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Jian Zou,&ast; Jia-Yun Zhong,&ast; Yan-Xin Liu, Yu Liu, Dan Huang, Bian-Tiao Xu, Xi-Wen Li, Wen-Jun Gong, Jia Tao Department of Clinical Pharmacy, The People’s Hospital of Pengzhou, Chengdu, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Jian Zou, The People’s Hospital of Pengzhou, No. 255 Second Section of South Third Ring Road, Chengdu, People’s Republic of China, Tel +86 28 86239898, Email 70336641@qq.comPurpose: Quality control circle (QCC) has acquired success in many fields in healthcare industry as a process management tool, whereas its efficacy in surgical antimicrobial prophylaxis (SAP) remains unknown. This study aimed to implement QCC interventions to improve the appropriateness of SAP.Methods: A QCC activity team was established to grasp the current situation of SAP in clean surgery procedure, set target, formulate corresponding countermeasures and implement and review them in stages. The plan-do-check-act (PDCA) method was cyclically applied.Results: The appropriateness of antibiotic prophylaxis before (January to December 2020) and after (January to December 2021) the implementation of QCC activities were evaluated based on relevant international and Chinese SAP guidelines. The overall SAP appropriateness was significantly improved from 68.72% before QCC to 93.7% post QCC implementation (P< 0.01). A significant improvement (P< 0.05) was also determined for each category: selection (from 78.82% to 96.06%), duration (from 90.15% to 96.46%), indication (from 94.09% to 97.64%), timing of first dose (from 96.55% to 99.21%), antimicrobial usage (from 96.8% to 99.41%), re-dosing of antimicrobial (from 96.55% to 99.21%).Conclusion: Implementation of a QCC program can optimize the use of antibiotics and improve the appropriateness of SAP and is of practical importance to their standardization.Keywords: surgical antimicrobial prophylaxis, quality control circle, appropriateness

Background: Diabetic cardiomyopathy (DbCM) is one of the common complications in diabetic patients, but there is no effective treatment for it up to now. Ketone bodies such as β-OHB have been widely reported to be beneficial for metabolic diseases including various diabetic complications. However, the role of ketone metabolism, especially the relevant enzymes, in the pathogenesis of DbCM is poorly understood., Methods and Results: In this study, we firstly observed BDH1, the rate-limiting enzyme of ketone metabolism, was markedly diminished in cardiac tissues from db/db mice and diabetic patients, as well as in H9C2 cells treated with palmitic acid. Genetic deletion of BDH1 aggravated, whereas AAV-mediated BDH1 overexpression attenuated, the diastolic dysfunction and pathogenic progression including apoptosis, fibrosis and inflammation of hearts from db/db mice. Likewise, BDH1 knockdown promoted, whereas BDH1 overexpression reversed, the palmitic acid-induced lipotoxicity in H9C2 cells. Transcriptome analysis revealed that BDH1 negatively regulated LCN2 expression and LCN2 overexpression largely abrogated BDH1 overexpression-mediated myocardial protection in vitro and in vivo. Mechanistically, BDH1 overexpression reprogrammed ketone metabolism with increased AcAc and decreased β-OHB, thereby resulting in decreased β-hydroxybutyrylation of H3K9 on promoter region of LCN2, which repressed transcription of LCN2 and ultimately inhibited NF-κB activity through weakening interaction between NF-κB and RPS3. Furthermore, oral administration of β-hydroxybutyrylation inhibitor A485 to diabetic mice mitigated the cardiac injury concurrently with decreased expression of LCN2., Conclusion: Our results uncovered a novel mechanism whereby myocardial BDH1 ameliorates DbCM via epigenetic regulation of LCN2, which highlights the potential of BDH1/LCN2-based therapeutics in DbCM., Competing Interests: Declarations. Ethics approval and consent to participate: All procedures that involved human samples were approved by the Affiliated Hospital of Southwest Medical University Ethics Committee (KY2023221). Animal experiments were approved by the Institutional Animals Ethics Committees of Southwest Medical University (20220225-014). Consent for publication: Not applicable. Competing interests: The authors declare no competing interests., (© 2025. The Author(s).)

This letter discusses the research conducted by Abdel-Razeq et al , highlighting a significant association between Helicobacter pylori ( H. pylori ) infection and metabolic dysfunction-associated steatohepatitis (MASH) in individuals with a prior history of H. pylori infection. Using a comprehensive patient database, the study establishes an independent correlation between H. pylori and an elevated risk of MASH, even after adjusting for coexisting conditions such as obesity, type 2 diabetes, and dyslipidemia. Notably, the findings suggest that H. pylori may worsen liver pathology through inflammatory pathways, contributing to hepatic insulin resistance and lipid accumulation. Although the study provides strong evidence for this association, limitations related to diagnostic heterogeneity indicate a need for further research to clarify the underlying mechanisms and to explore the potential roles of genetic and microbiome factors in this relationship., Competing Interests: Conflict-of-interest statement: The authors declare that they have no conflict of interest., (©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.)

This letter discusses the recent study by Mukherjee et al , which identifies a significant prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) among newly diagnosed type 2 diabetes mellitus (T2DM) patients in Bihar, India, and underscores the pressing need for integrated MASLD management within T2DM care. With 72.3% of the study cohort affected by MASLD, implementing routine liver function tests and ultrasound screenings is recommended as a standard practice in diabetes care, especially in regions with high prevalence rates. The study also advocates for dietary and lifestyle modifications, particularly the reduction of saturated fats, to slow MASLD progression. Patient education on monitoring body mass index and waist circumference, coupled with the integration of these metrics into digital health records, could enhance patient involvement and support proactive health management. Moreover, the letter emphasizes the advantages of developing a region-specific MASLD risk model that incorporates local dietary patterns and socioeconomic factors. Continued research into genetic and environmental determinants of MASLD remains essential for advancing our understanding of its etiology and informing targeted public health strategies., Competing Interests: Conflict-of-interest statement: The authors declare that they have no conflict of interest., (©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.)

This article discusses the interplay between colorectal cancer (CRC) stem cells, tumor microenvironment (TME), and gut microbiota, emphasizing their dynamic roles in cancer progression and treatment resistance. It highlights the adaptability of CRC stem cells, the bidirectional influence of TME, and the multifaceted impact of gut microbiota on CRC. The manuscript proposes innovative therapeutic strategies focusing on these interactions, advocating for a shift towards personalized and ecosystem-targeted treatments in CRC. The conclusion underscores the importance of continued research in these areas for developing effective, personalized therapies., Competing Interests: Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article., (©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.)

Nonalcoholic fatty liver disease (NAFLD) is a group of chronic liver disease which ranges from simple steatosis (NAFL) to non-alcoholic steatohepatitis (NASH) and is characterized by lipid accumulation, inflammation activation, fibrosis, and cell death. To date, a number of preclinical studies or clinical trials associated with therapies targeting fatty acid metabolism, inflammatory factors and liver fibrosis are performed to develop effective drugs for NAFLD/NASH. However, few therapies are cell death signaling-targeted even though the various cell death modes are present throughout the progression of NAFLD/NASH. Here we summarize the four types of cell death including apoptosis, necroptosis, pyroptosis, and ferroptosis in the NAFLD and the underlying molecular mechanisms by which the pathogenic factors such as free fatty acid and LPS induce cell death in the pathogenesis of NAFLD. In addition, we also review the effects of cell death-targeted therapies on NAFLD. In summary, our review provides comprehensive insight into the roles of various cell death modes in the progression of NAFLD, which we hope will open new avenues for therapeutic intervention., (© 2024. The Author(s).)

Flame-retardant materials that are mechanically robust, low cost and non-toxic from green and renewable resources are highly demanded in many fields. In this work, aerogels of alginate extracted from seaweeds were fabricated and reinforced with nanoclay. The nanoclay particles increase the molecular ordering (crystallinity) of the aerogels through physical interactions with alginate molecules. They also served as cross-linkers and flame-retardant additives to improve the mechanical strength, elasticity, thermal stability and flame-retarding properties of the aerogels. Under exposure to a butane flame (750 °C), the aerogels maintained their structural integrity and did not produce drips. An optimal loading of nanoclay which led to the best flame retardancy (non-flammable) of the aerogel was determined. The results of this work demonstrate that alginate-nanoclay composite aerogels can be promisingly used as flame-retardant thermal insulation materials., Competing Interests: There are no conflicts to declare., (This journal is © The Royal Society of Chemistry.)

A ketogenic diet (KD) and β-hydroxybutyrate (βOHB) have been widely reported as effective therapies for metabolic diseases. β-Hydroxybutyrate dehydrogenase 1 (BDH1) is the rate-limiting enzyme in ketone metabolism. In this study, we examined the BDH1-mediated βOHB metabolic pathway in the pathogenesis of diabetic kidney disease (DKD). We found that BDH1 is downregulated in the kidneys in DKD mouse models, patients with diabetes, and high glucose- or palmitic acid-induced human renal tubular epithelial (HK-2) cells. BDH1 overexpression or βOHB treatment protects HK-2 cells from glucotoxicity and lipotoxicity by inhibiting reactive oxygen species overproduction. Mechanistically, BDH1-mediated βOHB metabolism activates NRF2 by enhancing the metabolic flux of βOHB-acetoacetate-succinate-fumarate. Moreover, in vivo studies showed that adeno-associated virus 9-mediated BDH1 renal expression successfully reverses fibrosis, inflammation, and apoptosis in the kidneys of C57 BKS db/db mice. Either βOHB supplementation or KD feeding could elevate the renal expression of BDH1 and reverse the progression of DKD. Our results revealed a BDH1-mediated molecular mechanism in the pathogenesis of DKD and identified BDH1 as a potential therapeutic target for DKD.

Diabetes mellitus is a metabolic disease characterized by long-term hyperglycaemia, which leads to microangiopathy and macroangiopathy and ultimately increases the mortality of diabetic patients. Endothelial dysfunction, which has been recognized as a key factor in the pathogenesis of diabetic microangiopathy and macroangiopathy, is characterized by a reduction in NO bioavailability. Oxidative stress, which is the main pathogenic factor in diabetes, is one of the major triggers of endothelial dysfunction through the reduction in NO. In this review, we summarize the four sources of ROS in the diabetic vasculature and the underlying molecular mechanisms by which the pathogenic factors hyperglycaemia, hyperlipidaemia, adipokines and insulin resistance induce oxidative stress in endothelial cells in the context of diabetes. In addition, we discuss oxidative stress-targeted interventions, including hypoglycaemic drugs, antioxidants and lifestyle interventions, and their effects on diabetes-induced endothelial dysfunction. In summary, our review provides comprehensive insight into the roles of oxidative stress in diabetes-induced endothelial dysfunction., (© 2023. BioMed Central Ltd., part of Springer Nature.)

Cannabidiol (CBD) reportedly exerts protective effects against many psychiatric disorders and neurodegenerative diseases, but the mechanisms are poorly understood. In this study, we explored the molecular mechanism of CBD against cerebral ischemia. HT-22 cells or primary cortical neurons were subjected to oxygen-glucose deprivation insult followed by reoxygenation (OGD/R). In both HT-22 cells and primary cortical neurons, CBD pretreatment (0.1, 0.3, 1 μM) dose-dependently attenuated OGD/R-induced cell death and mitochondrial dysfunction, ameliorated OGD/R-induced endoplasmic reticulum (ER) stress, and increased the mitofusin-2 (MFN2) protein level in HT-22 cells and primary cortical neurons. Knockdown of MFN2 abolished the protective effects of CBD. CBD pretreatment also suppressed OGD/R-induced binding of Parkin to MFN2 and subsequent ubiquitination of MFN2. Overexpression of Parkin blocked the effects of CBD in reducing MFN2 ubiquitination and reduced cell viability, whereas overexpressing MFN2 abolished Parkin's detrimental effects. In vivo experiments were conducted on male rats subjected to middle cerebral artery occlusion (MCAO) insult, and administration of CBD (2.5, 5 mg · kg -1 , i.p.) dose-dependently reduced the infarct volume and ER stress in the brains. Moreover, the level of MFN2 within the ischemic penumbra of rats was increased by CBD treatment, while the binding of Parkin to MFN2 and the ubiquitination of MFN2 was decreased. Finally, short hairpin RNA against MFN2 reversed CBD's protective effects. Together, these results demonstrate that CBD protects brain neurons against cerebral ischemia by reducing MFN2 degradation via disrupting Parkin's binding to MFN2, indicating that MFN2 is a potential target for the treatment of cerebral ischemia., (© 2022. The Author(s), under exclusive licence to Shanghai Institute of Materia Medica, Chinese Academy of Sciences and Chinese Pharmacological Society.)