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Background and aims: Chinese herbal medicine (CHM) was used to prevent and treat coronavirus disease 2019 (COVID-19) in clinical practices. Many studies have demonstrated that the combination of CHM and Western medicine can be more effective in treating COVID-19 compared to Western medicine alone. However, evidence-based studies on the prevention in undiagnosed or suspected cases remain scarce. This systematic review and meta-analysis aimed to investigate the effectiveness of CHM in preventing recurrent, new, or suspected COVID-19 diseases. Methods: We conducted a comprehensive search using ten databases including articles published between December 2019 and September 2023. This search aimed to identify studies investigating the use of CHM to prevent COVID-19. Heterogeneity was assessed by a random-effects model. The relative risk (RR) and mean differences were calculated using 95% confidence intervals (CI). The modified Jadad Scale and the Newcastle-Ottawa Scale (NOS) were employed to evaluate the quality of randomized controlled trials and cohort studies, respectively. Results: Seventeen studies with a total of 47,351 patients were included. Results revealed that CHM significantly reduced the incidence of COVID-19 (RR = 0.24, 95% CI = 0.11-0.53, p = 0.0004), influenza (RR = 0.37, 95% CI = 0.18-0.76, p = 0.007), and severe pneumonia exacerbation rate (RR = 0.17, 95% CI = 0.05-0.64, p = 0.009) compared to non-treatment or conventional control group. Evidence evaluation indicated moderate quality evidence for COVID-19 incidence and serum complement components C3 and C4 in randomized controlled trials. For the incidence of influenza and severe pneumonia in RCTs as well as the ratio of CD4+/CD8+ lymphocytes, the evidence quality was low. The remaining outcomes including the disappearance rate of symptoms and adverse reactions were deemed to be of very low quality. Conclusion: CHM presents a promising therapeutic option for the prevention of COVID-19. However, additional high-quality clinical trials are needed to further strengthen evidential integrity.
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Chronic obstructive pulmonary disease (COPD) is a lung disease caused by limited airflow that leads to difficulty breathing. It is a major chronic disease that affects human quality of life and even endangers life. However, the exact cause of COPD is still unclear. The present study aimed to identify characteristic genes in COPD, assess the level of immune cell infiltration in COPD samples, and explore the association between characteristic genes and infiltrating immune cells. In this paper, we used dataset GSE76925 to identify 452 differentially expressed genes (DEGs) (including 407 downregulated and 45 upregulated DEGs). Gene Ontology (GO) enrichment analysis showed that the functions mainly include leukocyte migration, protein folding, negative regulation of cell activation, transcription regulator complex, collagen-containing extracellular matrix, RNA polymerase II transcription regulator complex, guanyl nucleotide binding, guanyl ribonucleotide binding, ubiquitin protein ligase binding, etc. In the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, pathways identified by DEGs mainly focused on Basal transcription factors, Arachidonic acid metabolism, Nucleocytoplasmic transport, Glutamatergic synapse, Ether lipid metabolism, alpha-Linolenic acid metabolism, etc. Next, we constructed a weighted gene co-expression network, identified six gene modules, found that the module with the highest correlation was the MEturquoise, and obtained 51 hub module genes. Further, 43 overlapping genes were obtained after the intersection of 452 DEGs and 51 hub genes in MEturquoise module, and seven characteristic DEGs (C-DEGs) (LOC649214, LOC440563, LOC643431, LOC642585, KRT18P17, LOC648057 and UBASH3B) were identified by the Least absolute shrinkage and selection operator (LASSO) regression method. In addition, we assessed the infiltration of 28 immune cells in 111 COPD samples and 40 NC samples, calculated and visualized the correlation between the expression of 7 C-DEGs and the infiltration level of 28 immune cells. These results will contribute to our further understanding of the molecular immunopathogenesis of COPD and have potential reference value for the development of molecular drug targets in the future.
Subject(s)
Pulmonary Disease, Chronic Obstructive , Quality of Life , Humans , Pulmonary Disease, Chronic Obstructive/genetics , DyspneaABSTRACT
The combined index of hemoglobin, albumin, lymphocyte, and platelet (HALP) is a novel indicator reflecting systemic inflammation and nutritional status. To explore the relationship between HALP score and ICU mortality risk in patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD). A total of 1533 AECOPD patients from the eICU Collaborative Research Database (eICU-CRD) between 2014 and 2015 were included in this retrospective cohort study. Univariate and multivariate Cox proportional hazards models were utilized to investigate the association of HALP score, platelet-to-lymphocyte ratio (PLR) score, and lymphocyte-to-monocyte ratio (LMR) score with the ICU mortality risk in patients with AECOPD. Stratified analyses were performed based on patients' ICU admission type, body mass index (BMI), and Acute Physiology, Age and Chronic Health Evaluation IV (APACHE IV) score. Of these 1533 AECOPD patients, 123 (8.00%) patients died in the ICU. Low HALP score [hazard ratio (HR) = 1.69; 95% confidence interval (CI) 1.14-2.53] and low LMR score (HR = 1.60; 95% CI 1.07-2.39) were associated with an increased ICU mortality risk in patients with AECOPD after adjusting for all confounders. Stratified analyses indicated that low HALP score were still associated with a higher ICU mortality risk in patients admitted to ICU by emergency (HR = 1.81; 95% CI 1.11-2.96), obese patients (HR = 2.81; 95% CI 1.29-6.10), and patients with low APACHE scores (HR = 2.87; 95% CI 1.75-4.69). Low HALP score was associated with an increased risk of ICU mortality in patients with AECOPD, suggesting that the HALP score may be a novel prognostic predictor in patients with AECOPD.
Subject(s)
Lymphocytes , Pulmonary Disease, Chronic Obstructive , Humans , Retrospective Studies , Prognosis , Albumins , Hemoglobins/analysis , Intensive Care UnitsABSTRACT
INTRODUCTION: Cisplatin, a chemotherapeutic drug, is widely used for the treatment of various malignant tumors with good effects. However, cisplatin-induced nephrotoxicity is a major dose-limiting factor and a significant adverse event. Mannitol is used to reduce cisplatin-induced nephrotoxicity, which is controversial. This study aimed to evaluate the efficacy and safety of a hydration regimen containing mannitol against cisplatin-induced nephrotoxicity through a meta-analysis. METHODS: Potential records from PubMed, EMBASE, Cochrane Library, and ClinicalTrials that met the inclusion criteria were included from inception to May 2021. Cochrane Collaboration tools were used to assess the risk of bias in the included studies. Jadad's and NOS scores were applied to assess the quality of randomized controlled trials (RCTs) and case-control studies. A random-effects model or fixed-effects model was used depending on the heterogeneity. Subgroup analyses were performed to evaluate the potential study characteristics. The pooled odds ratios (ORs) and 95% confidence intervals (CIs) were evaluated. RESULTS: Four RCTs and seven case-control studies involving 4168 patients were included. Pooled results showed that mannitol use could reduce the incidence of cisplatin-induced nephrotoxicity (OR = 0.66, 95% CI [0.45-0.97], p = 0.03), especially reducing grade 3 nephrotoxicity events according to CTCAE 4.0 (OR = 0.37,95% CI [0.16-0.84]). Moreover, mannitol use was not significantly associated with creatinine clearance, serum creatine, and electrolyte disturbance (p > 0.05). Gastrointestinal cancer (OR = 0.36, 95% CI [0.15-0.83], p = 0.02) and urinary tract cancer (OR = 0.32,95% CI [0.14-0.73], p = 0.007) may be more sensitive to mannitol, although the test for overall effect was significantly different (OR = 0.66, 95% CI [0.49-0.89], p = 0.007). For patients with diabetes and hypertension, mannitol may worsen renal function (OR = 1.80, 95% CI [1.18-2.72], p = 0.006; OR = 2.19, 95% CI [1.50, 3.19], p < 0.0001, respectively). Mannitol may have a better protective effect when doses of mannitol were ≥ 25 g (OR = 0.58, 95% CI [0.39-0.88], p = 0.01) and doses of cisplatin < 75 mg/m2 (OR = 0.59, 95% CI [0.36-0.94], p = 0.03). It revealed that mannitol use was likely to cause nausea or vomiting (OR = 1.86, 95% CI [1.20-2.89], p = 0.006). CONCLUSION: Current evidence revealed that mannitol was an effective and safe drug to reduce cisplatin-induced nephrotoxicity events, especially Grade 3 events. However, it may cause more nausea/vomiting events and deteriorate renal function in patients with diabetes or hypertension. We also found that mannitol had the best effect when mannitol was ≥ 25 g in total or cisplatin was < 75 mg/m2. Meanwhile, mannitol may have a better effect on gastrointestinal and urinary tract cancers. SYSTEMATIC REVIEW REGISTRATION: crd. york. ac. uk/PROSPERO, CRD 42021253990.
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Long non-coding RNAs (lncRNA) and microRNAs (miRNAs) are a subject of active investigation in neurodegenerative disorders including Parkinson's disease (PD). We hypothesized a regulatory role of lncRNA H19 with involvement of hypoxanthine phosphoribosyltransferase 1 (HPRT1) in dopaminergic neuron loss in PD model mice obtained by 6-hydroxydopamine (6-OHDA) lesions. We predicted the differentially expressed genes and related mechanisms by microarray analysis. We measured the expression of tyrosine hydroxylase (TH) and proneural genes in the substantia nigra of lesioned mice before and after treatment with lentiviral oe-HPRT1, agomir-miR-301b-3p and inhibition of the Wnt/ß-catenin pathway. We also evaluated the relationship among lncRNA H19, HPRT1 and miR-301b-3p as well as the Wnt/ß-catenin signaling pathway in these mice. The obtained results predicted and further confirmed a low level of HPRT1 in lesioned mice. We found low expression of lncRNA H19 and showed that its forced overexpression regulated HPRT1 by binding to miR-301b-3p. The overexpression of HPRT1 increased TH expression and inhibited dopaminergic neuron loss via activating the Wnt/ß-catenin pathway, as reflected by increased expressions of Nurr-1, Pitx-3, Ngn-2 and NeuroD1. Thus, overexpressed lncRNA H19 protects against dopaminergic neuron loss in this PD model through activating the Wnt/ß-catenin pathway via impairing miR-301b-3p-targeted inhibition of HPRT1 expression.
Subject(s)
Dopaminergic Neurons , Hypoxanthine Phosphoribosyltransferase/metabolism , MicroRNAs , Parkinson Disease/metabolism , RNA, Long Noncoding , Animals , Disease Models, Animal , Dopaminergic Neurons/cytology , Dopaminergic Neurons/metabolism , Male , Mice , Mice, Inbred C57BL , MicroRNAs/genetics , MicroRNAs/metabolism , RNA, Long Noncoding/genetics , RNA, Long Noncoding/metabolism , Substantia Nigra/chemistry , Substantia Nigra/metabolism , Substantia Nigra/pathology , Wnt Signaling Pathway/physiologyABSTRACT
An efficient Fe-catalyzed esterification of primary, secondary, and tertiary amides with various alcohols for the preparation of esters was performed. The esterification process was accomplished with FeCl3·6H2O, which is a stable, inexpensive, environmentally friendly catalyst with high functional group tolerance.