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Researchers at the University of Maryland have identified how the pathogenic bacterium Pseudomonas aeruginosa uses tension-activated membrane channels to stop itself from swelling up and bursting when it is suddenly exposed to water. The study, which will be published April 19 in The Journal of General Physiology, helps explain how this bacterium—a major cause of hospital-acquired infections—persists in a variety of different environments.

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Researchers in France have developed a new method that will allow doctors to detect minute amounts of a protein called interferon- in patient samples. The technique, which is described in the study “Detection of interferon- protein reveals differential levels and cellular sources in disease” published April 18 in The Journal of Experimental Medicine, will aid the diagnosis and treatment of numerous autoimmune diseases, including systemic lupus erythematosus (SLE) and dermatomyositis.

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Researchers from Harvard Medical School have discovered that the body’s immune system initially detects the presence of anthrax spores by recognizing RNA molecules that coat the spores’ surface. But this prompts an unfavorable immune response that hinders the body’s fight against anthrax once the spores have germinated into live bacteria, according to the study “TLR sensing of bacterial spore-associated RNA triggers host immune responses with detrimental effects,” which will be published April 11 in The Journal of Experimental Medicine.

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Researchers in Germany have developed a transgenic mouse that could help scientists identify new influenza virus strains with the potential to cause a global pandemic. The mouse is described in a study, “In vivo evasion of MxA by avian influenza viruses requires human signature in the viral nucleoprotein,” that will be published April 10 in The Journal of Experimental Medicine.

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Researchers at Bascom Palmer Eye Institute, part of the University of Miami Miller School of Medicine, have identified a new molecule that induces the formation of abnormal blood vessels in the eyes of diabetic mice. The study, “Secretogranin III as a disease-associated ligand for antiangiogenic therapy of diabetic retinopathy,” which will be published March 22 in The Journal of Experimental Medicine, suggests that inhibiting this molecule may prevent similarly aberrant blood vessels from damaging the vision of not only diabetics, but also premature infants.

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Researchers in China have discovered that a metabolic enzyme called AKR1B1 drives an aggressive type of breast cancer. The study, “AKR1B1 promotes basal-like breast cancer progression by a positive feedback loop that activates the EMT program,” which has been published in The Journal of Experimental Medicine, suggests that an inhibitor of this enzyme currently used to treat diabetes patients could be an effective therapy for this frequently deadly form of cancer.

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Researchers in Germany have discovered that a tumor suppressor protein thought to prevent acute myeloid leukemia (AML) can actually promote a particularly deadly form of the disease. The study, “RUNX1 cooperates with FLT3-ITD to induce leukemia,” which will be published online February 17 in The Journal of Experimental Medicine, suggests that targeting this protein could be an effective treatment for certain AML patients.

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Researchers at Cold Spring Harbor Laboratory in New York have discovered that a protein called Importin-11 protects the anti-cancer protein PTEN from destruction by transporting it into the cell nucleus. The study, “The nuclear transport receptor Importin-11 is a tumor suppressor that maintains PTEN protein,” which will be published online February 13 in The Journal of Cell Biology, suggests that the loss of Importin-11 may destabilize PTEN, leading to the development of lung, prostate, and other cancers.

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Boston Children’s Hospital researchers have uncovered a new molecular pathway that inhibits the myelination of neurons in the brains of patients with the rare genetic disorder tuberous sclerosis complex (TSC). The study, “Neuronal CTGF/CCN2 negatively regulates myelination in a mouse model of tuberous sclerosis complex,” which will be published online February 9 in The Journal of Experimental Medicine, suggests new ways to treat some of the neurological symptoms associated with TSC, including autism and epilepsy.

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Researchers from the Chinese Academy of Sciences have discovered that the metabolic enzyme phosphoglycerate mutase 1 (PGAM1) helps cancer cells repair their DNA and found that inhibiting PGAM1 sensitizes tumors to the cancer drug Olaparib (Lynparza). Their findings in the study “Phosphoglycerate mutase 1 regulates dNTP pool and promotes homologous recombination repair in cancer cells,” which has been published in The Journal of Cell Biology, suggest that this FDA-approved ovarian cancer medicine has the potential to treat a wider range of cancer types than currently indicated.

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Defects in the body’s regulatory T cells cause inflammation and autoimmune disease by altering the type of bacteria living in the gut, researchers from the University of Texas Health Science Center at Houston have discovered. The study, which will be published online December 19 in The Journal of Experimental Medicine, suggests that replacing the missing gut bacteria, or restoring a key metabolite called inosine, could help treat children with a rare and often fatal autoimmune disease called IPEX syndrome.

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Researchers have discovered that mice with Huntington’s disease (HD) suffer defects in muscle maturation that may explain some symptoms of the disorder. The study, “Progressive Cl− channel defects reveal disrupted skeletal muscle maturation in R6/2 Huntington’s mice,” which will be published online November 29 in The Journal of General Physiology, suggests that HD is a disease of muscle tissue as well as a neurodegenerative disorder and that therapies targeting skeletal muscle may improve patients’ motor function.

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Conventional, high-dose chemotherapy treatments can cause the fibroblast cells surrounding tumors to secrete proteins that promote the tumors’ recurrence in more aggressive forms, researchers have discovered. Frequent, low-dose chemotherapy regimens avoid this effect and may therefore be more effective at treating certain types of breast and pancreatic cancer, according to the murine study “Metronomic chemotherapy prevents therapy-induced stromal activation and induction of tumor-initiating cells,” which will be published online November 23 in The Journal of Experimental Medicine.

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Researchers from the University of Toronto have discovered that mice infected with the common gut parasite Tritrichomonas muris are at an increased risk of developing inflammatory colitis. Their findings, which have been published online in The Journal of Experimental Medicine, expand the type of gut-resident microorganism that can affect the health of their host and suggest that related parasites may cause gastrointestinal disease in humans.

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Researchers at Stanford University School of Medicine have identified several new biological markers to measure the progression of the inherited neurodegenerative disorder Huntington’s disease. Their findings, which will be published online November 7 ahead of issue in The Journal of Experimental Medicine, could benefit clinical trials that test new treatments for the disease.

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Researchers in Japan have discovered that the adrenergic nervous system controls when white blood cells circulate through the body, boosting the immune response by retaining T and B cells in lymph nodes at the time of day when they are most likely to encounter foreign antigens. The study, “Adrenergic control of the adaptive immune response by diurnal lymphocyte recirculation through lymph nodes,” will be published online October 31 ahead of issue in The Journal of Experimental Medicine.

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Researchers in France have identified a molecular motor that controls the release of inflammatory factors that cause severe and fatal allergic reactions. The study, “Kinesin-1 controls mast cell degranulation and anaphylaxis through PI3K-dependent recruitment to the granular Slp3/Rab27b complex,” which will be published online October 24 ahead of issue in The Journal of Cell Biology, suggests that targeting this motor may be a new way to treat patients undergoing anaphylactic shock.

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Researchers from The Ohio State University have discovered that spinal cord injury alters the type of bacteria living in the gut and that these changes can exacerbate the extent of neurological damage and impair recovery of function. The study, “Gut dysbiosis impairs recovery after spinal cord injury,” by Kristina A. Kigerl et al., which will be published online October 17 ahead of issue in The Journal of Experimental Medicine, suggests that counteracting these changes with probiotics could aid patients’ recovery from spinal cord injuries.

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Researchers have discovered that an enzyme called uracil-DNA glycosylase (UNG) protects the ends of B cell chromosomes to facilitate the proliferation of these antibody-producing cells in response to infection. The study “UNG protects B cells from AID-induced telomere loss,” which will be published online October 3 ahead of issue in The Journal of Experimental Medicine, also suggests that targeting this enzyme may help treat certain types of non-Hodgkin’s lymphoma.

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Researchers have built a three-dimensional map of the anthrax toxin that may explain how it efficiently transfers its lethal components into the cytoplasm of infected cells. The study, “Structure of anthrax lethal toxin prepore complex suggests a pathway for efficient cell entry,” which will be published online September 26 ahead of print in The Journal of General Physiology, suggests that the bacterial protein acts as a “conveyer belt” that allows toxic enzymes to continuously stream across cell membranes.