Genomic Islands of Divergence Between Drosophila yakuba Subspecies are Predominantly Driven by Chromosomal Inversions and the Recombination Landscape.

During the early stages of local adaptation and speciation, genetic differences tend to accumulate at certain regions of the genome leading to the formation of genomic islands of divergence (GIDs). This pattern may be due to selection and/or difference in the rate of recombination. Here, we investigate the possible causes of GIDs in Drosophila yakuba mayottensis, and reconfirm using field collection its association with toxic noni (Morinda citrifolia) fruits on the Mayotte island.

Gene family amplification facilitates adaptation in freshwater unionid bivalve Megalonaias nervosa.

Freshwater unionid bivalves currently face severe anthropogenic challenges. Over 70% of species in the United States are threatened, endangered or extinct due to pollution, damming of waterways and overfishing. These species are notable for their unusual life history strategy, parasite-host co-evolution and biparental mitochondrial inheritance.

Social Stress Affects Colonic Inflammation, the Gut Microbiome, and Short-chain Fatty Acid Levels and Receptors.

Objectives: Gastrointestinal disorders, such as inflammatory bowel diseases (IBDs) and functional gastrointestinal disorders (FGIDs), involve disrupted homeostatic interactions between the microbiota and the host. Both disorders are worsened during stress, and in laboratory mice, stress exposure has been shown to change the composition of the gut microbiome. Stress-induced changes to the microbiome exacerbate intestinal inflammation and alter intestinal motility in mice.

Prolonged restraint stressor exposure in outbred CD-1 mice impacts microbiota, colonic inflammation, and short chain fatty acids.

Stressor-exposure has been shown to exacerbate inflammation and change the composition of the gastrointestinal microbiota; however stressor-induced effects on microbiota-derived metabolites and their receptors are unknown. Thus, bacterial-produced short chain fatty acids (SCFAs), as well as microbial community composition, were assessed in the colons of mice exposed to stress during infection with Citrobacter rodentium. Mice were exposed to overnight restraint on 7 consecutive nights, or left undisturbed as a control.

MicroRNA expression following activated protein C treatment during septic shock.

Background: Sepsis induces systemic stress by augmenting inflammatory and procoagulant responses, resulting in microvascular dysfunction and end organ failure, events modulated by the protein C pathway. MicroRNAs (miRNAs) are small noncoding RNAs involved in post-transcriptional regulation of genes; yet, their role in sepsis is poorly defined. We hypothesized that activated protein C (aPC) selectively alters specific miRNA expression implicated in protection of hepatic function during septic shock.

Pyrrolidine dithiocarbamate improves mortality in a rat model of severe hemorrhage.

Background: Hemorrhagic shock is a life threatening condition characterized by diminishing organ function. The aim of this study was to determine whether an effective pyrrolidine dithiocarbamate (PDTC) treatment protocol could be established to decrease organ dysfunction and mortality in a lethal hemorrhagic shock-resuscitation (HSR) model.

Materials And Methods: Sprague-Dawley rats were randomized into three experimental groups; HSR alone (HSR), PDTC (100 mg/kg) administered 12 h pre-HSR (PDTC-12), and PDTC administered 1 h post-shock prior to resuscitation (PDTC+1).

Activated protein C restores hepatic microcirculation during sepsis by modulating vasoregulator expression.

Activated protein C (aPC) promotes fibrinolysis while inhibiting coagulation and inflammation. In septic patients, aPC levels are depleted, and aPC treatment has emerged as a therapeutic option. To better understand the mechanism(s) by which aPC improves survival in sepsis, we sought to determine the effect of aPC treatment on hepatic vasoactive gene and protein expression, leading to changes in hepatic vascular responsiveness in a septic animal model.

Nonmuscle myosin II regulates migration but not contraction in rat hepatic stellate cells.

Aim: To identify and characterize the function of nonmuscle myosin II (NMM II) isoforms in primary rat hepatic stellate cells (HSCs).

Methods: Primary HSCs were isolated from male Sprague-Dawley rats by pronase/collagenase digestion. Total RNA and protein were harvested from quiescent and culture-activated HSCs.

Activated protein C alters inflammation and protects renal function in sepsis.

Background: Activated protein C (aPC) confers survival benefit in patients with sepsis, yet its protective mechanism(s) remain unclear. Herein, we determined time-dependent severity of renal dysfunction during polymicrobial sepsis. We hypothesized aPC restores renal function by preserving organ architecture and reducing inflammation.

Opioid-like compound exerts anti-fibrotic activity via decreased hepatic stellate cell activation and inflammation.

Hepatic fibrosis is characterized by excess type I collagen deposition and exacerbated inflammatory response. Naltrexone, an opioid receptor antagonist used for treating alcohol abuse, attenuates hepatocellular injury in fibrotic animal models, which can be accompanied by deleterious side effects. Additionally, opioid neurotransmission is upregulated in patients with inflammatory liver disease.

Daily genetic profiling indicates JAK/STAT signaling promotes early hepatic stellate cell transdifferentiation.

Aim: To identify signaling pathways and genes that initiate and commit hepatic stellate cells (HSCs) to transdifferentiation.

Methods: Primary HSCs were isolated from male Sprague-Dawley rats and cultured on plastic for 0-10 d. Gene expression was assessed daily (quiescent to day 10 culture-activation) by real time polymerase chain reaction and data clustered using AMADA software.