EVB DNA fragments from 3 biopsies obtained from Vietnamese patients with NPC have been examined by PCR detection method, using a mixture of primers TH1,2. PRC products were cloned by using vector PCM TM II and were sequenced on Automated sequencer. The result showed that our PCR products were similar to the specific sequence of EBV have been reported in EMBL data library, confirmed that PCR products are specific fragments of EBV, we can successfully use the mixture of primers TH1,2 in PCR detection of EBV DNA in biopsies of NPC patients
Nasopharyngeal Neoplasms ; Base Sequence

Background: Heart failure is a common clinical condition and is the late stage of most cardiovascular diseases. Heart rate disorder is one of the causes of deaths in patients with chronic heart failure. There is few number of studies on Heart Rate Variability (HRV) in Vietnam. Objective: To study the change of HRV time in patients with chronic heart failure. Subject and Method: A prospective, descriptive and cross-sectional study was carried out on 105 subjects including 73 patients with chronic heart failure and 42 normal persons as controls. Time domain measurements of HRV were calculated from 24 hour electrocardiographic Holter (Holter WIN P-V, USA) on all 105 subjects. In the chronic heart failure group, there were 51 men and 22 women with the mean age of 62.8+/-11.2, control group including 30 men and 12 women with the mean age of 61.5+/-5.7. Results and conclusion: (1) There was a decrease of time domain of HRV showed the decrease of parasympathetic tone in patients with chronic heart diseases. (2) The higher degree of heart failure, the lower the time domain of HRV.
Chronic heart disease ; heart rate variability

Balanophora laxiflora Hemsl. (Balanophoraceae) is a traditional medicinal plant with a diverse array of biological activities. In our exploration of new bioactive constituents from B. laxiflora, we isolated five compounds, including a new lignan, balanophorone (5), and four known phenolic compounds (1–4). The chemical structures of these compounds were determined by extensive spectroscopic analyses, including 1D and 2D NMR, HR-ESI-MS, and CD. In addition, we evaluated the effects of each of the isolates (1–5) on the messenger RNA expression levels of tumor necrosis factor (TNF)-α and cyclooxygenase (COX)-2 in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages and cytotoxicity against MCF-7 and MDA-MB-231 breast cancer cells. Compound 2 showed significant inhibition of LPS-induced COX-2 and TNF-α expression in RAW 264.7 macrophages, while compound 4 showed moderate cytotoxicity against MCF-7 and MDA-MB-231 breast cancer cells, with IC 50 values of 18.3 and 30.7 μM, respectively. No significant effects on the viability of normal mammary epithelial cells were observed.

Balanophora laxiflora Hemsl. (Balanophoraceae) is a traditional medicinal plant with a diverse array of biological activities. In our exploration of new bioactive constituents from B. laxiflora, we isolated five compounds, including a new lignan, balanophorone (5), and four known phenolic compounds (1–4). The chemical structures of these compounds were determined by extensive spectroscopic analyses, including 1D and 2D NMR, HR-ESI-MS, and CD. In addition, we evaluated the effects of each of the isolates (1–5) on the messenger RNA expression levels of tumor necrosis factor (TNF)-α and cyclooxygenase (COX)-2 in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages and cytotoxicity against MCF-7 and MDA-MB-231 breast cancer cells. Compound 2 showed significant inhibition of LPS-induced COX-2 and TNF-α expression in RAW 264.7 macrophages, while compound 4 showed moderate cytotoxicity against MCF-7 and MDA-MB-231 breast cancer cells, with IC 50 values of 18.3 and 30.7 μM, respectively. No significant effects on the viability of normal mammary epithelial cells were observed.

Conjoined twins are rare, and each set of conjoined twins has a unique conjoined anatomy. It is necessary to perform separation to increase the chance of patient survival. Tissue expansion is an advanced technique for providing sufficient soft tissue and skin for wound closure. We report the successful application of rapid tissue expansion in 10-month-old xipho-omphalopagus conjoined twins in Vietnam. A tissue expander was placed on the anterior body between the sternum and umbilicus with a baseline of 70 mL sterile saline (0.9% NaCl). The first injection into the tissue expander began on the 6th day after expander insertion, and injections continued every 2 days with approximately 30–70 mL per injection according to the expansion of the skin. The expander reached 335 mL after six injections and within 10 days. In order to prepare for surgical separation, expansion was completed on the 15th day after insertion. The expanded skin area was estimated to be 180 cm2, which was sufficient to cover both patients’ skin deficiencies. The twins presented for surgical separation 6 days following the completion of tissue expansion. Both babies were discharged in good health 1 month after separation.

Conjoined twins are rare, and each set of conjoined twins has a unique conjoined anatomy. It is necessary to perform separation to increase the chance of patient survival. Tissue expansion is an advanced technique for providing sufficient soft tissue and skin for wound closure. We report the successful application of rapid tissue expansion in 10-month-old xipho-omphalopagus conjoined twins in Vietnam. A tissue expander was placed on the anterior body between the sternum and umbilicus with a baseline of 70 mL sterile saline (0.9% NaCl). The first injection into the tissue expander began on the 6th day after expander insertion, and injections continued every 2 days with approximately 30–70 mL per injection according to the expansion of the skin. The expander reached 335 mL after six injections and within 10 days. In order to prepare for surgical separation, expansion was completed on the 15th day after insertion. The expanded skin area was estimated to be 180 cm2, which was sufficient to cover both patients’ skin deficiencies. The twins presented for surgical separation 6 days following the completion of tissue expansion. Both babies were discharged in good health 1 month after separation.

The 5th outbreak of trichinosis occurred in a mountainous area of North Vietnam in 2012, involving 24 patients among 27 people who consumed raw pork together. Six of these patients visited several hospitals in Hanoi for treatment. Similar clinical symptoms appeared in these patients within 5-8 days after eating infected raw pork, which consisted of fever, muscle pain, difficult moving, edema, difficult swallowing, and difficult breathing. ELISA revealed all (6/6) positive reactions against Trichinella spiralis antigen and all cases showed positive biopsy results for Trichinella sp. larvae in the muscle. The larvae detected in the patients were identified as T. spiralis (Vietnamese strain) by the molecular analysis of the mitochondrial cytochrome c oxidase subunit III (cox3) gene.
Adult ; Animals ; Antigens, Helminth/analysis/immunology ; *Disease Outbreaks ; Electron Transport Complex IV/genetics ; Enzyme-Linked Immunosorbent Assay ; Female ; Humans ; Larva ; Male ; Meat/*parasitology ; Mitochondria/genetics ; Muscles/parasitology/pathology ; Swine ; Trichinella spiralis/genetics/immunology/*isolation & purification ; Trichinellosis/*epidemiology/parasitology/pathology ; Vietnam/epidemiology

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.