[Serum adenosine deaminase in human immunodeficiency virus infection. Its relationship with CD4+ lymphocytes and beta 2-microglobulin]. / Adenosina desaminasa sérica en la infección por el virus de la inmunodeficiencia humana. Su relación con los linfocitos CD4+ y la beta 2-microglobulina.

BACKGROUND: The activity of the deaminase adenosine enzyme (ADA) has principally been related with the functionalism and replication of the T lymphocytes. Its serum behavior and possible clinical use in infection by the human immunodeficiency virus type 1 (HIV-1) was studied. METHODS: A multicenter study in which the serum values of ADA were examined and compared with those of two reference markers (CD4+ lymphocytes and beta 2-microglobulin) in 35 presumably healthy donors used as controls, in 60 intravenous drug users (IVDU) seronegative for HIV-1, in 69 HIV-1 asymptomatic seropositive intravenous drug users (HIV-1+) and in 48 patients with AIDS. RESULTS: The serum values of ADA were as follows: control group 10.9 +/- 4.2 U/I; IVDU group 17.6 +/- 7.4 U/I; asymptomatic HIV-1+ group 32.7 +/- 10.2 U/I, AIDS group 46.2 +/- 18.2 U/I. Differences between the different groups were statistically significant in themselves and in relation to the control group. A negative correlation was observed (r = 0.47, p < 0.01) with the number of CD4+ lymphocytes and a positive correlation was found with respect to beta 2-microglobulin (r = 0.76, p < 0.001). The values of serum ADA activity in patients with AIDS and tuberculosis (47.4 +/- 17.2 U/I) were not significantly higher (p < 0.05) to those of patients with AIDS without this second infection (45.9 +/- 19.3 U/I). CONCLUSIONS: Serum deaminase adenosine may be a useful evolutive marker for human immunodeficiency virus type 1 given that its activity increases significantly in infected patients in agreement with the grade of immunodeficiency and its values correlate well with those of reference markers (CD4+ lymphocytes and beta 2-microglobulin).

[Posterior hypothalamus action on gastric secretion (author's transl)]. / Influencia del hipotálamo posterior en la secreción gástrica

Three groups of cats with surgically created total gastric pouches were employed in this experiment. They were divided as follows: in one group the innervation of the pouch was left intact; in another group the symphathetic innervation of the pouch was removed; and in the third group the pouch was completely denervated. It was seen that an infusion of histamine induced gastric secretion in all three groups. And when the secretion became constant it proved to be less acidic and more abundant in the sympathectomized group and also in the group that had suffered complete denervation. It was observed now that stimulating the posterior hypothalamus of the innervated group produced, in all of the cats, a decrease in the amount of acid secreted per unit of time. Consequently, it was seen that a symphathectomy did not eliminate the gastric effects produced when the posterior hypothalamus was stimulated. Specifically, stimulation of the posterior hypothalamus produced an increase in the amount of secretion rather than a decrease. The increase produced in these animals can be shown not to be due to irradiation of the anterior hypothalamus as the same response is obtained when a symphathectomy is combined with a vagotomy. It is, therefore, believed that it may be concluded that the Posterior hypothalamus does not produce its effect exclusively through its nervous pathways. It is believed its effect may possibly be mediated by an unknown substance liberated upon stimulation which then reaches the stomach by way of its blood supply.