IntroductionTraumatic Brain Injury (TBI) is an important public health problem in the United States (US) resulting in disabling conditions and long-term societal costs. Thus, there a compelling need for prevention, treatment and rehabilitation initiatives informed by national, population-based data.ObjectiveTo estimate the prevalence and incidence of TBI in the US utilizing several nationally representative data sets.MethodsTo produce national estimates, we averaged and analysed data from 2002–2006 for TBI-related visits to hospital-based emergency departments (EDs), hospitalisations, and deaths from the National Hospital Ambulatory Medical Care Survey, the National Hospital Discharge Survey, and the National Vital Statistics System, respectively.ResultsFor 2002–2006, the estimated average annual incidence of TBI was 1.7 million, including 52 000 deaths, 275 000 hospitalisations, and 1 365 000 ED visits. For all age groups, the leading external causes were as follows: falls (35.2%); motor vehicle traffic (17.3%); struck by/against events (16.5%); assaults (10%). Rates were higher for males than females in all age groups. Falls produced the greatest number of TBI-related ED visits, (523 043) and hospitalizations (62 334). Motor vehicle traffic was the leading cause of TBI death, with rates highest among those 20–24 years. Children 0–4 years, adolescents 15–19 years, and adults >65 years were most likely to sustain a TBI and adults >75 years had the highest rate for hospitalisation and death. Annually, almost half a million TBI-related ED visits, 473 947, were made by children aged 0–4 years. TBI was a contributing factor to one third of all injury related deaths in the US.

Viral diarrhea is a great threat to children's health in developing countries. We conducted a prospective surveillance study of acute diarrhea of young children at Tianjin Children's Hospital from April 2008 to April 2009. Viral infections were detected in 356 of the total 766 collected stool specimens (46.48%). Rotavirus infections were the most common (27.94%; predominant type G1), followed by adenovirus infections (17.62%; predominant type Ad41), norovirus infections (5.87%; predominant type GII-4/2006 b), and astrovirus infections (3.15%; only HAstV-1). Children younger than 1 year old were the most susceptible population to viral infections (87.9%). Diarrhea, vomiting, and fever were the most frequent clinical symptoms among the infected patients. The viral infections had no age, sex, or regional differences. Most infection rates were higher in the autumn, winter, and spring. This study supported that the rotavirus vaccine should be included in the Expanded Programme on Immunization in China.

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The comorbidity of depression and addiction has become a serious public health issue, and the relationship between these two disorders and their potential mechanisms has attracted extensive attention. Numerous studies have suggested that depression and addiction share common mechanisms and anatomical pathways. The nucleus accumbens (NAc) has long been considered a key brain region for regulating many behaviors, especially those related to depression and addiction. In this review article, we focus on the association between addiction and depression, highlighting the potential mediating role of the NAc in this comorbidity via the regulation of changes in the neural circuits and molecular signaling. To clarify the mechanisms underlying this association, we summarize evidence from overlapping reward neurocircuitry, the resemblance of cellular and molecular mechanisms, and common treatments. Understanding the interplay between these disorders should help guide clinical comorbidity prevention and the search for a new target for comorbidity treatment.

BackgroundEndothelial barrier dysfunction is central to the pathogenesis of sepsis-associated acute lung injury (ALI). Microtubule (MT) dynamics in vascular endothelium are crucial for the regulation of endothelial barrier function. Unfractionated heparin (UFH) possesses various biological activities, such as anti-inflammatory activity and endothelial barrier protection during sepsis.MethodsHere, we investigated the effects and underlying mechanisms of UFH on lipopolysaccharide (LPS)-induced endothelial barrier dysfunction. C57BL/6 J mice were randomized into vehicle, UFH, LPS and LPS + UFH groups. Intraperitoneal injection of 30 mg/kg LPS was used to induce sepsis. Mice in the LPS + UFH group received intravenous UFH 0.5 h prior to LPS injection. Human pulmonary microvascular endothelial cells (HPMECs) were cultured for analyzing the effects of UFH on LPS-induced and nocodazole-induced hyperpermeability, F-actin remodeling, and LPS-induced p38 MAPK activation.ResultsUFH pretreatment significantly attenuated LPS-induced pulmonary histopathological changes, and increased the lung W/D ratio and Evans blue accumulation in vivo. Both in vivo and in vitro studies showed that UFH pretreatment blocked the LPS-induced increase in guanine nucleotide exchange factor (GEF-H1) expression and myosin phosphatase target subunit 1 (MYPT1) phosphorylation, and microtubule (MT) disassembly in LPS-induced ALI mouse model and human pulmonary microvascular endothelial cells (HPMECs). These results suggested that UFH ameliorated LPS-induced endothelial barrier dysfunction by inhibiting MT disassembly and GEF-H1 expression. In addition, UFH attenuated LPS-induced hyperpermeability of HPMECs and F-actin remodeling. In vitro, UFH pretreatment inhibited LPS-induced increase in monomeric tubulin expression and decrease in tubulin polymerization and acetylation. Meanwhile, UFH ameliorates nocodazole-induced MTs disassembly and endothelial barrier dysfunction.Additionally, UFH decreased p38 phosphorylation and activation, which was similar to the effect of the p38 MAPK inhibitor, SB203580.ConclusionsUFH exert its protective effects on pulmonary microvascular endothelial barrier dysfunction via microtubule stabilization and is associated with the p38 MAPK pathway.