ROS, which would, in turn, contribute to neurodegeneration.

ROS are molecules that, in high levels, have been shown to damage proteins, lipids, and DNA, thus causing oxidative stress.

The team did find a correlation between the reduced activity of the sodium-calcium exchanger and increased neuronal death.

Additionally, in the mouse model, the scientists found that right before the onset of Alzheimer's, the gene that encodes the exchanger was significantly less active. A decrease in this gene's expression further suggests that the protein exchanger plays a key role in the progression of the disease.

Finally, the scientists also tested this mechanism in an Alzheimer's-affected cell culture model, by artificially boosting the levels of the exchanger.

As hypothesized, the affected cells recovered to a point where they were almost identical to healthy cells. Furthermore, the levels of adenosine triphosphate (ATP) increased, the ROS levels decreased, and fewer neurons died.

ATP is a molecule considered to be the "energy currency of life" by some biologists, as it is required by every activity our body engages in.

John Elrod, a co-author of the study, explains the significance of the findings:

"No one has ever looked at this before using these model systems. It is possible that alterations in mitochondrial calcium exchange may be driving the disease process."

The study may also pave the way for new treatment options, Elrod explains. The team is currently working to reverse the neurodegeneration typical of Alzheimer's disease in mouse models by stimulating the expression of the gene that encodes the sodium-calcium exchanger. This could be achieved with new drugs or gene therapy.

"Our hope is that if we can change either the expression level or the activity of this exchanger, it could be a viable therapy to use early on to perhaps impede Alzheimer's disease development - that is the home run," Elrod says. "We are not even close to that, but that would be the idea."

Learn how scientists can stop and reverse Alzheimer's-related brain damage in mice.

Written by Ana Sandoiu

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

Posted: February 15, 2017 at 8:46 am

February 14, 2017 5:15 PM By Marcus Washington

BALTIMORE (WJZ) The family of Henrietta Lacks issuing Johns Hopkins Medicine for using Lacks blood cells without her permission 66 years ago.

For years, Henriettas oldest son along with his son say they have been turned down by attorneys who have declined to help them because of the statute of limitation on the case. They now have an attorney who has agreed to help and take on John Hopkins.

The stories of Henrietta Lacks often surround her blood cells used by doctors to help create many medical advances for more than 60 years.

But to her oldest son, Lawrence, she is just mom.

I remember she was very strict and she was a very loving mother, said Lawrence Lacks.

At the age of 15, his world changed when his mother was diagnosed with cervical cancer.

I didnt know what it was all about, said Lacks. I [knew] I would have to stay home most of the time to take care of my brothers and sisters, because my father was taking her back and forth to Johns Hopkins all the time.

Within a year, Henrietta Lacks died, but her legacy would live on, not just with her family, but in the field of medicine.

Doctors at Johns Hopkins found that Henriettas cells were a type of immortal cell line that would later go on to help develop vaccines for many diseases, such at polio.

It wasnt until 2010, with the publishing of a book about Henrietta and her HeLa cells, that family members found out what had been going on for nearly 50 years.

Who wouldnt want their loved ones to have a cure for this or that, said Ron Lacks, Henriettas grandson.I mean, everybody was on board with that.

In a statement responding to Lacks familys claims, Johns Hopkins says in part:

Johns Hopkins Medicine celebrates and honors the incredible contribution to advances in biomedical research made possible by Henrietta Lacks.

Johns Hopkins never patented HeLa cells, and therefore does not own rights to the HeLa cell line. Johns Hopkins also did not sell or profit from the discovery or distribution of Hela cells.

Lacks family attorney, Francis Lanasa, thinks this goes beyond the money.

Fundamentally, its someone took someone elses property, and theyve continued to use that property to this day, said Lanasa. Its our understanding that the NIH (National Institutes of Health) and other entities have given Hopkins grants in the terms of hundreds of thousands of dollars to keep doing the research, so they have benefited financially by this.

Thats why we want to open our own foundation so we can get recognition for helping others, said Ron Lacks. You want to take control of your grandmothers legacy.

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Marcus Washington joined WJZ Eyewitness News in June 2014 as the weekend evening anchor and reporter. Dreams of becoming one of the people who tells the news came early for Marcus. He still remembers sitting in his living room at the age ...

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Researchers identify cells linked to the development of the heart’s ventricular chambers – Medical Xpress

Posted: February 14, 2017 at 10:43 am

February 14, 2017 The left image is of an embryonic mouse heart, showing the four chambered structure with atria at the top and ventricles at the bottom. The right image is the fluorescent lineage tracing reporter, showing that our newly discovered progenitor cell population contributes specifically to the ventricular chambers of the heart. Credit: Mount Sinai Health System

A population of cells in early development may give rise to the ventricular chambers of the heart, but not the atria, according to a study led by researchers from the Mindich Child Health and Development Institute at the Icahn School of Medicine at Mount Sinai and published today in Nature Communications.

Congenital heart defects are the most common type of birth defect, affecting 35,000 babies in the United States each year, according to the U.S. Department of Health and Human Services. Many of these defects originate as the heart chambers are forming. While much is known about the development of the heart, the formation of the four distinct chambers of the heart has lacked thorough understanding.

Using a model that traces cell lineage in mice, investigators studied the protein-coding gene Foxa2, primarily associated with endoderm and ectoderm development during embryogenesis. They discovered a population of progenitor cells expressing Foxa2 during early development that gave rise to cardiovascular cells of both the left and right ventricular chambers, but not the atria. Their research showed that atrial-ventricular segregation may occur long before the morphological establishment of differentiated cardiac structures.

"An in-depth understanding of the formation of the heart chambers will enable us to better comprehend the biology behind detrimental heart defects and how best to address them," said lead investigator Nicole Dubois, PhD, Assistant Professor in the Department of Cell, Developmental and Regenerative Biology at the Icahn School of Medicine at Mount Sinai. "In addition to informing our understanding of early heart development, we hope that these findings will also lead to new protocols for the generation of ventricular cardiomyocytes in cell culture that could potentially be used in therapeutic settings."

"There is a lot we still don't understand about this population, or the function of Foxa2 during the formation of the heart, but we think these findings provide a powerful new system to answer some of the most relevant open questions about how early heart development occurs," said Evan Bardot, PhD student and first author of the Nature Communications study.

Explore further: New mouse model helps explain gene discovery in congenital heart disease

More information: Nature Communications, DOI: 10.1038/NCOMMS14428

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Interesting that in the development from fertilized egg to fully grown human being we witness true evolution - changes from a single ancestor cell into an extreme highly complex life form. Right before our eyes, in our lifetime. Fully observed, repeatable and verifiable. No need to invent non-existing missing links since it's all there - right in front of us. Everywhere. True, full blooded, indisputable evolution - one kind into another into another into another into another.............all programmed to the last tee by a superlatively ingenious super intelligent being otherwise known as the Creator. Strange then that highly educated scientists do not want to see or acknowledge the evidence for the existence of said Creator.

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