22 research outputs found

    Assessment of cattle marketing in Ea Kar district, Daklak, Vietnam in 2008

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    This paper describes and discusses the results of a Cattle Market Study conducted in Ea Kar district, Daklak province of Vietnam in 2008. Since 2000, CIAT, TNU and NIAH, in partnership with the Ea Kar Extension Service and District Government, have worked in Ea Kar to introduce the concept of cultivating forage grasses and legumes on farmers’ land for improved smallholder beef cattle production. By 2007, more than 2400 smallholder farmers had adopted cultivated forages to feed to their animals. This new feed resource has enabled farmers to change their cattle production system. They have intensified their production systems from grazing to pen-fed cattle using planted forages as the main feed for fattening, and by changing from local breeds to raising Laisind and cross-bred cattle

    Efficient and precise CRISPR/Cas9-mediated MECP2 modifications in human-induced pluripotent stem cells

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    Patients with Rett syndrome (RTT) have severe mental and physical disabilities. The majority of RTT patients carry a heterozygous mutation in methyl-CpG binding protein 2 (MECP2), an X-linked gene encoding an epigenetic factor crucial for normal nerve cell function. No curative therapy for RTT syndrome exists, and cellular mechanisms are incompletely understood. Here, we developed a CRISPR/Cas9-mediated system that targets and corrects the disease relevant regions of the MECP2 exon 4 coding sequence. We achieved homologous recombination (HR) efficiencies of 20% to 30% in human cell lines and iPSCs. Furthermore, we successfully introduced a MECP2(R270X) mutation into the MECP2 gene in human induced pluripotent stem cells (iPSCs). Consequently, using CRISPR/Cas9, we were able to repair such mutations with high efficiency in human mutant iPSCs. In summary, we provide a new strategy for MECP2 gene targeting that can be potentially translated into gene therapy or for iPSCs-based disease modeling of RTT syndrome

    Prevalence and risk factors for carriage of antimicrobial-resistant Escherichia coli on household and small-scale chicken farms in the Mekong Delta of Vietnam

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    Objectives: To describe the prevalence of antimicrobial resistance among commensal Escherichia coli isolates on household and small-scale chicken farms, common in southern Vietnam, and to investigate the association of antimicrobial resistance with farming practices and antimicrobial usage. Methods: We collected data on farming and antimicrobial usage from 208 chicken farms. E. coli was isolated from boot swab samples using MacConkey agar (MA) and MA with ceftazidime, nalidixic acid or gentamicin. Isolates were tested for their susceptibility to 11 antimicrobials and for ESBL production. Risk factor analyses were carried out, using logistic regression, at both the bacterial population and farm levels. Results: E. coli resistant to gentamicin, ciprofloxacin and third-generation cephalosporins was detected on 201 (96.6%), 191 (91.8%) and 77 (37.0%) of the farms, respectively. Of the 895 E. coli isolates, resistance to gentamicin, ciprofloxacin and third-generation cephalosporins was detected in 178 (19.9%), 291 (32.5%) and 29 (3.2%) of the isolates, respectively. Ciprofloxacin resistance was significantly associated with quinolone usage (OR = 2.26) and tetracycline usage (OR = 1.70). ESBL-producing E. coli were associated with farms containing fish ponds (OR = 4.82). Conclusions: Household and small farms showed frequent antimicrobial usage associated with a high prevalence of resistance to the most commonly used antimicrobials. Given the weak biocontainment, the high prevalence of resistant E. coli could represent a risk to the environment and to humans

    Tetrahydrobiopterin enhances mitochondrial biogenesis and cardiac contractility via stimulation of PGC1 alpha signaling

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    Tetrahydrobiopterin (BH4) shows therapeutic potential as an endogenous target in cardiovascular diseases. Although it is involved in cardiovascular metabolism and mitochondrial biology, its mechanisms of action are unclear. We investigated how BH4 regulates cardiovascular metabolism using an unbiased multiple proteomics approach with a sepiapterin reductase knock-out (Spr(-/-)) mouse as a model of BH4 deficiency. Spr(-/-) mice exhibited a shortened life span, cardiac contractile dysfunction, and morphological changes. Multiple proteomics and systems-based data-integrative analyses showed that BH4 deficiency altered cardiac mitochondrial oxidative phosphorylation. Along with decreased transcription of major mitochondrial biogenesis regulatory genes, including Ppargc1a, Ppara, Esrra, and Tfam, Spr(-/-) mice exhibited lower mitochondrial mass and severe oxidative phosphorylation defects. Exogenous BH4 supplementation, but not nitric oxide supplementation or inhibition, rescued these cardiac and mitochondrial defects. BH4 supplementation also recovered mRNA and protein levels of PGC1 alpha and its target proteins involved in mitochondrial biogenesis (mtTFA and ERR alpha), antioxidation (Prx3 and SOD2), and fatty acid utilization (CD36 and CPTI-M) in Spr(-/-) hearts. These results indicate that BH4-activated transcription of PGC1 alpha regulates cardiac energy metabolism independently of nitric oxide and suggests that BH4 has therapeutic potential for cardiovascular diseases involving mitochondrial dysfunction.11Nsciescopu
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