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L Quijada

Publications and source records attributed to L Quijada.

At least 37 records · Page 2Linked to original sources
PubMed1995

Mapping of the linear antigenic determinants from the Leishmania infantum histone H2A recognized by sera from dogs with leishmaniasis.

Antibodies reacting against the H2A histone protein were frequently observed in the sera from dogs naturally infected with the protozoan parasite Leishmania infantum. Using synthetic peptides covering the complete sequence of the protein we have identified the amino terminal region, comprising from amino acids 1 to 20, and the carboxyl terminal region, comprising from amino acids 106 to 132, as conforming the antigenic determinants of the protein. Those regions, exposed in the nucleosome surface, are highly divergent in sequence relative to the mammalian H2A histones. The anti-H2A histone antibodies present in the sera of these dogs specifically recognize the L. infantum H2A histone and they do not react with mammalian histones. The present data indicate that, in spite of the evolutionary conservation of the H2A histone protein among eukaryotic organisms, the humoral response against this protein during natural infection is specifically triggered by the parasite protein antigenic determinants.

Amino Acid Sequence↗
PubMed1995

During active viscerocutaneous leishmaniasis the anti-P2 humoral response is specifically triggered by the parasite P proteins.

In this work we show that in the sera from dogs naturally infected with the protozoan parasite Leishmania infantum there are antibodies that react specifically against the parasite acidic ribosomal proteins LiP2a and LiP2b, and that each one of the Leishmania P proteins elicits a specific humoral immune response. Using synthetic peptides, the antigenic epitope of these proteins has been mapped in a single region located adjacent to the C-terminal domain highly conserved among the eukaryotic P proteins. The anti-P antibodies elicited during the Leishmania infection do not recognize the conserved C-terminal domain of the parasite P proteins, in contrast with the findings reported in Chagas' disease or systemic lupus erythematosus. The antigenic epitopes of the LiP2a and LiP2b are almost identical in amino acid sequence. No reactivity against Trypanosoma cruzi and human P proteins was found in sera from L. infantum-infected dogs.

Amino Acid Sequence↗
PubMed1993

Calcium channel antagonists and adenosine analogues decrease tolerance to opiate pentazocine and U 50488H.

1. A single dose of pentazocine induces cross-tolerance the analgesic effects of the kappa agonist U 50488H. Tolerance is observed by means of the hot plate test or by the i.p. administration of acetic acid 6 or 24 hr after the priming dose, respectively. 2. The administration of the calcium channel antagonists, diltiazem, nifedipine or verapamil, reduces the degree of tolerance as assessed by the hot plate test or acetic acid administration. 3. The adenosine agonist N6-cyclopentyl adenosine significantly reduced the intensity of the process; in contrast, N6-cyclohexyladenosine antagonized the analgesic response to the opiate obscuring its influence on the process. 4. The results are discussed in relation to the interaction of calcium channel function in the analgesic response to the kappa opiates.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1993

Calcium channel modulators modify K opioid-induced inhibition of C-fiber-evoked spinal reflexes in rat.

The role of L-type Ca2+ channels on the kappa opioid-induced depression of spinal afferent transmission was assessed in spinalized rats, through recording of the C-fiber-evoked spinal flexor reflex. Six successive i.t. doses of the K agonist U-50,488H produced a dose-dependent decrease of the C-reflex duration (ID50: 25.7 nmol), the log dose-response relationship being shifted to left by pretreatment with 5 mg/kg i.v. of the calcium channel blocker verapamil, or to right by pretreatment with .25 mg/kg i.v. of the calcium channel agonist Bay K8644. Verapamil and Bay K8644, administered i.v. after U-50,488H i.t., respectively potentiated or antagonized the depressor effect of the K ligand on the reflex. The results point to a role for Ca2+ availability as a factor involved in depression of afferent nociceptive transmission by K opioids at the spinal cord.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1992

Effects of calcium channel antagonists and Bay K 8644 on the analgesic response to pentazocine and U 50488H.

1. The effects of diltiazem, nifedipine and verapamil and the calcium channel agonist Bay K 8644 on the analgesic responses to the subcutaneous (s.c.) or intracerebroventricular (i.c.v.) administration of pentazocine and U 50488H were investigated in mice. 2. The three calcium channel antagonists and Bay K 8644 reduced the number of writhes induced by the intraperitoneal administration of acetic acid. 3. The analgesic responses to the low doses of pentazocine (s.c.) were additive with the effects of diltiazem, nifedipine or Bay K 8644; while, in contrast, the higher doses produced underadditive responses. Only verapamil increased the effects of the i.c.v. administration of the opioid. 4. The effects of U 50488H (s.c.) were additive with those of diltiazem and Bay K 8644; verapamil only increased the response to the lower dose of the opioid. Nifedipine plus pentazocine always induced underadditive responses. The i.c.v. effects of U 50488H were only increased by verapamil. 5. These findings are discussed in relation with a possible interaction of kappa agonists with calcium channels in the central nervous system.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1992

Cryptosporidiosis among patients with acquired immunodeficiency syndrome in Zulia State, Venezuela.

We studied the prevalence of Cryptosporidium in 29 patients with acquired immunodeficiency syndrome (AIDS) from Zulia State, Venezuela. They ranged in age from five months to 46 years. Two were children and 27 were adults, of which six were women. Of the 21 men, 66.6% reported homosexual behavior. Three stool samples from each patient were examined, and modified Ziehl-Neelsen carbolfuchsin staining of formalinether stool concentrates was used to identify Cryptosporidium oocysts. To detect the presence of other intestinal parasites, direct wet mounts and iron-hematoxylin-stained smears were examined. Cryptosporidium was found in 12 (41.3%) of the patients and was identified as a single parasitic infection in seven of the 12 patients (58.3%). Other pathogenic parasites encountered were Giardia lamblia (3 of 12, 25%), Entamoeba histolytica (1 of 12, 8.3%), Ascaris lumbricoides, Trichuris trichiura, and Strongyloides stercoralis (each 1 of 12, 8.3%). Blastocystis hominis, an organism with an uncertain taxonomic position and pathogenicity, was observed in three of 12 patients (25%). An inflammatory exudate was observed in 10 of 12 patients infected with Cryptosporidium. Most of the patients with this infection presented with chronic watery diarrhea and weight loss. Our results suggest that Cryptosporidium is very common in AIDS patients with diarrhea in Venezuela. However, the role of this parasite as an enteropathogen in these patients is uncertain.

AIDS-Related Opportunistic Infections↗
PubMed1990

Influence of adenosine analogs on morphine tolerance and dependence in mice.

A number of adenosine agonists were investigated for possible actions on tolerance to morphine withdrawal in mice. The induction of tolerance to a sustained release preparation of morphine was assessed by measuring the analgesic effect induced by a test dose of the drug. The concomitant treatment with L- and D-phenylisopropyl adenosine, (L- and D-PIA), cyclopentyladenosine (CPA) or chloroadenosine (CADO) during the period of morphine absorption did not alter the induction of the process. In contrast cyclohexyladenosine (CHA) significantly decreased the intensity of tolerance. The administration of naloxone 30 hrs, after the priming dose of morphine induced an intense withdrawal reaction. The intensity of the abstinence syndrome was decreased by the administration of L-PIA, CHA or CADO; CPA and D-PIA were ineffective. These results suggest that adenosine analogs may interfere with the known morphine effects on calcium disposition in nerve terminals.

Adenosine↗
PubMed1978

Partial inhibition of the abstinence syndrome in morphine tolerant-dependent mice following pharmacological denervation.

Mice were chronically treated with either atropine, methysergide or pentobarbital in order to induce sensitivity changes resulting from adaptative adjustments in the central nervous system (CNS), and to examine the degree of tolerance to and physical dependence on morphine several days after the discontinuation of pretreatments. Subsequently to the chronic blockade of muscarinic or serotonergic receptors, the intensity of tolerance was unaffected, but some manifestations of the abstinence behavior induced by naloxone were reduced in part. This attenuation of the abstinence syndrome in the pretreated mice was reverted by an additional dose of either atropine or methysergide administered a few min before naloxone. Additional experiments with physostigmine or 5-hydroxytryptophan (5-HTP) in morphine-dependent mice yielded results compatible with the hypothesis that morphine physical dependence may be the manifestation of compensatory changes of sensitivity to serotonin and acetylcholine in the CNS. These results do not exclude the participation of other neurotransmitters or neurohormones in morphine dependence.

5-Hydroxytryptophan↗
PubMed1977

Effects of tricyclic compounds and other drugs having a membrane stabilizing action on analgesia, tolerance to and dependence on morphine.

Several drugs affecting nerve cell excitability, by opposing ion movements in membranes, were tested in mice rendered tolerant to or dependent on morphine. The purpose of the study was to investigate whether these drugs share the ability to attenuate morphine tolerance and dependence exhibited by tricyclic antidepressants. Tolerance to morphine was decreased by the administration of imipramine, doxepin, promethazine, propranolol, lidocaine and quinidine. Chlorpromazine and carbamazepine were ineffective. The intensity of the abstinence syndrome provoked by naloxone was decreased by chlorpromazine, imipramine, doxepin, lidocaine, quinidine and propranolol. Diphenyl. hydantion and carbamazepine had no effect. The results are discussed in relation with the blockade of ion conductance and their interference with the release of neurotransmitters produced by the drugs assayed.

Analgesia↗
PubMed1976

Biologic activities of rabbit immunoglobulin G in relation to domains of the Fc region.

Biologic properties of antibodies are known to be mediated by the Fc portion of the H chains. In the present study such properties as complement fixation, cutaneous anaphylaxis, and macrophage cytophilia were examined in relation to the CH2 and CH3 domains of rabbit IgG. Fragments containing but one of these domains were prepared from plasmin and papain digests. Facb fragments of anti-DNP antibodies, together with the antigen DNP-BSA, were able to fix complement by the classical pathway, a result which implicates the CH2 domain; however, guinea pig Fab fragments directed to regions of the rabbit antibody molecule other than CH2 were able to inhibit complement fixation. Facb fragments were unable to mediate PCA or reverse PCA reactions in guinea pigs, nor were CH3 fragments active in tests of reverse PCA or inhibition of PCA. These results suggest that the entire Fc region is needed for cutaneous anaphylaxis. The ability to bind to guinea pig lung macrophages was studied with a rosette technique. Facb fragments were active whereas CH3 fragments failed to inhibit. It is suggested that although some effector functions of antibodies can be assigned to individual domains, others require the entire Fc region.

Animals↗
PubMed1975

Sensitivity changes to morphine and other drugs induced by cholinergic blockade.

Mice were given several atropine injections at a high dosage level. After 2 to 5 days of cessation of treatment the effects of morphine, arecoline, amphetamine, pentylenetetrazol, reserpine, and hexobarbital were determined and compared with those found in saline injected controls. The influence of atropine treatment on tolerance development to morphine was also studied. After withdrawal of atropine a reduction of the analgesic responses to morphine and arecoline was observed. A decrease in hexobarbital sleeping time was also found. There was no significant influence on the analgesic effect of amphetamine, on the depressant action of reserpine, and on the convulsant effect of pentylenetetrazol. The influence of the administration and further withdrawal of atropine on tolerance development to morphine was masked by the concomitant reduction of morphine analgesia. It was impossible to observe a supersensitivity to the pharmacological agents studied.

Amphetamine↗