Glucose supply from blood is mandatory for brain functioning and its interruption during acute hypoglycemia or cerebral ischemia leads to brain injury. Alternative substrates to glucose such as the ketone bodies (KB), acetoacetate (AcAc), and β-hydroxybutyrate (BHB), can be used as energy fuels in the brain during hypoglycemia and prevent neuronal death, but the mechanisms involved are still not well understood. During glucose deprivation adaptive cell responses can be activated such as autophagy, a lysosomal-dependent degradation process, to support cell survival. However, impaired or excessive autophagy can lead to cell dysfunction. We have previously shown that impaired autophagy contributes to neuronal death induced by glucose deprivation in cortical neurons and that D isomer of BHB (D-BHB) reestablishes the autophagic flux increasing viability. Here, we aimed to investigate autophagy dynamics in the brain of rats subjected to severe hypoglycemia (SH) without glucose infusion (GI), severe hypoglycemia folagic flux and decreases AMPK activity reducing autophagy initiation. D-BHB also reduced the number of degenerating cells. Together, data suggest different autophagy dynamics after GI in rats subjected to SH or the hypoglycemic coma and support that D-BHB treatment can modulate autophagy dynamics favoring the autophagic flux.Microglia are the brain resident immune cells; they can produce a large variety of growth factors (GFs) to prevent neuronal damages and promote recovery. In neurodegenerative diseases, microglia can play both benefic and deleterious roles, depending on different factors and disease context. In multiple sclerosis, microglia are involved in both demyelination (DM) and remyelination (RM) processes. Recent studies suggest a beneficial role of microglia in regenerative processes. These include the regenerative development of myelin after DM. This review gives an overlook of how microglia and GFs can influence the RM properties.Neural stimulation modulates the depolarization of neurons, thereby triggering activity-associated mechanisms of neuronal plasticity. Activity-associated mechanisms in turn play a major role in post-mitotic structure and function of adult neurons. Our understanding of the interactions between neuronal behavior, patterns of neural activity, and the surrounding environment is evolving at a rapid pace. Brain derived neurotrophic factor is a critical mediator of activity-associated plasticity, while multiple immediate early genes mediate plasticity of neurons following bouts of neural activity. New research has uncovered genetic mechanisms that govern the expression of DNA following changes in neural activity patterns, including RNAPII pause-release and activity-associated double stranded breaks. Discovery of novel mechanisms governing activity-associated plasticity of neurons hints at a layered and complex molecular control of neuronal response to depolarization. Importantly, patterns of depolarization in neuronction after trauma, disease, or age-related functional decline.Inflammatory bowel diseases (IBD) usually affect women in their fertile years and, therefore, have implications for their fertility and pregnancy. The presence of IBD during pregnancy has been shown to adversely affect pregnancy outcomes, and increased rates of preterm delivery and of spontaneous abortion have been reported. An onset of acute severe colitis in pregnancy has rarely been seen. We present the case of a 42-year-old woman who conceived after 9 attempts of in vitro fertilization and whose pregnancy was the result of a donated oocyte. Shortly after conception, she was diagnosed with severe active ulcerative colitis, and biologic therapy was introduced in the 28th week of pregnancy. Although therapy for IBD in pregnancy is considered safe for most drugs, this was not very well known in 2015. We also consider our case exceptional because we now have a 5-year follow-up of our patient and her child after having begun biologic therapy during late pregnancy.Pill-induced esophagitis or esophageal ulcers are considered when patients have retrosternal chest pain or odynophagia following the ingestion of suspicious medications.  https://www.selleckchem.com/products/l-ornithine-l-aspartate.html  Various drugs have been reported to induce esophageal ulcers. However, amoxycillin-clavulanic acid-induced esophagitis or esophageal ulcer has not been reported in literature. Hence, we report the case of a 30-year-old Thai male who presented with acute, severe odynophagia and retrosternal chest pain. He had a history of taking amoxycillin-clavulanic acid for 12 days. An esophagogastroduodenoscopy was performed and revealed geographic clean-based ulcers, with a kissing-ulcer appearance at the level of the mid-esophagus. A biopsy was taken and revealed inflamed granulation tissue and an ulcer with neither infection nor malignancy. Thus, the diagnosis of an amoxycillin-clavulanic acid-induced esophageal ulcer was made according to the clinicopathologic report.Heterotopic gastric tissue can be found throughout the intestinal tract, and when it is present in the small intestine, it can present with symptoms that include gastrointestinal bleeding, chronic abdominal pain, diarrhea, and chronic dyspepsia. This finding is incredibly rare in pediatrics, but if present, it can lead to significant morbidity and mortality. This can be especially true if a patient presents with a comorbidity of a bleeding disorder. We here present the case of a teenage male with a history of severe factor VII deficiency who was found to have iron deficiency anemia resulting in multiple blood transfusions from an occult lower gastrointestinal bleed. He was ultimately found to have a bleeding gastric heterotopic polyp in his duodenum that was successfully removed via surgery.Immunoglobulin G4-related disease (IgG4-RD) is a fibroinflammatory condition that becomes more recognized as multi-systemic disorders, characterized by three histological hallmarks of IgG4-positive lymphoplasmacytic tissue infiltrate, storiform fibrosis, and obliterative phlebitis. This disease has been reported in virtually every organ system, but the hepatic manifestations remain poorly defined. Moreover, IgG4-RD can mimic many malignancies, inflammatory disorders and infectious diseases. This report revealed IgG4-related liver disease with atypical presentation presenting with multiple liver abscesses and linear tracts mimicking parasitic infection.