Category Archives: Cell Biology

Cell Biology

Natural Infant Formula On The Horizon: How To Copy What Nature Put In Mothers Milk – Forbes

Novel ingredients that are built with biology

Photo by Lucy Wolski on Unsplash

Synthetic biology has already created a world of new foods that would have sounded impossible not so long ago. Today you can sink your teeth into a plant-based burger that bleeds with vegan cheese, then enjoy cow-free dairy ice cream for dessert. But what if bioengineering could make nutrition not just healthier and more humane, but more naturalcloser to original biology?

Of all the milk produced by mammals, human milk is the most complex. Refined over millions of years of evolution, it contains more than 200 unique sugars for infant nutrition, quadruple that of the 50 in cows milk. Studies of breastfeeding show that mothers milk plays a key role in boosting infant nutrition, immune system development, and gut health. In the modern era, however, breastfeeding is not always an option for caregivers.

Thats why the gold standard of infant formula is to create a product as similar to breast milk as possible, so babies can get the complex blend of nutrients that were tailored for them by nature. Thats exactly what Conagen has accomplished, again, with two synthetic biology breakthroughs that bring infant formula even closer to actual human milk.

Earlier this year, I wrote about Conagens breakthrough production of lactoferrin, a milk protein crucial to infant nutrition. Now, Conagen is tackling two more compounds found in breast milk: naturally occurring complex sugars called human milk oligosaccharides (HMOs), and a tasteless, odorless fatty acid called FBA that supports gut and immune system development. After lactoferrin, these are Conagens second and third offerings for fortifying infant formula.

HMOs serve an important signaling function in a newborns body: they help the young immune system tell the difference between dangerous foreign bodies, such as bacteria, and beneficial nutrients from food. The immune systems ability to distinguish friend from foe is what prevents the emergence of food allergies at a young age. Meanwhile, FBA promotes the production of butyrate, a pre- and postbiotic that supports healthy cellular development of the gut lining.

If mothers milk came with a nutrition facts label, HMOs would be the fourth ingredient after water, fat, and lactose. The most prevalent HMO in mothers milk is known as 2-FL. Because this HMO is not found in cows milk, infant formula needs to be supplemented with lab-made 2-FL. Producing 2-FL has required the use of genetically modified organisms (GMOs)until now.

In a process similar to how cheese is made by adding enzymes to milk, Conagen uses bioconversion to synthesize and then purify 2-FL. Unlike its competitors, Conagen can perform this chemistry outside of a living cell. This results in a more reliable and streamlined production process.

For Casey Lippmeier, VP of innovation at Conagen, reproducing the benefits of natural mothers milk is a personal goal. A father and a scientist, Dr. Lippmeier has been studying how to improve infant formula for his entire career. Mothers who dont have any other option than to use formula can feel better and better with every new improvement we make on health, he says. Manufacturers can expect Conagens HMOs to be available in the next few months, or partner with Conagen in the licensing of FBAs for other applications.

From pharmaceuticals to supplements to flavors, Conagens fermentation process has already put synthetic biology on the map within industrial manufacturing. Now, with its latest human milk compounds, the company continues to bring infant formula closer to the optimal nutrition of mothers milk. A healthier world for every newborn: thats building a better world with biology.

Subscribe to my weekly synthetic biology newsletter. Thank you to Desiree Ho for additional research and reporting in this article. Im the founder of SynBioBeta, and some of the companies that I write about, including Conagen, are sponsors of the SynBioBeta Global Synthetic Biology Summit and digest.

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Natural Infant Formula On The Horizon: How To Copy What Nature Put In Mothers Milk - Forbes

Cell Biology

Scientists uncover important disease-fighting role for cells in the liver – News-Medical.Net

Reviewed by Emily Henderson, B.Sc.Oct 19 2020

Scientists at Scripps Research have uncovered an important disease-fighting role for cells called hepatocytes, which constitute most of the liver. The discovery could potentially be harnessed to develop new medicines for viral illnesses.

According to the new study, which appears in Communications Biology, hepatocytes help control infections from common viruses called coxsackieviruses, and probably defend against many other viruses as well. The findings suggest these liver cells, long known for their role in deactivating chemical toxins in the blood, should also be viewed as a significant element of the immune system--an element that future drugs might be able to enhance to strengthen the body's defense against emergent viruses.

Hepatocytes may have evolved the ability to absorb and silence a variety of different viruses, to slow their spread in the body and reduce infection-related illness."

Taishi Kimura, PhD, postdoctoral research associate at Scripps Research and first author of the study

Kimura worked on the study while in the laboratory of J. Lindsay Whitton, MD, PhD, professor in the Department of Immunology and Microbiology at Scripps Research and senior author of the study.

Whitton and his lab have long studied coxsackieviruses, a family of polio-like viruses that spread via the fecal-oral route and can cause a broad array of symptoms including fever, sore throat, rash, diarrhea, meningitis, pancreatitis and inflammation of the heart muscle. The viruses are named for the New York town of Coxsackie, where virus specimens were initially isolated from patients in the late 1940s.

Recently Kimura and research assistant Claudia Flynn observed that mice experience significant liver damage, including damage to and deaths of hepatocytes, when infected with a type of coxsackievirus called coxsackievirus B3 (CVB3).

Hepatocytes, along with many other cell types, express a cell-surface protein called "coxsackievirus-adenovirus receptor" or CAR, which CVB3 uses to get into cells. So Kimura and Flynn genetically engineered mice whose hepatocytes--but no other cell types--lack CAR, and thus could not be infected by CVB3. Unsurprisingly, when these mutant mice were infected with CVB3, their hepatocytes were spared significant damage.

However, the CVB3 infection hit these mutant mice much harder on the whole, compared with non-mutant siblings. The mutants with protected hepatocytes swiftly showed high blood levels of virus, lost more weight, developed complications such as heart inflammation and were much more likely to die from the infection.

These findings showed that ordinary hepatocytes, when they are able to be infected by CVB3, help protect the rest of the body from the virus. In further experiments, the team found more support for this idea, observing that when hepatocytes absorb CVB3, they quickly shut down the virus's replication using an immune protein called IRF1. Although the infected hepatocytes are damaged by taking up the virus, the liver itself does not show the strong inflammation that is seen in other virus-infected organs, such as the heart and pancreas.

Virus researchers have known that other, much-less numerous cell types in the liver--such as so-called Kupffer cells--can trap and neutralize viruses that are circulating in the blood. Hepatocytes had not been thought to do this, but the study shows that they do.

Given the large size of the liver, hepatocytes constitute a major cell type in the body. To the researchers, it seems unlikely that this major cell type has evolved to defend against only one family of viruses. More likely, they say, it acts broadly, like an antiviral "sponge," soaking up any of a variety of virus types from the bloodstream early in infection, to help slow and limit the infection in the rest of the body. Hepatocytes that absorb viruses in this way may be damaged or die, the researchers add, but the harm to the liver is perhaps only temporary.

"Hepatocytes have an extraordinary capacity for regeneration, and this may be an adaptation that has more to do with their antiviral role than with their better-known role against toxins," Whitton says. "Toxins may not have been enough of a threat during animal evolution to create pressure for such an adaptation, but viruses probably have been."

Whitton and Kimura also note that other common viruses, including the SARS-CoV-2 coronavirus that causes COVID-19, can cause modest and often temporary liver damage, much like that observed for CVB3. This again hints that hepatocytes' defensive role may extend far beyond coxsackieviruses. Though Whitton is retiring this year, Kimura intends to continue this line of research into whether--and how--hepatocytes defend against SARS-CoV-2 and other viruses.

"The protein IRF1, which hepatocytes use to silence CVB3, works by activating a broad set of antiviral genes, and it may be that each of these antiviral genes is adapted to silence a different set of viruses," Whitton says.

By actively taking up virus that is circulating in the blood, hepatocytes may also serve as a first-alert mechanism that helps activate other immune system elements, Kimura says. In principle, Kimura adds, future drug treatments might enhance hepatocytes' uptake of viruses to limit serious infections when no other option is available, such as with new human-infecting viruses.

"This hepatocyte response might turn out to be a key element of the human immune response against emergent viruses," he says.

Source:

Journal reference:

Kimura, T., et al. (2020) Hepatocytes trap and silence coxsackieviruses, protecting against systemic disease in mice. Communications Biology. doi.org/10.1038/s42003-020-01303-7.

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Scientists uncover important disease-fighting role for cells in the liver - News-Medical.Net

Cell Biology

Fate Therapeutics’ and Celyad’s CAR therapies in oncology offer potential – pharmaceutical-technology.com

by Manasi Vaidya in New York.

Fate TherapeuticsandCelyadsnatural killer (NK) cell biology-focused cell therapies could overcome cell persistence challenges and consequent efficacy concerns with redosing strategies, experts said.

One of Fate Therapeutics lead products, FT596, is an allogeneic, multitargeted, chimeric antigen receptor (CAR) NK cell product. Celyads autologous CYAD-01 and CYAD-02 and allogeneic CYAD-101 are CAR T cell products using NK cell specificity to target T-cells. One analyst considered the potential to redose allogeneic products as a key item to consider while assessing clinical potential. While clinical data establishing the additive efficacy advantages of giving multiple doses is still preliminary, redosing allogeneic products could increase their expansion and persistence, experts said. Autologous therapies carry source constraints, so the ability to manufacture and administer allogeneic therapies is an advantage, they said.

While past NK cell therapy data has been mixed, experts saw potential in CAR NKs like FT596 or CAR T-cell products engineered to express NKG2D like CYAD-101, given the advancements in cell production.

Phase I FT596 results in B-cell lymphomas/ CLL are expected at either the American Society of Hematology (ASH) meeting in December or an investor meeting in early 2021, as per a second analyst report. Phase I data for CYAD-01 and CYAD-02 in relapsed/refractory (r/r) acute myeloid leukaemia (AML) and myelodysplastic syndrome (MDS) are expected by YE20, as per the companys August corporate presentation. Celyads allogeneic CYAD-101 is being tested in a Phase I alloSHRINK trial (NCT03692429) in metastatic colorectal cancer (CRC), which has a primary completion date of November 2020.

FT596s sales are expected to reach $136m in 2026, according to a GlobalData Consensus forecast. Celyad did not respond to a request for comment.

Increasing the persistence of cell therapies once they are infused into a patient has been a challenge, especially with NK cell-based therapies, experts said. The issue of persistence and consequent efficacy is significant because the potential efficacy with Celyad and Fate Therapeutics platforms remains largely unknown, they added.

Because the immune system can recognise foreign cells, cell products would not last for more than a few weeks, said Dr Marco Davila, medical oncologist, in the Department of Blood and Marrow Transplantation, Moffitt Cancer Center, Tampa, Florida. With CAR T-cell therapies, the expansion and persistence of CAR cells are said to correlate with the durability of response, said Dr David Sallman, assistant member, Department of Malignant Hematology, Moffitt Cancer Center.

Strategies involving multiple doses of cell therapies could maximise the total dose, improve duration, and increase efficacy magnitude with both autologous and allogeneic cell therapies, said Dr Tara Lin, associate professor of medicine, University of Kansas Medical Center, Kansas City. Multiple infusions of therapy could also potentially lead to complete remission, said Sallman. In Fate Therapeutics Phase I FT500 (NCT03841110) study, patients had been given up to six doses of the therapy, which was not found to be toxic, according to Fate Therapeutics CEO Scott Wolchko. Redosing has the potential to offer multiple infusions as maintenance therapy, said Dr Jeffrey Miller, professor of Medicine, Division of Hematology, Oncology and Transplantation, University of Minnesota, Minneapolis.

The persistence of allogeneic therapies is not well understood, and it is unknown how long cells need to persist to be effective or whether persisting cells confer durability of response, said Wolchko. Giving multiple doses is one way to overcome the lack of persistence if it is an important factor for efficacy, he said. In a 4Q19 call, the FDA said it was allowing the dose to be repeated on a patient-by-patient basis, Wolchko said. In the alloSHRINK study, CYAD-101 is administered three times with a two-week interval between each administration in metastatic CRC, as per ClinicalTrials.gov.

However, even if the engineered cells do not persist in the body, the response rate and ability to eradicate the disease should not be limited, said Davila. With a limited lifespan, allogeneic cell therapies would dissipate as the patients immune system recovers, said Dan Kaufman. With the incorporation of interleukin (IL)-12 or IL-15 into the cell product, the cell therapy could persist without exogenous cytokines, said Kaufman. The FT596 construct contains an IL-15 fusion protein.

Experts cited the data from a Phase I / II (NCT03056339) investigator-led effort at MD Anderson Cancer Center using cord blood-derived anti-CD19 CAR NK cells as an example of an effective CAR NK therapy. The study by Rezvani and colleagues showed a persistence challenge did not seem to hamper the response, because once a critical threshold for cell expansion is crossed, the activity can be mediated, Davila said. Eleven r/r patients with CD19-positive cancers, such as non-Hodgkins lymphoma or CLL, were treated with a single infusion; eight had a response, including seven with a complete remission (Rezvani et al. [2020] N Engl J Med, 382, pp. 545553). Even if the cells do not persist, they expand to sufficient levels to eradicate the disease before they are lost, Davila added.

In the Phase I THINK(NCT03018405) CYAD-01 data, decreased bone marrow blasts were observed in eight patients, including five objective responses and one stable disease for three or more months, as per the company presentation. Responding patients did have blast clearances, but some of the remissions were short-lived and the cells did not persist in the system, said Sallman. However, the short hairpin (sh) ribonucleic acid (RNA) technology employed CYAD-02, which could increase persistence and expansion, said Sallman (Fontaine et al., [2019]Blood, 134[Suppl 1], p. 3931). ShRNA technology allows T cell engineering without the need for gene editing to inhibit alloreactivity and increase persistence, according to Celyad.

Ongoing research on improving preconditioning regimens by combining additional drugs could also help with the persistence of allogeneic products, said Davila. It is not known whether every dose needs a conditioning regimen, but since conditioning regimens can suppress a patients immune system for several months, it may not be necessary before every therapy infusion, he added.

Patients will not have to receive a preconditioning regimen before every cell infusion, said Wolchko, adding redosing FT500 was found to be safe. Celyads protocol does not specify the preconditioning strategy for redosing. No predictive biomarkers are available to explain why some patients respond well and others do not, said Sallman, adding it is critical to identify potential responders. Nonetheless, there is no way to predict clinical efficacy based only on preclinical data, so data is still needed, said Miller.

The economic advantage to developing off-the-shelf therapies has driven interest in NK-cell based platforms, said Miller and Davila. If quick treatment is needed, then an allogeneic NK cell therapy would be better than an autologous therapy, which may take up to six weeks to manufacture, said Sallman. While the results with autologous CAR T-cell therapies have been significant, their scale-up and costs are challenging, said Kaufman. Related Report

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The ability to use induced pluripotent stem cell (iPSCs) or cord blood cells as a source would help scale up the cell manufacture and allow effective results, said Kaufman. iPSCs provide advancement in expansion protocols, which can provide multiple doses, Miller added. Fate Therapeutics has an iPSC-derived NK cell franchise. Also, since T cell therapies require donor apheresis to collect cells in a process lasting four to five hours, it is not feasible to keep going back to the same donor, said Miller.

Moreover, newer platforms are expected to improve on past NK cell therapy trials, specifically those showing mixed efficacy. Past studies had feasibility limitations in getting the required number of cells, said Miller. Those small studies were conducted at a time when cell isolation and production systems were not as advanced as they are now, said Davila.

Manasi Vaidya is a Senior Reporter for Clinical Trials Arena parent company GlobalDatas investigative journalism team. A version of this article originally appeared on the Insights module of GlobalDatas Pharmaceutical Intelligence Center. To access more articles like this, visit GlobalData.

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Fate Therapeutics' and Celyad's CAR therapies in oncology offer potential - pharmaceutical-technology.com

Cell Biology

Combination of peptides and antibiotics could be key to eliminating Leishmania parasites – News-Medical.net

Reviewed by Emily Henderson, B.Sc.Oct 16 2020

A combination of peptides and antibiotics could be key to eliminating the parasite causing leishmaniasis and avoiding the toxicity to people and animals caused by current drugs. The study, coordinated by researchers at the UAB, opens the door to new, more effective treatments against this disease.

Leishmaniasis is caused by the protozoan Leishmania parasites which are transmitted by the bite of an infected sandfly. Although in rich countries this disease mainly affects dogs, in other countries it can wreak havoc on the health of humans, causing anything from ulcers to damage to the bone marrow, liver or spleen, all which could be fatal.

The WHO estimates that there are currently over one billion people living in areas in which leichmaniasis is endemic and that there are over one million new cases each year. There is therefore an urgent need to find new, efficient and selective alternatives to leishmaniasis chemotherapy which can reduce the adverse side effects of existing drugs such as paromomycin and miltefosine.

Lecturers Rosa Maria Ortuo and Ona Illa from the UAB Department of Chemistry were in charge of coordinating a multidisciplinary research into finding new anti-Leishmania therapies. Also involved in the study were the groups of lecturer Jean-Didier Marchal, from the same department, and of lecturer Carme Nogus, from the UAB Department of Cell Biology, Phyisology and Immunology, as well as researchers Luis Rivas from the CIB Margarita Salas - CSIC (Madrid) and Mriam Royo from the IQAC - CSIC (Barcelona).

The study consisted in the preparation and biological evaluation of new cell-penetrating peptides (CPPs) which, with an antibiotic conjugation, serve as a vehicle or vector for the drug, enabling it to enter the parasite's cell membrane and be released inside, thus causing its death. The result is greater effectiveness, while at the same time a lower number of oral doses of the drug are needed. In addition, the synthesised CPPs are not toxic for mammal cells, but are for the Leishmania.

Although the idea of using CPPs in the treatment of leishmaniasis is not unknown, the importance of this study lies in its high cell-penetrating capacity and the selectivity (mammal vs parasite cells) of the new synthesised and studied peptides."

Rosa Maria Ortuo, Lecturer, UAB Department of Chemistry

In particular, the research has served to study peptides made up of non-protein amino acids with a covalent conjugate of doxorubicin (Dox), a drug which is also used in cancer treatments. While Dox in its free form is not active when incubated with Leishmania because it is not capable of penetrating its interior, the Dox-PPC conjugate has demonstrated to be toxic in very low concentrations. Its cell-penetrating capacity has been rationalised through molecular modelling studies. The results are highly promising, and "a great deal of research is still needed before thinking about new drugs, but we are now a little bit closer of our objective", concludes Ortuo.

Source:

Journal reference:

Illa, O., et al. (2020) Chiral Cyclobutane-Containing Cell-Penetrating Peptides as Selective Vectors for Anti-Leishmania Drug Delivery Systems. International Journal of Molecular Sciences. doi.org/10.3390/ijms21207502.

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Combination of peptides and antibiotics could be key to eliminating Leishmania parasites - News-Medical.net

Cell Biology

Remnants of Ancient Parasites Could Be Shaping Our Response to the COVID-19 Coronavirus – SciTechDaily

Packard Fellowship recipient Ed Chuong, assistant professor of molecular, cellular and developmental biology, works in his lab with undergraduate student Isabella Horton. Credit: Glenn Asakawa/CU Boulder

Why are some people more resilient to viruses than others?

The answer has eluded scientists for centuries and, in the age of COVID-19, has come to represent one of the holy grails of biomedical research.

Ed Chuong, an assistant professor of molecular, cellular and developmental biology at CU Boulder, proposes an intriguing answer: Exposure to ancient parasites by our ancestors forever altered our genome, shaping the varied responses of our immune systems today.

If you look closely at our genome, viruses have been shaping not only our lives but also our biology and evolution for hundreds of millions of years, said Chuong, who today was awarded the prestigious $875,000 Packard Fellowship to explore the idea. Its possible that ancient viral sequences from past pandemics are now lending a hand in helping us fight modern ones.

Say the word genome and most people think of the roughly 20,000 genes that encode the proteins necessary for life. But in reality, notes Chuong, we may be more virus than human. Previous research shows that at least half the human genome is made up bits of DNA left behind by viruses and other virus-like parasites, known as transposons, which slipped into cells of our primate ancestors over the past 50 million years.

In the human genome we can see traces of these invasions everywhere, like a fossil record of infections, said Chuong.

Ed Chuong in the lab with his research team. Credit: Glenn Asakawa/CU Boulder

Among those invaders were so-called endogenous retroviruses. As viruses do, they behaved selfishly at first, coaxing their host cells to make more copies so they could rip through the body and infect others. Over time, they lost their ability to sicken and spread, but infiltrated germ cells like sperm or eggs baking their genetic recipe into generations to come.

Scientists long assumed those remnants were useless junk DNA.

But in recent years, Chuong and others have discovered that, in some cases, they were coopted by mammalian hosts for evolutionary gain, influencing everything from cognition to reproduction to immune response.

In one landmark study, which sparked Chuongs interest in the field, scientists discovered a protein called Syncytin, derived from an endogenous retrovirus, which made the development of human placental tissue possible. Chuongs follow-up research, published in the journal Nature Genetics, found that endogenous retroviruses also serve as on-off switches for gene networks that influence placental development.

The development of the placenta enabled live birth in mammals and was a major step in the evolution of our species and these ancient viruses played a key role, he said.

Chuong has since shifted his attention to the immune system, showing in 2016 that ancient viruses helped shape the interferon response the cellular alarm system that sounds within hours of infection.

We found fragments of old viruses that normally lay silent but turn on during infection, and when they do, they turn on nearby immune genes, he said.

Notably, when those viral fossils are removed and the cell is then infected, the immune response is muted.

Our study was one of the first demonstrations of an ancient virus being co-opted for host defense and now necessary to fight modern viruses, he said.

Chuong, who arrived at the BioFrontiers Institute in 2018, was working under stay-at-home orders early in the pandemic when he began to think more about why different people respond to infection, including SARS-CoV-2, differently.

He wondered: Could these ancient retroviruses provide another hidden layer of explanation?

Chuong wrote a grant proposal centered around that question. On Thursday, the David and Lucile Packard Foundation named him among 20 early-career scientists across the nation to receive their award.

In a year when we are confronted by the devastating impacts of a global pandemic, racial injustice and climate change, these 20 scientists and engineers offer us a ray of hope for the future, said Frances Arnold, chair of the Packard Fellowships Advisory Panel.

Chuong suspects that ancient parasites could be influencing human immunity today in one of two ways: Either different populations were exposed to different viruses in their evolutionary history, leaving them with different cellular machinery with which to fight off new threats; or they share the same bits of ancient DNA but much newer influences (in utero or in the environment) have silenced or awakened that immune machinery in ways that make some resilient and others vulnerable.

To learn more, he and his team will amass population-wide datasets of immune cells from humans and other mammals and apply high-powered computing techniques to sequence their genome, looking not only at genes present but also at transposons.

He has pioneered a mind-blowing new way of thinking about how genomics works, said Lee Niswander, chair of the Department of Molecular, Cellular and Developmental Biology. For him to be able to follow his nose and see where the science takes him is really exciting.

While the science is young, Chuong hopes that it ultimately could lead to new diagnostic tests or even new treatments.

Learning how and why immune responses vary within a population could transform our ability to predict individual responses to infection and autoimmune diseases, Chuong said. To get this kind of recognition that these ideas are worth pursuing is incredible.

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Remnants of Ancient Parasites Could Be Shaping Our Response to the COVID-19 Coronavirus - SciTechDaily

Cell Biology

Researchers report the discovery of innate immune signaling pathway in fibroblasts – News-Medical.net

Reviewed by Emily Henderson, B.Sc.Oct 16 2020

Vanderbilt University researchers have reported the counterintuitive discovery that certain chemotherapeutic agents used to treat tumors can have the opposite effect of tissue overgrowth in normal, intact mammary glands, epidermis and hair follicles. The researchers also are the first to report the discovery of an innate immune signaling pathway in fibroblasts--the spindle-shaped cells responsible for wound healing and collagen production--that causes cells to proliferate. Such signaling pathways previously were attributed only to immune cells.

The article describing the research, "DNA Damage Promotes Epithelial Hyperplasia and Fate Mis-specification via Fibroblast Inflammasome Activation," was published in the journal Developmental Cell on Oct. 13.

The findings of this work, led by postdoctoral fellow Lindsey Seldin and Professor and Chair of the Department of Cell and Developmental Biology Ian Macara, have broad implications for diseases associated with the immune system like psoriasis, as well as cancer and stem cell research.

Understanding the functionality of stem cells and the way that their behavior is regulated has been a longstanding research interest for Seldin. "Normal stem cells have an amazing ability to continuously divide to maintain tissue function without forming tumors," she explained. "We wanted to understand what happens to these cells in their native environment when subjected to damage, and if the response was connected to a specific tissue."

By testing perturbations to the epidermis, mammary gland and hair follicles vis--vis mechanical damage or DNA damage through chemotherapeutic agents, the researchers saw a paradoxical response: Stem cells, which otherwise would divide slowly, instead divided rapidly, promoting tissue overgrowth.

When the tissues were subjected to DNA damage, their stem cells overly proliferated, giving rise to different cells than they normally would.

This was a very perplexing result. We were determined to figure out if this was a direct response by the stem cells themselves or by inductive signals within their environment."

Lindsey Seldin, the paper's lead author

The key clue was that stem cells isolated from the body did not behave the same way as in intact tissue--an indication that the response must be provoked from signals being sent to the stem cells from other surrounding cell types.

The investigators turned their attention to fibroblasts, the predominant component of the tissue microenvironment. When fibroblasts in the epidermis were removed, the stem cell responsiveness to DNA damage was diminished, indicating that they played an important role. RNA sequencing revealed that fibroblasts can signal by way of inflammasomes--complexes within cells that help tissues respond to stress by clearing damaged cells or pathogens, which also in this case caused stem cells to divide. "This is an astounding discovery," said Macara. "Inflammasome signaling has previously been attributed only to immune cells, but now it seems that fibroblasts can assume an immune-like nature."

Seldin intends to replicate this work in the mammary gland to determine whether fibroblasts initiate the same innate immune response as in the epidermis, and more broadly how fibroblasts contribute to the development of cancer and other diseases associated with the immune system.

Source:

Journal reference:

Seldin, L & Macara, I (2020) DNA Damage Promotes Epithelial Hyperplasia and Fate Mis-specification via Fibroblast Inflammasome Activation. Developmental Cell. doi.org/10.1016/j.devcel.2020.09.021.

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Researchers report the discovery of innate immune signaling pathway in fibroblasts - News-Medical.net

Cell Biology

Cell Biology Cloud Computing Market with Potential Impact of Coronavirus (COVID19) & Trends That Will Drive Success in 2020 – The Think Curiouser

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Cell Biology Cloud Computing Market with Potential Impact of Coronavirus (COVID19) & Trends That Will Drive Success in 2020 - The Think Curiouser

Cell Biology

Science professor named recipient of NIH New Innovator Award for cancer research – Observer Online

The National Health Institute (NIH) announced in October plans to give out nearly $251 million in grants over five years to 85 different scientists in their High-Risk, High Reward Research Program. Notre Dames Katharine White was on the list.

White is an assistant professor of chemistry and biology at the University of Notre Dame, as well as a 2007 graduate from Saint Marys, whose innovative research caught the attention of the NIH.

She was awarded the Directors New Innovators Award, a prestigious grant with a particular emphasis on supporting young researchers with big ideas.

The award funds exceptionally creative, early career-investigators, so thats people that propose innovative risk but also high reward research, White said. Its research thats innovative, and risky, but has a huge potential impact in human health and improving human health. Broadly, and in this case, improving the treatment of cancer.

Whites research focuses on comparing the relationship of the pH levels within cancer cells to normal cells.

Our research platform in general is at the interface of chemistry and cell biology. We design new chemical tools to manipulate cell biology, White said. Our focus is on understanding how intracellular pH dynamics [regulate] normal cell biology as well as how dysregulated pH dynamics drive diseases like cancer.

Junior Michael Siroky, who has been working in Whites lab since June 2019, said this research has the potential to find new ways to reverse the effects of cancer growth.

Were very interested in how the dysregulation of pH in cancer cells affects a lot of the hallmarks of cancer, like growth and metastasis and different metabolic adaptations, Siroky said. Were primarily focused on how those changes come about and to some extent like how to reverse them.

There are many smaller projects under the umbrella of Whites area of research. Junior Jessamine Kuehn has been a member of Whites lab since spring 2019 and has been working on one of the sub-projects.

My project was working with a particular mutation thats found in 70% of gliomas, Kuehn said. It was a point mutation that changed an arginine, a really basic amino acid, to a histidine, pH near-neutral amino acid, that could actually function as a molecular switch to change, with small changes in the intracellular pH of the cell, the function of the mutated protein.

With the influx of resources the grant will give her lab, White said she will be abled to dive into new avenues and sub-topics of her research. In particular, White said she would be looking into how heterogeneity drives single-cell migration and metastasis events or how the diversity of shape and function of cancer cells impacts their ability to spread in the body.

Furthermore, Siroky said this grant will give the lab the power to increase the specificity of their results and generate new opportunities to share their findings.

Receiving the NIH grant has been an aim for White since its inception. She said she believes her research is unique from other cancer research because it is the intersection between two areas of study applying the usage of chemical tools to gain a better understanding of cellular behavior.

I think one of the key reasons my work is potentially highly innovative [is] because it exists at this interface between chemistry and cell biology, White said.

Kuehn works closely with White as she learns new skills for the projects she takes on in the lab.

I have a lot of one on one [time], like learning procedures with [White]. Its really nice that shes available for that kind of guidance. I really appreciated that, Kuehn said.

Siroky said he is glad to see Whites hard work pay off.

Its pretty gratifying, especially knowing how hard [White] works inside and outside the lab, Siroky said. Shes always fighting for all of these opportunities; its really good to see one of them thats this important pay off because she definitely deserves it to the fullest extent.

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Science professor named recipient of NIH New Innovator Award for cancer research - Observer Online

Cell Biology

The Time-resolved Fluorescence Microscope market to Transcend the Covid-19 Barrier from 2021 onwards – PRnews Leader

Time-resolved Fluorescence Microscope Market: Introduction

Increasing demand for the advanced, efficient, and high-resolution diagnostic tools in the medical and life science industry leads to significant demand for the fluorescence microscopy. Time-resolved fluorescence microscope seems to be a promising diagnostic tool and have rapid and fast analysis ability which can be used in several fields of medical applications. Time-resolved fluorescence microscopes have emerged as the choice of the researcher to analyze biologic systems and cell biology researches. Time-resolved fluorescence microscope is an efficient tool for the analysis of the fluorescence properties of the sample. Time-resolved fluorescence microscope is generally used to measure the fluorescence properties of the sample or molecules. Time-resolved fluorescence microscope is widely used to analyze organic compounds medical laboratories and used for drug screening applications. Time-resolved fluorescence microscopes are gaining demand for map interactions between lipids, proteins, DNA, RNA, enzymes

Time-resolved Fluorescence Microscope Market: Drivers and Restraints

Increasing adoption of the advance and new technologies among researcher has led to the tremendous growth of the time-resolved fluorescence microscope market. Increasing life science-based research to diagnose the various disease are creating significant demand for the time-resolved fluorescence microscope. Advancement of the Time-resolved fluorescence microscope leads to significant demand for the devices among researchers and medical industry manufacturers. The growing number of biopharmaceutical research and drug discovery are the major factor expected to boost up the demand for the time-resolved fluorescence microscope market. Growing demand for time-resolved fluorescence microscope in medical areas such as molecular and cellular biology, proteomics, biochemistry boost up the growth of the time-resolved fluorescence microscope market. However, factors such as the high cost of the devices and less profitability are some of the factors negatively impact the growth of the time-resolved fluorescence microscope market.

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Time-resolved Fluorescence Microscope Market: Segmentation

Tentatively, the global time-resolved fluorescence microscope market can be segmented on the basis of product type, application, end user, and geography.

Based on product type, the global time-resolved fluorescence microscope market is segmented as:

Based on application, the global Time-resolved Fluorescence Microscope market is segmented as:

Based on end users, the global Time-resolved Fluorescence Microscope market is segmented as:

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Time-resolved Fluorescence Microscope Market: Overview

Since few years time-resolved fluorescence lifetime spectrometry technique applications are continuously growing in the pharmaceutical and biotechnology industry as well as in a laboratory. Time-resolved fluorescence microscopes are used for different applications such as forensic, drug discovery, biologics research, cell biology and biomolecules based researches and more. Moreover, Time-resolved fluorescence microscopes have substantial demand in the academic and research institutes as a growing number of researches and study on the diverse biologic particles.

Time-resolved Fluorescence Microscope Market: Regional Outlook

North America expected to dominate the global time-resolved fluorescence microscope market as high demand for technologically advanced tools for the research purpose. Europe expected to register second higher market value share in global time-resolved fluorescence microscope market as increasing number medical research, molecular and drug discovery. Asia Pacific market expected to register higher opportunities for time-resolved fluorescence microscope market players as increasing healthcare and research funding for medical researches. China, India, South Korea are the major countries in the Asia Pacific market which grow at a faster pace in the medical science and research industry. Japan is the established market for the time-resolved fluorescence microscope market players as high adoption of new technologies in clinical laboratories.

Time-resolved Fluorescence Microscope Market: Key Players

Examples of some of the key players operating in the global time-resolved fluorescence microscope market are Agilent Technologies, Inc, PicoQuanT GmbH, Carl Zeiss AG, Danaher Corporation, Olympus Corporation, Edinburgh Instruments Ltd., HORIBA Scientific, Aurora Biomed Inc., Thermo Fisher Scientific, Malvern Panalytical Ltd. and other companies.

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Cell Biology

CIRM Bridges to Stem Cell Research & Therapy The Bridge to Everywhere (in biomedicine) OP-ED – The Silicon Valley Voice

In a recent clinical trial for an immune cell therapy for lymphoma, 62% of patients experienced complete cancer clearance in spite of the fact that some of them were on their 5th line of treatment. Stem cell therapies have the potential to enact more of these paradigm-shifting treatments. Proposition 14 will continue to advance these therapies and bring them to full development as available cures.

The vision of stem cell therapy is that a physician can just as easily grab an IV bag full of therapeutic cells as they might draw a drug into a syringe. Conceived through Proposition 71 in 2004, the California Institute for Regenerative Medicine (CIRM) serves as a vehicle to support all aspects of stem cell research. Medical progress requires not just well-designed clinical studies but also a well-trained workforce, educated at the intersection of stem cell biology, engineering, and chemistry.

Since 2008, CIRM has supported the training of nearly 1300 Community College and California State University students for the emerging field of Regenerative Medicine through the Bridges to Stem Cell Research and Therapy Program. The Bridges Training Program has functioned as a pathway for first-generation and underrepresented students from Humboldt to San Diego, to all of the biomedical sectors startup and cell therapy companies, academic research institutes, graduate and medical school, and more. Exposure to hands-on labs, advanced seminar discussions, and a required paid internship fully prepares these students for entering the stem cell workforce. Over 80% of Bridges alumni have either advanced to graduate school or joined the biomedical workforce in industry or academic institutions. These Programs bring a greater return than the initial cost of training.

SPONSORED

Consider Vahid Hamzeinejad, a bright high school student, headed to UC Berkeley to begin his college career. Enter the Great Recession; Vahid found himself back at home, working non-stop to help keep his parents restaurant afloat. Not giving up on his commitment to an education, he enrolled at the College of the Canyons. After completing an Associates degree, Vahid transferred to Cal Poly, hoping to join the Bridges Program. After receiving the Bridges core training, Vahid started his internship at ViaCyte, where he continues to work today, as a critical member of the team supporting ViaCytes clinical development of a functional cure for diabetes. The nearly $30 billion that California currently spends on diabetes treatments could be significantly reduced, in no small part due to the efforts of a student that cost taxpayers $36,000 to educate. That is before considering the benefit to patients quality of life that would occur by replacing insulin pumps, glucose monitors, and constant vigilance with a stem-cell-derived tissue that regulates blood sugar levels biologically making and secreting its own insulin.

Passing Proposition 14 will enable this and other unparalleled treatments for diabetes, heart disease, cancer, and neurological disorders.

Signed,

Robert Kam and the CIRM Bridges Program

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