An assessment of oral cancer prevention curricula in U.S. medical schools.

BACKGROUND: Oral cancer is readily detectable through routine examination, but five-year survival rates remain low. Physicians bear the same responsibilities as dentists in the early detection of oral cancers, because high-risk patients utilize medical services more often than dental services. METHODS: Because physicians' practices are largely influenced by their training, this study assessed the level of oral cancer education provided to undergraduate U.S. medical students. Health history and physical diagnosis course curricula were assessed for relevant content. RESULTS: The response rate from the U.S. medical schools was 63.2%. When compared with the "gold standard," the average score was 43% of the optimum. Seven percent of the schools did not require inspection of the mouth, 29% required inspection of all oral structures, and intraoral palpation was advocated by 43% of the schools. Although most schools included questions about alcohol and tobacco use, only 13% asked about sunlight exposure. CONCLUSION: Preliminary oral cancer training in medical schools regarding physical assessment and elicitation of signs, symptoms, and high-risk behaviors lacks both adequacy and comprehensiveness.

A single arginine residue determines species specificity of the human growth hormone receptor.

Although growth hormone (GH) receptors (GHRs) in many species bind human (h) GH as well as their own GH, the hGHR only binds primate GH. Arg43 in hGHR interacts with Asp171 of hGH. Nonprimates have a His in the position equivalent to residue 171 of primate GH and a Leu in position 43 of primate GHR. To determine whether Arg43 accounts for the species specificity of the hGHR, point mutations that changed Leu43 to Arg were introduced into the cDNAs encoding the bovine (b) GHR or the rat GH binding protein (GHBP) and these mutants or their wild-type (WT) counterparts were expressed in mouse L cells. Binding of hGH or bGH to transfected cells or to GHBP secreted into the incubation medium was assessed by displacement of 125I-labeled hGH. WT and mutant bGHR bound hGH with similar affinity, but the affinity of the mutant receptors for bGH was reduced 200-fold. Likewise, WT and mutant GHBP bound hGH with equal affinity, but only WT GHBP bound bGH. Cross-linking of 125I-labeled hGH to WT or mutant GHR produced a 141-kDa labeled complex whose appearance was blocked by unlabeled hGH, but bGH blocked cross-linking only to WT receptors. Both hGH and bGH stimulated tyrosine phosphorylation of a 95-kDa protein in cells transfected with WT GHR, but bGH was less effective in cells expressing mutant GHR. We conclude that incompatibility of Arg43 in the hGHR with His171 in nonprimate GH is the major determinant of species specificity.

Inmunología de la enfermedad de Chagas / Inmunology of Chagas's disease

Después de examinar los conocimientos actuales de la morfología, multiplicación y transmisión del Trypanosoma cruzi, este artículo trata sobre los modelos animales que pueden servir para comprender los mecanismos inmunitarios que actúan en la enfermedad de Chagas. Se estudia la función de los anticuerpos circulantes y de la inmunidad por mediación celular en la protección contra el parásito, junto con la posibilidad de que algunas de las lesiones observadas en los pacientes con esta enfermedad se deban a mecanismos inmunopatológicos. Asimismo se mencionan los métodos de inmunodiagnóstico disponibles y la posibilidad de producir una vacuna para uso humano a la luz de los recientes resultados obtenidos en animales. Por último, se formula una serie de recomendaciones para investigaciones futuras (AU)