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Background Abdominal aortic aneurysm (AAA) is a deadly disease in the elderly population. Currently, the association between single nucleotide polymorphisms (SNPs) and the presence of AAAs has become a hot topic and is a concern for many researchers. Method We performed a document retrieval in PubMed, EMBASE, and the Cochrane Library (to January 2020). A total of 17 case-control reports on SNPs of AAAs and eight SNPs of correlation factors were selected. All essential data, including race, age, country, criteria of AAA diagnosis, method of AAA measurement, method of genotype detection, name of SNPs, minor allele frequency (MAF), Hardy Weinberg equilibrium (HWE) of the control group, and number of cases and control groups were extracted by two reviewers independently. The fixed-effect model and random-effect model were used to calculate the overall odds ratios (ORs) and 95% confidence intervals (CIs). The association between selected SNPs and the presence of AAAs was evaluated under different genetic models (dominant, codominant, recessive, overdominant, and allele models). Results A total of 17 articles (sample size ranging from to 42–665 AAA cases and 49–2,297 controls) and 23 SNPs of related factors were identified. Eight SNPs were assessed in at least two studies and were selected for further meta-analysis. We found that the A allele of interleukin (IL)-10 (−1082 G/A) (OR: 1.35, 95% CI: 1.18–1.54, p < 0.0001) was a risk factor for AAAs under random and fixed-effect models. In addition, partial genetic models of these SNPs were confirmed to be related to the presence of AAA. Subgroup analysis revealed that haptoglobin (HP)-1 was a risk factor for AAAs (OR: 1.30, 95% CI: 1.04–1.63, p = 0.02) in the European population. No association was found between the occurrence of AAA and the other SNPs. Conclusion In our current meta-analysis, we speculated that the genotype distribution of IL-10 (−1082 G/A) may be associated with the emergence of AAA.

BACKGROUND Studies have been carried out to assess the efficacy of high-volume hemofiltration (HVHF) among critically ill patients. However, it is currently unclear whether HVHF is really valuable in critically ill patients. MATERIAL AND METHODS Randomized controlled trials evaluating HVHF for critically ill adult patients were included in this analysis. Three databases were searched up to July 27, 2018. The relative risk (RR), mean difference (MD), and 95% confidence intervals (CI) were determined. RESULTS Twenty-one randomized controlled trials were included in this analysis. Overall, HVHF was associated with lower mortality compared with control measures (RR=0.88, 95% CI=0.81 to 0.96, P=0.004) in critically ill patients. Sub-analysis revealed HVHF reduced mortality in sepsis and acute respiratory distress syndrome patients, but no similar effect in other diseases. HVHF decreased levels of plasma tumor necrosis factor and interleukin 6. The heart rate of the HVHF group after treatment was slower than the control group, while we found higher mean arterial pressure in the HVHF group, but oxygenation index was not significantly different between the two groups. HVHF had no remarkable influence on acute physiological and chronic health evaluation score (APACHE II score) compared with the control group. CONCLUSIONS HVHF might be superior to conventional therapy in critically ill patients.

Previous studies suggest an association of cardiac microvascular endothelial cells (CMECs) hyperpermeability with sepsis-related cardiac injury. Our results showed that CMECs permeability was dependent upon concentration and time of lipopolysaccharides (LPS) stimulation. Integrin ανβ3 expression decreased after LPS stimulation. Pretreatment with anti-integrin ανβ3 antibody enhanced LPS-induced hyperpermeability. Upregulation of integrin ανβ3 decreased LPS-induced hyperpermeability. F-actin remodeling was enhanced after LPS stimulation and was inhibited by up-regulation of integrin ανβ3. Inhibition of Src or Rac1 reduced CMECs permeability after LPS stimulation, but there were no differences in the phosphorylation of Src and Rac1 when over-expressing or blocking integrin β3. After pretreatment with Src or Rac1 inhibitor, no significant difference was found in the expression of integrin ανβ3 in LPS-induced CMECs. These finding suggested that integrin ανβ3 overexpression decreased LPS-stimulated CMECS permeability by inhibition of cytoskeletal remodeling, but the mechanism might not be mediated via Src/Rac1 signaling.

Background Cerebral salt-wasting syndrome (CSWS), which usually secondary to cerebral diseases, is characterized by hyponatremia and hypovolemia. In clinical practice, it is quite difficult to distinguish CSWS from other hyponatremia syndrome, especially in Intensive Care Unit (ICU) where the conditions of patients are more complicated. Nonetheless, it is crucial because treatments might be fundamentally different. Case presentation We discuss a case of patient who presented with refractory hyponatremia and hypovolemia after traumatic brain injury, finally was diagnosed with CSWS, and successfully treated with corticotropin. Conclusions This case report provides a unique opportunity to observe the trigger of subdural effusion-induced CSWS, and also it provides the classical therapy for CSWS in a critically ill patient. In view of the difficulty to tell CSWS from other similar diseases in ICU, ICU doctors should be aware of such condition.