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Biomedical subjects

A Zapata

Publications and source records attributed to A Zapata.

At least 37 records · Page 2Linked to original sources

Titanium levels in rats implanted with Ti6Al4V treated samples in the absence of wear.

The effect of implantation time and implant nitriding on titanium ion concentration in several tissues of rats carrying Ti6Al4V implants was studied by means of inductively coupled plasma-mass spectroscopy (ICP-MS). Histological studies were also performed in order to check for tissue degeneration due to the Ti6Al4V implantation. The animals were divided into four groups: one received Ti6Al4V implants, the second received nitrided Ti6Al4V implants, the third group received nitrided and descaled Ti6Al4V implants and the last one was the control group. Half the animals of the implanted groups received the Ti6Al4V implant for 30 days, while the other half received the implant for 120 days. Spleen, muscle, kidney, lung, brain and bone samples were retrieved from these rats as well as the control group. Ion concentration measures did not show significant differences between control and implanted rats for the studied period of time, although histological studies showed minor differences, especially on liver tissue samples.

Journal Article↗

Region-specific and calcium-dependent increase in dialysate choline levels by NMDA.

NMDA receptor-induced excitotoxicity has been hypothesized to mediate abnormal choline (Cho) metabolism that is involved in alterations in membrane permeability and cell death in certain neurodegenerative disorders. To determine whether NMDA receptor overactivation modulates choline metabolism in vivo, we investigated the effects of NMDA on interstitial choline concentrations using microdialysis. Perfusion of NMDA by retrodialysis increased dialysate choline (approximately 400%) and reduced dialysate acetylcholine (Ach) (approximately 40%). Choline levels remained increased for at least 2.5 hr, but acetylcholine returned to pretreatment values 75 min after NMDA perfusion. The NMDA-evoked increase in dialysate choline was calcium and concentration dependent and was prevented with 1 mM AP-5, a competitive NMDA antagonist, but was not altered by mepacrine, a phospholipase A2 inhibitor. NMDA increased extracellular choline levels four- to fivefold in prefrontal cortex and hippocampus, produced a slight increase in neostriatum, and did not modify dialysate choline in cerebellum. Perfusion with NMDA for 2 hr produced a delayed, but not acute, reduction in choline acetyltransferase activity in the area surrounding the dialysis probe. Consistent with a lack of acute cholinergic neurotoxicity evoked by this treatment, basal acetylcholine levels were unaltered by 2 hr of continuous NMDA perfusion. Prolonged NMDA perfusion produced a 34% decrease in phosphatidylcholine content in the lipid fraction of the tissue surrounding the dialysis probe. These results show that NMDA modulates choline metabolism, eliciting a receptor-mediated, calcium-dependent, and region-specific increase in extracellular choline from membrane phospholipids that is not mediated by phospholipase A2 and precedes delayed excitotoxic neuronal cell death.

2-Amino-5-phosphonovalerate↗

Body fat distribution, insulin mediated suppression of non-esterified fatty acids and plasma triglycerides in obese subjects.

Triglyceride levels and free fatty acid metabolism are influenced by body fat distribution. To test whether the pattern of fat distribution in obese subjects results in distinct insulin mediated suppression of non-esterified fatty acids which could account for differences in plasma triglycerides, we studied 59 obese subjects who were classified according to waist-to-hip ratio. Non-esterified fatty acids and insulin response to a 75 g oral glucose tolerance test were higher in abdominal obesity. Total non-esterified fatty acids response, after adjustment for sex, showed a positive association with waist-to hip ratio (r = 0.292; p < 0.05). The abdominal obese group had higher fasting triglycerides (1.74+/-0.83 versus 1.11+/-0.71 mmol/L; p = 0.003) and lower glucose/insulin ratio (5.2+/-2.3 versus 7.1+/-2.4; p = 0.003). Stepwise multiple regression analysis showed that triglyceride levels are explained by fasting and 120 min non-esterified fatty acids and by glucose/insulin ratio. We conclude that abdominal obesity is associated with a higher resistance to insulin mediated suppression of non-esterified fatty acids in obese subjects. Variation of triglyceride concentrations in obesity is dependent on both fasting and 120 min non-esterified fatty acids as well as on insulin sensitivity to glucose utilization.

Adolescent↗

Glycine site antagonists and partial agonists inhibit N-methyl-D-aspartate receptor-mediated [3H]arachidonic acid release in cerebellar granule cells.

Activation of N-methyl-D-aspartate (NMDA) receptors is known to produce arachidonic acid release, which has been implicated in excitotoxicity. Antagonists and partial agonists at the glycine site of the NMDA receptor, despite exhibiting functional differences in electrophysiological studies, inhibit glutamate-induced neurotoxicity and ischemia-induced neurodegeneration. The objective of this study was to investigate the effects of both glycine site antagonists and partial agonists on NMDA receptor-mediated [3H]arachidonic acid (AA) release evoked by glutamate, NMDA or a competitive inhibitor of the glutamate/aspartate uptake carrier. The [3H]AA release evoked by a maximally effective concentration of glutamate (100 microM) was blocked by the glycine site antagonists 7-chlorokynurenic acid (7-CKYN) and 5,7-dichlorokynurenic acid (5,7-DCKYN) and by a low intrinsic efficacy glycine partial agonist (+)-1-hydroxy-3-aminopyrrolid-2-one [(+)-HA-966]. 1-Aminocyclopropanecarboxylic acid (ACPC), a high intrinsic efficacy glycine partial agonist, did not modify [3H]AA release evoked by 100 microM glutamate. However, ACPC blocked (in a glycine reversible manner) the [3H]AA release induced by NMDA (100 microM) with an IC50 of 131 +/- 2 microM. Furthermore, L-trans-pyrrolidine-2,4-dicarboxylate (PDC), a competitive inhibitor of the glutamate transporter, also released [3H]AA (Emax and EC50 of 127 +/- 4% and 30 +/- 1 microM, respectively). ACPC, 7-CKYN and (+/-)-2-amino-7-phosphonoheptanoic acid (AP-7), a competitive NMDA receptor antagonist, inhibited [3H]AA release evoked by PDC. These results demonstrate that both glycine site antagonists and partial agonists can inhibit NMDA receptor-mediated [3H]AA release in cerebellar granule cells, an action consistent with the neuroprotective effects of these compounds.

Amino Acids↗

[Occlusion of the right common carotid artery due to oral estrogen overdose].

INTRODUCTION: Continuous use of oral anticontraceptive agents has been related to adverse vascular changes in the form of venous or arterial thromboses and cerebrovascular accidents (CVA). In our case, we describe a CVA due to occlusion of the common carotid artery after an acute massive overdose of estrogens due to error of dosage when using Yuzpe's system or emergency post-coital therapy. CLINICAL CASE: We describe a 26 year old woman with no previous clinical history, who smoked 20 cigarettes per day, did not take oral contraceptive pills and suffered an acute left facial-brachial-crural hemiplegia together with reduced level of consciousness. Imaging tests showed acute occlusion of the right common carotid artery. Etiological study of the patient's cerebral vascular accident was negative. The only etiopathogenic factor to be related was having taken oral contraceptive agents for three days after coitus as emergency post-coital treatment. This treatment was incorrect, since the dose of estrogens was four times that recommended. CONCLUSIONS: The continued use of estrogens, especially at doses over 30 micrograms per day, was considered responsible for approximately 10% of CVAs in young people. The risk of cerebral vascular accident is greater when there is associated migraine and/or smoking. We describe a patient who showed that the acute use of high doses of estrogens may also cause arterial occlusion, in this case in the common carotid artery.

Administration, Oral↗

Clinical comparison of dexketoprofen trometamol and dipyrone in postoperative dental pain.

A total of 125 outpatients with moderate to severe pain after surgical removal of one impacted third molar were randomly assigned to receive dexketoprofen trometamol 12.5 or 25 mg or dipyrone 575 mg. For first-dose assessments, patients rated their pain intensity and its relief at regular intervals. From 60 min post dose to the end of the 6-h observation period, both doses of dexketoprofen trometamol had higher pain relief scores than dipyrone: Between 3 and 6 h the differences were statistically significant. In addition, peak measures (PIDmax and PARmax) were statistically superior after both doses of dexketoprofen trometamol compared to dipyrone. The overall efficacy assessed at the end of the first-dose phase was rated as good or excellent by 90%, 83.3%, and 70% of patients receiving dexketoprofen trometamol 25 mg, dexketoprofen trometamol 12.5 mg, and dipyrone, respectively. The number of patients who required remedication during the 6-h period was significantly lower in both dexketoprofen groups. Repeated-dose data were also obtained. No significant differences were found in the efficacy after repeated doses, the number of doses taken, or the mean time elapsed between doses. The overall efficacy at the end of the repeated-dose phase was rated as good or excellent by 84.2%, 66.7%, and 70% of patients receiving dexketoprofen trometamol 25 mg, dexketoprofen trometamol 12.5 mg, and dipyrone, respectively. The frequency of adverse events was similar for all treatments and no serious adverse events were reported during the study.

Adolescent↗

Effects of NMDA-R1 antisense oligodeoxynucleotide administration: behavioral and radioligand binding studies.

The effects of an antisense phosphodiester oligodeoxynucleotide (ODN) directed to the NR1 subunit of the NMDA receptor mRNA and of its corresponding sense ODN were investigated in mice. Treatment with the antisense ODN significantly increased the time mice spent in the open arms of an elevated maze while the total number of arm entries was unaltered. Furthermore, seizure latencies after the administration of an ED100 dose of NMDA (150 mg/kg) were significantly higher in antisense treated animals compared to vehicle controls. At the same time, treatment with NR1 antisense ODN significantly reduced the Bmax of [3H]CGS-19755 binding (2101 fmol/mg protein) compared to both vehicle (2787 fmol/mg protein) and sense (2832 +/- 39 fmol/mg protein) controls without any significant change in KD (33 nM). A corresponding reduction of [3H]CGP-39653 binding was also observed after treatment with NR1 antisense compared to both sense and vehicle controls. In contrast, neither antisense nor sense ODNs altered the proportion of high affinity glycine sites or the potency of glycine at either high or low affinity glycine binding sites to inhibit [3H]CGP-39653 binding. These results show that in vivo treatment with NR1 antisense ODNs to the NMDA receptor complex reduces antagonist binding at NMDA receptors and has pharmacological effects similar to those observed with some NMDA receptor antagonists. These results also suggest that treatment with antisense ODNs may provide another means to investigate allosteric modulation of receptor subtypes in vivo.

2-Amino-5-phosphonovalerate↗

Monoclonal antibodies specific for porcine monocytes/macrophages: macrophage heterogeneity in the pig evidenced by the expression of surface antigens.

Macrophages are widely distributed in most tissues of the body, where they play important roles in host defense and repair of tissue damage. In this report we describe the production and characterization of a panel of six monoclonal antibodies (mAb) against porcine macrophages and their use for phenotyping tissue macrophages. All mAbs were produced by immunizing mice with porcine alveolar macrophages. Three of them (2A10/11, 3B11/11 and 3F7/11) react mainly with macrophages and, at a lower extent, blood monocytes, whereas the others (1E12/11, 2C12/10 and 4E9/11) also recognize granulocytes. Antigens recognized by these antibodies could be characterized by Western blot and/or immunoprecipitation, with the exception of that one recognized by 2C12/10. By their behavior in SDS-PAGE under reducing and nonreducing conditions, all seem to be single polypeptides, whose apparent molecular weight under reducing conditions are: 1E12/11 and 3B11/11 larger than 204 kDa; 2A10/11, 150 kDa; 4E9/11, 125-170 kDa; and 3F7/11, 135 kDa. Immunohistochemical analyses of both lymphoid and non-lymphoid organs using these mAbs reveal important antigenic heterogeneity among tissue macrophages. These mAbs are, therefore, useful tools for the study of porcine macrophage maturation and differentiation and for determining their heterogeneity both in normal and pathological conditions.

Animals↗

Modulation of NMDA-induced cytosolic calcium levels by ACPC in cultured cerebellar granule cells.

The effect of 1-aminocyclopropanecarboxylic acid (ACPC) on the potentiation by glycine of N-methyl-D-aspartate (NMDA)-evoked increases in intracellular free calcium concentration [Ca2+]i was examined in cultured rat cerebellar granule cells. NMDA (50 microM) produced a rapid and sustained increase in [Ca2+]i from 72 +/- 3 to 205 +/- 18 nM. Addition of exogenous glycine potentiated (EC50 -2 microM) the effects of NMDA, increasing [Ca2+]i to an Emax of 323 +/- 5 nM. ACPC increased the EC50 of glycine from 2 microM (no ACPC) to 17 microM (400 microM ACPC). Concomitant with reduced potency of glycine, ACPC also inhibited the Emax of glycine to enhance NMDA-evoked cytosolic free calcium to values (224 +/- 1 nM) approaching those observed in the nominal absence of glycine. These results show that ACPC, a compound previously reported to prevent excitotoxic cell death, inhibits the glycine-induced increase of Ca2+ entry through NMDA receptors in cerebellar granule cells.

Animals↗

1-Aminocyclopropane-carboxylic acid reduces NMDA-induced hippocampal neurodegeneration in vivo.

The effect of systemic treatment with 1-aminocyclopro-panecarboxylic acid (ACPC), a partial agonist at the glycine site of the NMDA receptor, on convulsions and neurodegeneration induced by intrahippocampal injection of NMDA was investigated in mice. Five days after intrahippocampal NMDA infusion, 80-100% pyramidal cell death was observed in the CA1 region of the hippocampus. Pretreatment with ACPC prevented the lethal effects of NMDA and significantly reduced seizure induction. ACPC reduced cell death to 40% of that induced by a dose of NMDA (6 nmol) that damaged 80% of hippocampal CA1 neurones in untreated animals. These findings provide further evidence that ACPC can reduce NMDA receptor function in vivo and suggest that partial agonists at the glycine site of the NMDA receptor complex may be useful anticonvulsant and neuroprotective agents.

Amino Acids↗

Ultrastructural identification of the splenic follicular dendritic cells in the chicken.

BACKGROUND: There is a need to identify the follicular dendritic cells (FDC) of the chicken spleen at the ultrastructural level during a secondary immune response. METHODS: The cells were identified after intravenous priming BSA and boosting with biotinylated BSA conjugated to colloidal gold particles. Monoclonal antibodies raised specifically either to chicken IgG or IgM were used to characterize these immune complex-trapping cells. RESULTS: The FDC had an irregular morphology which varied through time, supporting the existence of two types of FDC in the chicken spleen, one showing filiform cell processes, the other provided with beaded dendrites. When the filiform dendrites were observed, the FDC bound the antigen on their surfaces. These dendrites showed an intrincate convoluted configuration, forming tightly wrapped networks near the cell body. The networks had the same features as those described in mammals as antigen retaining reticulum (ARR). In chickens, the ARR, which represents sites of antigen localization on FDC, reached maximum development on day 5 after the second injection of BSA and had disappeared by day 8. At this time FDC had beaded dendrites. CONCLUSIONS: Antigen is retained on FDC in the chicken spleen for long periods of time.

Animals↗

Histopathology of the thymus in Saprolegnia-infected wild brown trout, Salmo trutta L.

A comparative analysis was made of the thymic cytoarchitecture of healthy and Saprolegnia-infected wild brown trout. In Saprolegnia-infected fish, even when the thymus was not invaded by fungal hyphae, the thymic architecture was lost without signs of regionalization. Intercellular oedema, some thymocytes, hypertrophic and degenerated epithelial cells and increased phagocytic activity were also observed. In thymi invaded by the fungus, hyphae occurred isolated or in close apposition to epithelial cells, and the thymic disorganization was more noticeable. Most thymocytes were pyknotic and both epithelial cells and macrophages contained engulfed dead cells. However, no inflammatory response to the fungal invasion was observed. These results confirm the immunodepressed condition of Saprolegnia-infected wild brown trout previously observed in peripheral lymphoid organs. We discuss the secretion of fungal products and/or the high levels of corticosteroids observed in these fish as possible origins of the condition.

Animals↗

Gamma/delta T cells in fetal, neonatal, and adult rat lymphoid organs.

In the present study, we have analyzed the appearance and maturation of gamma/delta T cells, recognized with a new mAb V65, in the central and peripheral lymphoid organs of fetal, neonatal, and adult Wistar rats. Cytofluorometrical analysis demonstrated the first V65+ gamma/delta T cells in the thymus of 16-17-day embryonic rats, although by immunohistology, they were identified only in 19-day rat embryos in both the cortico-medullary border and thymic medulla. Phenotypically, gamma/delta thymocytes from fetal and neonatal thymus expressed CD3, CD2, and CD5, but only 60-80% were CD8+ and approximately 40-50% expressed the alpha chain (p55) of the IL-2R. In the periphery, the immunohistological study identified for the first time gamma/delta T cells in the splenic white pulp and the gut of 21-day fetal rats, where they occurred within the epithelium as well as in the lamina propria. After birth, gamma/delta lymphocytes appeared in the skin, where they were present as dendritic epidermal T cells in increasing numbers during postnatal life. Whereas these gamma/delta T cells formed the predominant T-cell population in the rat skin, gamma/delta T cells in peripheral lymphoid organs, BALT, or the gut only represented a minor T-cell population. These results are discussed in comparison to gamma/delta T cells of other vertebrate species.

Animals↗

Synthesis and investigation of the possible insulin-like activity of 1D-4-O- and 1D-6-O-(2-amino-2-deoxy-alpha-D-glucopyranosyl)-myo-inositol 1-phosphate and 1D-6-O-(2-amino-2-deoxy-alpha-D-glucopyranosyl)-myo-inositol 1,2-(cyclic phosphate).

The synthesis of the glycosyl-myo-inositol 1-phosphates 1 and 2 and of the glycosyl-myo-inositol 1,2-(cyclic phosphate) 3, starting from previously synthesized intermediates, is reported. Compound 3 was found to display proliferative effects on the early developing inner ear of chick embryo.

Animals↗

Establishment and characterization of cloned human thymic epithelial cell lines. Analysis of adhesion molecule expression and cytokine production.

The thymic stromal microenvironment is required for the generation of immunocompetent T lymphocytes. However, the different thymic stromal cell types have not been fully characterized and their roles regarding T-cell development are not completely understood. To address the phenotypic characteristics of the epithelial component of the human thymic microenvironment as well as its functional involvement in T-cell development, we have established cloned thymic epithelial cell (TEC) lines from fetal and postnatal human thymuses by an explant technique, repeated subculture, and limiting dilution cloning. These cloned TEC lines were shown to be derived from cortical epithelium and to express a number of cell-surface molecules including CD40, major histocompatibility complex (MHC) HLA-ABC and HLA-DR antigens, homing-associated cell-adhesion molecule (H-CAM), intercellular adhesion molecule-1 (ICAM-1), leukocyte function-associated antigen 3 (LFA-3), and beta 1 subfamily integrins. Finally, both postnatal and fetal TEC clones were shown to produce interleukin-1 alpha (IL-1 alpha), IL-6, and IL-7. These well-defined cloned TEC lines may provide useful tools for the study of TEC biology and for the understanding of the precise role played by TEC in human T-cell development.

Carrier Proteins↗

Struggling and flumazenil effects in the swimming test are related to the level of anxiety in mice.

The possible involvement of anxiety and learning/memory processes in escape-directed (struggling) behavior in a two-trial swimming test was investigated in mice, as well as the differential effects that low doses of flumazenil (a benzodiazepine receptor antagonist) could display depending on the animals' anxiety levels. Mice showing less anxiety in the plus-maze test exhibited less struggling behavior in the first swimming trial than the more anxious animals, suggesting a relationship between anxiety and struggling behavior in the swimming test. Flumazenil (5 mg/kg) given before the first swimming trial displayed differential effects depending upon the animals' anxiety levels. Thus, it increased struggling behavior in the first swimming trial in 'low-anxiety' mice whereas the opposite tendency was observed in 'high-anxiety' animals. Struggling decreased in the second swimming trial in all the animals, giving support to the involvement of learning/memory processes in the two-trial swimming test. That reduction in escape-directed behavior was greater in animals treated with flumazenil before the first swimming session, thus indicating a slight enhancement of retention.

Animals↗