Intensive care unit-acquired weakness (ICUAW) occurs frequently in the context of critical illness without alternative plausible cause and specific treatment options, and it is important to identify and summarize the independent risk factors for ICUAW. PubMed, Embase, Central, China Biological Medicine, China National Knowledge Infrastructure, VIP and Wanfang databases were searched from database inception until 10 July 2017. Prospective cohort studies on adult ICU patients who were diagnosed with ICUAW using either clinical or electrophysiological criteria were selected. Meta-analysis was performed using Stata version 12.0. The results were analysed using odds ratios (OR) and 95% confidence intervals (CI). Data were pooled using a random-effects model, and heterogeneity was assessed using the I statistic. Qualitative analysis and systematic review were used for risk factors that were deemed inappropriate to combine. Fourteen prospective cohort studies were included in this review. The meta-analysis showed that Acute Physiology and Chronic Health Evaluation II score (OR, 1.05; 95%CI, 1.01-1.10), neuromuscular blocking agents (OR, 2.03; 95%CI, 1.22-3.40) and aminoglycosides (OR, 2.27; 95%CI, 1.07-4.81) were found to be significantly associated with ICUAW. Other risk factors, including female, multiple organ failure, systemic inflammatory response syndrome, sepsis, electrolyte disturbances, hyperglycaemia, hyperosmolarity, high lactate level, duration of mechanical ventilation, parenteral nutrition and use of norepinephrine, were statistically significant on multivariable analysis in each single studies. This review provides a number of independent risk factors for ICUAW, which should be guided for early prediction and prevention of the disorder.
Background-The haplotypes in the gene vitamin K epoxide reductase complex subunit 1 (VKORC1) have been found to affect warfarin dose response through effects on the formation of reduced-form vitamin K, a cofactor for ␥-carboxylation of vitamin K-dependent proteins, which is involved in the coagulation cascade and has a potential impact on atherosclerosis. We hypothesized that VKORC1-dependent effects on the coagulation cascade and atherosclerosis would contribute to susceptibility for vascular diseases. Methods and Results-To test the hypothesis, we studied the association of polymorphisms of VKORC1 with stroke (1811 patients), coronary heart disease (740 patients), and aortic dissection (253 patients) compared with matched controls (nϭ1811, 740, and 416, respectively). Five common noncoding single-nucleotide polymorphisms of VKORC1 were identified in a natural haplotype block with strong linkage disequilibrium (DЈϾ0.9, r 2 Ͼ0.9), then single-nucleotide polymorphism (SNP) ϩ2255 in the block was selected for the association study. We found that the presence of the C allele of the ϩ2255 locus conferred almost twice the risk of vascular disease (odds ratio [OR] 1.95, 95% confidence interval [CI] .58 to 2.41, PϽ0.001 for stroke; OR 1.72, 95% CI 1.24 to 2.38, PϽ0.01 for coronary heart disease; and OR 1.90, 95% CI 1.04 to 3.48, PϽ0.05 for aortic dissection). We also observed that subjects with the CC and CT genotypes had lower levels of undercarboxylated osteocalcin (a regulator for the bone), probably vascular calcification, and lower levels of protein induced in vitamin K absence or antagonism II (PIVKA-II, a des-␥-carboxy prothrombin) than those with TT genotypes. Conclusions-The haplotype of VKORC1 may serve as a novel genetic marker for the risk of stroke, coronary heart disease, and aortic dissection.
BackgroundAlthough some trials assessed the effectiveness of aerobic exercise for Parkinson's disease (PD), the role of aerobic exercise in the management of PD remained controversial.ObjectiveThe purpose of this systematic review is to evaluate the evidence about whether aerobic exercise is effective for PD.MethodsSeven electronic databases, up to December 2013, were searched to identify relevant studies. Two reviewers independently extracted data and assessed methodological quality based on PEDro scale. Standardised mean difference (SMD) and 95% confidence intervals (CI) of random-effects model were calculated. And heterogeneity was assessed based on the I2 statistic.Results18 randomized controlled trials (RCTs) with 901 patients were eligible. The aggregated results suggested that aerobic exercise should show superior effects in improving motor actions (SMD, −0.57; 95% CI −0.94 to −0.19; p = 0.003), balance (SMD, 2.02; 95% CI 0.45 to 3.59; p = 0.01), and gait (SMD, 0.33; 95% CI 0.17 to 0.49; p<0.0001) in patients with PD, but not in quality of life (SMD, 0.11; 95% CI −0.23 to 0.46; p = 0.52). And there was no valid evidence on follow-up effects of aerobic exercise for PD.ConclusionAerobic exercise showed immediate beneficial effects in improving motor action, balance, and gait in patients with PD. However, given no evidence on follow-up effects, large-scale RCTs with long follow-up are warrant to confirm the current findings.
BackgroundObesity paradox refers to lower mortality in subjects with higher body mass index (BMI), and has been documented under a variety of condition. However, whether obesity paradox exists in adults requiring mechanical ventilation in intensive critical units (ICU) remains controversial.MethodsMEDLINE, EMBASE, China Biology Medicine disc (CBM) and CINAHL electronic databases were searched from the earliest available date to July 2017, using the following search terms: “body weight”, “body mass index”, “overweight” or “obesity” and “ventilator”, “mechanically ventilated”, “mechanical ventilation”, without language restriction. Subjects were divided into the following categories based on BMI (kg/m2): underweight, < 18.5 kg/m2; normal, 18.5–24.9 kg/m2; overweight, BMI 25–29.9 kg/m2; obese, 30–39.9 kg/m2; and severely obese > 40 kg/m2. The primary outcome was mortality, and included ICU mortality, hospital mortality, short-term mortality (<6 months), and long-term mortality (6 months or beyond). Secondary outcomes included duration of mechanical ventilation, length of stay (LOS) in ICU and hospital. A random-effects model was used for data analyses. Risk of bias was assessed using the Newcastle-Ottawa quality assessment scale.ResultsA total of 15,729 articles were screened. The final analysis included 23 articles (199,421 subjects). In comparison to non-obese patients, obese patients had lower ICU mortality (odds ratio (OR) 0.88, 95% CI 0.0.84–0.92, I2 = 0%), hospital mortality (OR 0.83, 95% CI 0.74–0.93, I2 = 52%), short-term mortality (OR 0.81, 95% CI 0.74–0.88, I2 = 0%) as well as long-term mortality (OR 0.69, 95% CI 0.60–0.79, I2 = 0%). In comparison to subjects with normal BMI, obese patients had lower ICU mortality (OR 0.88, 95% CI 0.82–0.93, I2 = 5%). Hospital mortality was lower in severely obese and obese subjects (OR 0.71, 95% CI 0.53–0.94, I2 = 74%, and OR 0.80, 95% CI 0.73–0.89, I2 = 30%). Short-term mortality was lower in overweight and obese subjects (OR 0.82, 95% CI 0.75–0.90, I2 = 0%, and, OR 0.75, 95% CI 0.66–0.84, I2 = 8%, respectively). Long-term mortality was lower in severely obese, obese and overweight subjects (OR 0.39, 95% CI 0.18–0.83, and OR 0.63, 95% CI 0.46–0.86, I2 = 56%, and OR 0.66, 95% CI 0.57–0.77, I2 = 0%). All 4 mortality measures were higher in underweight subjects than in subjects with normal BMI. Obese subjects had significantly longer duration on mechanical ventilation than non-obese group (mean difference (MD) 0.48, 95% CI 0.16–0.80, I2 = 37%), In comparison to subjects with normal BMI, severely obese BMI had significantly longer time in mechanical ventilation (MD 1.10, 95% CI 0.38–1.83, I2 = 47%). Hospital LOS did not differ between obese and non-obese patients (MD 0.05, 95% CI -0.52 to 0.50, I2 = 80%). Obese patients had longer ICU LOS than non-obese patients (MD 0.38, 95% CI 0.17–0.59, I2 = 70%). Hospital LOS and ICU LOS did not differ significantly in subjects with different BMI status.ConclusionsIn ICU patients receiving mechanical ventilation, higher BMI is associated...
Angiopoietin-1 is a vascular strengthening factor during vascular development and a protective factor for pathological vascular inflammation and leakage. Brain vascular leaking and inflammation are two important pathological processes of stroke; therefore, we hypothesized that variants of the microRNA-binding site in angiopoietin-1 would affect its expression and confer a risk of stroke. To test our hypothesis, a predicted microRNA-binding site was found in the 3'-UTR of angiopoietin-1 using bioinformatics; variant rs2507800 was identified to be located in the miR-211-binding site of angiopoietin-1. Secondly, the effects of the identified variant on angiopoietin-1 translation were assessed using a luciferase reporter assay and ELISA. We found that the A allele of rs2507800 suppressed angiopoietin-1 translation by facilitating miR-211 binding, but not the T allele. Subjects carrying the TT genotype had higher plasma angiopoietin-1 levels than those with the A allele. Finally, the association of the variant with stroke was tested in 438 stroke patients and 890 controls, and replicated in an independent population of 1791 stroke patients and 1843 controls. The TT genotype resulted in a significant reduction in overall stroke risk {OR, 0.51 [95% confidence interval (CI), 0.36-0.74], P = 0.0003}, ischemic stroke [OR, 0.56 (95% CI, 0.36-0.85), P = 0.007] and hemorrhagic stroke [OR, 0.46 (95% CI, 0.26-0.80), P = 0.007]. These results were confirmed in an independent study. Our results provide evidence that the TT genotype (rs2507800) in the 3'-UTR of angiopoietin-1 might reduce the risk of stroke by interfering with miR-211 binding.
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