Association Between Prognostic Nutritional Index and Prognosis in Patients With Heart Failure: A Meta-Analysis.

Background: The prognostic nutritional index (PNI) has been proposed as a marker of malnutrition and associated with the prognosis of cardiovascular disease. However, whether PNI can serve as a potential biomarker for the prognosis of heart failure (HF) upon those established risk factors were still controversial. This meta-analysis aimed to generate comprehensive evidence on the prognostic value of PNI in patients with HF. Methods: Multiple databases (PubMed, Embase, the Cochrane Library, and Google Scholar) were searched for related studies up to January 31, 2022. Observational studies accessed associations between PNI levels and the prognosis in patients with HF were included for meta-analysis. The hazard ratios (HRs) and 95% confidence intervals (CI) were calculated. Results: Fourteen studies, comprising 19,605 patients with HF were included for meta-analysis. The median follow-up duration was 18.5 months. Compared with those with higher PNI (normal nutritional status), patients with HF with lower PNI (malnourished) were associated with a higher risk of all-cause mortality (HR 1.53, 95% CI 1.27-1.85) and composite major adverse cardiac outcomes (MACEs; HR 2.26, 95% CI 1.54-3.31) in the multivariable-adjusted model. Furthermore, when PNI was defined as per 1 increment as a continuous metric, higher PNI was associated with a decrease in all-cause mortality (per 1 increment of PNI: HR 0.94, 95% CI 0.88-0.96) and MACEs (per 1 increment of PNI: HR 0.97, 95% CI 0.95-0.98). Conclusions: The PNI can serve as an easily calculated bedside "malnutrition-inflammation" biomarker in HF. Lower PNI was associated with a worse prognosis in patients with HF.

α-Linolenic Acid and Risk of Heart Failure: A Meta-Analysis.

Background: The α-linolenic acid is a plant origin n-3 fatty acid that may reduce the risk of cardiovascular disease. However, the effect of α-linolenic acid (ALA) on the risk of heart failure (HF) remains unclear. In this meta-analysis, we aimed to determine the role of ALA in the risk of incident HF. Methods: Electronic databases were searched for studies up to August 10, 2021. Studies were included for meta-analysis if the adjusted risk of HF in different dietary intake or circulating levels of ALA was reported. We used the random-effects model to calculate the estimated hazard ratios (HRs) and 95% CI for higher ALA. Results: A total of 6 studies (7 cohorts) comprising 135,270 participants were included for meta-analysis. After a median follow-up duration of 10 years, 5,905 cases of HF were recorded. No significant heterogeneity was observed among all the included studies. Random-effects model analyses showed that there was no significant association between ALA and the risk of incident HF, either assessed as quintiles (highest quintile vs. lowest quintile: HR = 0.95, 95% CI = 0.86-1.06) or per 1 SD increment (HR = 0.99, 95% CI = 0.95-1.01). Furthermore, we did not observe any association between ALA and the risk of HF in subgroup analyses performed according to age, sex, follow-up duration, and measuring method of ALA. Conclusions: We found no association between ALA and the risk of incident HF, suggesting that ALA might not be effective in the prevention of HF.

Resistance of Klebsiella pneumoniae Strains Carrying bla NDM-1 Gene and the Genetic Environment of bla NDM-1.

OBJECTIVE: Regional dissemination is the major cause of the widespread prevalence of a plasmid-encoding NDM-1 enzyme. We investigated the drug resistance, joint efficiency, and gene environment of a Klebsiella pneumoniae strain carrying bla NDM-1 gene. MATERIALS AND METHODS: Carbapenem-non-susceptible strains were analyzed using the VITEK 2 Compact. Strains carrying bla NDM-1 were identified using polymerase chain reaction and sequencing. Antimicrobial susceptibility testing and plasmid conjugation experiments were then conducted. Strains carrying bla NDM-1 were subjected to Southern blot analysis. After the gene mapping of bla NDM-1, library construction, and sequencing, plasmids were subsequently spliced and genotyped using the software Glimmer 3.0, and then analyzed using Mauve software. RESULTS: Among 1735 carbapenem-non-susceptible strains, 54 strains of bla NDM-1-positive bacteria were identified, which consisted of 44 strains of K. pneumoniae, 8 strains of Acinetobacter baumannii and 2 strains of Escherichia coli. Strains carrying bla NDM-1 had a resistance rate of more than 50% in most antibiotics. Plasmid conjugation between strains carrying bla NDM-1 and E. coli strain J53 had a success rate of 50%. Southern blot analysis indicated that each strain had multiple plasmids containing bla NDM-1. Among the five plasmids containing bla NDM-1 in K. pneumoniae for sequencing, two plasmids with complete sequences were obtained. The findings were as follows: (i) The p11106 and p12 plasmids were highly similar to pNDM-BTR; (ii) the p11106 and p12 plasmids showed differences in the 20-30 kb region (orf00032-orf00043) from the other six plasmids; and (iii) bla NDM-1 was located at orf00037, while ble was found at orf00038. Two tnpA genes were located in the upstream region, and orf00052 (tnpA) in the 36 kb region was in the downstream sequence. CONCLUSION: bla NDM-1-containing bacteria exhibit multidrug resistance, which rapidly spreads and is transferred through efficient plasmid conjugation; the multidrug resistance of these bacteria may be determined by analyzing their drug-resistant plasmids. The presence of ble and tnpA genes suggests a possible hypothesis that bla NDM-1 originates from A. baumannii, which is retained in K. pneumoniae over a long period by transposition of mobile elements.

The possible association between AQP9 in the intestinal epithelium and acute liver injury­induced intestinal epithelium damage.

The present study aimed to investigate the expression and function of aquaporin (AQP)9 in the intestinal tract of acute liver injury rat models. A total of 20 Sprague Dawley rats were randomly divided into four groups: Normal control (NC) group and acute liver injury groups (24, 48 and 72 h). Acute liver injury rat models were established using D­amino galactose, and the serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (Tbil) and albumin were determined using an automatic biochemical analyzer. Proteins levels of myosin light chain kinase (MLCK) in rat intestinal mucosa were investigated via immunohistochemistry. Pathological features were observed using hematoxylin and eosin (H&E) staining. MLCK, AQP9 and claudin­1 protein expression levels were detected via western blotting. Levels of ALT and AST in acute liver injury rats were revealed to steadily increase between 24 and 48 h time intervals, reaching a peak level at 48 h. Furthermore, TBil levels increased significantly until 72 h. Levels of ALT were revealed to significantly increase until the 48 h time interval, and then steadily decreased until the 72 h time interval. The acute liver injury 72 h group exhibited the greatest levels of MLCK expression among the three acute liver injury groups; however, all three acute liver injury groups exhibited enhanced levels of MLCK expression compared with the NC group. Protein levels of AQP9 and claudin­1 were enhanced in the NC group compared with the three acute liver injury groups. H&E staining demonstrated that terminal ileum mucosal layer tissues obtained from the acute liver injury rats exhibited visible neutrophil infiltration. Furthermore, the results revealed that levels of tumor necrosis factor­α, interleukin (IL)­6 and IL­10 serum cytokines were significantly increased in the acute liver injury groups. In addition, AQP9 protein expression was suppressed in acute liver injury rats, which induced pathological alterations in terminal ileum tissues may be associated with changes of claudin­1 and MLCK protein levels.

Oxidored-nitro domain-containing protein 1 promotes liver fibrosis by activating the Wnt/ß-catenin signaling pathway in vitro.

Hepatic fibrosis is a characteristic of various types of chronic liver diseases, and may further develop into liver cirrhosis and liver cancer. Oxidored­nitro domain­containing protein 1 (NOR1) expression levels are greater in hepatitis, cirrhosis and hepatocellular carcinoma samples compared with from normal liver samples. However, the importance of NOR1 in liver fibrosis remains to be elucidated. The present study aimed to investigate the effect of NOR1 on the proliferation and matrix expression of human hepatic stellate cells (HSCs) in vitro. Additionally, the molecular mechanisms underlying the role of NOR1 in the activation of HSCs was investigated. The present study determined that transforming growth factor ß1 (TGF­ß1) may induce NOR1 expression in HSCs in a dose­dependent manner, as determined by reverse transcription­quantitative polymerase chain reaction and western blot analysis. NOR1­small hairpin (sh)RNA was transfected into TGF­ß1­treated HSCs to knock down NOR1. The MTT assay revealed that TGF­ß1­induced cell proliferation was significantly inhibited in the NOR1­shRNA group. In addition, NOR1 knockdown significantly inhibited TGF­ß1­induced protein expression of fibrosis indexes, including collagen 1, 3 and α­smooth muscle actin (α­SMA). Subsequently, NOR1­pcDNA3.1 was transfected into HSCs to overexpress NOR1. It was revealed that NOR1 overexpression may activate the Wnt/ß­catenin pathway in HSCs. The gain­of function experiments demonstrated that NOR1 overexpression promoted cell proliferation and the expression of fibrosis indexes; however, these effects may be attenuated by dickkopf­1, an inhibitor of the Wnt/ß­catenin signaling pathway. In conclusion, the present study demonstrated that NOR1 activates HSCs and contributes to liver fibrosis in vitro and this effect was achieved through the activation of the Wnt/ß­catenin pathway. Therefore, the current study may provide a novel target for the treatment of chronic liver diseases.