RESUMEN
Hypoxia elicits hematopoiesis, which ultimately improves oxygen transport to peripheral tissues. In part because of this, altitude training has been used in the conditioning of elite endurance athletes for decades, despite equivocal evidence that such training benefits subsequent sea level performance. Recently, traditional live high-train high athletic conditioning has been implicated in a number of deleterious effects on training intensity, cardiac output, muscle composition, and fluid and metabolite balance--effects that largely offset hematopoietic benefits during sea level performance. Modified live high-train low conditioning regimens appear to capture the beneficial hematopoietic effects of hypoxic training while avoiding many of the deleterious effects of training at altitude. Because of the logistical and financial barriers to living high and training low, various methods to simulate hypoxia have been developed and studied. The data from these studies suggest a threshold requirement for hypoxic exposure to meaningfully augment hematopoiesis, and presumably improve athletic performance.
Asunto(s)
Altitud , Ejercicio Físico/fisiología , Hematopoyesis/fisiología , Hipoxia , Resistencia Física/fisiología , Adaptación Fisiológica , Gasto Cardíaco , Fenómenos Fisiológicos Cardiovasculares , Humanos , Fenómenos Fisiológicos Musculoesqueléticos , Fenómenos Fisiológicos RespiratoriosRESUMEN
The flaky skin (fsn) mutation in mice causes pleiotropic abnormalities including psoriasiform dermatitis, anemia, hyper-IgE, and anti-dsDNA autoantibodies resembling those detected in systemic lupus erythematosus. The fsn mutation was mapped to an interval of 3.9 kb on chromosome 17 between D17Mit130 and D17Mit162. Resequencing of known and predicted exons and regulatory sequences from this region in fsn/fsn and wild-type mice indicated that the mutation is due to the insertion of an endogenous retrovirus (early transposon class) into intron 14 of the Tetratricopeptide repeat (TPR) domain 7 (Ttc7) gene. The insertion leads to reduced levels of wild-type Ttc7 transcripts in fsn mice and the insertion of an additional exon derived from the retrovirus into the majority of Ttc7 mRNAs. This disrupts one of the TPRs within TTC7 and may affect its interaction with an as-yet unidentified protein partner. The Ttc7 is expressed in multiple types of tissue including skin, kidney, spleen, and thymus, but is most abundant in germinal center B cells and hematopoietic stem cells, suggesting an important role in the development of immune system cells. Its role in immunologic and hematologic disorders should be further investigated.
Asunto(s)
Anemia/genética , Autoinmunidad/genética , Mutación , Proteínas/genética , Psoriasis/genética , Secuencia de Aminoácidos , Animales , Secuencia de Bases , Cartilla de ADN , Expresión Génica , Ligamiento Genético , Humanos , Linfocitos/inmunología , Ratones , Ratones Endogámicos , Datos de Secuencia Molecular , Fenotipo , Homología de Secuencia de AminoácidoRESUMEN
Pulmonary tuberculosis (TB) is prevalent in Western urban centers, especially among immunocompromised patients and immigrants. However, TB enteritis is a rare sequela, occurring in less than 1 per cent of this population. Tuberculosis may affect any portion of the gastrointestinal (GI) tract, and 85 per cent of cases manifest in the ileocecal region. However, the stomach and duodenum are involved in just 0.3-2.3% of TB cases that affect the gut. Gastric outlet obstruction due to TB has been traditionally treated by a surgical bypass operation, followed by anti-TB chemotherapy. In a recent review of 17 cases of TB-related gastric outlet obstruction, gastrojejunostomy or duodenojejunostomy was performed in all patients. We present a case of gastric outlet obstruction due to TB that was treated successfully with a minimally invasive approach, without the need for a gastric bypass.