Search PubMed⌕ Search

Biomedical subjects

J Puente

Publications and source records attributed to J Puente.

At least 37 records · Page 2Linked to original sources
PubMed1994

Enhancement of natural killer cell activity in septic shock patients by a mixture of the calcium ionophore A23187 and the phorbol ester TPA: in vitro studies.

Preincubation of peripheral blood lymphocytes from drug-free, healthy volunteers with a mixture of the calcium ionophore A23187 (Io) and the phorbol ester TPA (12-O-tetradecanoylphorbol-13-acetate) consistently resulted in a significant enhancement (dose-dependent; maximum immunostimulation obtained with the Io + TPA final mixture concentration of 10 uM + 250 ng/ml, respectively) of natural killer cell activity (NKCA) (n = 8; mean +/- SD of 16.8 +/- 8.9 and 52.0 +/- 18.0, paired Student's t-test p < 0.005; effector-to-target cell ratio of 30:1). Results from the same protocol, but using samples from septic shock patients followed a similar trend; however, and perhaps reflecting the significantly lower baseline NKCA in this group of individuals (n = 7), the mean value reached for this cellular immune function after incubation with Io + TPA was significantly lower than that of the treated controls' group (mean +/- SD of 19.8 +/- 11.6 and 52.0 +/- 18.0, respectively, Student's t-test p < 0.005). As expected from the role of calcium in the activation of NKCA, incubation with the Io significantly increased baseline NKCA, which was largely unchanged by TPA. Expression of the CD56+ and CD16+ phenotypes in septic shock patients did not correlate directly with NKCA, suggesting that this condition may be associated with changes in the function rather than the quantity of these cellular markers.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Effect of the calcium channel blocker amlodipine on memory in mice.

Five experiments were performed to investigate the effects of amlodipine, a calcium channel antagonist of the 1,4-dihydropyridine class, on consolidation and retrieval of memory in mice. In a single-trial passive avoidance task, amlodipine was administered pretraining, posttraining, or pretesting. Results of temporal and dose-response studies showed that memory enhancement (significant increase in step-through latency) occurred when amlodipine (5, 7, 9, 15, and 30 mg/kg) was given either immediately post-training or (15 mg/kg) 15 min pretesting. Using a conditioned emotional response task, tone was paired with shock using Pavlovian conditioning procedures. Strength of conditioning was assessed by measuring suppression of drinking in the presence of a tone. Amlodipine (7 mg/kg) given immediately following both high- and low-intensity shock significantly enhanced conditioned suppression. In the third experiment thirsty mice were trained on a spatial discrimination task in a linear maze. Correct choices were reinforced with liquid reinforcement. Amlodipine (10 mg/kg) injected immediately after the training session produced a significant enhancement of discrimination performance on a 24-h retention test. In the fourth experiment mice were given 25 training trials in a two-way active avoidance task and were treated with either amlodipine (10 mg/kg) or saline after training. Amlodipine-treated mice made significantly more avoidances on the test session than control animals. The final experiment demonstrated that the deficit in approach-avoidance behavior seen in 18-month-old mice could be reversed by amlodipine treatment after the training session. These studies suggest that amlodipine can facilitate memory consolidation and retrieval.

Amlodipine↗
PubMed1993

In vitro studies of natural killer cell activity in septic shock patients. Response to a challenge with alpha-interferon and interleukin-2.

Natural killer cell activity (NKCA) in patients with septic shock was statistically significantly lower than the value recorded for a group of drug-free, healthy volunteers [9.1 +/- 7.8 (n = 20) and 20.6 +/- 16.6 (n = 15), respectively; Student's test, p < 0.05]. As expected, preincubation of peripheral blood lymphocytes from samples taken from a group of controls with either alpha-interferon or interleukin -2 resulted in an enhancement of NKCA for each and everyone of the subjects studied; however, results from a similar protocol using patient samples showed a lack of consistency, both in the direction and magnitude, in the elicited changes in NK lytic function. Whereas samples from same patient responded with either an increase or a decrease in NKCA to preincubation with both immunostimulators, others responded with NKCA upmodulation to one and downmodulation to other of these test substances. A better knowledge of the mechanism(s) responsible for the depressed expression of NKCA in septic shock patients, and its altered response to alpha-interferon and interleukin-2, could generate new modalities in the diagnosis and therapy of this condition.

Adult↗
PubMed1992

Changes in apyrase activity in uterus and mammary gland during the lactogenic cycle.

1. The purpose of this present research was to explore the possible roles of ATP-diphosphohydrolase (apyrase) in two tissues with high energetic demands during cell proliferation and differentiation. 2. Changes in apyrase activities during the pregnancy lactation cycle were examined in the rat uterus and mammary gland. 3. A significant decrease in apyrase activity (ATPase-ADPase) was observed in the pregnant uterus; this observation correlates with a minor inhibitory effect on platelet aggregation. 4. In mammary gland, the enzyme activity increases during lactation in parallel with an increase in blood supply, synthesis of glycoproteins and cell proliferation. 5. Apyrase activity did not change during the estrous cycle. Estradiol administration to rats slightly increased (20%) both ATPase-ADPase activities. 6. The probable function of apyrase is finally discussed, based on its substrate specificity and subcellular localization.

Animals↗
PubMed1992

Enhancement of human natural killer cell activity by opioid peptides: similar response to methionine-enkephalin and beta-endorphin.

We studied the effect of methionine-enkephalin (MET) and beta-endorphin upon human peripheral blood lymphocyte natural killer cell (NKC) activity in a group of healthy volunteers (n = 27; 17 male and 10 female, age +/- SD and range of 32 +/- 6, 25-43 years and 36 +/- 11, 22-65 years, respectively). Aliquots from some individual samples were preincubated separately with different concentrations of either peptide (n = 12), while others were tested with only one of these substances (MET, n = 6; beta-endorphin, n = 9). Using each individual as its own control, MET (10(-8) and 10(-6) M) and beta-endorphin (10(-10) and 10(-8) M) significantly increased NKC activity (NKCA) (at least 20% over base value, effector-to-target cell ratio, 40:1) in 7 out of 15 and 7 out of 19 subjects, respectively. Results obtained from the rest of the samples were mixed, e.g., changes observed in NKCA were not significant or showed significance with only one of the peptide concentrations studied. Cells from individuals showing a significant increase in NKC lytic function following preincubation with either MET or beta-endorphin responded similarly to the other peptide (in both cases 5 out of 6 subjects), suggesting that enhancement of NKCA by MET and beta-endorphin may work through a similar mechanism.

Adjuvants, Immunologic↗
PubMed1991

[Immunological defects in septic shock. Deficiency of natural Killer cells and T-lymphocytes].

It is well known that an immunosuppressive response occurs after acute trauma. Some cellular mediators participate in the pathogenesis of septic shock. However, the exact role of the lymphocyte subsets and natural killer (NK) activity in this condition is not clear. We studied NK cytolytic activity through a 51Cr liberation assay using K-562 target cells in 20 patients with initial septic shock (10 men and 10 females, mean age 41 years old). Lymphocyte subsets CD3 (T3), CD4 (T4), CD8 (T8), CD16 (Leu-11) and CD56 (Leu-19) were also studied by indirect immunofluorescence. Compared to results obtained in 20 healthy volunteers, patient's NK activity was decreased (4.6 +/- 3.9 vs 26.1 +/- 10, p less than 0.025), CD16 was lower (10%/187 vs 15%/280 per ul) and CD56 was also lower (6%/120 vs 12%/224 per ul), p less than 0.05. T lymphocyte subsets were also decreased: CD3 cells (1100 vs 1352 per ul) and CD4 cells (634 vs 873 per ul), p less than 0.05. Thus, a severe decrease in NK cells and NK cell function as well as decreases in CD3 and CD4 lymphocyte subsets are present in the initial stages of septic shock. The predictive value of these findings is currently under study.

Adolescent↗
PubMed1988

Studies of the in vitro human plasma degradation of methionine-enkephalin.

1. Incubation of [3H]tyrosine methionine-enkephalin (6 x 10(-9) M final concentration) with human platelet-poor plasma (1:9 ratio to Trizma Base buffer, pH 7.4) results mostly (greater than 95%) in hydrolysis of the tyrosyl-glycine peptide bond. This enzymatic reaction is essentially completed within 90 min, showing a half-life, Km and Vmax of 12.8 +/- 2.5 min, 0.70 +/- 0.01 mM and 17.90 +/- 1.05 mumol/L/min, respectively. These values are comparable to those previously reported for the human plasma degradation of leucine-enkephalin. 2. As expected hydrolysis of the methionine-enkephalin tyrosyl-glycine peptide bond was blocked by the known aminopeptidase inhibitors bestatin and puromycin (IC50 1.2 +/- 0.4 and 4.3 +/- 2.4 microM, respectively) but not by either thiorphan or captopril. 3. Neither the storing (up to 60 days) nor the freezing and thawing (up to ten times during a 60 days periods) significantly changed the above kinetic parameters, showing the stability of the plasma methionine-enkephalin degrading aminopeptidase.

Chromatography, Thin Layer↗
PubMed1988

Effects of enkephalin on lactating rat mammary gland: in vitro studies.

We studied the in vitro effects of methionine-enkephalin and D-ala-methionine-enkephalin upon lactating rat mammary gland milk product's secretion and intracellular cyclic AMP levels. Our results show that the lactating gland does not respond to the action of these peptides and suggest that during this period this tissue lacks enkephalin receptors.

Animals↗
PubMed1988

[Heterologous hormonal regulation in the mammary gland].

Mammary gland growth and differentiation are largely dependent on a complex and interrelated action of many different hormones which makes the mammary tissue a very suitable one for the study of heterologous hormonal regulation. This type of control is analyzed by two different approaches: 1. The participation of estradiol in prolactin action during lactation, and 2. The role of glucocorticoids and thyroid hormones in the control of functional activity of rat mammary gland beta-adrenergic receptors.

Animals↗
PubMed1987

The action of hormones on the rat uterus and mammary gland gamma-glutamyltranspeptidase activity.

The gamma-glutamyltranspeptidase activity of rat uterus and mammary gland was studied in ovariectomized, hypophysectomized and ovariectomized-hypophysectomized rats under different hormonal and drug treatments. The uterine enzyme appears to be mainly dependent on a direct action of estradiol and the mammary gland enzymatic activity is dependent on prolactin. Our result, however, do not exclude a possible role of estradiol in the regulation of prolactin effects on mammary gland enzymatic activity.

Animals↗
PubMed1986

Modulation of gamma-glutamyl cycle and glutathione levels in rat mammary gland explants.

The reduced glutathione levels and the enzymes gamma-glutamyl-transpeptidase, 5-oxoprolinase and gamma-glutamylcysteine synthetase, which participate in the metabolism of glutathione through the gamma-glutamyl cycle, were determined in explants from the lactating mammary gland of the rat. Significant activities of the enzyme were found. Two modulators of this cycle were used. L-2-Oxothiazolidine-4-carboxylate, an alternative substrate of 5-oxoprolinase and an intracellular cysteine delivery system, increased the reduced glutathione levels under the experimental conditions used. The other compound utilized, DL-buthionine-SR-sulphoximine, an inhibitor of gamma-glutamylcysteine synthetase, significantly decreased the glutathione levels. This effect is slowly reversible.

Amidohydrolases↗
PubMed1985

A role for adrenaline and calmodulin in modulating cyclic AMP levels during the lactogenic cycle.

The effect on lactose production of several external modulators of intracellular cyclic AMP was studied in rat mammary gland tissue slices and explants. Adrenaline, a beta-adrenergic receptor effector, forskolin, a direct adenylate cyclase activator and fluphenazine, a calmodulin inhibitor, all produced an increase in the intracellular level of cyclic AMP and a concomitant inhibition of lactose production. These results suggest a role for adrenaline and calmodulin in modulating cyclic AMP levels in mammary tissue during the lactogenic cycle.

Animals↗
PubMed1982

Enzymes of mercapturic acid production in rat mammary gland.

1. The enzymes glutathione S-transferase, gamma-glutamyl peptidyltransferase and dipeptidase, which participate in the detoxification pathway through mercapturic acid production, were measured in rat mammary gland during pregnancy and lactation. 2. Mammary-gland concentration of reduced glutathione showed, concomitantly with the enzyme activities, a significant increase during lactation. 3. The mammary-gland glutathione S-transferase exhibits characteristics quite similar to those described for the liver and kidney enzymes with respect to substrates, isoenzymes, molecular weight and probenecid and bilirubin inhibition. 4. In view of these similarities, mammary-gland glutathione S-transferase may play the same role as a cytoplasmic organic-anion receptor proposed for the hepatic enzyme. It may also represent a detoxification pathway for protecting the mammary tissue during the lactogenic cycle.

Acetylcysteine↗
PubMed1982

Glutathione and gamma-glutamyl cycle enzymes in rat mammary gland.

The main enzymes of the gamma-glutamyl cycle during the lactogenic cycle in rat mammary gland were studied. A significant increase was found in all of them with the onset of lactogenesis. The effect of methionine sulfoximine on reduced glutathione concentration was studied in tissue slices of lactating mammary gland. The findings suggest that this compound effects glutathione synthesis by inhibiting gamma-glutamylcysteine synthetase.

Animals↗