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Biomedical subjects

J Puente

Publications and source records attributed to J Puente.

47 records · Page 3Linked to original sources
PubMed1981

Properties of gamma-glutamyltranspeptidase, and glutathione levels in rat mammary gland.

gamma-Glutamyltranspeptidase activity and glutathione levels were studied in rat mammary gland during the lactogenic cycle; both increased during mid-lactation. The enzyme's specific activity with several amino acids showed that glutamine and methionine were the best substrates. Maleate decreased the transpeptidation reaction and increased the hydrolytic activity. These results suggest that gamma-glutamyltranspeptidase from the mammary gland is similar to the enzyme described in other tissues in relation to these properties and the physiological role proposed in amino acids transport.

Amino Acids↗
PubMed1977

Hydrolysis of synthetic pyrophosphoric esters by an isoenzyme of apyrase from Solanum tuberosum.

A highly purified isoenzyme of apyrase obtained from potatoes (Solanum tuberosum var. Pimpernel) exhibits a low specificity for the organic moiety of synthetic pyro- and triphosphates. Methyl di- and tri-phosphates were hydrolysed at higher rates than ADP and ATP, but their Km values were also higher. Steric hindrance at the carbon atom linked to the pyrophosphate chain decreases both binding and maximum rate, whereas length or polarity of the organic chain do not have systematic effects. t-Butyl diphosphate, inorganic pyrophosphate, adenosine 5'-[alpha,beta-methylene]triphosphate and adenosine 5'-[beta,gamma-methylene]triphosphate are competitive inhibitors of the hydrolysis of ATP and ADP.

Adenosine Triphosphatases↗
PubMedDate not supplied

In vitro studies of natural killer cell activity in post traumatic stress disorder patients. Response to methionine-enkephalin challenge.

Attempts to define biological parameters that may be specifically associated with the pathophysiology of post traumatic stress disorder (PTSD) have met with only limited success, reflecting perhaps the practical limitations resulting from the high frequency of comorbidity of this condition with Axis I, II and III psychiatric diagnoses. We now report our studies on natural killer cell activity (NKCA), and the response of this cellular immune function to an in vitro methionine-enkephalin (MET) challenge in a population of Vietnam veterans with PTSD. Due to the characteristics of our PTSD patients, our protocol included four sex-matched, age-comparable control groups: (1) chronic alcoholics, (2) chronic drug abusers excluding alcohol, (3) chronic users of alcohol and other drugs of abuse and (4) drug-free, healthy volunteers. Although these groups did not significantly differ in their "baseline" NKCA, significant findings emerged from their response to preincubation with MET (10(-10), 10(-8) and 10(-6) M; 40:1 effector-to-target cell ratio). To minimize interindividual variations in the expression of NKCA each subject was used as its own control. Whereas peptide challenge resulted in an increase in NK lytic function in a subpopulation of group four (one or more MET concentrations, 8 out of 22 subjects), it produced mixed results in samples from individuals in group 2, and in general failed to elicit NKCA changes in the samples from participants in groups 1 and 3. Nine of the thirteen PTSD patients responded to MET preincubation with decreases in NKCA, which in five of them reached values below 20% of baseline for the three peptide concentrations tested. These findings may suggest that the "stress factor" in Vietnam veterans with PTSD plays a role in downmodulating NK lytic function in response to an in vitro MET challenge, an effect that appears to be potentiated by the use of drugs of abuse other than alcohol. The possible clinical relevance of these findings, including the identification of a subgroup of PTSD patients on the basis of immunological tests such as the one described in this work, deserves further investigation.

Adult↗
PubMedDate not supplied

Enhancement of natural killer cell activity in HIV-1-infected subjects by a mixture of the calcium ionophore A23187 and the phorbol ester TPA: lack of response to a similar challenge with interleukin-2 or alpha-interferon.

When compared to controls (n = 30), human immunodeficiency virus type-1 (HIV-1)-positive individuals, either asymptomatic (n = 10) or diagnosed with acquired immunodeficiency syndrome (AIDS) (n = 10), showed a statistically significant decrease in the percentage and absolute number of CD4 ( + ) T-lymphocyte cells (flow cytometry, Becton Dickinson FACScan; mean +/- SD of 42.6 +/- 6.9 and 948.5 +/- 393.3, 19.5 +/- 8.7 and 269.8 +/- 174.3, 4.6 +/- 4.1 and 60.1 +/- 134.3, respectively; Student's t- test, p < 0.05). However, this decrease was less marked in asymptomatic patients; in fact, the percentage and number of the above cells in this group of subjects was significantly higher than in the AIDS patients (Student's t-test, p < 0.05). However, we failed to find significant differences in the percentage of natural killer cells (NKCs; CD15 ( + ) CD56 ( + ) ) between the HIV-1-infected asymptomatic or AIDS groups of patients, or when compared with the controls (mean +/- SD of 10.4% +/- 9.4%, 14.3% +/- 9.7%, and 14.8% +/- 6.4%, respectively). Whereas either group of patients had a lower number of NKCs per microliter than the control group (mean +/- SD of 137.8 +/- 87.6, 91.1 +/- 98.3, and 331. 5 +/- 266.5, respectively), this decrease only reached statistical significance for the AIDS patients (Student's t-test, p < 0.05). Healthy controls showed statistically significantly higher NKC activity than either the HIV-1-infected asymptomatic or AIDS group of patients (K-562 target cell; mean +/- SD and range values as percentage of specific lysis of 19.1% +/- 15.6% and 2.4%-58.2%, 3.4% +/- 3.2% and less than 0.1% [non-detectable]-10.3%, and 6.4% +/- 5. 5% and less than 0.1%-19.5%, respectively; Student's t-test, p < 0. 05). Challenge of samples from the control group with either interleukin-2, alpha-interferon, or with a mixture of the calcium ionophore A23187 (Io) plus the 12-O-tetradecanoylphorbol-13-acetate ester (TPA) resulted in every case in a statistically significant increase in NKC lytic function (mean +/- SD and range values as percentage of specific lysis of 19.1% +/- 15.6% and 2.4%-58.2%, 27. 6% +/- 17.4% and less than 0.1%-56.0%, 32.1% +/- 20.9% and 2.1%-76. 4%, and 62.6% +/- 24.0% and 16.7%-95.0%, respectively; Student's t-test, p < 0.05). A similar challenge for samples from the HIV-1-positive subjects, either asymptomatic or with AIDS, resulted in most cases in an enhanced NKC activity; however, this increase in NKC lytic function reached statistical significance only for the group of Io + TPA-incubated samples (Student's t-test, p < 0.05). These results indicate that control or patient baseline NKC activity, and the response of this cellular immune function to a challenge with different immunomodulators, are phenotype-independent. They also suggest an association between HIV-1 infection and alterations in the initial mechanisms responsible for NKC activation; a similar general explanation has been suggested to account for the abnormal NKC lytic function observed in various severe pathological conditions, e.g., extensive burns, polytrauma, and sepsis. Understanding the molecular mechanism involved in regulating initial NKC activation could provide the rational basis for the design of newer pharmacological strategies to treat these conditions.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Hormonal modulation of the rat mammary gland gamma-glutamyltranspeptidase.

1. The in vivo effect of estradiol and domperidone (a hypophysis stimulator of prolactin secretion) in immature ovariectomized-adrenalectomized and hypophysectomized rat mammary gland was studied. 2. gamma-Glutamyltranspeptidase activity was used to evaluate the role of estradiol in the specific response of the gland to prolactin. 3. Our results suggest that the activity of gamma-glutamyltranspeptidase, like casein and lactose synthetase, is part of the specific response of the gland to prolactin.

Adrenalectomy↗