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Cell Biology

An ion channel senses cell swelling and helps cells to choose a response – Washington University in St. Louis Newsroom

After a dry spell, a rainy day can feel rejuvenating. But for plants, a downpour can mean trouble. Faced with water suddenly rushing into its tissues, a plant must control its cells volume or risk them exploding.

New research from Washington University in St. Louis offers clues about how mechanosensitive ion channels in the plants cells respond to swelling by inducing cell death potentially to protect the rest of the plant.

The plants response to cell swelling has been studied for a long time and a lot is known about the signaling events. However, the sensor that detects cell swelling in the first place was not known, said Liz Haswell, professor of biology in Arts & Sciences.

The discovery reported by Haswell and Debarati Basu, postdoctoral research scholar in the Haswell lab, in the June 11 issue of Current Biology provides insight into how plants sense and respond to mechanical signals, such as cell swelling, rather than chemicals signals, such as nutrients or growth factors.

Plant cells are armed with a strong yet flexible outer cell wall that holds back the force of water pushing out from inside the cell. Lacking a skeleton, plants only have the force of water and cellulose to keep them upright. Without that force, they go limp. But as the pressure pushing out turgor pressure becomes too great, the cell swells and an imbalance occurs.

It has been documented in plants that cell swelling leads to a release of calcium into the cell cytoplasm and a buildup of reactive oxygen species, unstable molecules containing oxygen that can lead to cell death. As the cell responds to the swelling, specific genes get turned on or off.

But the player that senses cell swelling has been missing.

Sandwiched between the outer cell wall and the internal contents of the cell is the plasma membrane. Embedded in the plasma membrane are mechanosensitive ion channels or tunnels that release ions in a response to membrane stretch. Mechanosensitive ion channel 10 (MSL10) is one member of the family of mechanosensitive ion channels that is a focus of the Haswell lab.

Basu applied a chemical that would cause the cell wall to lose its strength and become soft. At the same time, she could increase the turgor pressure inside the cell and study the role of MSL10 in the initial steps involved in the cell swelling response.

Plant cells, carrying a mutation that made MSL10 overly active, responded to cell swelling similarly to wildtype plants calcium was released, reactive oxygen species made and gene expression changed. However, the response was more pronounced and missing when the plant cells lacked MSL10.

Basu and Haswell discovered that MSL10 is not only an ion transporter but also a primary responder to cell swelling.

MSL10 is an ion channel, so its tempting to think that it itself is transporting calcium. That may not be true, explained Basu. Our results propose the possibility that MSL10 senses the cell swelling and activates a different channel that then transports the calcium.

As the cell swelled, the cell wall failed to maintain the force of the turgor pressure. But it did not explode. Instead, the cell died. But only plants with functional MSL10 died. In plants lacking MSL10, death was avoided.

This might seem counterintuitive, Haswell said. Why is MSL10 required for cells to die youd expect it to save cells lives during swelling, not the other way around. The key is that cells werent dying a normal kind of death, they were undergoing programmed cell death.

Basu found that MSL10 activates programmed cell death a regulatory mechanism that originates from inside of the cell. Cell damage itself did not cause death; MSL10 triggered a program of cell suicide.

Why the plant triggers cell suicide in response to cell swelling is still a mystery. But Basu and Haswell have some intriguing hypotheses.

The plasma membrane has probably been damaged. So maybe the plant wants to recoup some of that material and incorporate it back into the plant through this regulated process, Basu offered.

Or perhaps these damaged cells are more susceptible to infection, and the plant commits cell suicide as a way to save the plant at the sacrifice of a few cells.

We already know that when a pathogen infects a plant, the plant will kill off a bunch of the cells that are infected to prevent the spread of the infection, Haswell said. This idea of cell suicide in response to mechanical stimuli is intriguing.

Original post:
An ion channel senses cell swelling and helps cells to choose a response - Washington University in St. Louis Newsroom

Cell Biology

bluebird bio : Majority of Evaluable Patients Across Genotypes Achieve Transfusion Independence and Maintain It with Near-Normal Hemoglobin Levels in…

89% of evaluable patients (17/19) with transfusion-dependent -thalassemia who do not have a 0/0 genotype achieved transfusion independence with 11.9 g/dL median weighted average total hemoglobin (Hb) level in HGB-207

Data from exploratory analyses of HGB-207 show improved markers of blood cell production and bone marrow function in patients who achieved transfusion independence

85% of patients (11/13) with a 0/0 genotype or IVS-I-110 mutation in HGB-212 have been transfusion-free for at least 7 months

bluebird bio, Inc. (Nasdaq: BLUE) today announced that new data from ongoing Phase 3 studies of betibeglogene autotemcel (beti-cel; formerly LentiGlobin for -thalassemia gene therapy) show pediatric, adolescent and adult patients with a range of genotypes of transfusion-dependent -thalassemia (TDT) achieve and maintain transfusion independence with hemoglobin (Hb) levels that are near-normal (10.5 g/dL). These data are being presented at the Virtual Edition of the 25th European Hematology Association (EHA25) Annual Congress.

With more than a decade of clinical experience evaluating gene therapy in patients with transfusion dependent -thalassemia across a wide range of ages and genotypes, we have built the most comprehensive understanding of treatment outcomes in the field, said David Davidson, M.D., chief medical officer, bluebird bio. Seeing patients achieve transfusion independence and maintain that positive clinical benefit over time with robust hemoglobin levels reflects our initial vision of the potential of beti-cel. The accumulating long-term data demonstrating improvements in bone marrow histology, iron balance and red cell biology support the potential of beti-cel to correct the underlying pathophysiology of transfusion-dependent -thalassemia.

A total of 60 pediatric, adolescent and adult patients across genotypes of TDT have been treated with beti-cel in the Phase 1/2 Northstar (HGB-204) and HGB-205 studies, and the Phase 3 Northstar-2 (HGB-207) and Northstar-3 (HGB-212) studies as of March 3, 2020. In studies of beti-cel, transfusion independence is defined as no longer needing red blood cell transfusions for at least 12 months while maintaining a weighted average Hb of at least 9 g/dL.

TDT is a severe genetic disease caused by mutations in the -globin gene that results in significantly reduced or absent adult hemoglobin (HbA). In order to survive, people with TDT maintain Hb levels through lifelong, chronic blood transfusions. These transfusions carry the risk of progressive multi-organ damage due to unavoidable iron overload.

Patients with transfusion-dependent -thalassemia do not make enough healthy red blood cells and cannot live without chronic transfusions; for patients that means a lifetime of necessary visits to a hospital or clinic and reliance on an often unreliable blood supply, which compounds the challenges of managing this disease, said presenting study author Professor John B. Porter, MA, M.D., FRCP, FRCPath, University College London Hospital, London, UK. These results showing patients free from transfusions and maintaining near-normal hemoglobin levels after treatment with beti-cel is a positive outcome for people living with transfusion-dependent -thalassemia. In addition, we now have more data that provide further evidence that most of these patients have a measurable improvement in markers of healthy red blood cell production.

Beti-cel is a one-time gene therapy designed to address the underlying genetic cause of TDT by adding functional copies of a modified form of the -globin gene (A-T87Q-globin gene) into a patients own hematopoietic (blood) stem cells (HSCs). This means there is no need for donor HSCs from another person, as is required for allogeneic HSC transplantation (allo-HSCT). Once a patient has the A-T87Q-globin gene, they have the potential to produce HbAT87Q, which is gene therapy-derived Hb, at levels that eliminate or significantly reduce the need for transfusions.

Northstar-2 (HGB-207) Efficacy

As of March 3, 2020, all 23 patients in HGB-207 were treated and have been followed for a median of 19.4 months. These patients ranged in age from four to 34 years, including eight pediatric (<12 years of age) and 15 adolescent/adult (>12 years of age) patients. Only 19 patients were evaluable for transfusion independence; four additional patients do not yet have sufficient follow-up to be assessed for transfusion independence.

Eighty-nine percent of evaluable patients (17/19) achieved transfusion independence, with median weighted average total Hb levels of 11.9 g/dL (min-max: 9.4 12.9 g/dL) over a median of 19.4 months of follow-up to date (min-max: 12.3 31.4 months). These 17 patients previously required a median of 17.5 transfusions per year (min-max: 11.5 37 transfusions per year).

Improved iron levels, as measured by serum ferritin and hepcidin levels (proteins involved in iron storage and homeostasis), were observed and trends toward improved iron management were seen. Over half of patients stopped chelation therapy, which is needed to reduce excess iron caused by chronic blood transfusions. Seven out of 23 patients began using phlebotomy for iron reduction.

Analysis of Healthy Red Blood Cell Production

In exploratory analyses, biomarkers of ineffective erythropoiesis (red blood cell production) were evaluated in patients who achieved transfusion independence in HGB-207.

The myeloid to erythroid (M:E) ratio in bone marrow from patients who achieved transfusion independence increased from a median of 1:3 (n=17) at baseline to 1:1.2 (n=16) at Month 12. Improvement of the M:E ratio, the ratio of white blood cell and red blood cell precursors in the bone marrow, suggests an improvement in mature red blood cell production. Images illustrating the bone marrow cellularity at baseline, Month 12 and Month 24 are available in the EHA25 presentation (abstract #S296): Improvement in erythropoiesis in patients with transfusion-dependent -thalassemia following treatment with betibeglogene autotemcel (LentiGlobin for -thalassemia) in the Phase 3 HGB-207 study.

Additionally, biomarkers of erythropoiesis continue to demonstrate a trend toward normalization in patients who achieved transfusion independence, including improved levels over time of erythropoietin, a hormone involved in red blood cell production; reticulocytes, immature red blood cells; and soluble transferrin receptor, a protein measured to help evaluate iron status. The continued normalization of red blood cell production over time among some patients who achieved transfusion independence supports the disease-modifying potential of beti-cel in patients with TDT.

Northstar-3 (HGB-212) Efficacy

As of March 3, 2020, 15 patients (genotypes: 9 0/0, 3 0/ +IVS1-110, 3 homozygous IVS-1-110 mutation) were treated and had a median follow-up of 14.4 months (min-max: 1.124.0 months). Median age at enrollment was 15 (min-max: 4 33 years).

Six of eight evaluable patients achieved transfusion independence, with median weighted average total Hb levels of 11.5 g/dL (min-max: 9.5 13.5 g/dL), and continued to maintain transfusion independence for a median duration of 13.6 months (min-max: 12.2 21.2 months) as of the data cutoff.

Eighty-five percent of patients (11/13) with at least seven months of follow-up had not received a transfusion in more than seven months at time of data cutoff. These 11 patients previously required a median of 18.5 transfusions per year (min-max: 11.0 39.5 transfusions per year). In these patients, gene therapy-derived HbAT87Q supported total Hb levels ranging from 8.814.0 g/dL at last visit.

Betibeglogene autotemcel Safety

Non-serious adverse events (AEs) observed during the HGB-207 and HGB-212 trials that were considered related or possibly related to beti-cel were tachycardia, abdominal pain, pain in extremities, leukopenia, neutropenia and thrombocytopenia. One serious event of thrombocytopenia was considered possibly related to beti-cel.

In HGB-207, serious events post-infusion in two patients included three events of veno-occlusive liver disease and two events of thrombocytopenia. In HGB-212, serious events post-infusion in two patients included two events of pyrexia.

Additional AEs observed in clinical studies were consistent with the known side effects of HSC collection and bone marrow ablation with busulfan, including SAEs of veno-occlusive disease.

In both Phase 3 studies, there have been no deaths, no graft failure, no cases of vector-mediated replication competent lentivirus or clonal dominance, no leukemia and no lymphoma.

The presentations are now available on demand on the EHA25 website:

About betibeglogene autotemcel

The European Commission granted conditional marketing authorization (CMA) for betibeglogene autotemcel (beti-cel; formerly LentiGlobin gene therapy for -thalassemia), marketed as ZYNTEGLO gene therapy, for patients 12 years and older with transfusion-dependent -thalassemia (TDT) who do not have a 0/0 genotype, for whom hematopoietic stem cell (HSC) transplantation is appropriate, but a human leukocyte antigen (HLA)-matched related HSC donor is not available. On April 28, 2020, the European Medicines Agency (EMA) renewed the CMA for ZYNTEGLO, supported by data from 32 patients treated with ZYNTEGLO, including three patients with up to five years of follow-up.

TDT is a severe genetic disease caused by mutations in the -globin gene that result in reduced or significantly reduced hemoglobin (Hb). In order to survive, people with TDT maintain Hb levels through lifelong chronic blood transfusions. These transfusions carry the risk of progressive multi-organ damage due to unavoidable iron overload.

Beti-cel adds functional copies of a modified form of the -globin gene (A-T87Q-globin gene) into a patients own hematopoietic (blood) stem cells (HSCs). Once a patient has the A-T87Q-globin gene, they have the potential to produce HbAT87Q, which is gene therapy-derived hemoglobin, at levels that may eliminate or significantly reduce the need for transfusions.

Non-serious adverse events (AEs) observed during clinical studies that were attributed to beti-cel included abdominal pain, thrombocytopenia, leukopenia, neutropenia, hot flush, dyspnea, pain in extremity and non-cardiac chest pain. Two serious adverse events (SAE) of thrombocytopenia was considered possibly related to beti-cel.

Additional AEs observed in clinical studies were consistent with the known side effects of HSC collection and bone marrow ablation with busulfan, including SAEs of veno-occlusive disease.

The CMA for beti-cel is valid in the 27 member states of the EU as well as UK, Iceland, Liechtenstein and Norway. For details, please see the Summary of Product Characteristics (SmPC).

The U.S. Food and Drug Administration (FDA) granted beti-cel orphan drug designation and Breakthrough Therapy designation for the treatment of transfusion-dependent -thalassemia. Beti-cel is not approved in the U.S.

Beti-cel continues to be evaluated in the ongoing Phase 3 Northstar-2 and Northstar-3 studies. For more information about the ongoing clinical studies, visit http://www.northstarclinicalstudies.com or clinicaltrials.gov and use identifier NCT02906202 for Northstar-2 (HGB-207) and NCT03207009 for Northstar-3 (HGB-212).

bluebird bio is conducting a long-term safety and efficacy follow-up study (LTF-303) for people who have participated in bluebird bio-sponsored clinical studies of betibeglogene autotemcel or LentiGlobin for SCD. For more information visit: https://www.bluebirdbio.com/our-science/clinical-trials or clinicaltrials.gov and use identifier NCT02633943 for LTF-303.

About bluebird bio, Inc.

bluebird bio is pioneering gene therapy with purpose. From our Cambridge, Mass., headquarters, were developing gene therapies for severe genetic diseases and cancer, with the goal that people facing potentially fatal conditions with limited treatment options can live their lives fully. Beyond our labs, were working to positively disrupt the healthcare system to create access, transparency and education so that gene therapy can become available to all those who can benefit.

bluebird bio is a human company powered by human stories. Were putting our care and expertise to work across a spectrum of disorders including cerebral adrenoleukodystrophy, sickle cell disease, -thalassemia and multiple myeloma using three gene therapy technologies: gene addition, cell therapy and (megaTAL-enabled) gene editing.

bluebird bio has additional nests in Seattle, Wash; Durham, N.C.; and Zug, Switzerland. For more information, visit bluebirdbio.com.

Follow bluebird bio on social media: @bluebirdbio, LinkedIn, Instagram and YouTube.

ZYNTEGLO, LentiGlobin, and bluebird bio are trademarks of bluebird bio, Inc.

bluebird bio Forward-Looking Statements

This release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Any forward-looking statements are based on managements current expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by such forward-looking statements. These risks and uncertainties include, but are not limited to: the risk that the COVID-19 pandemic and resulting impact on our operations and healthcare systems will affect the execution of our development plans or the conduct of our clinical studies; the risk that the efficacy and safety results observed in the patients treated in our prior and ongoing clinical trials of beti-cel may not persist; and the risk that the efficacy and safety results from our prior and ongoing clinical trials will not continue or be repeated with additional patients in our ongoing or planned clinical trials or in the commercial context; the risk that the FDA will require additional information regarding beti-cel, resulting in a delay to our anticipated timelines for regulatory submissions, including submission of our BLA. For a discussion of other risks and uncertainties, and other important factors, any of which could cause our actual results to differ from those contained in the forward-looking statements, see the section entitled Risk Factors in our most recent Form 10-Q, as well as discussions of potential risks, uncertainties, and other important factors in our subsequent filings with the Securities and Exchange Commission. All information in this press release is as of the date of the release, and bluebird bio undertakes no duty to update this information unless required by law.

View source version on businesswire.com: https://www.businesswire.com/news/home/20200612005084/en/

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bluebird bio : Majority of Evaluable Patients Across Genotypes Achieve Transfusion Independence and Maintain It with Near-Normal Hemoglobin Levels in...

Cell Biology

Brain Tumor Diagnostics and Therapeutics Market Competitive Environment and Forecast 2017 2025 – 3rd Watch News

Global Brain Tumor Diagnostics and Therapeutics Market: Snapshot

The global market for the diagnostics and therapeutics is gaining traction from a number of factors, such as increasing prevalence of brain cancer, innovations in drug delivery to brain cancer cells, and widespread market for the treatment of brain cancer as well as its associated symptoms. On the other hand, the lack of brain cancer specific drugs, increasing use of generics in chemotherapy, and utterly high cost of brain tumor diagnosis and treatment are a few important challenges faced by the market before attaining its true potential. Nevertheless, in the near future, the vendors of this market are expected to gain new opportunities by improving the technology to reach the cancer tumor at unreachable parts of the brain, although surgery currently remains the most effective mode of treatment.

Based on cancer type, the global brain tumor diagnostics and therapeutics market can be segment into glioma including oligodendroglioma, astrocytoma, choroid plexus papilloma, and ependymoma, medulloblastoma, meningioma, schwannomas, and pituitary adenoma. On the basis of therapeutics, this market can be categorized into brain cancer including radiation therapy, chemotherapy, and targeted therapy. Geographically, the report takes stock of the potential of all important regions such as North America, Asia Pacific, and Europe.

This report on the global brain tumor diagnostics and therapeutics market has been developed by a group of professional market research analysts, with a solitary goal to represent the current scenario as well as the future prospects of the market to the stakeholders connected to the value chain. A number of leading companies operating in this market have also been profiled to highlight the competitive landscape.

Get Sample Copy of the Report @https://www.tmrresearch.com/sample/sample?flag=B&rep_id=1181

Global Brain Tumor Diagnostics and Therapeutics Market: Overview

Increased prevalence of symptoms associated with brain tumor has led to a growing demand for tests detecting the presence of tumors. Some of the common types of tests used for the diagnosis of brain tumor are magnetic resonance imaging (MRI), myelogram, electroencephalography (EEG), tissue sampling or biopsy of surgical removal of a tumor, CT scan, cerebral angiogram or cerebral anteriogram, molecular testing, positron emission tomography (also called PET or PET-CT scan), and neurocognitive assessment.

The growth drivers, opportunities, deterrents, and recent developments in the global market for brain tumor diagnostics and therapeutics have been analyzed in details. The report presents value chain analysis, the supply and demand ratio, market attractiveness, and the past and projected leading market segments. The prominent vendors have been evaluated in depth, considering their market shares, product portfolios, and recent business strategies.

Global Brain Tumor Diagnostics and Therapeutics Market: Drivers and Restraints

Recently, the healthcare sector has been displaying increasing public-private partnerships. These partnerships will prove to be beneficial for the growth of the global brain tumor diagnostics and therapeutics market as they are contributing towards the modernization of radiology and diagnostic imaging services. Research activities in the area of molecular diagnostics aimed at understanding cell biology and recognizing gene mutations related to malignancy are expected to boost growth. Technological advancements, increasing consumer base, advanced healthcare infrastructures, and growing health awareness among people are some of the major growth drivers of the global brain tumor diagnostics and therapeutics market.

On the other hand, the high cost of these tests and lack of trained personnel might restrain the growth of the global brain tumor diagnostics and therapeutics market. Nevertheless, opportunities are likely to materialize from the emergence of new technologies such as chemical exchange saturation transfer (CEST) and sodium magnetic resonance imaging (Na MRI). These technologies not only aid in the diagnosis of tumors, but also in therapies treating them.

Based on types of tumor, the anaplastic astrocytoma, anaplastic oligodendroglioma, low-grade (diffuse) astrocytoma, ependymoma, glioblastoma, and oligodendroglioma can be the major segments.

Read Comprehensive Overview of Report @https://www.tmrresearch.com/brain-tumor-diagnostics-therapeutics-market

Global Brain Tumor Diagnostics and Therapeutics Market: Regional Outlook

Based on region, the global brain tumor diagnostics and therapeutics market can be segmented into the Middle East and Africa, Latin America, North America, Asia Pacific, and Europe. North America, with the U.S at the forefront, is expected to witness significant growth. The increasing demand for brain tumor diagnostics and therapeutics from this region can be attributed to the rising incidence of brain tumors. According to the Central Brain Tumor Registry, the U.S. might witness approximately 79,270 new cases of primary non-malignant and malignant brain and CNS tumors by the end of 2017.

Furthermore, Asia Pacific is slated to expand considerably over the forecast period, as the awareness about the availability and significance of these tests is gradually spreading. The healthcare expenditures and per capita incomes of people in countries across Asia Pacific are also rising, promising further expansion of the brain tumor diagnostics and therapeutics market in the region.

Companies Mentioned in the Report

Some of the major market players operating in the global brain tumor diagnostics and therapeutics market are Philips Healthcare, Roche Diagnostics, GE Healthcare, Toshiba Corporation, Carestream Health, Bristol Myer Squibb, Hitachi, Ltd., and Siemens Healthineers.

About TMR Research:

TMR Research is a premier provider of customized market research and consulting services to business entities keen on succeeding in todays supercharged economic climate. Armed with an experienced, dedicated, and dynamic team of analysts, we are redefining the way our clients conduct business by providing them with authoritative and trusted research studies in tune with the latest methodologies and market trends.

Contact:

TMR Research,3739 Balboa St # 1097,San Francisco, CA 94121United StatesTel: +1-415-520-1050

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Brain Tumor Diagnostics and Therapeutics Market Competitive Environment and Forecast 2017 2025 - 3rd Watch News

Cell Biology

A protein that helps treat viruses can later interfere with lung tissue repair – News-Medical.Net

Jun 12 2020

Researchers at the Francis Crick Institute have found that a protein which is initially helpful in the bodys immune response to a virus, can later interfere with the repair of lung tissue. The work, published in Science, highlights the need for careful consideration regarding the use of this protein to treat viruses, including coronavirus.

Tissue sections of mouse lungs, after infection with influenza. The image on the left is the control and the image on the right is from mice without receptors for interferon lambda. The lungs where interferon lambda signalling is blocked (right) shows improved epithelial cell growth and differentiation (in red).

When a virus infects the lungs, the body attempts to defend itself and fight off the infection. One defensive mechanism is the activation of a protein, called interferon lambda, which signals to surrounding lung tissue cells to switch on anti-viral defenses.

Interferon lambda is currently being investigated in clinical trials as a potential treatment for COVID-19, so understanding the biology underlying its anti-viral effects is important.

The research team investigated the effects of this protein in the lab and found that if it is active for an extended period, it inhibits the repair of the lung tissue. This could prolong lung damage and increase the risk of subsequent bacterial infections.

The Crick scientists observed that in mice with influenza, having increased levels of this protein in their lungs meant that their epithelial cells multiplied less. These cells make up the lining of the airspaces in the lung and need to multiply to replace damaged cells and repair damage. This was the case for mice treated with the protein experimentally and also mice that had produced the protein naturally, as a result of their response to the virus.

Furthermore, cultures of human lung epithelial cells treated with this protein were also less able to grow.

This is a really potent protein with many different functions. At the beginning of a viral infection, it is protective, triggering functions that help to fight the virus. However, if it remains in the tissue for too long, it could become harmful.

This means, for any anti-viral treatment that uses this protein, there is a really careful balance that must be made. Clinicians should consider the timing of the treatment, the earlier this better, and the duration of treatment.

Andreas Wack, Author and group leader of the Immunoregulation lab at the Crick

While this research studied mice infected with influenza, the effects of this protein should be similar for other viruses that also cause lung damage, including coronavirus.

The paper has been published alongside research from Harvard Medical School, which found that severe COVID-19 patients showed strong expression of this protein in their lungs.

Understanding how our bodies respond to infection has never been more important. Differences in our immune responses have huge implications for whether a treatment will work and what the side effects might be.

Our results suggest that before pursuing treatment with interferon lambda, doctors should consider at what stage of the disease patients are, as treatment late in infection may increase the risk of prolonged damage.

Jack Major, Lead author and PhD student in the Immunoregulation lab at the Crick

The Crick researchers will continue to study inflammatory pathways in lung infections, including infection with coronavirus.

Source:

Journal reference:

Major, J., et al. (2020) Type I and III interferons disrupt lung epithelial repair during recovery from viral infection. Science. doi.org/10.1126/science.abc2061.

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A protein that helps treat viruses can later interfere with lung tissue repair - News-Medical.Net

Cell Biology

Neural circuits that control hibernation-like behaviors discovered in mice – News-Medical.Net

Reviewed by Emily Henderson, B.Sc.Jun 11 2020

The dream of suspended animation has long captivated the human imagination, reflected in countless works of mythology and fiction, from King Arthur and Sleeping Beauty to Captain America and Han Solo. By effectively pausing time itself for an individual, a state of stasis promises to enable the repair of lethal injuries, prolong life and allow for travel to distant stars.

While suspended animation may seem a fantasy, a strikingly diverse array of life has already achieved a version of it. Through behaviors like hibernation, animals such as bears, frogs and hummingbirds can survive harsh winters, droughts, food shortages and other extreme conditions by essentially entering into biological stasis, where metabolism, heart rate and breathing slow to a crawl and body temperature drops.

Now, Harvard Medical School neuroscientists have discovered a population of neurons in the hypothalamus that controls hibernation-like behavior, or torpor, in mice, revealing for the first time the neural circuits that regulate this state.

Reporting in Nature on June 11, the team demonstrated that when these neurons are stimulated, mice enter torpor and can be kept in that state for days. When the activity of these neurons is blocked, natural torpor is disrupted.

Another study published simultaneously in Nature by researchers from the University of Tsukuba in Japan also identified a similar population of neurons in the hypothalamus.

By better understanding these processes in mice and other animal models, the authors envision the possibility of one day working toward inducing torpor in humans--an achievement that could have a vast array of applications, such as preventing brain injury during stroke, enabling new treatments for metabolic diseases or even helping NASA send humans to Mars.

The imagination runs wild when we think about the potential of hibernation-like states in humans. Could we really extend lifespan? Is this the way to send people to Mars?"

Sinisa Hrvatin, study co-lead author, instructor in neurobiology in the Blavatnik Institute at HMS

"To answer these questions, we must first study the fundamental biology of torpor and hibernation in animals," Hrvatin said. "We and others are doing this--it is not science fiction."

To reduce energy expenditure in times of scarcity, many animals enter a state of torpor. Hibernation is an extended seasonal form of this. Unlike sleep, torpor is associated with systemic physiological changes, particularly significant drops in body temperature and suppression of metabolic activity. While common in nature, the biological mechanisms that underlie torpor and hibernation are still poorly understood.

The role of the brain, in particular, has remained largely unknown, a question that drove the research efforts of Hrvatin and colleagues, including co-lead author Senmiao Sun, a graduate student in the Harvard Program in Neuroscience, and study senior author Michael Greenberg, the Nathan Marsh Pusey Professor and chair of the Department of Neurobiology in the Blavatnik Institute at HMS.

The researchers studied mice, which do not hibernate but experience bouts of torpor when food is scarce and temperatures are low. When housed at 22 C (72 F), fasting mice exhibited a sharp drop in core body temperature and significant reduction in metabolic rate and movement. In comparison, well-fed mice retained normal body temperatures.

As mice began to enter torpor, the team focused on a gene called Fos--previously shown by the Greenberg lab to be expressed in active neurons. Labeling the protein product of the Fos gene allowed them to identify which neurons are activated during the transition to torpor throughout the entire brain.

This approach revealed widespread neuronal activity, including in brain regions that regulate hunger, feeding, body temperature and many other functions. To see if brain activity was sufficient to trigger torpor, the team combined two techniques--FosTRAP and chemogenetics--to genetically tag neurons that are active during torpor. These neurons could then be re-stimulated later by adding a chemical compound.

The experiments confirmed that torpor could indeed be induced--even in well-fed mice--by re-stimulating neurons in this manner after the mice recovered from their initial bout of inactivity.

However, because the approach labeled neurons throughout the entire brain, the researchers worked to narrow in on the specific area that controls torpor. To do so, they designed a virus-based tool that they used to selectively activate neurons only at the site of injection.

Focusing on the hypothalamus, the region of the brain responsible for regulating body temperature, hunger, thirst, hormone secretion and other functions, the researchers carried out a series of painstaking experiments. They systematically injected 54 animals with minute amounts of the virus covering 226 different regions of the hypothalamus, then activated neurons only in the injected regions and looked for signs of torpor.

Neurons in one specific region of the hypothalamus, known as the avMLPA, triggered torpor when activated. Stimulating neurons in other areas of the hypothalamus had no effect.

"When the initial experiment worked, we knew we had something," Greenberg said. "We gained control over torpor in these mice using FosTRAP, which allowed us to then identify the subset of cells that are involved in the process. It's an elegant demonstration of how Fos can be used to study neuronal activity and behavioral states in the brain."

The team further analyzed the neurons that occupy the region, using single-cell RNA sequencing to look at almost 50,000 individual cells representing 36 different cell types, ultimately pinpointing a subset of torpor-driving neurons, marked by the neurotransmitter transporter gene Vglut2 and the peptide Adcyap1.

Stimulating only these neurons was sufficient to induce rapid drops in body temperature and motor activity, key features of torpor. To confirm that these neurons are critical for torpor, the researchers used a separate virus-based tool to silence the activity of avMLPA-Vglut2 neurons. This prevented fasting mice from entering natural torpor, and in particular disrupted the associated decrease in core body temperature. In contrast, silencing these neurons in well-fed mice had no effect.

"In warm-blooded animals, body temperature is tightly regulated," Sun said. "A drop of a couple of degrees in humans, for example, leads to hypothermia and can be fatal. However, torpor circumvents this regulation and allows body temperatures to fall dramatically. Studying torpor in mice helps us understand how this fascinating feature of warm-blooded animals might be manipulated through neural processes."

The researchers caution that their experiments do not conclusively prove that one specific neuron type controls torpor, a complex behavior that likely involves many different cell types. By identifying the specific brain region and subset of neurons involved in the process, however, scientists now have a point of entry for efforts to better understand and control the state in mice and other animal models, the authors said.

They are now studying the long-term effects of torpor on mice, the roles of other populations of neurons and the underlying mechanisms and pathways that allow avMLPA neurons to regulate torpor.

"Our findings open the door to a new understanding of what torpor and hibernation are, and how they affect cells, the brain and the body," Hrvatin said. "We can now rigorously study how animals enter and exit these states, identify the underlying biology, and think about applications in humans. This study represents one of the key steps of this journey."

The implications of one day being able to induce torpor or hibernation in humans, if ever realized, are profound.

"It's far too soon to say whether we could induce this type of state in a human, but it is a goal that could be worthwhile," Greenberg said. "It could potentially lead to an understanding of suspended animation, metabolic control and possibly extended lifespan. Suspended animation in particular is a common theme in science fiction, and perhaps our ability to traverse the stars will someday depend on it."

Source:

Journal reference:

Hrvatin, S., et al. (2020) Neurons that regulate mouse torpor. Nature. doi.org/10.1038/s41586-020-2387-5.

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Neural circuits that control hibernation-like behaviors discovered in mice - News-Medical.Net

Cell Biology

Magenta Therapeutics Announces Collaboration with the National Marrow Donor Program/Be The Match to Advance Development of MGTA-145 for First-Line…

CAMBRIDGE, Mass. & MINNEAPOLIS--(BUSINESS WIRE)--Magenta Therapeutics (Nasdaq: MGTA) and the National Marrow Donor Program (NMDP)/Be The Match, the global leader in providing a cure to patients with life-threatening blood and marrow cancers like leukemia, lymphoma and other diseases, today announced a clinical collaboration agreement to evaluate the potential utility of MGTA-145, Magentas investigational first-line stem cell mobilization program, for mobilizing and collecting hematopoietic stem cells from donors in a single day and then using them for allogeneic transplants in patients. This life-saving procedure is currently used in approximately 28,000 patients in the U.S. and Europe each year, but approximately 62,000 additional eligible patients do not receive an allogeneic transplant due to challenges, including difficulty with the donation process.

Under the collaboration, Magenta and NMDP/Be The Match will run a Phase 2 clinical trial of MGTA-145 to mobilize and collect hematopoietic stem cells from donors which will then be transplanted into patients with blood cancers in need of a stem cell transplant. The number of stem cells mobilized, engraftment function and benefit to disease will be measured. Magenta will retain all commercial rights to MGTA-145.

MGTA-145, a CXCR2 agonist, works in combination with plerixafor, a CXCR4 antagonist, to harness the physiological mechanism of stem cell mobilization into peripheral blood. MGTA-145 achieved all of the safety and activity endpoints in the recently completed Phase 1 trials in over 100 volunteers. Results showed that MGTA-145, in combination with plerixafor, enabled safe, same-day dosing, mobilization and collection of superior functional hematopoietic stem cells for transplant compared to the current standard of care.

The NMDP/Be The Match is the leading stem cell transplant organization in the United States and facilitates more than 6,500 stem cell transplants per year, through its contracted global network of 187 transplant centers. Through Be The Match BioTherapies, the company also partners with cell and gene therapy companies, including Magenta, to advance the development and delivery of life-saving cell and gene therapies. This most recent collaboration builds on the existing partnership between the two organizations announced in May 2017, which is based on shared missions to ensure more patients receive curative stem cell transplants. This collaboration will combine Magentas leadership in developing medicines for immune system reset with NMDP/Be The Matchs expertise in managing more than 100,000+ stem cell transplants to-date, expansive global networks and the worlds largest and most diverse registry of more than 22 million potential blood stem cell donors.

Magenta is delighted to build upon its successful partnership with NMDP/Be The Match through this clinical collaboration. The NMDP/Be The Match team brings unparalleled experience in stem cell transplant, operating the largest and most diverse marrow registry in the world, with a global network of 187 transplant centers. We are excited to collaborate with them to explore MGTA-145 in allogeneic transplant, which makes up nearly half of the transplants that take place each year in the U.S. and Europe, said John Davis Jr., M.D., M.P.H., M.S., Head of Research & Development and Chief Medical Officer, Magenta. MGTA-145 mobilizes robust numbers of functional stem cells in a single day, allowing donors to potentially avoid multiple visits to infusion centers or hospitals, which has been a major concern for donors during the COVID-19 pandemic. The large number of functional cells may also result in faster recovery and improved outcomes for patients undergoing a life-saving allogeneic transplant.

There is a significant need for new medicines for stem cell mobilization for patients and stem cell donors, and this need is only exacerbated during the COVID-19 pandemic as donors in particular prefer to avoid the hospital setting. Clinical data generated with MGTA-145 to date suggest that its robust mobilization of functional stem cells in a single day could improve both the donor experience and patient outcomes, said Steven Devine, M.D., Chief Medical Officer, NMDP/Be The Match. We are pleased to partner with Magenta to further transform the practice of stem cell transplant. We look forward to initiating this Phase 2 study.

About Magenta Therapeutics

Magenta Therapeutics is a clinical-stage biotechnology company developing medicines to bring the curative power of immune system reset through stem cell transplant to more patients with autoimmune diseases, genetic diseases and blood cancers. Magenta is combining leadership in stem cell biology and biotherapeutics development with clinical and regulatory expertise, a unique business model and broad networks in the stem cell transplant world to revolutionize immune reset for more patients. Magenta is based in Cambridge, Mass. For more information, please visit http://www.magentatx.com. Follow Magenta on Twitter: @magentatx.

About the National Marrow Donor Program/Be The Match

We save lives through cellular therapy. As the global leader in providing a cure to patients with life-threatening blood and marrow cancers like leukemia, lymphoma and other diseases, we manage the worlds largest registry of potential blood stem cell donors and cord blood units. We work with a global network to connect patients to their donor match for a life-saving transplant. Through Be The Match BioTherapies, we partner with cell and gene therapy companies to support the development and delivery of new therapies. And, we conduct research through our research program, CIBMTR (Center for International Blood and Marrow Transplant Research), in collaboration with Medical College of Wisconsin. The NMDP/Be The Match is an investor in Magenta Therapeutics.

Magenta Therapeutics Forward-Looking Statements

This press release may contain forward-looking statements and information within the meaning of The Private Securities Litigation Reform Act of 1995 and other federal securities laws, including, without limitation, statements regarding the clinical collaboration agreement between Magenta and NMDP/Be The Match, including the timing, progress and success of the collaboration contemplated under the agreement, the commercial terms under the agreement, and Magentas strategy and business plan. The use of words such as may, will, could, should, expects, intends, plans, anticipates, believes, estimates, predicts, projects, seeks, endeavor, potential, continue or the negative of such words or other similar expressions can be used to identify forward-looking statements. The express or implied forward-looking statements included in this press release are only predictions and are subject to a number of risks, uncertainties and assumptions, including, without limitation, risks set forth under the caption Risk Factors in Magentas most recent Annual Report on Form 10-K filed on March 3, 2020, as updated by Magentas most recent Quarterly Report on Form 10-Q and its other filings with the Securities and Exchange Commission, as well as risks, uncertainties and assumptions regarding the impact of the COVID-19 pandemic to Magentas business, operations, strategy, goals and anticipated timelines, including, without limitation, Magentas ongoing and planned preclinical activities, ability to initiate, enroll, conduct or complete ongoing and planned clinical trials and timelines for regulatory submissions. In light of these risks, uncertainties and assumptions, the forward-looking events and circumstances discussed in this press release may not occur and actual results could differ materially and adversely from those anticipated or implied in the forward-looking statements. You should not rely upon forward-looking statements as predictions of future events. Although Magenta believes that the expectations reflected in the forward-looking statements are reasonable, it cannot guarantee that the future results, levels of activity, performance or events and circumstances reflected in the forward-looking statements will be achieved or occur. Moreover, except as required by law, neither Magenta nor any other person assumes responsibility for the accuracy and completeness of the forward-looking statements included in this press release. Any forward-looking statement included in this press release speaks only as of the date on which it was made. We undertake no obligation to publicly update or revise any forward-looking statement, whether as a result of new information, future events or otherwise, except as required by law.

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Magenta Therapeutics Announces Collaboration with the National Marrow Donor Program/Be The Match to Advance Development of MGTA-145 for First-Line...

Cell Biology

IIT-M researchers identify role of microRNA in tongue cancer – Zee News

Chennai: Indian Institute of Technology Madras (IIT-M) on Monday said its researchers have identified a specific microRNA (miRNAs) called `miR-155 that is over-expressed in tongue cancer.

According to the researchers, miRNAs affect cancer growth by inhibiting or enhancing the functions of certain proteins. For example, it has been seen that a type of protein called `programmed cell death 4` --pdcd4-- helps in stopping cancer cells from growing and spreading.

Inhibition of this protein has been known to cause the spread of oral, lung, breast, liver, brain and colon cancers.

For the current study, IIT Madras collaborated with researchers from Cancer Institute and Sree Balaji Dental College and Hospital at Chennai and Indian Institute of Science at Bengaluru.

"MicroRNAs (miRNAs) are short non-coding RNAs containing 20?24 nucleotides that participate in virtually all biological pathways in animals," study lead researcher Devarajan Karunagaran, Head, Department of Biotechnology, IIT Madras, said in a statement.

"They have been found to play important roles in many cancers, in carcinogenesis (start of cancer), malignant transformation and metastasis - the development of secondary cancer. The miRNAs associated with cancer are called `Oncomirs`," Karunagaran added.

According to the researchers, many of the oncomirs affect cancer by suppressing the performance of tumour suppressing agents that can prevent growth and spread of cancer cells, although some oncomirs are also involved in preventing tumour growth itself.

It is therefore important to identify the types of miRNAs that are associated with both suppression and proliferation of cancer cells.

For the findings, published in the peer-reviewed journal Molecular and Cellular biology, the research team went beyond showing the connection between miR-155 and pdcd4.

They have also shown that knocking out miR-155 causes death of cancer cells, arrests the cell cycle, and regresses tumour size in animal models and reduces cell viability and colony formation in benchtop assays.

"While it has been long suspected that miR-155 downregulates Pdcd4, there have, hitherto, been no evidence for such interaction," said study researcher Shabir Zargar.

The research team has shown beyond doubt that miR-155 is overexpressed in tongue cancer cells and tongue tumour tissues.

This `overactivity` of miR-155 hinders the action of pdcd4, which in turn causes spread and growth of cancer of the tongue.

"Our study has shown that the restoration of Pdcd4 levels through molecular manipulation of miR-155 can lead to potential therapeutic developments for cancers, especially of tongue cancer," Karunagaran added.

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IIT-M researchers identify role of microRNA in tongue cancer - Zee News

Cell Biology

Neuroscientists Discover Neural Circuits That Control Hibernation-Like Behaviors in Mice – Newswise

At a glance:

Newswise The dream of suspended animation has long captivated the human imagination, reflected in countless works of mythology and fiction, from King Arthur and Sleeping Beauty to Captain America and Han Solo. By effectively pausing time itself for an individual, a state of stasis promises to enable the repair of lethal injuries, prolong life and allow for travel to distant stars.

While suspended animation may seem a fantasy, a strikingly diverse array of life has already achieved a version of it. Through behaviors like hibernation, animals such as bears, frogs and hummingbirds can survive harsh winters, droughts, food shortages and other extreme conditions by essentially entering into biological stasis, where metabolism, heart rate and breathing slow to a crawl and body temperature drops.

Now, Harvard Medical School neuroscientists have discovered a population of neurons in the hypothalamus that controls hibernation-like behavior, or torpor, in mice, revealing for the first time the neural circuits that regulate this state.

Reporting in Nature on June 11, the team demonstrated that when these neurons are stimulated, mice enter torpor and can be kept in that state for days. When the activity of these neurons is blocked, natural torpor is disrupted.

Another study published simultaneously in Nature by researchers from the University of Tsukuba in Japan also identified a similar population of neurons in the hypothalamus.

By better understanding these processes in mice and other animal models, the authors envision the possibility of one day working toward inducing torpor in humansan achievement that could have a vast array of applications, such as preventing brain injury during stroke, enabling new treatments for metabolic diseases or even helping NASA send humans to Mars.

The imagination runs wild when we think about the potential of hibernation-like states in humans. Could we really extend lifespan? Is this the way to send people to Mars? said study co-lead author Sinisa Hrvatin, instructor in neurobiology in the Blavatnik Institute at HMS.

To answer these questions, we must first study the fundamental biology of torpor and hibernation in animals, Hrvatin said. We and others are doing thisit is not science fiction.

To reduce energy expenditure in times of scarcity, many animals enter a state of torpor. Hibernation is an extended seasonal form of this. Unlike sleep, torpor is associated with systemic physiological changes, particularly significant drops in body temperature and suppression of metabolic activity. While common in nature, the biological mechanisms that underlie torpor and hibernation are still poorly understood.

The role of the brain, in particular, has remained largely unknown, a question that drove the research efforts of Hrvatin and colleagues, including co-lead author Senmiao Sun, a graduate student in the Harvard Program in Neuroscience, and study senior author Michael Greenberg, the Nathan Marsh Pusey Professor and chair of the Department of Neurobiology in the Blavatnik Institute at HMS.

Neural TRAP

The researchers studied mice, which do not hibernate but experience bouts of torpor when food is scarce and temperatures are low. When housed at 22 C (72 F), fasting mice exhibited a sharp drop in core body temperature and significant reduction in metabolic rate and movement. In comparison, well-fed mice retained normal body temperatures.

As mice began to enter torpor, the team focused on a gene called Fospreviously shown by the Greenberg lab to be expressed in active neurons. Labeling the protein product of the Fos gene allowed them to identify which neurons are activated during the transition to torpor throughout the entire brain.

This approach revealed widespread neuronal activity, including in brain regions that regulate hunger, feeding, body temperature and many other functions. To see if brain activity was sufficient to trigger torpor, the team combined two techniquesFosTRAP and chemogeneticsto genetically tag neurons that are active during torpor. These neurons could then be re-stimulated later by adding a chemical compound.

The experiments confirmed that torpor could indeed be inducedeven in well-fed miceby re-stimulating neurons in this manner after the mice recovered from their initial bout of inactivity.

However, because the approach labeled neurons throughout the entire brain, the researchers worked to narrow in on the specific area that controls torpor. To do so, they designed a virus-based tool that they used to selectively activate neurons only at the site of injection.

Focusing on the hypothalamus, the region of the brain responsible for regulating body temperature, hunger, thirst, hormone secretion and other functions, the researchers carried out a series of painstaking experiments. They systematically injected 54 animals with minute amounts of the virus covering 226 different regions of the hypothalamus, then activated neurons only in the injected regions and looked for signs of torpor.

Neurons in one specific region of the hypothalamus, known as the avMLPA, triggered torpor when activated. Stimulating neurons in other areas of the hypothalamus had no effect.

When the initial experiment worked, we knew we had something, Greenberg said. We gained control over torpor in these mice using FosTRAP, which allowed us to then identify the subset of cells that are involved in the process. Its an elegant demonstration of how Fos can be used to study neuronal activity and behavioral states in the brain.

Worthwhile goal

The team further analyzed the neurons that occupy the region, using single-cell RNA sequencing to look at almost 50,000 individual cells representing 36 different cell types, ultimately pinpointing a subset of torpor-driving neurons, marked by the neurotransmitter transporter gene Vglut2 and the peptide Adcyap1.

Stimulating only these neurons was sufficient to induce rapid drops in body temperature and motor activity, key features of torpor. To confirm that these neurons are critical for torpor, the researchers used a separate virus-based tool to silence the activity of avMLPA-Vglut2 neurons. This prevented fasting mice from entering natural torpor, and in particular disrupted the associated decrease in core body temperature. In contrast, silencing these neurons in well-fed mice had no effect.

In warm-blooded animals, body temperature is tightly regulated, Sun said. A drop of a couple of degrees in humans, for example, leads to hypothermia and can be fatal. However, torpor circumvents this regulation and allows body temperatures to fall dramatically. Studying torpor in mice helps us understand how this fascinating feature of warm-blooded animals might be manipulated through neural processes.

The researchers caution that their experiments do not conclusively prove that one specific neuron type controls torpor, a complex behavior that likely involves many different cell types. By identifying the specific brain region and subset of neurons involved in the process, however, scientists now have a point of entry for efforts to better understand and control the state in mice and other animal models, the authors said.

They are now studying the long-term effects of torpor on mice, the roles of other populations of neurons and the underlying mechanisms and pathways that allow avMLPA neurons to regulate torpor.

Our findings open the door to a new understanding of what torpor and hibernation are, and how they affect cells, the brain and the body, Hrvatin said. We can now rigorously study how animals enter and exit these states, identify the underlying biology, and think about applications in humans. This study represents one of the key steps of this journey.

The implications of one day being able to induce torpor or hibernation in humans, if ever realized, are profound.

Its far too soon to say whether we could induce this type of state in a human, but it is a goal that could be worthwhile, Greenberg said. It could potentially lead to an understanding of suspended animation, metabolic control and possibly extended lifespan. Suspended animation in particular is a common theme in science fiction, and perhaps our ability to traverse the stars will someday depend on it.

Additional authors include Oren Wilcox, Hanqi Yao, Aurora Lavin-Peter, Marcelo Cicconet, Elena Assad, Michaela Palmer, Sage Aronson, Alexander Banks and Eric Griffith.

The study was supported by the National Institutes of Health (R01 NS028829, R01 MH114081, R01 DK107717) and a Warren Alpert Distinguished Scholar Award.

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Neuroscientists Discover Neural Circuits That Control Hibernation-Like Behaviors in Mice - Newswise

Embryology

The NHS worker from Croydon who needs to find 40k to take up her place at Oxford University – MyLondon

Being accepted to Oxford was a life changing moment for this 22-year-old from Thornton Heath.

But if Leighann Nesbeth, an NHS admin worker, cant raise the 40,000 needed to pay for the fees, her dream may not become a reality.

Inspired by her work in the gynocology oncology department at Guys Hospital, she hopes taking a masters in Clinical Embryology at Oxford will set her on a path where she can help women struggling to get pregnant.

She said: I find with a lot of patients with ovarian cancer their fertility is affected, and going to an assisted fertility unit is the first point of contact before they have cancer treatment so they can preserve their fertility.

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I found I was really interested in that and I was looking for a positive way to impact the lives of women so fertility is definitely my calling.

Leighann was determined to pursue a career in clinical medicine from a young age despite being told by a teacher to aim lower.

Her sights remained high even after being rejected from medical school multiple times.

Instead she chose to study for a degree in Medical Physiology in Nottingham where she graduated with first class honours.

She explained that accepted to Oxford has boosted her confidence in what shes capable of, but the huge fees nearly stopped her from applying at all.

She said: When I did my research and I found out it was 40,000 I honestly wasnt even going to apply. I thought theres no way I could afford it. I spoke to my mum and dad about it and we thought it was just impossible.

It was only an encouraging message on the day of the deadline that prompted Leighann to submit her application.

There are some scholarships available, she said, but she wont know if she has been granted any until just two weeks before the day her fees need to be paid at the end of June.

In terms of the money, it does make me feel very disheartened, she said.

Its just such a huge barrier. If the only thing thats stopping me is the finance it seems like Ive come so far to just not be able to get it.

Leighann has raised just over 6,000 towards her target on her Go Fund Me page. You can help get her Oxford by donating here.

Do you have a story you think MyLondon should cover? If so, email danielle.manning@reachplc.com.

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The NHS worker from Croydon who needs to find 40k to take up her place at Oxford University - MyLondon

Embryology

Merck Foundation Together With 18 African First Ladies Respond to the Coronavirus Pandemic in Four Main Areas – Devdiscourse

Mumbai, Maharashtra, India & Monrovia, Liberia Business Wire India Merck Foundation, the philanthropic arm of Merck KGaA Germany has raced to respond to the Coronavirus pandemic in partnership with 18 African First Ladies, Ministries of Health, Information and Education focusing on four main areas: 1. Community Support: Merck Foundation partners with African First Ladies to support livelihood of thousands of women and casual workers affected by Coronavirus lockdown. 2. Healthcare Capacity Building: Merck Foundation started Coronavirus healthcare capacity building by providing online one-year diplomas and two-year masters degree in Respiratory Medicines and Acute Medicines for African Doctors 3. Community Awareness through media Awards: Merck Foundation announced, Stay at Home Media Recognition Awards in Africa, Middle East, Asia & Latin America to raise awareness about Coronavirus.

4. Community awareness for Children and Youth: Merck Foundation launched an inspiring storybook Making the Right Choice in partnership with African First Ladies to sensitize children and youth about Coronavirus Merck Foundation has partnered with the African First Ladies of Liberia, Ghana, DR Congo, Zimbabwe, Niger, Sierra Leone, Malawi and Burkina Faso to support livelihood of thousands of women and families of casual and daily workers who are most affected by the Coronavirus (COVID -19) lockdown. The relief contribution was also undertaken in Egypt with the aim to support 500 families. Dr. Rasha Kelej, CEO of Merck Foundation explained, Lockdown imposed in most countries has hit the daily workers and women the most, making it very difficult for them to survive. Therefore, Merck Foundation decided to partner with the African First Ladies to support up to 1000 women and casual workers families in each country, with the aim to save their livelihood as part of Separated but Connected Merck Foundation Initiative. Speaking of women being impacted by the lockdown, Dr. Rasha Kelej explained, I am sad to know that the pandemic has led to a horrifying increase in violence against women. The confinement at home with an abusive partner has resulted in not only physical violence but also emotional violence against women which can have disastrous consequences for their health and well-being. Therefore, we decided to focus on supporting women in our coronavirus community intervention and strongly continue empowering infertile and childless women as part of our signature campaign Merck More than a Mother. We know they now need our support more than ever. We strongly believe that building professional healthcare capacity is the right strategy to improve access to quality and equitable healthcare specially during this vicious pandemic, Dr. Kelej added.

Therefore, Merck Foundation will strongly continue their current capacity advancement programs and will specially focus on building Coronavirus healthcare capacity through providing African and Asian medical postgraduates with one-year online diploma and two-year online Master degree in both of Respiratory Medicines and Acute Medicines at one of the UK Universities. This program is in partnership with African First Ladies, Ministers of Health and Academia across the two continents. As part of their strategy of responding to coronavirus lockdown, Merck Foundation scaled up to more African and Asian medical postgraduates to provide online medical specialization scholarships.

During this lockdown, Merck Foundation will focus more on these online scholarships which will be for one-year diploma and two year master degree in several specialties such as: Diabetes, Cardiovascular Preventive Medicines, Endocrinology and Sexual and Reproductive Medicines. To apply for these scholarships, please email us on: submit@merck-foundation.com Merck Foundation has also launched Stay at Home Media Recognition Awards in partnership with African First Ladies of Ghana, Nigeria, Democratic Republic of Congo (DRC), Malawi, Namibia, Niger, Guinea Conakry, Burundi, Central African Republic (C.A.R.), Chad, Zimbabwe, Zambia, The Gambia, Liberia and Congo Brazzaville, Angola, Mali, Mozambique for English, French, Portuguese and Arabic Speaking African countries. The awards have been also announced for Middle Eastern, Asian countries and in Spanish for Latin American Countries. The theme of the awards is Raising Awareness on how to Stay Safe and Keep Physically and Mentally Healthy during Coronavirus Lockdown with the aim to separate facts from myths and misconceptions to apply for these awards email: submit@merck-foundation.com Dr. Rasha Kelej emphasized, We strongly believe that media plays a critical role in raising awareness about sensitive and pressing issues such as Coronavirus. I am looking forward to receive the creative and informative work of our winners so that they become Merck Foundation health champions in their countries. Merck Foundation has also launched an inspiring storybook called Making the Right Choice in partnership with 18 African First Ladies. The story aims to raise awareness about coronavirus prevention amongst children and youth as it provides facts about the pandemic and how to stay safe and healthy during the outbreak. It also promotes honesty, hard-work and the ability to make the right choices even during the most challenging times. The story released in three languages: English, French and Portuguese. To read the storybook please click on below links: English: https://www.merck-foundation.com/servlet/servlet.FileDownload?retURL=%2Fapex%2FMF_MainPage%3FstartURL%3D%252FNews-Article%252FMerck-Foundation-together-with-African-First-Ladies-continue-their-strategy-to-provide-specialty-training-for-African-doctors-to-better-manage-Diabetes-and-Hypertension-patients-who-are-Coronavirus-risk-groups.&file=00P1r00002YfRDrEAN French: https://www.merck-foundation.com/servlet/servlet.FileDownload?retURL=%2Fapex%2FMF_MainPage%3FstartURL%3D%252FNews-Article%252FMerck-Foundation-together-with-African-First-Ladies-continue-their-strategy-to-provide-specialty-training-for-African-doctors-to-better-manage-Diabetes-and-Hypertension-patients-who-are-Coronavirus-risk-groups.&file=00P1r00002YfzaGEAR Portuguese: https://www.merck-foundation.com/servlet/servlet.FileDownload?retURL=%2Fapex%2FMF_MainPage%3FstartURL%3D%252FNews-Article%252FMerck-Foundation-together-with-African-First-Ladies-continue-their-strategy-to-provide-specialty-training-for-African-doctors-to-better-manage-Diabetes-and-Hypertension-patients-who-are-Coronavirus-risk-groups.&file=00P1r00002YfzeUEAR About Merck Oncology Fellowship and Master Degree Program A part of Merck Cancer Access, the program focuses on building professional cancer care capacity with the aim to increase the limited number of Oncologists in Africa. Oncology Fellowship Program of one year, one and half years, two years in India, Malaysia, Kenya and Master Degree in Medical Oncology for three years in Egypt in partnership with African Ministries of Health, Local Governments and Academia.

Launched in 2016, over 80 candidates from more than 26 African countries have been enrolled in the Merck Oncology Fellowship Program. The program will continue to build cancer care capability in African countries such as Botswana, Burundi, Cameroon, CAR, Chad, Congo Brazzaville, DRC, Ethiopia, Gabon, The Gambia, Ghana, Guinea, Kenya, Liberia, Mauritius, Namibia, Niger, Nigeria, Rwanda, Senegal, Sierra Leone, South Africa, Tanzania, Uganda, Zambia & Zimbabwe. About Merck Fertility & Embryology Training Program Merck Fertility & Embryology Training Program was launched in 2016 as part of Merck More Than a Mother. Under this program, Merck Foundation has been providing hands-on practical training to candidates from Africa and Asia, in partnership with the Indonesian Reproductive Science Institute (IRSI), Indonesia; International Institute for Training and Research in Reproductive Health (IIRRH), India; Manipal Academy of Higher Education (MAHE), India and Indira IVF Hospitals, India.

Through this program, Merck Foundation is making history in many African and Asian countries where they never had fertility specialists or specialized fertility clinics before Merck More Than a Mother intervention, to train the first fertility specialists such as; in Sierra Leone, Liberia, The Gambia, Niger, Chad, Guinea, Ethiopia, Myanmar and Uganda. So far, Merck Foundation has provided for more than 180+ candidates, clinical and practical training for fertility specialists and embryologists in more than 35 countries across Africa and Asia such as: Bangladesh, Benin, Burkina Faso, Burundi, Cameroon, Chad, CAR, Cote D'IVOIRE, DRC, Congo Brazzaville, Ethiopia, Ghana, Guinea, Kenya, Malaysia, Liberia, Mali, Myanmar, Namibia, Nepal, Nigeria, Niger, Philippines, Russia, Rwanda, Senegal, Sierra Leone, Sri Lanka, The Gambia, Togo, Tanzania, Uganda, Zambia & Zimbabwe. About Merck Diabetes Blue Points Project Merck Diabetes Blue Points Project in partnership with African First Ladies, Ministries of Health and Academia to help improve access to equitable and quality diabetes care nationwide in African countries. Candidates from different provinces, countries or districts of the respective countries are provided with one-year Online Postgraduate Diabetes Diploma in English for English Speaking countries, or an Online Master course on Clinical Management of Diabetes in French and Portuguese for 3 months duration, for French and Portuguese speaking countries respectively, ensuring geographical coverage of the whole country to help improve the landscape of diabetes care in Africa.

Download the Merck Foundation App now Google Play - https://play.google.com/store/apps/details?id=de.merck.foundation.googleplay App Store - https://apps.apple.com/no/app/merck-foundation/id1297299793 Join the conversation on our social media platforms below and let your voice be heard Facebook: Merck Foundation Twitter: @Merckfoundation YouTube: MerckFoundation Instagram: Merck Foundation Flickr: Merck Foundation Website: http://www.merck-foundation.com About Merck Foundation The Merck Foundation, established in 2017, is the philanthropic arm of Merck KGaA Germany, aims to improve the health and wellbeing of people and advance their lives through science and technology. Our efforts are primarily focused on improving access to quality & equitable healthcare solutions in underserved communities, building healthcare and scientific research capacity and empowering people in STEM (Science, Technology, Engineering, and Mathematics) with a special focus on women and youth. All Merck Foundation press releases are distributed by e-mail at the same time they become available on the Merck Foundation Website. Please visit http://www.merck-foundation.com to read more. To know more, reach out to our social media: Merck Foundation; Facebook, Twitter, Instagram, YouTube and Flicker. To View the Image Click on the Link Below: Dr. Rasha Kelej, CEO of Merck Foundation with H.E. DJN COND, The First Lady of Guinea; H.E. FATIMA MAADA BIO; The First Lady of Sierra Leone; H.E. Prof. GERTRUDE MUTHARIKA, The First Lady of Malawi; H.E. FATOUMATTA BAH-BARROW, The First Lady of The Gambia; H.E. DENISE NKURUNZIZA, The First Lady of Burundi; H.E. ASSATA ISSOUFOU MAHAMADOU, The First Lady of Niger; H.E. BRIGITTE TOUADERA, The First Lady of Central African Republic; H.E. REBECCA AKUFO-ADDO, The First Lady of Ghana; H.E. CLAR MARIE WEAH, The First Lady of Liberia; H.E. ANTOINETTE SASSOU-NGUESSO, The First Lady of Congo Brazzaville; H.E. MONICA GEINGOS, The First Lady of Namibia; H.E. AUXILLIA MNANGAGWA, The First Lady of Zimbabwe; H.E. NEO JANE MASISI, The First Lady of Botswana; H.E. Dr. ISAURA FERRO NYUSI, The First Lady of Mozambique and Former First Lady of Mauritania PWR PWR.

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Merck Foundation Together With 18 African First Ladies Respond to the Coronavirus Pandemic in Four Main Areas - Devdiscourse