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[This corrects the article DOI: 10.3389/fneur.2023.1252259.].
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Cytokeratin-18 (CK-18) is a marker of hepatic cell death. Serum CK-18 could serve as a prognostic marker for patients with advanced liver disease (ALD). This meta-analysis aims to explore the association between total CK-18 (M65) and caspase-cleaved CK-18 (M30) levels with the prognosis of ALD patients. Relevant longitudinal observational studies were identified through comprehensive searches of the Medline, Web of Science, and Embase databases. A random-effects model was utilized to synthesize the findings, accommodating heterogeneity among studies. The analysis included 14 datasets from 11 studies. Elevated serum CK-18 levels at admission were linked to a higher risk of death or liver transplantation during follow-up. This association was consistent for both M65 (risk ratio [RR] 1.99, 95% confidence interval [CI] 1.65 to 2.40, p < 0.001; I2 = 43%) and M30 (RR 1.94, 95% CI 1.57 to 2.40, p < 0.001; I2 = 46%). Subgroup analysis revealed that the relationship between serum M65 levels and adverse outcomes was attenuated in studies using multivariate analysis compared to those using univariate analysis (RR 1.78 vs. 2.80, p for subgroup difference = 0.03). Further subgroup analyses indicated that the prognostic significance of CK-18 for ALD patients was not significantly influenced by study design, methods of determining CK-18 cutoff values, or follow-up durations. Elevated serum CK-18 levels at admission indicate a poor prognosis in patients with ALD. This finding holds for both M65 and M30.
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Biomarcadores , Queratina-18 , Queratina-18/sangre , Humanos , Pronóstico , Biomarcadores/sangre , Hepatopatías/sangre , Hepatopatías/diagnóstico , Hepatopatías/mortalidad , Trasplante de Hígado , Fragmentos de PéptidosRESUMEN
[This corrects the article DOI: 10.3389/fneur.2023.1252259.].
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BACKGROUND: Many KOA patients have not reached indications for surgery, thus we need to find effective non-surgical treatments. Acupuncture is thought to have the potential to modulate inflammation and cytokines in KOA through the immune system. However, the mechanisms have not been elucidated, and there is no network Meta-analysis of acupuncture on KOA animals. So we evaluate the effect and mechanism of acupuncture-related therapy in KOA animals. METHODS: A comprehensive search was conducted in multiple databases including PubMed, Web of Science, Embase, CBM, CNKI, WanFang, and VIP Database to identify relevant animal studies focusing on acupuncture therapy for KOA. The included studies were assessed for risk of bias using SYRCLE's Risk of Bias tool. Subsequently, pair-wise meta-analysis and network meta-analysis were performed using Stata 15.0 software, evaluating outcomes such as Lequesne index scale, Mankin score, IL-1ß, TNF-α, MMP3, and MMP13. RESULTS: 56 RCTs with 2394 animals were included. Meta-analysis showed that among the 6 outcomes, there were significant differences between acupuncture and model group; the overall results of network meta-analysis showed that the normal group or sham operation group performed the best, followed by the acupotomy, acupuncture, and medicine group, and the model group had the worst effect, and there were significant differences between 6 interventions. CONCLUSIONS: Acupuncture-related therapy can be a possible treatment for KOA. The mechanism involves many immune-inflammatory pathways, which may be mediated by DAMPs/TLR/NF-κB/MAPK,PI3K/Akt/NF-κB pathway, or IFN-γ/JAK-STAT pathway. It needs to be further confirmed by more high-quality animal experiments or meta-analysis. SYSTEMATIC REVIEW REGISTRATION: PROSPERO identifier: CRD42023377228.
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Terapia por Acupuntura , Osteoartritis de la Rodilla , Animales , Humanos , Osteoartritis de la Rodilla/terapia , Metaanálisis en Red , Quinasas Janus , FN-kappa B , Fosfatidilinositol 3-Quinasas , Factores de Transcripción STAT , Transducción de Señal , Terapia por Acupuntura/métodos , Modelos AnimalesRESUMEN
Background: More than half of cancer patients develop severe chemotherapy-induced peripheral neuropathy (CIPN), resulting in low quality of life, negative effects on function, and challenges in treatment compliance. Most recent studies have shown that exercise therapy has a positive impact on reducing CIPN symptoms and can also improve quality of life, balance, and activity levels. The aim of this meta-analysis was to evaluate the effect of exercise therapy on the efficacy of CIPN. Methods: Computerized search of Embase, Web of Science, CNKI, Wan Fang Data, VIP, CBM for RCTs on exercise therapy for CIPN from database creation to November 2022, without language restriction. The Cochrane Handbook 5.3 risk of bias assessment tool was used to evaluate the quality of the included studies. Then Revman 5.3 software was used to evaluate the quality of the included studies. The heterogeneity of the research results is tested by I2, continuous variables were presented as weighted mean difference or standard mean difference, and confidence intervals were set at 95%. Stata15.0 was utilized to conduct a meta-analysis. Results: A total of 15 RCTs with 1,124 patients were included. Meta-analysis showed that the test group was superior to the control group in terms of total symptom score (SMD: -0.62; 95% Cl: -0.99, -0.24), numbness, tingling, quality of life score (total score, physical, function), pain, balance, and neurotoxicity function assessment (FACT/GOG-NTX) questionnaire (p < 0.05). Limitations: The duration and frequency of treatment are different every week, which may have some impact on the results. Conclusion: Exercise therapy can be effective in treating CIPN by improving symptom score (total symptom score, numbness, tingling), quality of life score (total score, physical function), pain, balance, and FACT/GOG-NTX questionnaires. It still needs to be refined and validated by more high-quality, multicenter, large-sample RCTs in the future. Systematic review registration: https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42022373131, identifier: CRD42022373131.
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BACKGROUND: Fluorofenidone (AKF-PD) is a novel pyridone agent. The purpose of this study is to investigate the inhibitory effects of AKF-PD on dimethylnitrosamine (DMN)-induced liver fibrosis in rats and the involved molecular mechanism related to hepatic stellate cells (HSCs). MATERIALS AND METHODS: Wistar rats were randomly divided into normal control, DMN, DMN/AKF-PD treatment and DMN/pirfenidone (PFD) treatment groups. AKF-PD and PFD treatments were, respectively, performed for two activated HSCs lines, rat CFSC-2G and human LX2. The cell proliferation was analysed by MTT. The expression of collagen I was determined by immunohistochemical staining and real-time RT-PCR. The expression of α-smooth muscle actin (α-SMA), tissue inhibitor of metalloproteinases-1 (TIMP-1), extracellular signal regulated kinase (ERK1/2), p38 MAPK (p38), and c-Jun N-terminal kinase/stress-activated protein kinase (JNK) were also detected by real-time RT-PCR and/or Western blot. RESULTS: AKF-PD significantly reduced PDGF-BB-induced proliferation and activation of HSCs, as determined by reducing protein expression of α-SMA and TIMP-1. AKF-PD treatment attenuated PDGF-BB-induced upregulation of phosphorylation of ERK1/2, p38 and JNK. In fibrotic rat liver, AKF-PD reduced the degree of liver injury and hepatic fibrosis, which was associated with reduced the expression of collagen I, α-SMA, TIMP-1 at both mRNA and protein levels. CONCLUSION: AKF-PD treatment inhibits the progression of hepatic fibrosis by suppressing HSCs proliferation and activation via MAPK signalling pathway.