PubMed Health⌕ Search

Biomedical subjects

R Ramirez

Publications and source records attributed to R Ramirez.

At least 37 records · Page 2Linked to original sources
PubMed1998

Serum levels of intercellular adhesion molecule 1 (ICAM-1) in patients with colorectal cancer: inhibitory effect on cytotoxicity.

A positive correlation between the level of ICAM-1 in serum and the stage of neoplastic processes has been demonstrated. We studied ICAM-1 serum concentration in 27 colorectal cancer patients and investigated the effect of this molecule on cellular aggregation and toxicity. ICAM-1 serum concentration in the group of patients was significantly higher (P < 0.01) than in normal controls and was related to tumour stage. Patient sera inhibited both the formation of cellular aggregates and the percentage of specific lysis, the effect being lost when the serum was depleted of ICAM-1. These results suggest that the release of soluble ICAM-1 may represent a mechanism of tumour escape.

Aged↗
PubMed1998

Plasma growth hormone secretion is impaired in obesity-prone rats before onset of diet-induced obesity.

Sprague-Dawley rats, which become obese (obesity prone) when fed a moderately high-fat (MHF; 32.5% of kcal as fat) diet, have decreased growth hormone (GH) concentrations compared with obesity-resistant rats fed the same diet. To determine whether plasma GH concentrations are different in obesity-prone rats compared with obesity-resistant rats before diet-induced obesity occurs, total integrated GH concentrations were determined in male Sprague-Dawley rats before exposure to the MHF diet. After initial blood sampling, rats were fed an MHF diet for 15 wk, over which time the animals were separated into two discrete populations based on body weight gain. Analysis of GH in episodic blood samples showed that the obesity-prone group had a GH secretion deficit before the onset of obesity (115.2 +/- 12.9 ng . ml-1 . 200 min-1) compared with obesity-resistant rats (237.2 +/- 47.1 ng . ml-1 . 200 min-1). The GH concentration difference was due to a decrease in mean GH peak height in rats that later became obese (34.8 ng/ml) compared with rats that remained lean (74.2 ng/ml). The results suggest that GH secretion impairment exists before dietary challenge or onset of obesity and may contribute to the susceptibility to obesity observed in these animals.

Animals↗
PubMed1998

Reduction of the Human Placental Vascular Relaxation to Progesterone by Gestational Diabetes

>Background: We have recently described a dose-dependent, endothelium-independent relaxation to progesterone in human placental arteries and veins. This receptor-operated, cAMP-mediated relaxation may be of value in maintaining adequate blood flow in the placental circulation.Objective: To investigate if gestational diabetes alters this relaxation to progesterone.Study design: Isolated human placental vessels from pregnancies complicated by gestational diabetes and well matched controls (uncomplicated term pregnancies), incubated in Krebs-bicarbonate buffer and submaximally precontracted with KCl, were exposed to cumulative doses of progesterone (0.01-30 µmol/liter), nitroglycerin (0.001-1 µmol/liter), arachidonic acid (0.01-10 µmol/liter), forskolin (0.01-10 µmol/liter) and 5-hydroxytryptamine (serotonin, 0.01-10 µmol/liter).Results: The relaxation to progesterone in vessels from patients with gestational diabetes was reduced by 50-100% in both arteries and veins compared with control (for example, relaxation to 10 µmol/liter progesterone was reduced from 52 +/- 7 to 18.8 +/- 5.4% in arteries and from 58 +/- 8 to 19 +/- 5.2% in veins, n = 7-13, P < 0.05), whereas responses to the other vasoactive agents were unchanged.Conclusion: Based on these results, gestational diabetes significantly reduces the relaxation to progesterone in human placental vessels. This alteration of the relaxation to progesterone may lead to an increase in placental vascular resistance and possibly to a reduction of placental blood flow.

Journal Article↗
PubMed1997

Vertical transmission of toxoplasma by human immunodeficiency virus-infected women.

OBJECTIVE: Our goal was to determine the frequency of mother-to-child transmission of Toxoplasma gondii from human immunodeficiency virus-infected mothers who are also chronically infected with T. gondii. STUDY DESIGN: One hundred thirty-eight women were entered into a prospective study of human immunodeficiency virus infection in pregnancy. The women were seen at enrollment, during the third, sixth, and eighth months of pregnancy (except those enrolled later in pregnancy or at delivery), at 2 and 6 months post partum, and at 6-month intervals thereafter through 4 years after delivery. Standardized interviews and physical examinations were performed, and blood was drawn at each visit. Toxoplasma serologic testing was performed on the sample drawn earliest in pregnancy; the Sabin-Feldman dye test for immunoglobulin G antibodies and enzyme-linked immunoassays for immunoglobulins M, A, and E were used. Univariate analysis for categoric variables was performed with chi2 and two-tailed Fisher exact tests, and for continuous variables the Student t test was used. Statistical Analysis System procedures were followed. RESULTS: Twenty-eight of 138 (20.2%) women who had positive test results for human immunodeficiency virus had positive findings of the Sabin-Feldman dye test. Serologic status for T. gondii did not correlate with age, immune status, parity, or drug use. One of 27 children born to women who were seropositive for both human immunodeficiency virus and T. gondii (one child's serologic status for T. gondii was unknown) had Sabin-Feldman dye test antibodies beyond age 6 months (3.7%, 95% confidence interval 0.09% to 18.9%). Among the cohort of human immunodeficiency virus-infected mothers the rate of mother-to-child human immunodeficiency virus transmission did not vary with maternal Toxoplasma status. However, with sample sizes of 28 and 110, respectively, for the mothers who were T. gondii seropositive and seronegative, the power to detect a difference in the human immunodeficiency virus transmission rate between these groups would be relatively small. CONCLUSIONS: Transmission of T. gondii from a chronically infected mother can occur in the setting of a human immunodeficiency virus infection, but this is not a common phenomenon. In a small cohort of human immunodeficiency virus-infected women we did not observe its occurrence among those without severe immunocompromise.

Adult↗
PubMed1997

Lymphokine-activated killer (LAK) cell generation from peripheral blood stem cells by in vitro incubation with low-dose interleukin-2 plus granulocyte-macrophage colony-stimulating factor.

Previous reports have demonstrated granulocyte-macrophage colony-stimulating factor (GM-CSF)-mediated enhancement of lymphokine activated killer (LAK) cell function. Based on these studies we have developed a model of LAK cell generation from peripheral blood stem cells (PBSC) from cancer patients by in vitro incubation with low-dose interleukin-2 (IL-2) + GM-CSF. PBSC from seven patients were incubated for 48 h at 37 degrees C in serum-free culture medium supplemented with IL-2 at increasing concentrations (10, 100 or 1000 IU/ml) in the presence or absence of 10 IU/ml GM-CSF. LAK activity generated in cultures with 10 IU/ml IL-2 + GM-CSF was significantly higher than that generated by 10 IU/ml IL-2 and did not differ from LAK generation at optimal concentrations of IL-2 (100 and 1000 IU/ml). PBSC from five additional patients were incubated with low-dose IL-2 + GM-CSF after sequential depletion of the CD4+ and CD8+ T cell subsets. LAK activity was significantly reduced by depletion of both CD4+ and CD8+ T cells and almost completely abolished after depletion of both subsets, suggesting that T cells and not NK cells are the main LAK precursors in this model. Six patients have received two courses of LAK cells generated in vitro by low-dose IL-2 + GM-CSF on day +1 and +8 after PBSC transplant in combination with GM-CSF and IL-2 administration in vivo. The mean LAK activity in peripheral blood of these patients dramatically increased immediately after transplant from a mean of 10% to 43.2% on day +2 and remained increased during the period studied. These results are encouraging and suggest that the administration of in vitro generated LAK cells early after transplant may have a role in the control of minimal residual disease.

Adolescent↗
PubMed1997

Upregulation of acidic fibroblast growth factor during development of experimental lung fibrosis.

Fibroblast proliferation and extracellular matrix accumulation are crucial in the pathogenesis of lung fibrosis. Fibroblast growth factor (FGF)-1 participates in both processes, but its role in lung fibrogenesis has not been evaluated. We analyzed the expression of FGF-1 and of FGF receptor (FGFR) in a model of lung fibrosis induced in rats with paraquat plus hyperoxia. Experimental and control animals were killed at 48 h and 2, 4, and 8 wk, and the lungs were studied by in situ hybridization, immunohistochemistry, and Northern blot. In normal lungs, scattered macrophages contained FGF-1. In contrast, at all times examined, the injured lungs exhibited FGF-1 transcript and the immunoreactive protein, mainly in alveolar epithelial cells and macrophages. In advanced fibrotic lesions, fibroblasts also appeared stained. Northern blot corroborated the upregulation of FGF-1 mRNA. FGFR was not observed in normal lungs, whereas it was strongly increased in the damaged lungs and was virtually immunolocalized in the same cell types as the corresponding ligand. These findings suggest that FGF-1 and FGFR are actively synthesized during the development of pulmonary fibrosis.

Animals↗
PubMed1997

C1-esterase inhibitor prevents early pulmonary dysfunction after lung transplantation in the dog.

The success of lung transplantation to a large extent depends on effective protection of the graft from ischemic injury after reperfusion. Although mechanisms have not been clarified, the pathologic findings of ischemic injury after reperfusion are similar to adult respiratory distress syndrome, a condition in which the blood coagulation contact system is activated. This study evaluates the effect of C1-esterase inhibitor (C1-INH), the main inhibitor of the blood coagulation contact system, on short-term lung function in a dog model of orthotopic lung transplantation. Twelve lung transplantations were performed after 24 h of ischemic time. Dogs were randomly assigned to receive either vehicle (Control) or C1-INH. After the lung transplantation in the control group, Pao2 decreased by 84% and both the AaPO2 and the Qs/Qt% increased (340 and 530%, respectively, p < 0.01); these parameters remained unchanged in the C1-INH group. The hypoxemia observed in control animals was associated with decreased blood coagulation contact factors, complement consumption, increased expression of adhesion glycoproteins in leukocytes, and extensive intraalveolar and interstitial neutrophil infiltration. In contrast, C1-INH administration prevented hypoxemia, the decrease in blood coagulation contact factors, the activation of the complement system, the increase in expression of leukocyte adhesion molecules, and inflammatory cell infiltrate. This study has demonstrated that in a dog model of lung transplantation, the administration of C1-INH prevents early pulmonary dysfunction, and it suggests that activation of blood coagulation contact system and complement are important mechanisms causing ischemic injury after reperfusion.

Animals↗
PubMed1997

Common Caucasoid HLA-A1B8DR3 linkage group and immune responsiveness in a hybrid Venezuelan population: preliminary data.

A study performed on Venezuelans reveals a correlation between the common Caucasoid linkage group HLA-A1 B8 (A*0101, B*0801, DR3-) and increased lymphoproliferative activity stimulated by several concentrations of phytohemagglutin and concanavalin A in comparison to the group of persons possessing either the HLA-A1 (A*0101) antigen or the HLA-B8,DR3 (B*0801,DRB1*03012) haplotype. The increased lymphoproliferative activity was simultaneously present with increased CD16 cell counts and decreased CD3 and total mononuclear counts. A further comparison of lymphocyte population and subpopulation counts in peripheral blood and serum Ig G,A,M levels in the HLA-A1+ B8+ versus the HLA-A1-B8-high-responder individuals revealed increased CD16 cell counts and IgM levels in persons with the common Caucasoid haplotype (HLA-A1 B8). The data may suggest that some of the genes responsible for these levels or genes controlling their expression could be localized in or along the length of the common Caucasoid haplotype HLA-A1 B8 between the A and B loci of the MHC.

Adult↗
PubMed1996

The coupling of metabolic to secretory events in pancreatic islets. Glucose-induced changes in mitochondrial redox state.

Mitochondrial NAD+, NADH, NADP+ and NADPH were measured in dispersed pancreatic islet cells incubated in the absence or presence of D-glucose and then exposed for 20 s to 0.5 mg/ml digitonin. The latter treatment resulted in the full release of lactate dehydrogenase without any detectable loss of glutamate dehydrogenase. The permeabilized cells were separated from the incubation medium by centrifugation through an oil layer and their content in pyridine nucleotides measured by a radioisotopic procedure coupled to the classical cycling technique. Relative to basal value, D-glucose, in concentrations of 2.8 and 16.7 mM, caused a concentration-related increase in both the NADH/NAD+ and NADPH/NADP+ ratio. These findings provide the first direct evidence for the induction of a more reduced mitochondrial redox state in glucose-stimulated pancreatic islets.

Animals↗
PubMed1996

Anti-CD69 antibodies enhance phorbol-dependent glucose metabolism and Ca2+ levels in human thymocytes. Antagonist effect of cyclosporin A.

The human activation antigen CD69 is an early inducible surface glycoprotein acquired by T cells in the thymus at the stage of positive selection and during activation of mature lymphoid cells both in vivo and in vitro. We have studied the regulatory influence of CD69 activation pathway on the glycolytic process and transduction signals of thymocytes. Treatment of human thymocytes with different anti-CD69 monoclonal antibodies (mAbs), in the presence of submitogenic doses of phorbol ester, produced an enhanced release of lactate without significant alterations in Fru 2,6-P2 levels or phosphofructokinase-2 (PFK-2) and pyruvate kinase activities. A small increase in phosphofructokinase-1 (PFK-1) activity was also detected. Furthermore, anti-CD69 mAb increased the glucose detritiation from [2-3H] and [3-3H]glucose, thus indicating an enhanced flux through hexokinase and PFK-1 steps. In addition, de novo synthesis of diacylglycerol and intracellular Ca2+ levels increased after anti-CD69 mAb treatment. The stimulatory effects of anti-CD69 mAb on both glycolysis and Ca2+ levels were inhibited by cyclosporin A. Because CD69 molecules are present in certain subset populations of immature thymocytes, the ability of anti-CD69 mAb to stimulate the glycolysis, the synthesis of diacylglycerol and the intracellular Ca2+ levels suggest that the activation signals delivered through CD69 molecules could play a role in the thymus cells maturation.

Antibodies, Monoclonal↗
PubMed1996

Alteration of human placental vascular tone by antiarrhythmic medications in vitro.

INTRODUCTION: Antiarrhythmic medications are commonly used during pregnancy for treatment of maternal or fetal arrhythmias, but little is known about their effect on human placental vascular tone and, consequently, placental blood flow. The objective of this study was to evaluate the tone responses caused by antiarrhythmic medications in human placental vessels from normal term pregnancies in vitro. METHODS AND RESULTS: Isolated human placental arteries and veins from uncomplicated term pregnancies incubated in Krebs'-bicarbonate under 5% oxygen/5% carbon dioxide/balance nitrogen (PO2 35 to 38 torr) were exposed to cumulative doses of quinidine, procainamide, lidocaine, flecainide, propranolol, amiodarone, verapamil, digoxin, and adenosine after submaximal contraction with 5-hydroxytryptamine. The study was conducted both in the presence and absence of endothelium. The addition of the tested medications caused a significant, dose-dependent relaxation of human placental arteries and veins except for adenosine, which induced a sustained, dose-dependent contraction of human placental vessels regardless of the presence or absence of tone. Removal of the endothelium did not alter these responses. CONCLUSIONS: Based on these results, the medications tested should have no decremental effect on placental blood flow, with the possible exception of adenosine, which causes significant, dose-dependent contraction of human placental vessels in vitro. Should similar contraction be present in vivo, it may have an adverse effect on the fetus when administering adenosine to pregnant women at term or during labor.

Anti-Arrhythmia Agents↗
PubMed1996

Study of Abbott Toxo IMx system for detection of immunoglobulin G and immunoglobulin M toxoplasma antibodies: value of confirmatory testing for diagnosis of acute toxoplasmosis.

We compared the Abbott Toxo immunoglobulin G (IgG) and IgM IMx assays with the Sabin-Feldman dye test and an IgM enzyme-linked immunosorbent assay (ELISA) in 398 serum samples previously tested in our laboratory (retrospective group) and 1,000 consecutive serum samples, tested as they were received in our laboratory in 1995 (prospective group). In the retrospective group, the IgG IMx had a sensitivity of 100%, specificity of 99.0%, positive predictive value of 99.0%, negative predictive value of 100%, and overall agreement of 99.5%. The percentages for the IgM IMx were 97.8, 99.0, 98.9, 98, and 98.4%, respectively. In the prospective group, the IgG IMx had a sensitivity of 97.8%, specificity of 98.7%, positive predictive value of 97.8%, negative predictive value of 98.7%, and overall agreement of 98.4%. The percentages for the IgM IMx were 88.3, 95.9, 74.7, 98.3, and 95%. A serological profile (IgA and IgE antibodies and the differential agglutination [AC/HS] test) was performed in an attempt to resolve discrepancies. Of 21 serum samples that were positive in the IgM IMx and negative in the IgM ELISA, 19 had serological profiles which were most compatible with an infection acquired in the distant past. Of 8 serum samples which were positive in the IgM ELISA and negative in the IgM IMx, 5 had serological profiles which were most compatible with an infection acquired in the distant past. Of the 55 serum samples that were positive in both IgM tests, 21 were from patients who had serological profiles which were most compatible with an infection acquired in the distal past. In conclusion, our data highlight the importance of confirmatory testing for the diagnosis of recently acquired infection with Toxoplasma gondii. When compared with the dye test and IgM ELISA, the Toxo IgG and IgM IMx assays, respectively, revealed high overall agreement in the retrospective and prospective study.

Acute Disease↗
PubMed1996

Inhibition of apoptotic cell death in B-CLL by interferon gamma correlates with clinical stage.

Apoptosis was evaluated in B cells from 41 patients with B-CLL and 20 healthy aged-matched controls. B cells were cultured with and without gamma-IFN and other cytokines; apoptosis was quantified at regular intervals throughout a 5-day culture period. According to Rai's criteria, 17 patients were classified as good risk, 16 as intermediate and eight as high risk. In vitro, purified B cells from B-CLL patients were evaluated for apoptosis. Maximal apoptosis (44.12%) was observed at day 5 in cells from patients with poor prognosis. The addition of gamma-IFN to the culture media prevented apoptosis in a dose-dependent manner. Maximal inhibition of apoptosis was achieved with 100 IU/ml of gamma-IFN. The degree of inhibition of apoptosis by gamma-IFN was greater in cells from the high-risk group patients than in those from the intermediate and good prognosis group (P < 0.0001). The expression of gamma-IFN receptors in B-CLL cells was evaluated using a MnAb against the extracellular domain of gamma-IFN receptor. After 4 days in culture with gamma-IFN, only cells from the intermediate- and high-risk groups showed an increase in the density of gamma-IFN receptors (P < 0.001). gamma-IFN was not detected in the sera of our study patients. However gamma-IFN was detectable in the media from both normal B cells and B-CLL cells in culture; there was no difference in the amount of gamma-IFN released by cells from the three groups of patients studied. Our results show that in vivo gamma-IFN inhibits apoptosis of B cells from B-CLL patients. The inhibitory effect of gamma-IFN on apoptosis correlates directly with the severity of the disease and this is likely explained by a marked upregulation of gamma-IFN receptors in cells from patients in the high-risk group.

Aged↗
PubMed1995

Hexose metabolism in pancreatic islets: effect of D-glucose on the mitochondrial redox state.

The mitochondrial NADH/NAD+ ratio for free nucleotides in rat pancreatic islets was judged from the cell content in L-glutamate and L-alanine, 2-ketoglutarate and pyruvate, and NH4+. At a physiological concentration of D-glucose, such a ratio averaged 9.6 +/- 1.1%. A rise in hexose concentrations, above a threshold value in excess of 5.6 mM, caused a rapid, sustained and rapidly reversible decrease in the mitochondrial NADH/NAD+ ratio. It is speculated that in the process of glucose-stimulated insulin release, the latter change participates in the coupling between metabolic and secretory events by favouring both the activity of key mitochondrial dehydrogenases and the translocation of Ca2+ from the mitochondria into the cytosol.

Animals↗
PubMed1995

Hexose metabolism in pancreatic islets: regulation of the mitochondrial NADH/NAD+ ratio.

In rat pancreatic islets, D-glucose in concentrations exceeding 5.6 mM caused a concentration-related decrease of the mitochondrial NADH/NAD+ ratio, as judged from the changes in the islet content of glutamate, NH4+, and 2-ketoglutarate, and assuming that the glutamate dehydrogenase reaction is near equilibrium with the mitochondrial NAD system. The concentration dependency of the response to D-glucose was vastly different in islet and parotid cells, respectively. L-Leucine, 2-ketoisocaproate, BCH (a nonmetabolized but insulinotropic analog of L-leucine) and 3-phenylpyruvate also lowered the mitochondrial NADH/NAD+ ratio. In the presence of D-glucose, the latter ratio was also decreased by NH4+ or the absence of extracellular Ca2+, but dramatically increased by aminooxyacetate. Taking into account prior metabolic findings, the nutrient-induced fall in the mitochondrial redox state is thought to reflect an increased clearance of mitochondrial NADH through both the respiratory chain and malate-aspartate shuttle. The nutrient-induced decrease in the mitochondrial NADH/NAD+ ratio might favor both the circulation of metabolites in the Krebs cycle and the exit of Ca2+ from the mitochondria.

Amino Acids↗
PubMed1995

Properties of a progesterone-induced relaxation in human placental arteries and veins.

To study the effects of progesterone on placental vascular tone, we used isolated (1-2 mm in diameter) placental arteries and veins from term uncomplicated pregnancies. These vessels, incubated in Krebs buffer (pH 7.4) under 5% O2-5% CO2 (balance N2, PO2 approximately 35 torr) and precontracted with serotonin were exposed to incremental doses of progesterone (0.01-30 mumol/L) in the presence or absence of endothelium, 10 mumol/L indomethacin (inhibits prostaglandin synthesis), 10 mumol/L methylene blue (a soluble guanylate cyclase inhibitor), 100 mumol/L nitro-L-arginine (inhibits L-arginine metabolism), 1 mmol/L isobutylmethylxanthine (a cAMP phosphodiesterase inhibitor), or 30 mumol/L mifepristone (RU 38486, an antiprogestin). Progesterone elicited an acute dose-dependent relaxation in both arteries and veins that was not altered by removal of the endothelium or pretreatment with indomethacin, nitro-L-arginine, or methylene blue, excluding a role for prostaglandins, L-arginine products, or cGMP in mediating this relaxation. However, isobutylmethylxanthine significantly enhanced the relaxation in response to progesterone, suggesting a role for cAMP. RU 38486 inhibited the relaxation by 50-100%, depending on the progesterone dose, consistent with a role for progesterone receptors. These results suggest that progesterone causes a dose-dependent endothelium-independent relaxation of human placental arteries and veins. This relaxation seems to be mediated by a receptor-activated cAMP mechanism and could be physiologically important in maintaining low resistance and adequate blood flow in the placental circulation.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1995

Macroscopic effects of percutaneous trigeminal ganglion compression (Mullan's technique): an anatomic study.

After the use of Mullan's technique, macroscopic changes take place on the gasserian ganglion and the surrounding structures. These changes were studied on 20 trigeminal nerves of 10 fresh adult cadavers. Changes took place on the dura as well as in the neural elements. There was compression on the ganglion and on the trigeminal nerve, and there were changes in the position of the trigeminal root, with shortening of its cisternal segment. When the balloon was inflated to capacity (0.75-1.0 ml), dural stretching in an area of 15 x 10 mm took place. This stretching of the dura extended from the lateral wall of the cavernous sinus to the level of the porus trigemini. Despite these important mechanical effects, we never found a rupture or tear on the dura or the trigeminal nerve fibers. We discuss the relationship between mechanical effects and clinical results.

Adult↗