Salivary flow rates by mechanical stimulation with forced spitting method and by chemical stimulation with 10% citric acid were determined in 25 healthy adult subjects with a history of chronic tobacco-betel-lime "quid" chewing and in 25 healthy control adults with no history of chewing. The chewers secreted more saliva as compared to nonchewers on chemical, but not on mechanical stimulation. The salivary amylase, potassium, and sodium levels were lower in chewers, but the reductions of the first two components only were significant. These reductions were thought to be due to increased salivary flow with its dilutional effect. There was no difference between the two groups with respect to salivary pH. The salivary flow rates by either method had significant positive correlation with the duration of chewing, but not with the amount of tobacco chewed. Salivary potassium was inversely correlated with the amount of tobacco chewed. It was concluded that chronic tobacco-betel-lime quid chewing induces excessive secretion of more watery saliva leading to a concomitant decrease in enzyme and electrolyte content. One or more of the following factors were considered to be operating in causing increased salivary flow in chewers effect of nicotine or tobacco on other constituents of the quid, chronic salivary gland hyperplasia, or chronic hypertrophy of the muscles of mastication.
Diabetes-Cooke et al. MEDICALSJOUNLThe fact that the inheritance of diabetes does not conform to the pattern expected on the single-gene hypothesis is of importance in the study of potential diabetes.We have shown that the offspring of two diabetic parents are at a relatively low risk of becoming clinically diabetic. They cannot all be assumed to be future diabetics, and it is therefore unjustifiable to .refer to them as prediabetic. A recent study of " prediabetes " (Taton et al., 1964) assumed that children of two diabetic parents and identical twins of diabetics could be regarded as equally at risk. Yet only 5 % of the former are diabetic, as compared with about 50% of the latter (Joslin et al., 1959; Harvald and Hauge, 1963).Our results suggest that no more than one-quarter of the children of conjugal diabetics will become diabetic, assuming that they develop the disease at the same ages as is true of the general diabetic-clinic population-and it may well be that the number will be less. However, it seems that the children of young-onset diabetics are more likely to develop the disorder than those of older onset.We are collecting more data in order to get a clearer idea of the risk of diabetes developing in the children of patients of different ages (and will welcome news of diabetic couples).
SummaryA cooperative study of the children of conjugal diabetic couples has been made on behalf of the British Diabetic Association. Of 362 children of 164 couples both of whom were diabetic 16 (4.4%) were diagnosed as having diabetes. This is a greater number than was found in control couples in whom neither or one parent was diabetic.Diabetes is commoner in the children of diabetic parents who develop diabetes early in life than in those of older couples.If diabetes depends upon a single recessive gene all the offspring of the conjugal diabetic pairs should eventually become diabetic. However, the incidence so far suggests that only about one-quarter will do so.We are grateful to the physicians who sent us the material upon which this report is based, and to Miss Mary Wall for statistical advice.
Dose-response curves for the effect of continuous intravenous infusion of histamine on the gastric acid secretion was obtained in nine healthy volunteers of Indian origin. Each subject was studied with 5 doses (20, 40, 60, 80, and 100 μg/kg/h) of histamine acid phosphate administered for 3 h, on separate days, in random fashion. The plateau of secretion occurred in the 2nd h of infusion. The analysis of variance revealed that acid output significantly increased with increasing dose of histamine; the increase in acid output was significant at all dose levels except between 80 and 100 μg/kg/h. The analysis of data using dose of histamine independent of body weight gave a poorer fit to the regression line than that obtained with histamine dose on the basis of body weight, suggesting that dose of histamine should be administered on the basis of body weight. The estimate of calculated Vmax and the dose of histamine producing a response 50% of Vmax or (Km) by the three different transformations of the Michaelis-Menten equation gave somewhat different values for both these constants. All these were slightly different from direct estimation of Vmax and Km with analysis of curvilinear regression. The linear transformation using the plot of Cs/v versus Cs gave the best results. The double reciprocal plot underestimated both the constants. The value of Km in Indian subjects was almost six times the value in Western subjects, indicating the relative insensitivity of the parietal cells to histamine in our subjects.
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