Case Report Open Access 15 Methaemoglobinaemia is a rare but potentially life -threatening cause of hypoxemia that may be overlooked in emergency settings. We report a case of acquired methaemoglobinaemia in a 36 - year-old man following inhalation of an alkyl nitrite –containing recreational product (“Super Rush ”). The patient presented with cyanosis and hypoxemia on pulse oximetry despite minimal symptoms and preserved arterial oxygen tension. Diagnosis was confirmed by co -oximetry demonstrating elevated methaemoglobin levels. Prompt treatment with intravenous methylene blue led to rapid clinical and biochemical improvement. This case highlights the importance of suspecting and recognising recreational inhalants as a cause of methaemoglobinaemia and the utility of co -oximetry in patients with unexplained cyanosis and a saturation gap

Case Report Open Access 15 Methaemoglobinaemia is a rare but potentially life -threatening cause of hypoxemia that may be overlooked in emergency settings. We report a case of acquired methaemoglobinaemia in a 36 - year-old man following inhalation of an alkyl nitrite –containing recreational product (“Super Rush ”). The patient presented with cyanosis and hypoxemia on pulse oximetry despite minimal symptoms and preserved arterial oxygen tension. Diagnosis was confirmed by co -oximetry demonstrating elevated methaemoglobin levels. Prompt treatment with intravenous methylene blue led to rapid clinical and biochemical improvement. This case highlights the importance of suspecting and recognising recreational inhalants as a cause of methaemoglobinaemia and the utility of co -oximetry in patients with unexplained cyanosis and a saturation gap

Background and Objectives: SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms. Methods: Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes. Results: The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes. Conclusions This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.

Background and Objectives: SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms. Methods: Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes. Results: The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes. Conclusions This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.

Background and Objectives: SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms. Methods: Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes. Results: The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes. Conclusions This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.

Background and Objectives: SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms. Methods: Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes. Results: The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes. Conclusions This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.

Objectives: The rapid and widespread development of social networking sites has created a potential venue for an increase in cyberbullying among adolescents. While much research has been done on middle school/high school students, this issue for college/university students has yet to receive much attention. The present study described the prevalence of cyberbullying and associated factors among Hanoi Medical University students. Methods: Data were obtained from an online survey of conveniently selected Hanoi Medical University students. A total of 736 students participated and finished a structured questionnaire based on the Cyberbullying Victimization Scale (CVS). Results: The prevalence of cyberbullying victims among Hanoi Medical University students was 17.4%, and 9.0% of the students had engaged in cyberbullying behaviors. Research also indicated that there is an association between cyberbullying behavior and factors such as internet usage duration and frequency of monitoring violent information. Gender didn't have any relationship with cyberbullying victimization but had a significant association with cyberbullying perpetration (OR = 2.37, 95%CI = 1.42 – 3.96). Conclusion: Cyberbullying has become an important phenomenon related to internet usage duration and violent information among students of Hanoi Medical University. Therefore, it is necessary to build healthy internet habits and manage online information to reduce cyberbullying prevalence and promote student health in the digital age.

Background: Depression, anxiety, and stress have become major public health concerns among adolescents, particularly in the aftermath of the COVID-19 pandemic. Understanding their prevalence and determinants is essential to inform prevention and intervention strategies. Objectives: To describe the prevalence and associated factors of depression, anxiety, and stress among adolescents from 2022 to 2023. Methods: This is a scoping review. We synthesize scientific studies on depression, anxiety, stress in adolescents aged 10-24 years published in journals from three data bases: PubMed, Cochrane, Embase. Results: A total of 34 studies on depression, anxiety, and stress in adolescents were included in the review. This scoping review indicates that prevalence of depression ranged from 12.5% to 90.9%, that of anxiety was between 15.2% and 74.7%, and that of stress ranged from 3.2% to 75.3%. The mean age of participants across studies ranged from 14.5 to 21.9 years. Several factors have been identified in different studies as exacerbating these symptoms among adolescents, including age, gender, education related factors, family background, and risk behaviors. Conclusion: The findings of this review provide valuable insights for parents and health professionals to design effective strategies that mitigate mental health symptoms and foster adolescents’ healthy development.

Purpose: Simple virilizing congenital adrenal hyperplasia (SV-CAH) due to 21-hydroxylase deficiency (21-OHD) is an autosomal recessive disease caused by pathogenic variants of the CYP21A2 gene. Children with SV-CAH often experience delayed diagnosis, presenting with pseudo-precocious puberty in males and genital virilization in females. Genotyping is essential for diagnosis, treatment, optimization, and phenotype prediction. This study describes the clinical and genetic characteristics of SV-CAH to guide treatment strategies. Methods: From November 2016 to March 2023, 79 children (accounting for 34.3% of 230 CAH cases in the overall children’s cohort) from 75 families were classified as SV-CAH due to 21-OHD at the Vietnam National Children's Hospital. Forty-three children underwent CYP21A2 mutation analysis using multiplex ligation-dependent probe amplification and complete gene sequencing to detect pathogenic variants. Results: Median age at diagnosis was 4.5 years (interquartile range, 1 day–22.3 years). There were 38.0% males and 62.0% females. The most common symptoms were penile enlargement in males (53.3%) and clitoromegaly (87.8%) in females; the height standard deviation (SD) at diagnosis was 1.90±1.79 SD (-2.02 to 5.43) according to the World Health Organization; and bone age advancement was 4.65±2.59 years. Genetic analysis identified 21 pathogenic variants and 22 genotypes in 43 children. The most common variant was p.I173N (47.7%); the most common genotype was p.I173N/p.I173N (16.3%). Conclusion Children with SV-CAH are often diagnosed late. To avoid that, early genetic analysis should be prioritized, especially for children diagnosed through newborn screening programs. Determining the genotype is crucial for optimizing treatment strategies, ensuring personalized management, and avoiding overtreatment.

This study aims to describe the feasibility of inserting an oblique lumbar interbody fusion (OLIF) cage through biportal endoscopic lumbar interbody fusion (BE-LIF) and to illustrate the key surgical steps through a case-based video demonstration. BE-LIF is a safe and effective minimally invasive fusion technique. Among the factors influencing successful fusion, the cage footprint plays a critical role—a larger cage increases endplate contact area, maintains disc height, and enhances segmental stability. The OLIF cage offers these biomechanical advantages; however, inserting it through a biportal endoscopic approach is technically demanding and requires several strategic considerations. These include meticulous preoperative planning of portal positions to optimize visualization and working angles, adequate preparation of the disc space window for cage insertion, precise endplate preparation, and safe neural manipulation within a confined surgical field. A 56-year-old female presented with chronic low back pain and bilateral leg symptoms unresponsive to conservative treatment. Imaging revealed severe L4–5 central canal stenosis, foraminal narrowing, and instability. She underwent BE-LIF with OLIF cage insertion and percutaneous pedicle screw fixation. The step-by-step surgical video demonstrates portal placement, decompression, endplate preparation, bone grafting, and cage insertion under combined endoscopic and fluoroscopic guidance. The operation lasted 180 minutes, with an estimated blood loss of 150 mL. The patient was mobilized on postoperative day 1 and discharged on day 5 with marked improvement. Follow-up radiographs confirmed restoration of disc height, correct cage positioning, and adequate decompression. This case demonstrates that BE-LIF with OLIF cage insertion is feasible and may enhance fusion potential by combining the minimally invasive benefits of biportal endoscopy with the biomechanical advantages of a large-footprint cage. However, the procedure remains technically demanding and is best suited for experienced endoscopic spine surgeons.