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Context: Although cancer and HIV/AIDS are common causes of death in Vietnam, limited data exist on their palliative care needs. As palliative care becomes part of Universal Health Coverage, evidence is needed to scale up appropriate care.Objectives: To elicit from people with cancer or HIV/AIDS in Vietnam, and their caregivers, the specific multidimensional symptoms and concerns that cause serious health-related suffering.Methods: Semistructured, qualitative, in-depth interviews were conducted with stage III or IV cancer patients, people with HIV/AIDS, and their caregivers at three cancer treatment centers and two HIV/AIDS treatment centers in northern, central, and southern Vietnam. Interviews were analyzed using thematic analysis.Results: Sixty people were interviewed (21 cancer patients, 20 people with HIV/AIDS, 19 caregivers). Pain and other physical symptoms severely impacted their daily lives. Psychological distress-including sadness, depression, worry, and a feeling of having no future-was mentioned frequently, and it was exacerbated by disease progression and by social problems such as financial difficulties and, among people with HIV/AIDS, stigma. Caregivers also suffered physically and psychosocially. Spirituality emerged as a source of strength for patients. Findings highlighted patients' and family caregivers' desire for more information about diagnosis, prognosis, and treatment, a shift toward individual decision-making.Conclusion: The findings demonstrate common, multidimensional, and severe suffering among people living with cancer or HIV/AIDS and their caregivers in Vietnam. These qualitative data should guide development of optimum clinical assessment tools and palliative care services for these populations. [ABSTRACT FROM AUTHOR]

SUMMARY: Biological fish can create high forward swimming speed due to change of thrust/drag area of pectoral fins between power stroke and recovery stroke in rowing mode. In this paper, we proposed a novel type of folding pectoral fins for the fish robot, which provides a simple approach in generating effective thrust only through one degree of freedom of fin actuator. Its structure consists of two elemental fin panels for each pectoral fin that connects to a hinge base through the flexible joints. The Morison force model is adopted to discover the relationship of the dynamic interaction between fin panels and surrounding fluid. An experimental platform for the robot motion using the pectoral fin with different flexible joints was built to validate the proposed design. The results express that the performance of swimming velocity and turning radius of the robot are enhanced effectively. The forward swimming velocity can reach 0.231 m/s (0.58 BL/s) at the frequency near 0.75 Hz. By comparison, we found an accord between the proposed dynamic model and the experimental behavior of the robot. The attained results can be used to design controllers and optimize performances of the robot propelled by the folding pectoral fins. [ABSTRACT FROM AUTHOR]

Since there is currently a lack of data on the natural history of Odorrana chapaensis, an amphibian species listed in the IUCN Red List (2019), we herein provided the feeding ecology of this amphibian species is virtually lacking. We herein provide data about the diet of O. chapaensis based on the results of our field work in Ngoc Chien Commune, Muong La District and Xim Vang Commune, Bac Yen District, Son La Province, Vietnam. We used the stomach-flushing method to obtain the stomach contents of 85 individuals at two survey sites. A total of 20 prey categories with 334 items, comprising 299 items of invertebrates and 35 unidentified items, were found in the stomachs of O. chapaensis. The dominant prey items of O. chapaensis were Araneae, Polydesmida, insect larvae, Blattodea, Coleoptera, Dermaptera, Lepidoptera, Hymenoptera, and Orthoptera. The importance index for these categories ranged from 3.5% to 32.5%. Coleoptera was the category with the highest frequency of prey items and its representatives were found in 45 stomaches. [ABSTRACT FROM AUTHOR]

Emery-Dreifuss muscular dystrophy (EDMD) is a degenerative neuromuscular disease associated with at least nine genes, including EMD, LMNA, FHL1, TMEM43, SUN1, SUN2, TTN, SYNE1, and SYNE2. Herein, we identified a heterozygous missense LMNA mutation (NM_170707.4: c.1357C>T,p.R453W) in three members of a Vietnamese family using whole-exome sequencing (WES), in which the proband was an 11-year-old girl presenting humeroperoneal muscle weaknesses and generalized contracture. Her father and one other relative also exhibited multiple signs of muscular atrophy and contracture. Sanger sequencing in the extended family verified the causative nature of this mutation, establishing a confirmed diagnosis of autosomal dominant Emery-Dreifuss muscular dystrophy (EDMD2). The clinical presentations of each patient in this study are different from each other, demonstrating the intrafamilial phenotypic variability of this mutation. Early identification of the underlying genetic course of the disease by sequencing, combined with clinical findings provides solid evidence to diagnosis process, genetic counseling and management strategy. [ABSTRACT FROM AUTHOR]

Leigh syndrome is a rare inherited, heterogeneous and progressive neurometabolic disorder that is mainly caused by specific mutations in nuclear DNA (nDNA) or mitochondrial DNA (mtDNA). The present study reported a case of childhood Leigh syndrome with a point mutation at bp 8,993 in the mitochondrial ATPase6 gene. A 21‑month‑old male child had developed epilepsy, muscular weakness and vomiting, which was accompanied by high fever. Magnetic resonance imaging indicated typical characteristics of Leigh syndrome, including a symmetric abnormal signal in the dorsal medulla oblongata and Sylvian fissure enlargement in association with an abnormal signal in the periventricular white matter and in the putamina and caudate heads. The diagnosis was further supported with genetic tests including polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP), sequencing, and quantitative PCR. The patient was found to carry a mitochondrial T8993C (m.T8993C) mutation in peripheral blood with 94.00±1.34% heteroplasmy. Eight of his relatives were also subjected to quantification of the m.T8993C mutation. The percentages of heteroplasmy in samples taken from the grandmother, mother, aunt, cousin 1, and cousin 2 were 16.33±1.67, 66.81±0.85, 71.66±3.22, 87.00±1.79, and 91.24±2.50%, respectively. The mutation was not found in samples taken from the father, the husband of the aunt, or the grandfather of the patient. The obtained data showed that the mutation was maternally inherited and accumulated through generations. Even though the heteroplasmy levels of his mother, aunt, cousin 1, and cousin 2 were relatively high (66.81‑91.24%), they remained asymptomatic, indicating that the threshold at which this mutation shows effects is high. To the best of our knowledge, this is the first report of a case of Leigh syndrome in a Vietnamese individual harboring a mtDNA mutation at the 8,993 bp site, and showing a correlation between the heteroplasmy and clinical phenotype. These findings may be useful in helping to improve the clinical diagnosis and treatment of Leigh syndrome. [ABSTRACT FROM AUTHOR]

Vietnamese patients (106) tentatively diagnosed with encephalomyopathy were screened for the presence of 15 common point mutations in mitochondria using PCR-RFLP. The screened mutations include A3243G, T3271C and T3291C for Mitochondrial Encephalopathy, Lactic Acidosis and Stroke-like episodes (MELAS); A8344G and T8356C for Myoclonus Epilepsy and Rag-Red Fibers (MERRF); G11778A, G3460A and T14484C for Leber's Hereditary Optic Neuropathy (LHON); T8993G/C and T9176G for Leigh syndrome; A1555G for deafness syndrome; G4298A, T10010C, T14728C and T14709C for neuromuscular syndrome. As a result, 6 cases of A3243G (5.7%) and 2 cases of T14727C (3.9%) were found. The 6 cases of A3243G mutation were heteroplasmic at different levels (4.23–80.85%). The T14727C change was discovered for the first time in the MTTE gene encoding for tRNAGluand showed homoplasmy. The T14727C change was probably a mutation because it was further confirmed as vertically inherited from the mother and not the result of isolated polymorphism. [ABSTRACT FROM AUTHOR]

The A3243G mitochondrial mutation is the major cause of mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS). The severity of the disease is correlated with the heteroplasmy level of the mutation. Here we describe for the first time the validation of a real-time polymerase chain reaction (PCR) assay with Taqman locked nucleic acid (LNA) fluorescent (FAM for mutant, HEX for wild type) probes for quantification of heteroplasmy levels in a total of 18 family members from 5 Vietnamese MELAS patients carrying A3243G. Almost no background of FAM signals was detected in normal samples, indicating that the probes were allele-specific. Standard curves indicate sensitive detection at 0.1% mutants and high reliability with R > 0.985. The correlation line between measured % mutant and expected % mutant was highly reliable, with a slope of 0.993 and R of 0.998. All positive A3243G mutant samples pre-screened by PCR-restriction fragment length polymorphism (RFLP) were confirmed, and their heteroplasmy levels quantified to be from 3.68 to 80.85%. The heteroplasmy levels in patients were higher than in their family members and generally correlated well with the severity of their clinical symptoms. Overall, this work is the first demonstration of the application of LNA probes for sensitive and highly reliable quantification of heteroplasmy levels in human mitochondria. [ABSTRACT FROM AUTHOR]