PubMed Health⌕ Search

Biomedical subjects

V Sandoval

Publications and source records attributed to V Sandoval.

11 recordsLinked to original sources
PubMed2001

[Results of treatment with 2-chlorodeoxyadenosine in refractory or relapsed Langerhans cell histiocytosis. Study of 9 patients].

BACKGROUND: To analyse the results of the treatment with 2-chlorodeoxyadenosine (2CdA) in 9 patients with refractory or relapsed Langerhans cell histiocytosis (LCH) tracted in 8 Spanish hospitals between 1993 and 1999. PATIENTS AND METHOD: In the 9 patients the following data were recorded: age, sex, organ involvement by LCH, first treatment and response, dose, number of cycles and schedule of administration 2CdA, response to 2CdA treatment, toxicity, disease-free survival (DFS) and overall survival (OS). RESULTS: Median age was 25 years (range, 6-63). All patients had multiorganic involvement by LCH, with severe organ dysfunction in 4. 2CdA was administered as second line treatment in 7 cases and as third line in 2. The 2CdA dose was 0.1 mg/kg per day during 5 days in the majority of patients, and interval between cycles was 4 weeks. In 2 cases a complete remission (CR) was achieved and 4 cases attained a partial remission (PR) (overall response rate 66%). The main toxicity was hematologic, with neutropenia grade > 2 in 5 cases and thrombocytopenia > 2 in 5. Four patients had infections, with fatal evolution in one of them. After a median follow-up of 8 months (range 2-17), 2 patients remained in CR (12 months both), 4 in PR (range 2-12 months) and one had active disease (17 months). The other two died due to progressive disease and Aspergillus spp. sepsis, respectively. The actuarial probabilities of DFS and OS were 58% (95% CI, 38-78%) and 71% (95% CI, 54-88%), respectively. CONCLUSIONS: 2CdA is an active drug for patients with refractory or relapsed LCH, and its main toxicity is myelosuppression. The usefulness of 2CdA, isolated or in combination with other drugs, in patients with refractory or relapsed LCH must be assessed in controlled studies.

Adolescent↗
PubMed2001

Methamphetamine-induced rapid and reversible changes in dopamine transporter function: an in vitro model.

This laboratory has demonstrated that a single methamphetamine (METH) injection rapidly and reversibly decreases the activity of the dopamine transporter (DAT), as assessed ex vivo in synaptosomes prepared from treated rats. This decrease does not occur because of residual drug introduced by the original injection or nor is it associated with a change in binding of the DAT ligand WIN35428. The purpose of this study was to elucidate the mechanism or mechanisms of this METH effect by determining whether direct application of this stimulant to synaptosomes causes changes in DAT similar to those observed ex vivo. Similar to the ex vivo effect, incubation of striatal synaptosomes with METH decreased DAT activity, but not WIN35428 binding: the effect on activity was not eliminated by repeated washing of synaptosomes. Also, as observed ex vivo, incubation with 3,4-methylenedioxymethamphetamine, but not cocaine or methylphenidate, caused a METH-like reduction in DAT function. The rapid and reversible METH-induced diminution in DAT activity did not occur because of a change in membrane potential, as assessed in vitro and ex vivo by [(3)H]tetraphenylphosphonium accumulation. However, the METH-related decline in DAT function may be attributed to phosphorylation because NPC15437, a protein kinase C inhibitor, attenuated the METH-induced decline in DAT function. Similarities between previously reported effects ex vivo of a single METH injection on serotonin and norepinephrine transporter function and effects of direct METH application in vitro were also found. Together, these data demonstrate that the in vitro incubation model mimics the rapid and reversible effects observed after a single METH injection.

3,4-Methylenedioxyamphetamine↗
PubMed2000

Methamphetamine decreases mouse striatal dopamine transporter activity: roles of hyperthermia and dopamine.

Multiple methamphetamine administrations rapidly decrease rat striatal dopamine transporter activity. To determine the species specificity of this phenomenon, the present studies examined effects of this stimulant on the dopamine transporter in mice. As in rats, multiple methamphetamine injections rapidly reduced striatal dopamine transporter activity; a decrease that was partially reversed 24 h later. Moreover, methamphetamine decreased binding of the dopamine transporter ligand, WIN35428, but to a lesser degree than the change in dopamine transporter function. These decreases did not appear to result from residual methamphetamine introduced by the original drug treatment. As in rats, hyperthermia contributed to this phenomenon. Unlike in rats, a role for dopamine was not observed in mice as dopamine depletion, resulting from alpha-methyl-p-tyrosine pretreatment, did not prevent this decrease. In addition, unlike in rats, pretreatment with either a dopamine D1 or D2 receptor antagonist (SCH23390 or eticlopride, respectively) did not attenuate the methamphetamine-induced reduction in dopamine uptake. These findings demonstrate both similarities and differences in the acute effects of methamphetamine on dopamine transporter function in mice and rats, and suggest the mouse as an additional model for assessing the acute effects of methamphetamine on the dopamine transporter.

Animals↗
PubMed1996

[Post-transfusion purpura. Description of 2 cases diagnosed at the same hospital in a 6-month period].

Two new cases of postransfusional purpura diagnosed at the same hospital within the space of six months are described. This finding supports the idea that despite being an infrequent disorder, a substantial rise in PTP cases inside and outside our country, has been recorded. This increase has coincided with a greater interest in platelet immunology and, particularly, in complications associated with blood transfusion. Both cases constitute an example of the clinical epidemiological profile which characterizes the patients suffering from this disorder. The patients are two women aged 74 and 60 years who after 8 and 9 days, respectively, of being transfused with red cells developed a severe thrombocytopenia accompanied by generalized haemorrhagic diathesis. The serological studies performed revealed the presence, in both patients, of an HPA-1a platelet specific antibody. The platelet genotyping enabled us to confirm this specificity after detecting an HPA-1 (a-b+) platelet genotype. The treatment with immunoglobulins at high doses proved to be effective in both cases. The adsorption-elution experiments of the antibody versus HPA-1 (a + b) platelets were positive in the patient with the highest antibody titre (1024). This finding support the most recent hypothesis concerning the pathogenic mechanism of PTP. According to this theory, the antibody, which is detected in the acute phase of the PTP, would not yet have acquired the restricted specificity corresponding to it. This could enable it to react with a structure shared by the HPA-1a positive and HPA-1a negative platelets.

Aged↗
PubMed1988

Ligand-induced desensitization of B-cell membrane immunoglobulin-mediated Ca2+ mobilization and protein kinase C translocation.

Binding of ligand to B-cell membrane immunoglobulin (mIg) can lead to activation of a number of distinct biologic responses, including altered expression of genes encoding c-fos, c-myc, and Ia, as well as proliferation and immunologic tolerance. Tolerance could reflect a functional uncoupling of receptors from systems that generate intracellular second messengers (i.e., receptor desensitization). To better understand the molecular basis of immune regulation, we examined the ability of mIg to function as a signal transducer after the cell's initial contact with mIg-binding ligand. The results show that ligand binding to as little as 2-10% of mIgM or mIgD renders the cell unresponsive to ligand binding to the reciprocal isotype as judged by Ca2+ mobilization and protein kinase C translocation responses. This heterologous receptor desensitization lasts longer than 24 hr and does not reflect loss of receptor from the cell surface. Studies with the calcium ionophore ionomycin, 1,2-dioctanoyl-sn-glycerol, and the protein kinase inhibitor staurosporine indicate that both protein kinase C-dependent and protein kinase C-independent (staurosporine-insensitive) mechanisms mediate heterologous desensitization after mIg crosslinking.

Animals↗
PubMed1986

BSF1 induces membrane protein phosphorylation but not phosphoinositide metabolism, Ca2+ mobilization, protein kinase C translocation, or membrane depolarization in resting murine B lymphocytes.

The findings presented in this study provide evidence that BSF1 receptors and mIg transmit signals via dissimilar transduction mechanisms that result in a common biologic response, hyper-Ia expression. Specifically, BSF1-containing supernatant does not induce PtdInsP2 hydrolysis as determined by measurement of PtdOH and InsP3. Additionally, BSF1 does not stimulate Ca2+ mobilization, PKC translocation from cytosol to membrane, or membrane depolarization. All of these metabolic events appear to play a central role in hyper-Ia expression mediated by mIg and are initiated after treatment of resting B cells with anti-Ig antibodies. In vitro phosphorylation studies with partially purified plasma membranes from resting B cells revealed that BSF1 interaction with membrane receptors stimulates a membrane-associated protein kinase that phosphorylates an endogenous protein of 44 KDa. Anti-Ig does not stimulate phosphorylation of the 44 KDa protein, suggesting that it does not activate the membrane-associated protein kinase. This observation provides the first evidence of a signal transduction mechanism associated with BSF1-receptor ligation. It indicates that although BSF1 does not modulate events associated with PKC activation, it may function via activation of a membrane-associated protein kinase. This provides a focal point for further studies directed at elucidating signal transduction resulting from BSF1-receptor interaction.

Animals↗
PubMedDate not supplied

[Multiple paragangliomas. The problem of its localization. Report of the first case studied with 131I meta-iodobenzylguanidine in our milieu and review of the literature].

We report the case of a young woman, with an 8 year history of paroxysmal episodes of dyspnea, palpitations, blurred vision, tremors, precordial oppression and hypertension; the diagnosis of a chromaffin tumor was established, with an increase in serum and urine catecholamines level. She had three surgical interventions and also the following studies: abdominal and pelvic ultrasound, computed tomography, cavography; selective arteriography, and infusion of the meta iodobenzyl-guanidine 131, which localizes tissues hypersecretors rich in catecholamines.

3-Iodobenzylguanidine↗
PubMedDate not supplied

[Chronic cardiac actinomycosis. Case report and review of the literature].

We report the case of a young man in whom a right paracardiac mass was resected. The histopathologic study was compatible with actinomycosis. He developed severe cardiac failure, pulmonary edema and pericardial effusion. He was treated with penicillin, during 12 months. He did well afterwards, however, the echocardiographic follow-up revealed chronic pericardial effusion and thickening and fusion of the pericardium to the epicardial wall.

Actinomycosis↗