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A new study in mice shows that activation of the brain's reward system boosts beneficial antibacterial immunity in the periphery. These findings provide biological insights into the association between psychological and physical well-being.
Two recent studies have shown that alterations in muscle stem cell–niche interactions during aging underlie the functional decline in regenerative potential. The reconstitution of this communication restores stem cell function and enhances skeletal muscle repair.
Little is known about the regulatory mechanisms of antifungal host defense. Two complementary studies show that the E3 ubiquitin ligase CBLB targets dectin-1 and dectin-2 for degradation, and thus exerts a strong anti-inflammatory effect.
A new study provides the first insights into epigenetic heterogeneity in AML. The study highlights a striking independence of genetic and epigenetic variation, and links the kinetics of epigenetic change to clinical outcome.
Reservoirs of virally infected cells that are resistant to standard antiretroviral therapy make HIV-1 infection an incurable disease. A new study shows that follicular T helper cells in lymph node germinal centers are prime niches for HIV-1 persistence during antiviral therapy.
Two recent studies provide novel insights into the mechanism of action of thalidomide analogs in multiple myeloma and del(5q) myelodysplastic syndrome. They show that the role of the chaperone function of cereblon, and a calcium- and calpain-dependent pathway, are important in anticancer functions.
A recent study has shown that a single dose of fibroblast growth factor (FGF) 1 into the central nervous system (CNS) of various mouse and rat models of type 2 diabetes results in profound and exceptionally long-lasting reductions in blood glucose. This work raises the possibility of truly revolutionary therapies for individuals with type 2 diabetes that target the brain FGF system.
Two new studies in mice show that the gut microbiota produces metabolites from dietary tryptophan that regulate inflammation in the gut and central nervous system.
A recent study shows that skeletal muscle responds to tumor-secreted factors by undergoing a change in fatty acid metabolism, and that blocking this metabolic response in mice inhibits muscle wasting.
A new study of the impact of cytotoxic T lymphocyte (CTL) escape mutations suggests that holes in the host immune repertoire contribute to poor disease outcomes, owing to a gradual deterioration of the host anti-HIV-1 immune response. This should be accounted for in HIV-1 vaccine development strategies.
A new study in humans links genetic variants associated with schizophrenia to changes in the expression of two genes, arsenite methyltransferase (AS3MT) and BLOC-1 related complex subunit 7 (BORCS7). Subsequent investigations provide compelling evidence that AS3MT is involved in the etiology of schizophrenia.
A recent study identifies differences in human induced pluripotent stem cell (hiPSC)-derived cardiomyocytes from patients with breast cancer who were treated with doxorubicin and either did or did not develop cardiotoxicity. The results open up new avenues for the development of personalized therapy and the prevention of cardiotoxicity.
Pancreatic ductal adenocarcinoma (PDAC) is characterized by an extensive stromal component that hinders treatment. A new study shows how the genetic identity of pancreatic tumors might influence the physical properties of the associated stroma to promote tumor progression.
A new study shows in mice that tumor necrosis factor (TNF) superfamily member 11 (TNFSF11, also known as RANKL), which stimulates osteoclasts to remove bone, binds to the G-protein-coupled receptor LGR4 to prevent excessive bone removal. In mouse models of osteoporosis, a recombinant LGR4 ectodomain reduces bone loss.
A new study with patient stem cell–based modeling of Smith-Lemli-Opitz syndrome (SLOS) shows that the accumulation of a specific cholesterol precursor dysregulates the Wnt/b-catenin pathway, which in turn leads to precocious neural differentiation.
Ablation of the tumor suppressor phosophatase and tensin homlog (PTEN) unexpectedly suppresses the development of pre-B acute lymphoblastic leukemia (ALL).
