Background: While advanced age is a known risk factor for postoperative complications following hip arthroplasty, its role as an independent predictor versus a surrogate for comorbidity remains unclear, particularly in developing countries. This study aimed to investigate the independent impact of age on postoperative outcomes and explore the mediating role of key comorbidities in a resource-limited setting. Methods: We retrospectively reviewed 769 adult patients undergoing hip arthroplasty at a Vietnamese tertiary hospital (2021–2024), categorized into three groups: younger adults (18–64 years), older adults (65–79 years), and oldest old (≥80 years). The primary outcome was a composite of major postoperative complications. Multivariable logistic regression and structural equation modeling were used to identify independent predictors and assess mediation effects. Results: Among 769 patients, 363 were younger (47.2%), 241 older adults (31.3%), and 165 oldest old (21.5%). Complication rates increased significantly with age (18.7%, 36.9%, and 60.0%, respectively; p<0.001). However, multivariable adjustment showed that age was not an independent predictor. Instead, heart failure (adjusted odds ratio [aOR]=5.49, 95% confidence interval [CI] 2.19–13.74) and preoperative anemia (aOR=1.77, 95% CI 1.21– 2.59) were identified as independent risk factors. Mediation analysis revealed that the effect of age on complications was significantly mediated through preoperative anemia. Conclusion Increased postoperative risk in older adults is driven by comorbidity burden rather than chronological age. Preoperative anemia and heart failure are critical, independent predictors, with anemia acting as a key mediator for the effects of age. Individualized correction of modifiable comorbidities may be more beneficial than using age alone to assess surgical risk.

Mirizzi syndrome type IV, a rare and complex form of biliary obstruction, has traditionally required major open surgery. This case report describes a groundbreaking alternative: a 44-year-old woman successfully treated using a minimally invasive laparoscopic approach.The less invasive procedure resulted in rapid, complication-free recovery, with no evidence of biliary stricture at the 6-month follow-up. This outcome challenges conventional management and demonstrates that a minimally invasive approach can be both feasible and highly effective in carefully selected patients.

Background: Aspiration pneumonia (AP), which can be caused by gastric content inhalation into the lower airways, causes acute lung injury (ALI) through complex mechanisms, including inflammation, oxidative stress, and apoptosis. Here, we evaluated the efficacy of exosomes derived from human placental mesenchymal stem cells (hpMSCs) in mitigating ALI in a murine model of AP. We also investigated the role of hsa-let-7i-5p, the most abundant miRNA in hpMSC-derived exosomes, in this respect. Methods: Adult male C57BL/6 mouse AP models were administered hpMSC-derived exosomes (APExo group) or phosphate-buffered saline (AP group) intra-tracheally. After 48 h, the mice were euthanized and evaluated. The effects of hsa-let-7i-5p were assessed by specific inhibition or overexpression. Results: Compared with the APExo group, the AP group exhibited significantly greater ALI, as evidenced by histological damage, increased lung injury scores, impaired lung function, increased leukocyte infiltration, and elevated tissue edema (all P < 0.05). The untreated AP group also showed more inflammation, characterized by nuclear factor-κB upregulation, macrophage M1 polarization, and cytokine level elevation (tumor necrosis factor-α, interleukin-1β, and interleukin-6), as well as increased oxidation and activation of the apoptosis pathway (all P < 0.05). Notably, the therapeutic effects of hpMSC-derived exosomes were compromised by specific inhibition of hsa-let-7i-5p. Furthermore, engineered exosomes derived from genetically modified RAW264.7 overexpressing hsa-let-7i-5p demonstrated therapeutic effects against AP similar to those obtained with hpMSC-derived exosomes. Conclusions In a murine AP model, intra-tracheal administration of hpMSC-derived exosomes has ALI-mitigating effects, involving inflammation, oxidation, and apoptosis modulation, with hsa-let-7i-5p playing a pivotal mediating role.

Background: Nonalcoholic fatty liver disease, a progressive condition caused by the accumulation of fat in the liver, begins with simple steatosis and can potentially progress to metabolic dysfunction-associated steatohepatitis (MASH) in the presence of inflammation and fibrosis, ultimately leading to cirrhosis or hepatocellular carcinoma. Increasing evidence indicates that sodiumglucose cotransporter 2 (SGLT2) inhibitors effectively alleviate MASH in mouse models. However, there is a lack of research on the effects of enavogliflozin on liver disease. In the present study, we investigated the effects of SGLT2 inhibitors on MASH induced by a high-fat, high-cholesterol (HFHC) diet in mice. Methods: Male C57BL/6 mice were fed a normal chow diet, HFHC diet, or HFHC diet with enavogliflozin for 12 weeks. LX-2 and HepG2 cells were treated with enavogliflozin in the presence of various pathological stimuli. Results: The HFHC diet induced excessive hepatic lipid accumulation, inflammation, and severe fibrosis. Administration of enavogliflozin not only ameliorated hepatic steatosis and fibrotic conditions but also suppressed the production of inflammatory cytokines. Positive outcomes were also observed in in vitro experiments, where enavogliflozin demonstrated the ability to impede the activation of hepatic stellate cells and alleviate lipid accumulation in hepatocytes. The potential pathway through which enavogliflozin attenuated liver fibrosis development may be associated with the transforming growth factor β1/Smad signaling pathway. Conclusion Our results suggest that enavogliflozin is effective in a mouse model of MASH by attenuating hepatic steatosis, suppressing inflammation, and improving liver fibrosis.

Nonobstructive azoospermia (NOA) affects about 60% of men with azoospermia, representing a severe form of male infertility. The current approach to manage NOA primarily involves testicular sperm retrieval methods such as conventional testicular sperm extraction (c-TESE) and microdissection testicular sperm extraction (micro-TESE). While combining testicular sperm retrieval with intracytoplasmic sperm injection (ICSI) offers hope for patients, the overall sperm retrieval rate (SRR) stands at around 50%. In cases where micro-TESE fails to retrieve sperm, limited options, like donor sperm or adoption, can be problematic in certain cultural contexts. This paper delves into prospective treatments for NOA management. Gene editing technologies, particularly clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated (Cas) protein 9 (CRISPR/Cas9), hold potential for correcting genetic mutations underlying testicular dysfunction. However, these technologies face challenges due to their complexity, potential off-target effects, ethical concerns, and affordability. This calls for research to address key challenges associated with NOA management within the clinical settings. This also necessitate ongoing research essential for developing more sensitive diagnostic tests, validating novel treatments, and customizing current treatment strategies for individual patients. This review concluded that the future of NOA management may entail a combination of these treatment options, tailored to each patient's unique circumstances, providing a comprehensive approach to address NOA challenges.
Humans ; Male ; Gene Editing/methods* ; Azoospermia/genetics* ; Sperm Retrieval ; Sperm Injections, Intracytoplasmic ; CRISPR-Cas Systems ; Spermatozoa ; Stem Cells

Objectives: The objective of this study was to characterize mental health issues among Vietnamese healthcare workers (HCWs) and to identify related factors. Methods: A cross-sectional study was conducted with 990 HCWs in 2021. Their mental health status was measured using the Depression, Anxiety, and Stress Scale. Results: In total, 49.9%, 52.3%, and 29.8% of respondents were found to have depression, anxiety, and stress, respectively. The multivariable linear regression model revealed that factors associated with increased anxiety scores included depression scores (β, 0.45; 95% confidence interval [CI], 0.39 to 0.51) and stress scores (β, 0.46; 95% CI, 0.41 to 0.52). Factors associated with increased depression scores included being frontline HCWs (β, 0.57; 95% CI, 0.10 to 1.10), stress scores (β, 0.50; 95% CI, 0.45 to 0.56), and anxiety scores (β, 0.41; 95% CI, 0.36 to 0.47), while working experience was associated with reduced depression scores (β, -0.08; 95% CI, -0.16 to -0.01). Factors associated with increased stress scores included working experience (β, 0.08; 95% CI, 0.00 to 0.16), personal protective equipment interference with daily activities (β, 0.55; 95% CI, 0.07 to 1.00), depression scores (β, 0.54; 95% CI, 0.48 to 0.59), and anxiety scores (β, 0.45; 95% CI, 0.39 to 0.50), while age was associated with reduced stress scores (β, -0.12; 95% CI, -0.20 to -0.05). Conclusions Specific interventions are necessary to enhance and promote the mental health of HCWs so they can successfully cope with the circumstances of the pandemic.

Aims: The objective of the study was to isolate bacteriophages and conduct a comprehensive analysis of their potential against Xanthomonas oryzae pv. oryzae (Xoo) strains in the Mekong Delta, Vietnam. Methodology and results: Twelve Xoo strains were isolated from rice fields located in the Mekong Delta, Vietnam. Among these strains, three strains Xoo L019, L020 and L024, showed the highest disease index of bacterial blight. Four phages specific to Xoo were isolated from soil, water and leaf samples, and their morphologies were determined. In a test against 12 Xoo strains, phage L541, MLA23 or W41 could infect 10 of the 12 Xoo strains, while phage LBH01 could infect 8 of the 12 Xoo strains. The stability of the phages to pH, organic solvents, UV-A and UV-B was also evaluated. Conclusion, significance and impact of study The initial characterization of the phages indicates their potential as biocontrol agents against bacterial blight in rice. The study is one of the very first studies about Xoo phages in rice in Vietnam.

Background: Liver fibrosis is a common outcome of chronic liver disease and is primarily driven by hepatic stellate cell (HSC) activation. Irisin, a myokine released during physical exercise, is beneficial for metabolic disorders and mitochondrial dysfunction. This study aimed to explore the effects of irisin on liver fibrosis in HSCs, a bile duct ligation (BDL) mouse model, and the associated mitochondrial dysfunction. Methods: In vitro experiments utilized LX-2 cells, a human HSC line, stimulated with transforming growth factor-β1 (TGF-β1), a major regulator of HSC fibrosis, with or without irisin. Mitochondrial function was assessed using mitochondrial fission markers, transmission electron microscopy, mitochondrial membrane potential, and adenosine triphosphate (ATP) production. In vivo, liver fibrosis was induced in mice via BDL, followed by daily intraperitoneal injections of irisin (100 μg/kg/day) for 10 days. Results: In vitro, irisin mitigated HSC activation and reduced reactive oxygen species associated with the TGF-β1/Smad signaling pathway. Irisin restored TGF-β1-induced increases in fission markers (Fis1, p-DRP1) and reversed the decreased expression of TFAM and SIRT3. Additionally, irisin restored mitochondrial membrane potential and ATP production lowered by TGF-β1 treatment. In vivo, irisin ameliorated the elevated liver-to-body weight ratio induced by BDL and alleviated liver fibrosis, as evidenced by Masson’s trichrome staining. Irisin also improved mitochondrial dysfunction induced by BDL surgery. Conclusion Irisin effectively attenuated HSC activation, ameliorated liver fibrosis in BDL mice, and improved associated mitochondrial dysfunction. These findings highlight the therapeutic potential of irisin for the treatment of liver fibrosis.

Background: Liver fibrosis is a common outcome of chronic liver disease and is primarily driven by hepatic stellate cell (HSC) activation. Irisin, a myokine released during physical exercise, is beneficial for metabolic disorders and mitochondrial dysfunction. This study aimed to explore the effects of irisin on liver fibrosis in HSCs, a bile duct ligation (BDL) mouse model, and the associated mitochondrial dysfunction. Methods: In vitro experiments utilized LX-2 cells, a human HSC line, stimulated with transforming growth factor-β1 (TGF-β1), a major regulator of HSC fibrosis, with or without irisin. Mitochondrial function was assessed using mitochondrial fission markers, transmission electron microscopy, mitochondrial membrane potential, and adenosine triphosphate (ATP) production. In vivo, liver fibrosis was induced in mice via BDL, followed by daily intraperitoneal injections of irisin (100 μg/kg/day) for 10 days. Results: In vitro, irisin mitigated HSC activation and reduced reactive oxygen species associated with the TGF-β1/Smad signaling pathway. Irisin restored TGF-β1-induced increases in fission markers (Fis1, p-DRP1) and reversed the decreased expression of TFAM and SIRT3. Additionally, irisin restored mitochondrial membrane potential and ATP production lowered by TGF-β1 treatment. In vivo, irisin ameliorated the elevated liver-to-body weight ratio induced by BDL and alleviated liver fibrosis, as evidenced by Masson’s trichrome staining. Irisin also improved mitochondrial dysfunction induced by BDL surgery. Conclusion Irisin effectively attenuated HSC activation, ameliorated liver fibrosis in BDL mice, and improved associated mitochondrial dysfunction. These findings highlight the therapeutic potential of irisin for the treatment of liver fibrosis.

Background: Liver fibrosis is a common outcome of chronic liver disease and is primarily driven by hepatic stellate cell (HSC) activation. Irisin, a myokine released during physical exercise, is beneficial for metabolic disorders and mitochondrial dysfunction. This study aimed to explore the effects of irisin on liver fibrosis in HSCs, a bile duct ligation (BDL) mouse model, and the associated mitochondrial dysfunction. Methods: In vitro experiments utilized LX-2 cells, a human HSC line, stimulated with transforming growth factor-β1 (TGF-β1), a major regulator of HSC fibrosis, with or without irisin. Mitochondrial function was assessed using mitochondrial fission markers, transmission electron microscopy, mitochondrial membrane potential, and adenosine triphosphate (ATP) production. In vivo, liver fibrosis was induced in mice via BDL, followed by daily intraperitoneal injections of irisin (100 μg/kg/day) for 10 days. Results: In vitro, irisin mitigated HSC activation and reduced reactive oxygen species associated with the TGF-β1/Smad signaling pathway. Irisin restored TGF-β1-induced increases in fission markers (Fis1, p-DRP1) and reversed the decreased expression of TFAM and SIRT3. Additionally, irisin restored mitochondrial membrane potential and ATP production lowered by TGF-β1 treatment. In vivo, irisin ameliorated the elevated liver-to-body weight ratio induced by BDL and alleviated liver fibrosis, as evidenced by Masson’s trichrome staining. Irisin also improved mitochondrial dysfunction induced by BDL surgery. Conclusion Irisin effectively attenuated HSC activation, ameliorated liver fibrosis in BDL mice, and improved associated mitochondrial dysfunction. These findings highlight the therapeutic potential of irisin for the treatment of liver fibrosis.