Prediction Models for Sarcopenia in Patients with Maintenance Hemodialysis: A Systematic Review and Meta-Analysis.

BACKGROUND: This systematic review and meta-analysis investigated all prediction models for sarcopenia in Maintenance Hemodialysis (MHD) patients. METHODS: This study used the Systematic Reviews and Meta-Analysis statement (PRISMA) for systematic review. DATA SOURCES: PubMed, Web of Science, Embase, Cochrane Library and Medline databases up to September 2023. DATA ANALYSIS: Risk of bias (ROB) was evaluated using the Prediction model Risk Of Bias ASsessment Tool (PROBAST). Random effect models were calculated due to high heterogeneity identified. RESULTS: Fifteen models from twelve studies were analyzed. All studies had high ROB and three of them posed a high risk in terms of applicability. The pooled AUC, sensitivity, and specificity were 0.715, 0.583 and 0.656 respectively. The diagnostic criteria (P=0.0046), country (P=0.0046), and study design (P=0.0087) were significant sources of the heterogeneity. Analysing purely from the data perspective, grouping by diagnostic criterias, the AUC and specificity [(0.773, 95% CI 0.12-0.99, (0.652, 95% CI 0.641-0.664)] of the Asian Working Group for Sarcopenia (AWGS) group was lower than the European Working Group on Sarcopenia in Older People (EWGSOP) group [(0.859, 95% CI 0.12-1.00), (0.874, 95% CI 0.803-0.926)]. Grouping by styles of research, the AUC, sensitivity, and specificity in development group [(0.890, 95% CI 0.16-1.00), (0.751, 95% CI 0.697-0.800), (0.875, 95% CI 0.854-0.895)] were all higher than validation group [(0.715, 95% CI 0.09-0.98), (0.550, 95% CI 0.524-0.576), (0.617, 95% CI 0.604-0.629)]. CONCLUSIONS: Moving forward, there is a critical need to create low-ROB, high-applicability, and more accurate sarcopenia prediction models for MHD patients, customized for diverse global populations.

Effect of emodin on Aquaporin 5 expression in rats with sepsis-induced acute lung injury.

OBJECTIVE: To investigate the effects of emodin on aquaporin 5 (AQP5) expression in rats with sepsis-induced acute lung injury. METHODS: We divided 60 adult male Sprague-Dawley rats, weighing 200-230 g, into four groups: control, sham surgery, model and emodin groups (n = 15 for each). We created a sepsis model with cecal ligation and puncture; the sham surgery group had their cecums replaced after exposure outside the abdominal cavity. Each group was further divided into three subgroups (n = 5 for each) and expressions of AQP5 mRNA and proteins in lung tissue were measured by real-time fluorescence polymerase chain reaction and western blot at 6,12 and 24 h after surgery. RESULTS: AQP5 expression did not change over time in the control group and sham surgery group, but decreased over time in the model group. The lowest expression was found in 12-h subgroup, which significantly differed from the 6-h subgroup (P < 0.01). Compared with the model group, AQP5 expression in the emodin group was significantly higher in all the subgroups (all P < 0.01). Expressions in the 12-h subgroup were the highest, and significantly differed from the other subgroups. We found that lung tissue damage, such as pulmonary edema, alveolar damage and the exudation of red blood cells in pulmonary interstitium and alveolar, was significantly milder in the emodin group under light microscope than the model group. CONCLUSION: AQP5 expression was significantly down-regulated in rats with sepsis-induced acute lung injury induced by cecal ligation and puncture. Early prophylactic use of emodin can significantly enhance the AQP5 expression, thus effectively reducing the degree of pulmonary edema in septic rats.

AZD1480, a JAK inhibitor, inhibits cell growth and survival of colorectal cancer via modulating the JAK2/STAT3 signaling pathway.

Interleukin (IL)-6 and the downstream Janus kinase (JAK)/signal activator of transcription (STAT) pathway have been found to be important in the development of colorectal cancer (CRC). To develop novel therapies for CRC, we have explored the effects of a novel small-molecule JAK inhibitor (AZD1480) on IL-6/JAK/STAT3 pathway and its potential antitumor activity on the human CRC cell lines (HCT116, HT29 and SW480). The results showed that, AZD1480 effectively prevents constitutive and IL-6-induced JAK2 and STAT-3 phosphorylation and exerted antitumor functional effects by a decrease in proliferation and an increase in apoptosis in CRC cells. The inhibition of tumorigenesis was consistent with the decreased phosphorylated JAK2 and phosphorylated STAT3, and the decreased expression of STAT3­targeted genes c-Myc, cyclin D2 and IL-6. Thus, AZD1480 is a potential new clinical therapeutic agent for patients with CRC.