Two additional cases of metformin‐associated encephalopathy in patients with end‐stage renal disease undergoing hemodialysis

We report on two additional cases of metformin‐associated encephalopathy in patients with end‐stage renal disease (ESRD) undergoing hemodialysis. Two patients were seen at our hospital with abnormal neurological signs and symptoms. Magnetic resonance imaging (MRI) revealed the same pattern of high signal intensity in both basal ganglia in T2‐weighted images in the two patients. The two patients had started taking metformin 5 and 6 weeks earlier at the same dose of 1000 mg per day. Metformin was immediately stopped, and regular hemodialysis was conducted. Their signs and symptoms resolved completely after these measures. The high signal intensity in both ganglia in T2‐weighted MRI also disappeared. We should suspect metformin‐induced encephalopathy and withdraw the drug when presented with diabetic patients with chronic kidney disease and neurological signs and symptoms of unknown cause.     

Health burden of road traffic accidents,an analysis of clinical data on disability and mortality exposure rates in Flanders and Brussels

Statistics on road traffic accidents (RTAs) mainly come from police records. The police reported RTA statistics however are known to have a large degree of under-registration, underestimating the true risk of being injured in traffic accidents. The use of medical based datasets can provide a more accurate estimate of the actual traffic accident health risk. Exposure-based rates of the actual burden from Flanders and Brussels were calculated, comparing differences between road user, age, gender and type of injury sustained. Minimal Clinical Data (MCD) was selected for the years 2003–2007, as well as data from the mortality statistics. Disability Adjusted Life Years (DALY) were calculated and put into perspective with the passenger kilometres travelled.     

Lactobacillus casei MYL01 modulates the proinflammatory state induced by ethanol in an in vitro model

Accumulating studies have suggested that probiotics have beneficial effects on liver injury but the underlying mechanism has remained unclear. Toll-like receptors (TLR) expressed on immune cells and hepatocytes recognize bacterial components that are translocated from the gut into the portal vein. To date, it has been demonstrated that ethanol alone, without microbial components, is able to activate TLR, leading to promotion of proinflammatory cytokine production. Because the enhanced signaling of TLR triggers persistent inflammation, we hypothesized that development of hepatocyte TLR tolerance to repetitive stimulation plays an important role in protecting the liver from hypergeneration of proinflammatory cytokines. In this study, we showed that Lactobacillus casei MYL01 modulated the proinflammatory state induced by ethanol and investigated in detail the mechanism underlying the observation that L. casei MYL01 gave rise to TLR tolerance toward ethanol stimulation. The effects of L. casei MYL01 in the attenuation of ethanol-induced liver damage were due to enhancement of IL-10 production, which limited the proinflammatory process. Furthermore, better defense of hepatocytes against ethanol challenge by treatment of L. casei MYL01 was attributed to previous induction of toll interacting protein (TOLLIP) and suppressor of cytokine signaling (SOCS)1 and SOCS3 expression via activation of TLR1, TLR2, TLR6, and TLR9, an action that cross-regulated ethanol–TLR4–nuclear factor κB signal transduction events. This finding might help establish an in vitro platform for selecting hepatoprotective probiotic strains in terms of ethanol-induced liver damage.     

Neuroprotective Strategies for Traumatic Brain Injury: Improving Clinical Translation

Traumatic brain injury (TBI) induces secondary biochemical changes that contribute to delayed neuroinflammation, neuronal cell death, and neurological dysfunction. Attenuating such secondary injury has provided the conceptual basis for neuroprotective treatments. Despite strong experimental data, more than 30 clinical trials of neuroprotection in TBI patients have failed. In part, these failures likely reflect methodological differences between the clinical and animal studies, as well as inadequate pre-clinical evaluation and/or trial design problems. However, recent changes in experimental approach and advances in clinical trial methodology have raised the potential for successful clinical translation. Here we critically analyze the current limitations and translational opportunities for developing successful neuroprotective therapies for TBI.     

酸碱失衡与急性心血管疾病关系研究进展

急性心血管疾病作为内科常见疾病,病情进展快,病理变化复杂,常出现体内酸碱平衡紊乱,酸碱失衡尤其见于急性心肌梗死疾病中。临床研究表明,体内酸碱失衡可能会导致急性心血管系统损伤,影响疾病的预后,甚至导致心源性休克发生,因此各项酸碱监测指标对于急性心血管疾病的诊断、治疗监测和预后有着重要临床作用。     

Ranson评分对中重度高脂血症性急性胰腺炎分型的预测价值

目的探讨Ranson评分对高脂血症性急性胰腺炎(hyperlipidemic acute pancreatitis,HLAP)分型的早期预测价值。方法回顾性收集2014年1月至2018年10月在北京协和医院急诊科就诊的中重度HLAP患者资料,包括年龄、性别、血脂水平、血糖、白细胞、乳酸脱氢酶(lactate dehydrogenase, LDH)、谷草转氨酶(aspartate aminotransferase,AST)以及入院48 h后的血细胞比容、尿素氮、血钙、碱缺乏、液体丢失量。按照疾病严重程度分为中度和重度HLAP,并计算每例患者的Ranson评分。采用t检验比较中度和重度HLAP组间Ranson评分的差异,运用受试者工作特征(receiver operating characteristic,ROC)曲线分析得出最佳界值,计算其敏感度和特异度,以卡方检验验证其一致性。结果共计99例符合入选和排除标准的HLAP患者进入本研究,其中中、重度HLAP分别为45例和54例。重度HLAP组的Ranson评分显著高于中度组,差异具有统计学意义(5. 19±1. 33比3. 09±1. 35,P<0. 01)。ROC曲线分析显示4为最佳临界值,敏感度为75. 9%,特异度为84. 4%;以4为临界值,Ranson评分3～4者符合中度HLAP的表现,Ranson评分>4符合重度HLAP表现,中度和重度组的Ranson评分与疾病分型一致(P<0. 01)。结论 Ranson评分可用于中度和重度HLAP分型早期预测,3～4分提示中度HLAP,>4分提示重度HLAP。     

Aged Skeletal Muscle Retains the Ability to Remodel Extracellular Matrix for Degradation of Collagen Deposition after Muscle Injury

Aging causes a decline in skeletal muscle function, resulting in a progressive loss of muscle mass, quality, and strength. A weak regenerative capacity is one of the critical causes of dysfunctional skeletal muscle in elderly individuals. The extracellular matrix (ECM) maintains the tissue framework structure in skeletal muscle. As shown by previous reports and our data, the gene expression of ECM components decreases with age, but the accumulation of collagen substantially increases in skeletal muscle. We examined the structural changes in ECM in aged skeletal muscle and found restricted ECM degradation. In aged skeletal muscles, several genes that maintain ECM structure, such as transforming growth factor β (TGF-β), tissue inhibitors of metalloproteinases (TIMPs), matrix metalloproteinases (MMPs), and cathepsins, were downregulated. Muscle injury can induce muscle repair and regeneration in young and adult skeletal muscles. Surprisingly, muscle injury could not only efficiently induce regeneration in aged skeletal muscle, but it could also activate ECM remodeling and the clearance of ECM deposition. These results will help elucidate the mechanisms of muscle fibrosis with age and develop innovative antifibrotic therapies to decrease excessive collagen deposition in aged muscle.