81 research outputs found

    Efecto de la inulina en reemplazo de los antibióticos promotores de crecimiento sobre la calidad de la carne de cuy

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    Publicación a texto completo no autorizada por el autorRealiza un experimento en el galpón de cuyes de la EAP de Ingeniería Agroindustrial de la UNMSM con sede en San Juan de Lurigancho - Lima, con el objetivo de evaluar el efecto de la inulina en reemplazo de Antibiótico Promotor de Crecimiento (APC) sobre la calidad de la carne de cuy. Se emplea los siguientes tratamientos: T1: Control (con APC), T2: Sin inulina y sin APC, T3: 150 ppm de inulina, T4: 300 ppm de inulina y T5: 600 ppm de inulina; en un periodo de 5 semanas. Para ello se utiliza 40 cuyes machos genotipo Cieneguilla, de 28 +/- 2 días de edad, adquiridos de una granja de cuyes de Manchay.Tesi

    Neurological deficits and glycosphingolipid accumulation in saposin B deficient mice

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    Saposin B derives from the multi-functional precursor, prosaposin, and functions as an activity enhancer for several glycosphingolipid (GSL) hydrolases. Mutations in saposin B present in humans with phenotypes resembling metachromatic leukodystrophy. To gain insight into saposin B's physiological functions, a specific deficiency was created in mice by a knock-in mutation of an essential cysteine in exon 7 of the prosaposin locus. No saposin B protein was detected in the homozygotes (B−/−) mice, whereas prosaposin, and saposins A, C and D were at normal levels. B−/− mice exhibited slowly progressive neuromotor deterioration and minor head tremor by 15 months. Excess hydroxy and non-hydroxy fatty acid sulfatide levels were present in brain and kidney. Alcian blue positive (sulfatide) storage cells were found in the brain, spinal cord and kidney. Ultrastructural analyses showed lamellar inclusion material in the kidney, sciatic nerve, brain and spinal cord tissues. Lactosylceramide (LacCer) and globotriaosylceramide (TriCer) were increased in various tissues of B−/− mice supporting the in vivo role of saposin B in the degradation of these lipids. CD68 positive microglial cells and activated GFAP positive astrocytes showed a proinflammatory response in the brains of B−/− mice. These findings delineate the roles of saposin B for the in vivo degradation of several GSLs and its primary function in maintenance of CNS function. B−/− provide a useful model for understanding the contributions of this saposin to GSL metabolism and homeostasis

    Prolonged survival of a patient with active MDR-TB HIV co-morbidity: insights from a Mycobacterium tuberculosis strain with a unique genomic deletion

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    Coinfection of HIV and multidrug-resistant tuberculosis (MDR-TB) presents significant challenges in terms of the treatment and prognosis of tuberculosis, leading to complexities in managing the disease and impacting the overall outcome for TB patients. This study presents a remarkable case of a patient with MDR-TB and HIV coinfection who survived for over 8 years, despite poor treatment adherence and comorbidities. Whole genome sequencing (WGS) of the infecting Mycobacterium tuberculosis (Mtb) strain revealed a unique genomic deletion, spanning 18 genes, including key genes involved in hypoxia response, intracellular survival, immunodominant antigens, and dormancy. This deletion, that we have called “Del-X,” potentially exerts a profound influence on the bacterial physiology and its virulence. Only few similar deletions were detected in other non-related Mtb genomes worldwide. In vivo evolution analysis identified drug resistance and metabolic adaptation mutations and their temporal dynamics during the patient’s treatment course

    Infectious causes of microcephaly: epidemiology, pathogenesis, diagnosis, and management.

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    Microcephaly is an important sign of neurological malformation and a predictor of future disability. The 2015-16 outbreak of Zika virus and congenital Zika infection brought the world's attention to links between Zika infection and microcephaly. However, Zika virus is only one of the infectious causes of microcephaly and, although the contexts in which they occur vary greatly, all are of concern. In this Review, we summarise important aspects of major congenital infections that can cause microcephaly, and describe the epidemiology, transmission, clinical features, pathogenesis, management, and long-term consequences of these infections. We include infections that cause substantial impairment: cytomegalovirus, herpes simplex virus, rubella virus, Toxoplasma gondii, and Zika virus. We highlight potential issues with classification of microcephaly and show how some infants affected by congenital infection might be missed or incorrectly diagnosed. Although Zika virus has brought the attention of the world to the problem of microcephaly, prevention of all infectious causes of microcephaly and appropriately managing its consequences remain important global public health priorities

    Polymorphic Exact Tandem Repeat A (PETRA): a Newly Defined Lineage of Mycobacterium tuberculosis in Israel Originating Predominantly in Sub-Saharan Africa▿

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    As part of the Israel National Program for Prevention and Control of Tuberculosis, the molecular epidemiology of new tuberculosis cases is monitored. Prospective screening showed that about 20% of all new cases of culture-positive tuberculosis (43 of 222) in Israel in the year 2008 were caused by certain Mycobacterium tuberculosis strains of the central Asian (CAS) spoligotype lineage. The identity and similarity of these strains by mycobacterial interspersed repetitive-unit-variable-number tandem-repeat (MIRU-VNTR) typing form a lineage we call PETRA for polymorphic at locus ETR A. The name PETRA was given to 79 strains we have found since the year 2000, because the largest number of strains with MIRU-VNTR profiles identical other than at locus A formed three groups, including 5 of 10 strains that had deleted the ETR A region from their genomes. No PETRA strain was found to be multiple drug resistant (resistant to both isoniazid and rifampin [rifampicin]). Most patients (75% [58 of 77 patients of known origin]) infected with PETRA were of sub-Saharan African origins. The genotypes associated with the 79 PETRA lineage strains presented in this paper suggest that the PETRA lineage is a large, major contributor to new tuberculosis cases in Israel

    Association between parental smoking and child exposure to environmental tobacco smoke in Israel

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    Abstract Background Environmental tobacco smoke (ETS) exposure in children can cause delayed lung development and lifelong cardiovascular damage. The aim of this study was to measure ETS exposure in children in Israel in 2020–2021 using urinary cotinine (UC) measurements and to assess correlates of ETS exposure, including parental smoking. Methods In the framework of the National Human Biomonitoring Program, spot urine samples and questionnaire data were collected from 166 children aged 4–12 years, during the years 2020–2021. We collected urine samples in 233 adults, 69 of whom were parents of children included in the study. Parents of participating children were asked about parental smoking, child’s exposure to ETS and smoking policy at home. Cotinine and creatinine were measured in urine. Creatinine-adjusted and unadjusted urine cotinine (UC) geometric means were calculated. Associations between potential correlates and UC concentrations were analyzed in univariate and multivariate analyses. For 69 child-parent pairs, correlation between child and parental UC was analyzed. Results Based on urinary cotinine measurement, 65.2% of children of smokers are exposed to ETS, compared to 20.7% of children in non-smoking families. Greater numbers of smokers living in the home (beta = 1.27, p < 0.01), and low maternal education (beta = − 2.32, p < 0.01) were associated with higher levels of UC in a multivariate analysis. Spearman correlations showed a positive moderate correlation between UC in 69 child–parent pairs (r = 0.52, p < 0.01). Conclusions In order to reduce child exposure to ETS, smoking parents should be urgently targeted for smoking cessation and smoke-free home interventions. Further interventions are needed to protect all children from ETS
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