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Background: Medication adherence to inhaler therapy is pivotal for optimizing the management of Chronic Obstructive Pulmonary Disease (COPD). Individuals with COPD often have suboptimal adherence behaviors to inhaler therapy. Illness perception and beliefs about medicines have been proved to be associated with medication adherence. Nevertheless, the influence of illness perception and medication beliefs on adherence to inhaler therapy among elderly individuals with COPD in China remains unclear. Methods: A cross-sectional study was conducted on 252 elderly COPD participants in China from June 2022 to September 2023. The Test of Adherence to Inhalers (TAI), the Brief Illness Perception Questionnaire (B-IPQ) and the Belief about Medicines Questionnaire (BMQ) were utilized. Spearman correlations, regression analysis and parallel mediation analysis were employed to assess the correlations and mediating effects among beliefs about medicines, illness perception, and medication adherence to inhaler therapy. Results: Medication adherence to inhaler therapy exhibited a negative correlation with concerns beliefs, while showing positive correlations with illness perception, necessity beliefs and total BMQ scores. Mediating effects of concerns beliefs and necessity beliefs were observed in the relationship between perception of illness and medication adherence to inhaler therapy. Conclusions: This study suggests that essential interventions targeting beliefs about medicines in elderly individuals with COPD should be implemented to optimize the level of their inhaler adherence, particularly in those with low levels of necessity beliefs or high levels of concerns beliefs., (Copyright © 2024 by Daedalus Enterprises.)

BACKGROUND The results of previous studies that evaluated the association between pretreatment blood platelet-to-lymphocyte ratio (PLR) and clinical outcomes and chemosensitivity in patients with advanced gastric cancer are inconsistent. Therefore, this study was designed to investigate the association between pretreatment blood PLR and clinical outcomes and chemosensitivity in advanced gastric cancer patients. MATERIAL AND METHODS We performed a systematic literature search in PubMed, Web of Science, EMBASE, and the Cochrane Library up to Mar 9, 2021. Hazard ratios (HRs) for overall survival (OS) and disease-free survival (DFS) were pooled for meta-analysis. The quality of the included studies was measured by the Newcastle-Ottawa Quality Assessment Scale. RESULTS We included 17 studies comprising 3499 patients with advanced GC in this meta-analysis. Pooled results demonstrated that high PLR was correlated with poor OS (HR=1.429, 95% CI=1.246-1.639, P<0.001) and DFS (HR=1.47, 95% CI=1.14-1.88, P=0.003) compared with low PLR in patients with advanced GC. Moreover, high PLR was associated with a lower response to chemotherapy in patients with advanced GC (OR=1.395, 95% CI=1.056-1.841, P=0.019). However, there was no significant correlation between PLR and clinicopathological features. CONCLUSIONS This meta-analysis suggests that high PLR is a risk factor for unfavorable OS, DFS, and chemosensitivity in patients with advanced GC.

Purpose: Liver cancer or hepatocellular carcinoma (HCC) is considered as one of the most frequent malignancies with significantly high morbidity and mortality across the globe. MicroRNAs (miRs) are regarded as important regulators of liver cancer formation and its development. However, the full biochemical mechanism of their role is still very less understood. The main objective of the current research work was to examine the role of miR-16/cyclin-B1 axis in liver cancer regulation and how this pathway along with liver cancer migration and invasion are targeted by zingiberene molecule., Methods: Quantitative reverse transcriptase polymerase chain reaction was used to evaluate miR-16 expression in HCC cell lines. Western blotting was performed to evaluate the expression of the miR-16 target genes. Effects on cell migration and invasion were evaluated by in vitro wound healing assay and transwell Matrigel assay, respectively. Effects of zingiberene on HCC cell viability were evaluated by MTT assay., Results: Zingiberene treatment led to downregulation of miR-16 in HepG2 human hepatocellular carcinoma cells, accompanied by induction of G0/G1 cell cycle arrest targeting cyclin B1 as direct target. These effects were also accompanied by inhibition of cell migration and invasion, indicating that miR-16 can have a significant role as liver cancer suppressor after zingiberene treatment. Luciferase reporter assay confirmed that miR-16, which was one of HCC downregulated miRs, directly targeted Cyclin B1 in HCC cells., Conclusion: The current study indicates miR-16/cyclin B1 axis might have significant applications as a therapeutic target for patients with liver cancer.

Purpose: Gastric carcinoma is the fourth leading cause of cancer-related morbidity throughout the globe. There are limited clinical therapies for gastric cancer due to lack of effective drugs and ambiguity in molecular mechanisms. As such there is a pressing need for novel and effective anticancer drugs for gastric cancer. The main aim of the current research work was to investigate the anticancer effects of Lanostane natural product in MKN-45 human gastric cancer cells along with evaluating its effects on cell autophagy, apoptosis, and m-TOR/PI3K/AKT signalling pathway., Methods: MTT cytotoxicity assay was used to evaluate cell viability of MKN-45 human gastric cancer cells. Apoptosis was evaluated by fluorescence microscopy using Hoechst 33258 and Annexin-V/propidium iodide (PI) assay using flow cytometry. Autophagy was evaluated by transmission electron microscopy (TEM) and western blot method. Effects on m-TOR/PI3K/AKT related protein expression were evaluated by western blot method., Results: Lanostane molecule led to substantial and dose-dependent growth inhibitory effects onMKN-45 human gastric cancer cells. Clonogenic assay showed significant decrease in MKN-45 cell colonies. Hoechst 33258 and annexin V/PI revealed that lanostane induced dominant apoptotic effects in these cells and exhibited dose-dependence. TEM revealed that lanostane induced autophagy in MKN-45 cells by forming autophagosomes and autophagic vacuoles. Lanostane also targeted m-TOR/PI3K/AKT signalling pathway by altering the expression of some key proteins., Conclusion: Lanostane displayed strong anticancer effects in MKN-45 human gastric cancer cells by triggering apoptosis and autophagy and targeting m-TOR/PI3K/AKT signalling pathway.

Hepatitis B infection is a major global health problem and a primary cause of hepatocellular carcinoma (HCC). While various antiviral treatments have been explored, there is not yet a reliable method for preventing the progression of chronic hepatitis B infection into HCC. Hepatitis B virus X protein (HBx) plays a major role in viral replication, chronic inflammation and the pathogenicity of chronic liver disease. Modulation of purinergic receptors using their specific agonists has become a popular new strategy for modifying disease processes. In the present study, we investigated the involvement of the P2Y 11 receptor using its specific antagonist NF157 in some key aspects of HBx-induced liver disease in human MIHA hepatocytes, including mitochondrial dysfunction due to compromised mitochondrial membrane potential (MMP), oxidative stress resulting from overproduction of reactive oxygen species (ROS) and decreased antioxidant glutathione (GSH), production of proinflammatory cytokines and chemokines such as interleukin (IL)-6, monocyte chemoattractant protein (MCP)-1, and chemokine (C-X-C motif) ligand 2 (CXCL2), as well as activation of cellular signaling pathways including the p38/mitogen-activated protein kinase (p38/MAPK) and nuclear factor-κB (NF-κB) pathways. Our findings present a novel new strategy for the treatment and prevention of chronic liver infection and subsequent morbidities induced by HBx via specific antagonism of the P2Y 11 purinergic receptor., Competing Interests: None.

The major histocompatibility complex class I chain-related gene A transmembrane (MICA-TM) polymorphism has been implicated in susceptibility to cancer. However, the results are inconsistent. The aim of this meta-analysis is to evaluate the association between the MICA-TM polymorphisms and cancer risk. All eligible case-control studies published up to August 20, 2014 were identified by searching PubMed, Web of Science, CNKI and Wanfang databases. The cancer risk associated with the MICA polymorphism was estimated for each study by odds ratios (OR) together with its 95% confidence interval (CI), respectively. 21 studies from 19 publications with 3620 cases and 4903 controls were included. Overall, no significant associations between the MICA-TM polymorphism and cancer risk were found (A4 allele: OR = 0.97, 95% CI: 0.88-1.07; A5 allele: OR = 0.91, 95% CI: 0.81-1.04; A5.1 allele: OR = 1.03, 95% CI: 0.89-1.18; A6 allele: OR = 1.05, 95% CI: 0.95-1.15; A9 allele: OR = 0.96, 95% CI: 0.80-1.14; A10 allele: OR = 0.88, 95% CI: 0.43-1.79; del: OR = 2.50, 95% CI: 0.73-8.58; A7 allele: OR = 0.93, 95% CI: 0.43-2.00). When stratified by ethnicity, similar results were observed among Asians; however, there were significant association in Caucasian population for A5 (OR = 0.77, 95% CI: 0.68-0.87) and A9 allele (OR = 0.75, 95% CI: 0.66-0.85). This meta-analysis suggests that the MICA-TM A5 and A9 alleles may be an important protective factor for cancer in Caucasian populations.