Background: The aim of this meta-analysis was to assess if early mobilization and rehabilitation in the intensive care unit (ICU) could reduce ICU-acquired weakness (ICU-AW), improve functional recovery, improve muscle strength, shorten the length of ICU and hospital stays, and reduce the mortality rate. Methods: A comprehensive literature search in PubMed, Embase, Web of Science, SinoMed (Chinese BioMedical Literature Service System, China), and National Knowledge Infrastructure, China (CNKI) was performed. Results were expressed as a risk ratio (RR) with 95% confidence intervals (95% CIs) or weight mean difference (WMD) with 95% CIs. Pooled estimates were calculated using a fixed-effects or randomeffects model according to the heterogeneity among studies. Results: Fifteen randomized controlled trials involving a total of 1941 patients were included in this meta-analysis. Pooled estimates suggested that early mobilization significantly reduced the incidence of ICU-AW (RR = 0.49, 95% CI: 0.26, 0.91; P = .025),
Background: We studied patients with coronavirus disease 2019 (COVID-19) infected by severe acute respiratory syndrome coronavirus 2, a virus that originated in Wuhan, China, and is spreading over the country including Jiangsu Province. We studied the clinical characteristics and therapies of severe cases in Jiangsu Province. Methods: A multicenter retrospective cohort study was conducted to analyze clinical, laboratory data and treatment of 60 severe cases with COVID-19 infection in Jiangsu Province between January 24, 2020 and April 20, 2020. The improvement and deterioration subgroups were compared to identify predictors of disease progression. Results: A total of 653 infected cases with COVID-19 were reported in Jiangsu Province, of which 60 severe cases were included in this study. Up until April 20, 2020, the mortality of severe patients was 0%. The median age was 57 years. The average body mass index of these patients was 25 kg/m 2. White blood cell counts decreased in 45.0% of patients, lymphopenia in 63.3%, thrombocytopenia in 13.3% and procalcitonin levels in 88.3% of the patients were less than 0.5 ng/mL. There were no statistically significant differences in immunoglobulin therapy and GCs therapy between the improvement and deterioration subgroups. Logistic regression analysis identified higher levels of troponin T (odds ratio [OR]: 1.04; 95% confidence interval [
Background: Researchers had contradictory conclusions about the role of probiotics in preventing ventilator-associated pneumonia (VAP), which has led to the controversial use of probiotics in mechanically ventilated patients. Objective: To explore the efficacy and safety of probiotics in preventing VAP. Methods: A literature search was conducted in 7 medical databases. Two investigators assessed literature quality independently and collected data. The primary outcome was the incidence of VAP. Secondary outcomes included 16 measures. Sensitivity analysis and subgroup and meta-regression analyses were performed to analyze the source of heterogeneity. P values <0.05 were considered statistically significant, and CIs were set at 95%. A random-effects model was set when I2 <50%, otherwise a fixed-effects model was used. Results: A total of 20 randomized controlled studies with a total of 2428 patients were analyzed. Pooled results showed positive effects of probiotics on the reduction of VAP incidence (risk ratio [RR] = 0.672; P < 0.001; I2 = 11.3%), length of ICU stay (WMD = −1.417; P = 0.012; I2 = 90.7%), oropharyngeal (RR = 0.866; P = 0.031; I2 = 12.4%) and gastric (RR = 0.645; P < 0.001; I2 = 30.2%) colonization. Conclusions and Relevance: Probiotics can reduce the incidence of VAP and reduce oropharyngeal and gastric bacterial colonization. The results also suggest that probiotics do not cause adverse effects.
Sepsis is a systemic inflammatory response syndrome that can cause multiple-organ damage, including acute kidney injury (AKI). Studies have shown that the long non-coding RNA cancer susceptibility candidate 2 (cASc2) is involved in the occurrence and development of multiple human diseases, although its expression and role in AKI has not yet been reported. The present study demonstrated that the expression of CASC2 was significantly decreased in the serum of patients with sepsis compared with healthy subjects. In addition, the cASc2 level was negatively associated with the severity of AKI. Further experiments revealed that CASC2 promoted cell viability and inhibited inflammatory factor secretion, apoptosis and oxidative stress in lipopolysaccharide-stimulated human renal tubular epithelial HK-2 cells. Importantly, the current study observed that CASC2 was negatively associated with a pro-inflammatory microRNA (miR)-155. In addition, the upregulation of cASc2 significantly suppressed the nuclear factor κB (NF-κB) signaling pathway. In conclusion, the results of the present study suggested that cASc2 may serve as a potential target for treating sepsis-induced AKI by inhibiting the miR-155 and NF-κB pathway-mediated inflammation.
This study aimed to compare the preference of different methods of nutritional support for patients with severe acute pancreatitis (SAP). Patients with SAP were divided into the enteral nutrition group (EN group, 16 cases), total the parenteral nutrition group (TPN group, 14 cases), and the enteral plus total parenteral nutrition group (EN+TPN group, 15 cases). At 7 days after admisson, TPN and EN+TPN groups showed significantly increased Ranson scores compared with the EN group (p < .05). At 14 and 21 days after admisson, TPN and EN+TPN groups exhibited significantly increased Acute Physology and Chronic Health Evaluation (APACHE) II scores, Ranson scores, and intra-abdominal pressure compared with the EN group (p < .05 or p < .01). The incidences of multiple organ dysfunction syndrome and its complication in the EN group were significantly lower than the TPN and EN+TPN groups (p < .05). Hospital stay was significantly lower, but the incidences of abdominal distenson and regurgitation complications were significantly higher in the EN group than in the TPN and EN+TPN groups (p < .05). In concluson, early enteral nutrition could significantly improve nutritional status of patients with SAP, shorten the course of the disease, and reduce the incidences of infection, death, and complication, but also increase the risk of abdominal distenson and regurgitation.
For patients who have sepsis, acute lung injury (ALI) causes most of death. Metformin (Met) is an anti-hyperglycemic agent and it has extensive pharmacological properties. This study aimed to analyze the influence of Met on lipopolysaccharide (LPS) -induced ALI. Met (1, 2, and 4 mg/kg) were injected and LPS was injected 30 min later. The data suggested Met can reduce release of inflammatory cytokines and bronchoalveolar lavage fluid (BALF) protein expression, reduce lung wet/dry ratio, and significantly improve LPS-induced lung destruction during ALI. In addition, Met inhibits LPS-induced neutrophil and macrophage infiltration, reduces MPO activity, and promotes AMPK-α1 expression in lung tissues. Our data suggested that metformin alleviates capillary injury during ALI via AMPK-α1.
Sepsis is an acute systemic infectious disease engendered by infectious factors, which can cause the dysfunction of multiple organs, including acute kidney injury (AKI). Recently, more and more researchers are focusing on long non-coding RNA (lncRNA) that is closely associated with the development and progression of various diseases; however, the role and mechanism of lncRNA in sepsis-induced acute kidney injury is not fully understood. Here, we found a significant increase in the expression of lncRNA small nuclear RNA host gene 5 (SNHG5) in the serum of patients with sepsis than healthy controls. Similar results were obtained from mouse model of sepsis. Further investigations revealed that knockdown of SNHG5 improves the viability and reduces the rate of apoptosis and the generation of inflammatory cytokines in HK-2 and TCMK-1 cells treated with lipopolysaccharide (LPS). Mechanistically, we showed that SNHG5 can combine with microRNA-374a-3p (miR-374a-3p) which inhibits nuclear factor-κB (NF-κB) activity by targeting TLR4. In conclusion, our results demonstrate that SNHG5 may regulate sepsis-induced AKI via the miR-374a-3p/TLR4/NF-κB pathway, therefore providing a new insight into the treatment of this disease.
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