Globally, providing evidence on the economic burden of chronic obstructive pulmonary disease (COPD) is becoming essential as it assists the health authorities to efficiently allocate resources. This study aimed to summarize the literature on economic burden evidence for COPD from 1990 to 2019. This study examined the economic burden of COPD through a systematic review of studies from 1990 to 2019. A search was done in online databases, including Web of Science, PubMed/Medline, Scopus, and the Cochrane Library. After screening 12,734 studies, 43 articles that met the inclusion criteria were identified. General study information and data on direct, indirect, and intangible costs were extracted and converted to 2018 international dollars (Int$). Findings revealed that the total direct costs ranged from Int$ 52.08 (India) to Int$ 13,776.33 (Canada) across 16 studies, with drug costs rannging from Int$ 70.07 (Vietnam) to Int$ 8,706.9 (China) in 11 studies. Eight studies explored indirect costs, while one highlighted caregivers’ direct costs at approximately Int$ 1,207.8 (Greece). This study underscores the limited research on COPD caregivers’ economic burdens, particularly in developing countries, emphasizing the importance of increased research support, particularly in high-resource settings. This study provides information about the demographics and economic burden of COPD from 1990 to 2019. More strategies to reduce the frequency of hospital admissions and acute care services should be implemented to improve the quality of COPD patients’ lives and reduce the disease’s rising economic burden.

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.

Background: s/Aims: Parenchymal-sparing anatomical hepatectomy (Ps–AH) based on portal ramification of the right anterior section (RAS) is a new technique to avoid unnecessarily transecting too much liver parenchyma, especially in cases of major anatomical hepatectomy. Methods: We prospectively assessed 26 patients with primary hepatic malignancies having undergone major Ps–AH based on portal ramification of the RAS from August 2018 to August 2022 (48 months). The perioperative indications, clinical data, intra-operative index, pathological postoperative specimens, postoperative complications, and follow-up results were retrospectively evaluated. Results: Among the 26 patients analyzed, there was just one case that had intrahepatic cholangiocarcinoma The preoperative level of α– Fetoprotein was 25.2 ng/mL. All cases (100%) had Child–Pugh A liver function preoperatively. The ventral/dorsal RAS was preserved in 19 and 7 patients, respectively. The mean surgical margin was 6.2 mm. The mean surgical time was 228.5 minutes, while the mean blood loss was 255 mL. In pathology, 5 cases (19.2%) had microvascular invasion, and in the group of HCC patients, 92% of all cases had moderate or poor tumor differentiation. Six cases (23.1%) of postoperative complications were graded over III according to the Clavien–Dindo system, including in three patients resistant ascites or intra-abdominal abscess that required intervention. Conclusions Parenchymal-sparing anatomical hepatectomy based on portal ramification of the RAS to achieve R0-resection was safe and effective, with favorable short-term outcomes. This technique can be used widely in clinical practice.

Although the need for social and emotional development has existed for decades, implementing Social-Emotional Learning (SEL) in schools continues to get considerable attention as newer generations enter the educational system. The demand for development is presently increasing daily. No one challenges the significance of social-emotional learning and the influence of organizations on adolescent development today. Social-emotional learning matches accurately with the priorities in modern schools. In Vietnam, quantitative research was conducted on 350 high school students. This research aimed to determine how students evaluate the implementation of the Social-emotional learning model in soft skills education. The results revealed students’ interest in implementing the social-emotional learning model into soft skills education. In addition, the results indicated the obstacles to implementing the social-emotional learning model in soft skills education. This study’s findings suggested that school leaders and background educators should implement the social-emotional learning model and support, monitor, and evaluate program efficacy to ensure program objectives are reached and students acquire social and emotional abilities. In addition, the study suggested that specific strategies are necessary to limit the factors that prevent the implementation of the social-emotional learning model in high schools.

Alcohol-dependent patients face a risk of relapse after detoxification and alcohol dependence relapse is affected by many factors in different countries. The study aims to analyze some of the factors associated to the relapse in alcohol-dependent inpatients in northern Vietnam. Methods: A prospective study that monitored alcohol-dependent inpatient in northern Vietnam for six months. Results: Patients with education from high school and higher had a relapse rate of 0.65 times as compared to patients with education below high school (IRR=0.65; 95% CI: 0.43-0.99). Patients with four or more times of alcohol withdrawal had a relapse rate of 1.76 times compared with patients with less than four times of alcohol withdrawal (IRR=1.76; 95% CI: 1.09-2.84). Patients with severe and very severe depressive disorders on the Hamilton depression rating scale at one month after being discharge from hospital had a relapse rate of 4.27 times that of non-depressed patients. (IRR=4.27; 95% CI: 1.08-16.97). Conclusion: Alcohol-dependent patients had many previous alcohol withdrawal times, the cooccurrence of depressive disorder increased alcohol dependence relapse and relapse soon after recovering from alcohol dependence. In particular, higher education was a protective factor against relapse. These factors were depended on economic, medical, cultural and social characteristics in different countries.

Peritoneal dialysis-related peritonitis remains the most common complication and a key barrier to peritoneal dialysis’ long-term success. The present study aimed to report on the incidence of peritonitis and clinical outcomes in CKD patients on CAPD at a hospital in Vietnam’s south and evaluate the peritoneal membrane transport status before and after peritonitis therapy. This study was a cross-sectional study involving 141 participants sampled from the warded adult patients at An Giang center general hospital, in Vietnam. Peritonitis rate was measured in terms of incidences per patient-year. Dialysis fluid was drawn under aseptic conditions and treated using a culture approach to identify bacteria. The response treatment time for each episode of peritonitis after receiving empirical antibiotic medication. We use Peritoneal Equilibration Test (PET) to determine the peritoneal transport status. Peritonitis was found in 29.8% of the cases. The number of episodes of peritonitis per patient-year was 0.035. Negative bacteria account for 81.0 percent of all cases tested. It took an average of 3 to 5 days for a clinical response. Before and after peritonitis, there was no statistically significant connection between transport status groups. The rate of peritonitis identified in this study was significantly lower than that recommended by the International Society for Peritoneal Dialysis (ISPD) recommendations. More research is needed to fully understand the variables that influence the clinical outcomes of peritonitis and the remaining function of the peritoneal membrane.
Peritoneal Dialysis, Continuous Ambulatory

Glioblastoma (GBM) is the most aggressive malignant brain tumor and has a high mortality rate. Photodynamic therapy (PDT) has emerged as a promising approach for the treatment of malignant brain tumors. However, the use of PDT for the treatment of GBM has been limited by its low blood‒brain barrier (BBB) permeability and lack of cancer-targeting ability. Herein, brain endothelial cell-derived extracellular vesicles (bEVs) were used as a biocompatible nanoplatform to transport photosensitizers into brain tumors across the BBB. To enhance PDT efficacy, the photosensitizer chlorin e6 (Ce6) was linked to mitochondria-targeting triphenylphosphonium (TPP) and entrapped into bEVs. TPP-conjugated Ce6 (TPP-Ce6) selectively accumulated in the mitochondria, which rendered brain tumor cells more susceptible to reactive oxygen species-induced apoptosis under light irradiation. Moreover, the encapsulation of TPP-Ce6 into bEVs markedly improved the aqueous stability and cellular internalization of TPP-Ce6, leading to significantly enhanced PDT efficacy in U87MG GBM cells. An in vivo biodistribution study using orthotopic GBM-xenografted mice showed that bEVs containing TPP-Ce6 [bEV(TPP-Ce6)] substantially accumulated in brain tumors after BBB penetration via transferrin receptor-mediated transcytosis. As such, bEV(TPP-Ce6)-mediated PDT considerably inhibited the growth of GBM without causing adverse systemic toxicity, suggesting that mitochondria are an effective target for photodynamic GBM therapy.