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Biomedical subjects

E Alvarez

Publications and source records attributed to E Alvarez.

At least 235 records · Page 13Linked to original sources
PubMed1987

Field trial of vaccination against American trypanosomiasis (Chagas' disease) in domestic guinea pigs.

Domestically bred South American guinea pigs received 3 to 5 immunizing intradermal inocula of 28 X 10(6) live attenuated Trypanosoma cruzi epimastigotes (TCC strain) per kg. These inocula were unable to produce patent infections or to propagate through vectors. Groups of experimental and control guinea pigs were exposed to natural T. cruzi infection in a field yard for periods of up to 551 days. Xenodiagnoses were applied periodically to all animals. This showed that the incidence of natural T. cruzi infection was significantly lowered at various periods post-exposure. The final proportion of infected animals was 39% (20/51) among vaccinees vs. 63% (32/51) among controls (P less than 0.02). The protective effect was exerted particularly upon males and lasted for over a year in one experimental series (infection in 1/7 vaccinees vs. 6/7 controls, P = 0.014). Vaccination reduced vector transmission rates from 38% to 18% (P less than 0.001). These results agree with previous laboratory experiments in showing a partial resistance which does not eliminate residual T. cruzi infection. However, the field work indicates that even this kind of resistance may have epidemiological impact, reducing both the number of reservoirs spreading the disease and the rate of vector transmission.

Animals↗
PubMed1987

[Percutaneous microcatheters: experience in a neonatal pathology center].

We have performed 113 percutaneous catheterization in 87 newborn babies, locating them centrally in 60 cases (53%). In 69 (61%) cases the duration of catheter was as long as desired. Average duration was 14.65 days. No important complications were detected. We think that this in a useful technique that allows a long term circulatory access, even central venous lines. Aseptic procedure is mandatory as well as X-ray control of the distal tip of the catheter.

Catheterization, Central Venous↗
PubMed1987

[Hepatic lesions induced by drugs. Report of 26 cases].

Two thousand six hundred and seventy one liver biopsies were reviewed from 1972 to 1985 at the Hospital A. Posadas. There were 26 patients with drug-induced liver injury; those who fulfilled the following criteria were included: contact with a drug known to produce hepatotoxicity; clinic, biologic and histologic picture corresponding to the drug studied, complete recovery after the drug was stopped and no other hepatic toxics. Fourteen patients showed estrogen-induced intrahepatic cholestasis, 5 had hepatitis-like lesions due to: alphamethyldopa (3), ketoconazole (1) and indomethacin (1). Carbon tetrachloride caused fatty degeneration in two patients and phenylbutazone a granulomatous hepatitis in one patient and cholestatic hepatitis in other. The last three cases were cholestatic lesions after the administration of chlorpromazine allopurinol and penicillin respectively. The evolution in 24 patients was excellent after the drug was withdrawn. Two patients died because of surgical complications since they were operated on with the wrong diagnosis of extrahepatic cholestasis.

Adult↗
PubMed1987

[Systemic Candida infections].

Seven cases of neonatal systemic candidiasis are summarized. This means an incidence of 8.3% respect total amount of newborns admitted and 3.7% of babies admitted in the intensive care unit. Clinical presentation was not specific. Five blood cultures were positive and in two cases meningitis was recognized. Two cases died. Six cases were treated with amphotericin B and 5-fluorocytosine and in one case renal toxicity appear.

Amphotericin B↗
PubMed1986

Delayed appearance of liver growth hormone binding sites and of growth hormone-induced somatomedin production during rat development.

The present study was designed to determine whether the apparent paradox of high circulating growth hormone levels in the fetus and the minimal effect of this hormone on growth might reflect a diminished responsiveness of fetal target organs to GH. Specific uptake by rat liver of [125I] bGH was very low in fetuses as compared to suckling and adult rats. Also, liver uptake of the iodinated hormone decreased proportionally with the simultaneous injection of increasing amounts of growth hormone, but was not modified by the simultaneous injection of unlabelled chemically-related hormones. Since the water content is significantly greater in fetal than adult tissues, results were expressed by liver dry weight and again, [125I] bGH liver uptake continued to increase with age. After bovine growth hormone administration to adult rats, plasma somatomedin C concentrations increased significantly, while they had no effect in fetuses. These results suggest that reduced liver somatogenic binding sites in the fetus prevents growth hormone from inducing growth-promoting effects during intrauterine life.

Animals↗
PubMed1986

Characterization of insulin receptors in liver membranes and isolated hepatocytes during rat ontogenic development.

The studies described in this paper were undertaken to characterize the hepatic insulin receptors in liver membranes and isolated hepatocytes, during rat ontogenic development. In liver membranes insulin binding was found to be the same in fetal and greater in suckling rats as compared with adult animals. Modifications of insulin binding reflect changes in the number of receptors, but not in the affinity constants. Time courses of insulin association and dissociation from liver membranes were unaffected by development. Degradation of insulin by liver membranes was significantly lower in fetal than in adult rats, but this does not seem to be responsible for the differences observed in binding. No significant differences in the degradation of insulin receptors between different groups of liver membranes were found. Similar results were obtained with isolated hepatocytes except for a reduced number of insulin receptors in fetal cells. This could be explained by the smaller cell surface of younger cells, since when the results were expressed by micron 2, insulin binding was almost the same in fetal and adult rats. These findings suggest that the early hepatic development of insulin receptors may play a significant role in the metabolic growth processes of the fetus and in the availability of nutrients after birth.

Animals↗
PubMed1986

Glucose represses formation of delta-(L-alpha-aminoadipyl)-L-cysteinyl-D-valine and isopenicillin N synthase but not penicillin acyltransferase in Penicillium chrysogenum.

The content of alpha-aminoadipyl-cysteinyl-valine, the first intermediate of the penicillin biosynthetic pathway, decreased when Penicillium chrysogenum was grown in a high concentration of glucose. Glucose repressed the incorporation of [14C]valine into alpha-aminoadipyl-cysteinyl-[14C]valine in vivo. The pool of alpha-aminoadipic acid increased sevenfold in control (lactose-grown) penicillin-producing cultures, coinciding with the phase of rapid penicillin biosynthesis, but this increase was very small in glucose-grown cultures. Glucose stimulated homocitrate synthase and saccharopine dehydrogenase activities in vivo and increased the incorporation of lysine into proteins. These results suggest that glucose stimulates the flux through the lysine biosynthetic pathway, thus preventing alpha-aminoadipic acid accumulation. The repression of alpha-aminoadipyl-cysteinyl-valine synthesis by glucose was not reversed by the addition of alpha-aminoadipic acid, cysteine, or valine. Glucose also repressed isopenicillin N synthase, which converts alpha-aminoadipyl-cysteinyl-valine into isopenicillin N, but did not affect penicillin acyltransferase, the last enzyme of the penicillin biosynthetic pathway.

2-Aminoadipic Acid↗
PubMed1986

Insulin secretion stimulated by allogeneic lymphocytes in an inbred strain of mice.

Effects of intraperitoneal injection of allogeneic lymphocytes on insulin secretion were studied in incubated pancreas slices from BALB/c mice. Injection of allogeneic lymphocytes from C57BL/6J (H2b) mice increased insulin secretion, both in basal and 11-mM glucose-stimulated conditions. This effect was only present when at least 5 X 10(6) or 1 X 10(6) cells were injected (in basal and stimulated conditions, respectively). Glucose-induced insulin secretion (3.3-27.5 mM) was significantly increased in pancreata from mice injected with allogeneic lymphocytes. No effect was observed when glucose was not included in the incubation medium. Intraperitoneal injection of Dextran 70 produced no change in glucose-elicited insulin secretion. There were no differences in glucagon and somatostatin (SRIF) secretion obtained from pancreas of mice injected with allogeneic or syngeneic lymphocytes. Injection of allogeneic cells increases insulin secretion (basal and both phases of 11 mM glucose-stimulated secretion). Puromycin significantly inhibited the second phase of insulin secretion. These results suggest that: Injection of allogeneic lymphocytes raises both basal and glucose-stimulated insulin secretion. This effect seems to be connected with the major histocompatibility complex, and to be related to the number of allogeneic cells injected. Injection of allogeneic lymphocytes seems to sensitize the beta cell response to glucose stimulus. Neither glucagon nor SRIF secretion are altered by alloantigen injection. The stimulatory effect of allogeneic lymphocytes is related, at least in part, to insulin synthesis.

Animals↗
PubMed1986

Effect of maternal food restriction on circulating insulin and glucagon levels and on liver insulin and glucagon binding sites of fetal and suckling rats.

Food was restricted in pregnant and nursing rats in order to evaluate the effect of malnutrition on insulin and glucagon metabolism in fetal and suckling rats. Food restriction of the mothers induced a loss of body and liver weights in their offspring, which was more pronounced in suckling than in fetal rats. A significant decrease of circulating insulin and glucagon levels in fetal and suckling rats from food restricted mothers (FRM) was also observed. In liver membranes insulin binding was higher in control, fetal and suckling rats than in adult animals, but maternal food restriction decreased insulin binding to liver membranes of suckling rats, and no changes between control and fetuses from FRM were observed. By contrast, glucagon binding was higher in adult than in younger control animals; however maternal food restriction had no effect on glucagon binding to liver membranes of fetal rats, although they produced an increase in 10 day-old suckling rats. The modifications in insulin and glucagon binding reflect changes in the number of receptors, but not in the affinity constants. The time courses of insulin and glucagon association to liver membranes were unaffected by the development or by the nutritional status of the animals. Degradation of insulin and glucagon by liver membranes was significantly lower in young rats and in rats from FRM, but this does not seem to be responsible for the differences observed in binding. No significant differences in the degradation of insulin and glucagon receptors between different groups of liver membranes were found.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Glucagon-like peptide-1 does not have a role in hepatic carbohydrate metabolism.

Glucagon-like peptide-1 does not have specific, high-affinity receptors on rat liver membranes, does not displace glucagon from glucagon receptors on these membranes and does not stimulate the production of cyclic AMP by isolated rat hepatocytes. In the presence of glucagon, high concentrations of glucagon-like peptide-1 do not significantly alter the production of cyclic AMP. Thus, glucagon-like peptide-1 appears unlikely to have a direct action on hepatic carbohydrate metabolism.

Animals↗
PubMed1985

Immunochemical behaviour of a tumour-associated antigen obtained from an AKR mouse lymphoma.

A soluble tumour-associated antigen was prepared by homogenizing AKR lymphoma cells (L15) followed by treatment with acetone and glycine-HCl buffer pH 3. It was analyzed by immunoelectrophoresis, rocket electrophoresis in the presence of Concanavalin A and SDS-PAGE. It showed rapid electrophoretic mobility, and the major component had an estimated molecular weight of 70,000 daltons. The molecular composition of the antigen included a glycoprotein. Specific antibodies against this antigen were demonstrated in BALB/c mice in which the AKR lymphoma was conditioned to grow by introducing the L15 cells into a subcutaneously implanted glass cylinder. In this model antibodies were found in both tumour-bearing (progressor) and tumour-rejecting (regressor) animals. In vivo experiments showed that pretreatment of BALB/c mice with L15 acellular extracts, 10 days before tumour challenge, led to a significant increase in allogeneic tumour growth. A rabbit anti-tumour extract serum was prepared and was rendered tumour -specific by exhaustive absorption with normal AKR serum and tissues. It shared the same epitopic specificity with tumour progressor or regressor mouse sera since indirect immunofluorescence using L15 cells could be reciprocally inhibited.

Animals↗
PubMed1985

Induction of thymidine kinase activity in a spontaneously enzyme-deficient murine tumor cell line by exposure in vivo to the DNA-hypomethylating agent 5-aza-2'-deoxycytidine: implications for mechanisms of tumor progression.

We previously reported that thymidine kinase (TK) activity in a spontaneously TK-deficient (TK-) mouse tumor cell line (called L61-M) could be partially restored by brief exposure of the cells in vitro to the DNA-hypomethylating agent 5-azacytidine. We now show that similar results can be obtained by exposing L61-M cells growing in mice to the DNA-hypomethylating agent 5-aza-2'-deoxycytidine. The frequency of TK+ cells within the TK- L61-M cell population was increased approximately 26,000-fold by the in vitro 5-azacytidine treatment. The frequency of L61-M TK+ cells was increased from between 200- and 1000-fold depending upon the routes of tumor and drug inoculation following the in vivo administration of 5-aza-2'-deoxycytidine. 5-Aza-2'-deoxycytidine treatment increased the proportion of L61-M TK+ cells by the induction of TK activity and not as a result of the selection of any preexisting TK+ cells from within the L61-M tumor cell population. While 5-aza-2'-deoxycytidine treatment increased the frequency of L61-M TK+ cells within the tumor cell population, it had no effect upon the survival times of mice bearing the L61-M tumor line. These results indicate that some anticancer chemotherapeutic drugs may be able to promote the diversification of tumor cell populations in vivo through the activation of previously quiescent genes as a result of alterations in the methylation of DNA.

Animals↗