IL-4 Inhibits IL-1β-Induced Depressive-Like Behavior and Central Neurotransmitter Alterations

It has been known that activation of the central innate immune system or exposure to stress can disrupt balance of anti-/proinflammatory cytokines. The aim of the present study was to investigate the role of pro- and anti-inflammatory cytokines in the modulation of depressive-like behaviors, the hormonal and neurotransmitter systems in rats. We investigated whether centrally administered IL-1β is associated with activation of CNS inflammatory pathways and behavioral changes and whether treatment with IL-4 could modulate IL-1β-induced depressive-like behaviors and central neurotransmitter systems. Infusion of IL-4 significantly decreased IL-1β-induced anhedonic responses and increased social exploration and total activity. Treatment with IL-4 markedly blocked IL-1β-induced increase in PGE2 and CORT levels. Also, IL-4 reduced IL-1β-induced 5-HT levels by inhibiting tryptophan hydroxylase (TPH) mRNA and activating serotonin transporter (SERT) in the hippocampus, and levels of NE were increased by activating tyrosine hydroxylase (TH) mRNA expression. These results demonstrate that IL-4 may locally contribute to the regulation of noradrenergic and serotonergic neurotransmission and may inhibit IL-1β-induced behavioral and immunological changes. The present results suggest that IL-4 modulates IL-1β-induced depressive behavior by inhibiting IL-1β-induced central glial activation and neurotransmitter alterations. IL-4 reduced central and systemic mediatory inflammatory activation, as well as reversing the IL-1β-induced alterations in neurotransmitter levels. The present findings contribute a biochemical pathway regulated by IL-4 that may have therapeutic utility for treatment of IL-1β-induced depressive behavior and neuroinflammation which warrants further study

Clinical Characteristics and Genotypes of Rotaviruses in a Neonatal Intensive Care Unit

BackgroundThere are few reports on the symptoms of rotavirus infections in neonates. This study aims to describe clinical signs of rotavirus infections among neonates, with a particular focus on preterm infants, and to show the distribution of genotypes in a neonatal intensive care unit (NICU).MethodsA prospective observational study was conducted at a regional NICU for 1 year. Stool specimens from every infant in the NICU were collected on admission, at weekly intervals, and from infants showing symptoms. Rotavirus antigens were detected by enzyme-linked immunosorbent assay (ELISA), and genotypes were confirmed by Reverse transcription-Polymerase chain reaction (RT-PCR). The infants were divided into three groups: symptomatic preterm infants with and without rotavirus-positive stools [Preterm(rota+) and Preterm(rota–), respectively] and symptomatic full- or near-term infants with rotavirus-positive stools [FT/NT(rota+)]. Demographic and outcome data were compared among these groups.ResultsA total of 702 infants were evaluated for rotaviruses and 131 infants were included in this study. The prevalence of rotavirus infections was 25.2%. Preterm(rota+) differed from Preterm(rota–) and FT/NT(rota+) with respect to frequent feeding difficulty (p = 0.047 and 0.034, respectively) and higher percentage of neutropenia (p = 0.008 and 0.011, respectively). G4P[6] was the exclusive strain in both the Preterm(rota+) (97.7%) and FT/NT(rota+) (90.2%), and it was the same for nosocomial, institutional infections, and infections acquired at home.ConclusionSystemic illness signs such as feeding difficulty and neutropenia are specific for preterm infants with rotavirus infections. G4P[6] was exclusive, regardless of preterm birth or locations of infections. This study might be helpful in developing policies for management and prevention of rotavirus infections in NICUs

Fragility, Stokes-Einstein violation, and correlated local excitations in a coarse-grained model of an ionic liquid

Dynamics of a coarse-grained model for the room-temperature ionic liquid, 1-ethyl-3-methylimidazolium hexafluorophosphate, couched in the united-atom site representation are studied via molecular dynamics simulations. The dynamically heterogeneous behavior of the model resembles that of fragile supercooled liquids. At or close to room temperature, the model ionic liquid exhibits slow dynamics, characterized by nonexponential structural relaxation and subdiffusive behavior. The structural relaxation time, closely related to the viscosity, shows a super-Arrhenius behavior. Local excitations, defined as displacement of an ion exceeding a threshold distance, are found to be mainly responsible for structural relaxation in the alternating structure of cations and anions. As the temperature is lowered, excitations become progressively more correlated. This results in the decoupling of exchange and persistence times, reflecting a violation of the Stokes-Einstein relation.Comment: Published on the Phys. Chem. Chem. Phys. websit

Chronic Treatment with Squid Phosphatidylserine Activates Glucose Uptake and Ameliorates TMT-Induced Cognitive Deficit in Rats via Activation of Cholinergic Systems

The present study examined the effects of squid phosphatidylserine (Squid-PS) on the learning and memory function and the neural activity in rats with TMT-induced memory deficits. The rats were administered saline or squid derived Squid-PS (Squid-PS 50 mg kg−1, p.o.) daily for 21 days. The cognitive improving efficacy of Squid-PS on the amnesic rats, which was induced by TMT, was investigated by assessing the passive avoidance task and by performing choline acetyltransferase (ChAT) and acetylcholinesterase (AchE) immunohistochemistry. 18F-Fluorodeoxyglucose and performed a positron emission tomography (PET) scan was also performed. In the passive avoidance test, the control group which were injected with TMT showed a markedly lower latency time than the non-treated normal group (P < 0.05). However, treatment of Squid-PS significantly recovered the impairment of memory compared to the control group (P < 0.05). Consistent with the behavioral data, Squid-PS significantly alleviated the loss of ChAT immunoreactive neurons in the hippocampal CA3 compared to that of the control group (P < 0.01). Also, Squid-PS significantly increased the AchE positive neurons in the hippocampal CA1 and CA3. In the PET analysis, Squid-PS treatment increased the glucose uptake more than twofold in the frontal lobe and the hippocampus (P < 0.05, resp.). These results suggest that Squid-PS may be useful for improving the cognitive function via regulation of cholinergic enzyme activity and neural activity