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.

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.

Objectives: The prevalence of posttraumatic stress disorder (PTSD) has increased, particularly among individuals who have recovered from coronavirus disease 2019 (COVID-19) infection. Health literacy is considered a “social vaccine” that helps people respond effectively to the pandemic. We aimed to investigate the association between long COVID-19 and PTSD, and to examine the modifying role of health literacy in this association. Methods: A cross-sectional study was conducted at 18 hospitals and health centers in Vietnamfrom December 2021 to October 2022. We recruited 4,463 individuals who had recovered from COVID-19 infection for at least 4 weeks. Participants provided information about their sociodemographics, clinical parameters, health-related behaviors, health literacy (usingthe 12-item short-form health literacy scale), long COVID-19 symptoms and PTSD (Impact Event Scale-Revised score of 33 or higher). Logistic regression models were used to examine associations and interactions. Results: Out of the study sample, 55.9% had long COVID-19 symptoms, and 49.6% had PTSD.Individuals with long COVID-19 symptoms had a higher likelihood of PTSD (odds ratio [OR], 1.86; 95% confidence interval [CI], 1.63–2.12; p < 0.001). Higher health literacy was associated with a lower likelihood of PTSD (OR, 0.98; 95% CI, 0.97–0.99; p = 0.001). Compared to those without long COVID-19 symptoms and the lowest health literacy score, those with long COVID-19 symptoms and a 1-point health literacy increment had a 3% lower likelihood of PTSD (OR, 0.97; 95% CI, 0.96–0.99; p = 0.001). Conclusion Health literacy was found to be a protective factor against PTSD and modified the negative impact of long COVID-19 symptoms on PTSD.

Purpose: This study aimed to determine the occurrence rate of gestational trophoblastic neoplasia (GTN) and its related factors in aged women with hydatidiform mole (HM) in Tu Du Hospital, Vietnam. Materials and Methods: This retrospective cohort study included 372 women aged ≥40 years with HM diagnosed through postabortion histopathological assessment in Tu Du Hospital from January 2016 to March 2019. Survival analysis was used for GTN cumulative rate estimation, log-rank test for group comparison, and Cox regression model for determining GTN-related factors. Results: After a 2-year follow-up, 123 patients were found to have GTN at a rate of 33.06% [95% confidence interval (CI): 28.30– 38.10]. GTN occurrence meant that the time was 4.15±2.93 weeks with peaks at week 2 and 3 after curettage abortion. The GTN rate was remarkably higher in the ≥46-year age group than in the 40-to-45-year age group [hazard ratio (HR)=1.63; 95%CI: 1.09– 2.44], as was the vaginal bleeding group compared to the non-bleeding group (HR=1.85; 95%CI: 1.16–2.96). Preventive hysterectomy and preventive chemotherapy plus hysterectomy in the intervention group reduced the GTN risk compared to the no intervention group at HRs of 0.16 (95%CI: 0.09–0.30) and 0.09 (95%CI: 0.04–0.21), respectively. Chemoprophylaxis failed to decrease the GTN risk when comparing the two groups. Conclusion Post-molar pregnancy GTN rate in aged patients was 33.06%, much higher than that of the general population. Preventive hysterectomy or chemoprophylaxis plus hysterectomy are effective treatment methods to support GTN risk reduction.

CD46 is a membrane-bound complement regulatory protein (mCRP) possessing a regulatory role with the complement system. CD46 protects the host cells from damage by complement. Expression of CD46 is also highly maintained in many cancers, including bladder cancers, and thus functions as a receptor for many cancer therapeutic viruses.In this study we report a unique role of CD46 as a progression factor of cancer cells in bladder cancers. Resulting data from a DNA microarray using CD46-altered HT1376 bladder cancers demonstrated a pool of target genes, including complement C3  chain (C3), matrix Gla protein (MGP), AFAP-AS1, follicular dendritic cell secreted protein (FDCSP), MAM domain containing 2 (MAMDC2), gamma-aminobutyric acid A receptor pi (GABRP), transforming growth factor, beta-induced (TGFBI), a family of cytochrome P450 (CYP24A1), sialic acid binding Ig-like lectin 6 (SIGLEC6), metallothionein 1E (MT1E), and several members of cytokeratins. Subsequent studies using quantitative RT-PCR and Western blot analyses confirmed CD46-mediated regulation of C3, MGP, and keratin 13 (KRT13). MGP and KRT13 are known to be involved in cell migration and cancer cell metastasis. A cell migration assay demonstrated that CD46 enhanced migratory potential of bladder cancer cells. Taken all together, this report demonstrated that CD46 is generally overexpressed in bladder cancers and plays a unique role in the promotion of cancer cell migration. Further detailed studies are needed to be performed to clarify the action mechanism of CD46 and its application to cancer therapeutics.

Background: Buxus latistyla Gagnep. (Buxaceae) has been used as a remedy for treating malaria, haemoptysis, amoebic dysentery etc. However, its chemical constituents are still unknown. Thus, the aim of this study was to identify phytochemicals isolated from this plant. Materials and method: Aerial parts of B. latistyla were collected from Quang Tri province. Pure compounds were isolated using the combination of chromatographic methods. Structures of isolated compounds were identified by analyzing spectral data of nuclear magnetic resonance as well as by comparing with reported data. Results & Conclusion: Five triterpenes were isolated and identified including lupeol (1), lupenone (2), betulin (3), 20(29)-lupene-2α,3α-diol (4), 20(29)-lupene-2α,3α,28-triol (5). This is the first report about those phytochemicals of B. latistyla collected in Vietnam.

Background: The genus Alpinia is one of the diverse genera in Thua Thien Hue province, in which many species have been used as medicine. But until now, studies on A. vietnamica have rarely been reported. Objectives: The present study was aimed at the determination of microscopic characteristics and chemical compositions as well as evaluating the antioxidant and acetylcholinesterase inhibitory activities of A. vietnamica. Materials and methods: A. vietnamica was collected in Phong Dien district, Thua Thien Hue province. Anatomic structures and powder properties were determined by the microscopic method. Phytochemical screening was conducted by specific chemical reactions. The Folin-Ciocalteau method and the aluminum chloride-flavonoid assay, respectively, were used to quantify the total polyphenol (TPC) and total flavonoid contents (TFC). Antioxidant activity was assessed using the DPPH assay, while acetylcholinesterase (AChE) inhibitory activity was evaluated using the Ellman method. Results: The microscopic characteristics of this species have been described. Phytochemical analysis results revealed the presence of flavonoids, coumarins, and tannins in A. vietnamica. The ethanol extract from the aerial part of A. vietnamica had higher polyphenol and flavonoid contents than the underground part extract. Moreover, this extract also displayed a stronger DPPH radical scavenging and exhibited AChE inhibitory activities. Conclusion: This is the first report on the microscopic characteristics, chemical compositions, and biological activities of A. vietnamica.