Prolonged disease-free survival in bronchogenic carcinoma associated with HLA-Aw19 and HLA-B5. A two-year prospective study

Seventy patients with squamous carcinoma or adenocarcinoma of the lung were HLA typed at the time of their diagnosis and initial therapy. No abnormal HLA antigen frequencies were found. However, the possession of HLA-Aw19 or HLA-B5 was significantly correlated with two year disease-free survival. Twelve of 21 patients (57%) with either Aw 19 or B5 were disease-free at two years. In contrast, only six of 48 patients (13%) not having either antigen were disease-free (p less than .001). One patient was lost to follow-up. It is possible that Aw 19 and/or B5 confer resistance to progression of bronchogenic carcinoma on their possessors.     

Frequency of intestinal parasitosis in different communities the Federal District of Mexico

An electron-capture gas chromatographic method is described for the determination of naloxone and naltrexone as the perfluoroalkyl esters. Each compound serves as internal standard for determination of the other. The method permits quantitation of 2-100 ng of either compound. Conditions for derivatization with heptafluorobutyric anhydride (HFBA), pentafluoropropionic anhydride (PFPA), and trifluoroacetic anhydride (TFAA) have been investigated. When catalyzed with pyridine, derivatization with HFBA and PFPA at 70 degrees gives naloxone and naltrexone triesters. Evidence for triester formation was obtained from gas chromatography-methane chemical ionization mass spectrometry and infrared spectral analysis. It was found that both the HFB and PFP triesters are suitable for quantitation of the narcotic antagonists, the HFB derivatives having greater stability than the PFP derivatives. The TFA derivatives are substantially less stable.     

Clinical aspects of human Venezuelan equine encephalitis in Texas

The Venezuelan equine encephalitis epidemic which occurred in Texas in 1971 produced a wide range of predominantly mild clinical symptoms. This epidemic, which peaked on 13-14 July, was most intensely felt in the far-south counties of Cameron and Hidalgo. In all, 88 laboratory-confirmed human cases were reported to the U.S. Center for Disease Control by the Texas State Department of Health. The ratio of male to female cases was about two to one. An attack of 20.8 cases per 100,000, observed in both the 20-29 and 30-39 age groups, was higher than attack rates experienced by other age groups and by the population at large. Together, Cameron and Hidalgo counties experienced a much higher overall attack rate (21.7 cases por 100,000) than did affected counties in the Corpus Christi area (4.9 cases per 100,000). Knowledge about when various patients were first exposed points to an incubation period ranging from 27.5 hours to four days. In those 79 cases for which clinical data were available, the most common clinical manifestations were found to be fever, severe headache, myalgia, and chills. Evidence of mild to moderate central nervous system involvement was found in 10 out of 25 children and young people under 17 years of age, and in six out of 54 adults. Two children still had residual paralysis six weeks after onset of illness, but by 10 months these sequelae had disappeared. Seven of the 54 adults, however, still complained of tiring easily a year after onset of illness. Leukopenia, as demonstrated by a count of less rhan 4,500 white blood cells per cubic millimeter, was observed in 75 per cent of the patients examined.     

Dynamic lung function changes following long-term work in polluted environments

15N-labelled glycine, ammonium chloride, and L-aspartic acid were infused intravenously into a series of non-diabetic adults at a constant rate for 4 to 8 hours. Midway during the infusion, a pulse of 8-10 units of regular insulin was injected as a pulse or infused at a constant rate for the remainder of the 15N infusion period. Frequent urine specimens were collected during the infusion period. The 15N enrichment of the urinary urea, ammonia, and amino acids increased smoothly with time until the insulin was given. The pulse of insuline caused a downturn on the N enrichment. We concluded from this that a) the effect of a pulse of insulin on human urea and ammonia metabolism lasted for about one hour; and b) insulin affected glutamine distribution in the plasma.     

Regulation of amyloid precursor protein cleavage

Multiple lines of evidence suggest that increased production and/or deposition of the beta-amyloid peptide, derived from the amyloid precursor protein, contributes to Alzheimer's disease. A growing list of neurotransmitters, growth factors, cytokines, and hormones have been shown to regulate amyloid precursor protein processing. Although traditionally thought to be mediated by activation of protein kinase C, recent data have implicated other signaling mechanisms in the regulation of this process. Moreover, novel mechanisms of regulation involving cholesterol-, apolipoprotein E-, and stress-activated pathways have been identified. As the phenotypic changes associated with Alzheimer's disease encompass many of these signaling systems, it is relevant to determine how altered cell signaling may be contributing to increasing brain amyloid burden. We review the myriad ways in which first messengers regulate amyloid precursor protein catabolism as well as the signal transduction cascades that give rise to these effects.     

Variation of dorsal horn cell dendritic spread with map scale

OBJECTIVE: To examine the hypothesis that, in polycystic ovary syndrome (PCOS), ovarian steroids induce adrenal enzyme dysfunction or adrenal androgen hyperresponsiveness to ACTH. DESIGN: Prospective controlled clinical study. SETTING: Reproductive endocrinology unit of an academic medical center. PATIENTS: Twelve women with PCOS who had adrenal androgen excess were compared with five weight-matched ovulatory women. In half of the women with PCOS, prestudy screening was suggestive of mild 3 beta-hydroxysteroid dehydrogenase (HSD) deficiency. INTERVENTIONS: Basal and adrenal dynamic blood sampling before and after GnRH agonist (GnRH-a) administration for 6 months. MAIN OUTCOME MEASURES: Basal E2 and androgen levels as well as dexamethasone-suppressed, ACTH-stimulated 17 alpha-hydroxyprogesterone, 17 alpha-hydroxypregnenolone, and androgen levels before and after ovarian suppression. RESULTS: Although none of the subjects with PCOS proved to have mild 3 beta-HSD deficiency, the majority of them (58%) met the criteria for 17,20 lyase hyperactivity before and after GnRH-a therapy. As a group, the remaining subjects with PCOS exhibited an elevated DHEAS response to ACTH before GnRH-a treatment, which may have normalized after GnRH-a treatment. CONCLUSION: Adrenal androgen excess in PCOS may be heterogeneous in etiology, whereas 17,20 lyase hyperactivity appears to be an intrinsic adrenal disorder, adrenal androgen hyperresponsiveness to ACTH may be ovarian induced. Reliance on historical controls may lead to overdiagnosis of mild 3 beta-HSD deficiency.