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M Rodriguez

Publications and source records attributed to M Rodriguez.

At least 73 records · Page 4Linked to original sources
PubMed1997

Cross-resistance to pyrethroid and organophosphorus insecticides in the southern house mosquito (Diptera:Culicidae) from Cuba.

A sample of the southern house mosquito, Culex pipiens quinquefasciatus Say, from Cuba was subjected to lambda-cyhalothrin selection to evaluate the usefulness of this pyrethroid insecticide for mosquito control. High resistance developed after 6 generations of selection. Little or no cross-resistance was observed to other pyrethroids (deltamethrin and cypermethrin), to a carbamate (propoxur) and to some organophosphates (chlorpyrifos and pirimiphos-methyl), but high cross-resistance was found to malathion (organophosphate). Possible resistance mechanisms responsible for this phenomenon are discussed.

Animals↗
PubMed1997

Evidence for adaptation of the entire PTH-calcium curve to sustained changes in the serum calcium in haemodialysis patients.

BACKGROUND: Based on in vitro studies, the set point of calcium has often been considered to represent an intrinsic property of parathyroid gland function. However, in the dialysis patient, the serum calcium does not consistently reflect the magnitude of hyperparathyroidism; in addition, little information is available on whether the PTH-calcium curve is modified by sustained changes in the serum calcium. The present study in haemodialysis patients was designed to evaluate whether the set point of calcium and the dynamics of PTH secretion were modified by sustained changes in the serum calcium. METHODS: To accomplish the goal of the study and obtain a wide range of changes in the serum calcium, haemodialysis patients were dialysed with either a 1.75 mM (group I) or a 1.25 mM (group II) calcium dialysate for 2 weeks, and were then changed to a 1.25 mM (group I) or a 1.75 mM (group II) calcium dialysate for an additional 2 weeks. At the end of the first and second 2-week periods, low and high calcium studies were performed to obtain PTH-calcium curves. RESULTS: In group I, the serum ionized calcium decreased with the lower calcium dialysate (P < 0.02) and the set point of calcium was reduced (P < 0.02); in group II, the serum calcium did not change and the set point of calcium was not modified. When both groups were evaluated together, the delta serum calcium correlated directly with the delta set point of calcium (r = 0.87, P < 0.001) and inversely with the delta PTH (r = -0.73, P < 0.005); at the same time, an inverse correlation was observed between the delta PTH and the delta set point of calcium (r = -0.67, P < 0.01). Moreover, the delta serum calcium correlated with both the delta ratio of basal/maximal PTH (r = -0.71, P < 0.005) and the change in predialysis serum calcium necessary to maximally stimulate PTH (r = 0.84, P < 0.001); these latter two are indicators of the position of PTH along the PTH-calcium curve. Finally, in group I the entire PTH-calcium curve shifted to the left on the 1.25 mM calcium dialysate as compared with the 1.75 mM calcium dialysate. CONCLUSION: The findings of the present study indicate that: (1) the set point of calcium followed sustained changes in the serum calcium independently of PTH secretion, and (2) the parathyroid gland was able both to adjust the position of PTH secretion on the PTH-calcium curve and to adapt PTH secretion to the existing serum calcium concentration.

Adaptation, Physiological↗
PubMed1997

IgA from HIV+ haemophilic patients triggers intracellular signals coupled to the cholinergic system of the intestine.

IgA was obtained from HIV-infected haemophilic patients and the intracellular signals triggered by its reaction with isolated rat intestinal strips were studied. HIV+ IgA stained intestinal microvilli with a granular immunofluorescence pattern and bound to the muscarinic acetylcholine receptor (mAChR), displacing the specific muscarinic cholinergic antagonist QNB in a non-competitive manner. It triggered the signals that are the consequence of mAChR stimulation in the intestine. Thus, it decreased cAMP synthesis and increased guanosine 3':5'-cyclic monophosphate (cGMP) formation and phosphoinositide (PI) turnover of the intestine. In addition, it stimulated prostaglandin E2(PGE2) synthesis by intestinal strips. Through its effect on PGE2 synthesis, HIV+ IgA could have a dual action. On the one hand, it could enhance immunosuppression at a local level, favouring pathogen growth and subsequent intestinal dysfunction. On the other hand, PGE2 could directly increase intestinal motility and electrolyte/fluid loss. Both effects could be involved in intestinal damage in AIDS.

Animals↗
PubMed1997

Antiviral immune responses modulate the nature of central nervous system (CNS) disease in a murine model of multiple sclerosis.

The spectrum of disease is influenced by factors related to both the pathogen and the host, as well as the end points used in defining disease. In this article, the issue of disease resistance versus susceptibility will be examined in the framework that genetic manipulation of either the pathogen or the host immune response alters the balance from disease protection towards pathogenesis. The response of the host may trigger both a protective and a pathogenic immune response. The failure to mount a protective immune response predisposes the pathogen to persistence, which then becomes the target for immunopathology. This review will examine the factors involved both in virus-mediated pathogenesis and in disease protection in the Theiler's model of human multiple sclerosis. By manipulating the character of the virus pathogen and the specificity of the immune response, the entire spectrum of human demyelinating disease is reproduced.

Animals↗
PubMed1997

The immune system preferentially clears Theiler's virus from the gray matter of the central nervous system.

Infection of susceptible strains of mice with Daniel's (DA) strains of Theiler's murine encephalomyelitis virus (DAV) results in virus persistence in the central nervous system (CNS) white matter and chronic demyelination similar to that observed in multiple sclerosis. We investigated whether persistence is due to the immune system more efficiently clearing DAV from gray than from white matter of the CNS. Severe combined immunodeficient (SCID) and immunocompetent C.B-17 mice were infected with DAV to determine the kinetics, temporal distribution, and tropism of the virus in CNS. In early disease (6 h to 7 days postinfection), DAV replicated with similar kinetics in the brains and spinal cords of SCID and immunocompetent mice and in gray and white matter. DAV RNA was localized within 48 h in CNS cells of all phenotypes, including neurons, oligodendrocytes, astrocytes, and macrophages/microglia. In late disease (13 to 17 days postinfection), SCID mice became moribund and permitted higher DAV replication in both gray and white matter. In contrast, immunocompetent mice cleared virus from the gray matter but showed replication in the white matter of their brains and spinal cords. Reconstitution of SCID mice with nonimmune splenocytes or anti-DAV antibodies after establishment of infection demonstrated that both cellular and humoral immune responses decreased virus from the gray matter; however, the cellular responses were more effective. SCID mice reconstituted with splenocytes depleted of CD4+ or CD8+ T lymphocytes cleared virus from the gray matter but allowed replication in the white matter. These studies demonstrate that both neurons and glia are infected early following DAV infection but that virus persistence in the white matter is due to preferential clearance of virus from the gray matter by the immune system.

Animals↗
PubMed1997

Brain-infiltrating cytolytic T lymphocytes specific for Theiler's virus recognize H2Db molecules complexed with a viral VP2 peptide lacking a consensus anchor residue.

Mice expressing the H2b haplotype are resistant to infection with Theiler's murine encephalomyelitis virus (TMEV), which causes chronic demyelination in susceptible mice. The prominent cytolytic T-lymphocyte (CTL) response to the VP2 antigen encoded by TMEV led us to the identification of a class I-binding peptide derived from the VP2 antigen. Escherichia coli transformants overexpressing a series of 11 overlapping VP2 protein fragments were subjected to lysis and alkali digestion, and the resultant peptide pools were tested for their abilities to sensitize RMA-S targets for lysis by CTLs. The source of effector CD8+ T cells for the assays was either freshly harvested central nervous system-infiltrating lymphocytes (CNS-IL) or CNS-IL-derived VP2-specific CTL clones and lines. A 10-residue peptide at VP2 positions 121 to 130 (VP2(121-130)) (FHAGSLLVFM) was identified that sensitized targets for lysis and formed stable complexes with H2Db class I molecules. The VP2(121-130) peptide sensitized target cells for lysis by freshly harvested CNS-IL CTLs at femtomolar concentrations. Despite its relative high level of biological activity, the VP2(121-130) peptide is distinguished from other Db-binding peptides by its lack of an asparagine residue at position five, which had been previously proposed to be a requirement for Db-peptide complexing.

Amino Acid Sequence↗
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

Promotion of endogenous remyelination in multiple sclerosis.

Studies in both human and experimental models demonstrate that myelin repair occurs in the central nervous system and is a normal physiologic response to myelin injury. However, remyelination in MS is often incomplete and limited. The outcome of an actively demyelinating lesion depends on the balance between factors promoting myelin destruction and myelin repair. Experimental models of CNS demyelination provide an opportunity to investigate the morphologic, cellular and molecular mechanisms involved in remyelination. This review focuses on experiments using the Theiler's virus model of demylination which indicate that manipulation of the immune response has the potential to promote endogenous CNS remyelination and functional recovery in MS.

Animals↗
PubMed1997

Enhancement of central nervous system remyelination in immune and non-immune experimental models of demyelination.

Studies in both humans and experimental animals indicate that there is potential for full remyelination following CNS demyelination, but the factors that control the degree of myelin repair are unknown. In the Theiler's virus model of demyelination CNS remyelination can be promoted either by global immunosuppression or by selective immunoglobulin therapy. In this paper we discuss whether immunoglobulin-mediated remyelination is a characteristic of immune-mediated demyelination, or whether immunoglobulin-mediated remyelination also occurs in the toxic-traumatic model of lysolecithin-induced demyelination. Our data support the hypothesis that even in a non-primary immune model of demyelination, manipulating the immune system can be beneficial in myelin repair.

Animals↗
PubMed1997

Remyelination in multiple sclerosis.

Stimulation of remyelination in multiple sclerosis lesions may be one possible therapeutic approach. However, since the pathology and pathogenesis of multiple sclerosis may be heterogeneous, it is important to analyze in what patients and at what stages of the disease such a therapy can be reasonable and feasible. Spontaneous remyelination is pronounced in some MS patients. The extent of remyelination correlates well with the presence of oligodendrocytes in the lesions. Yet, the source and origin of the remyelinating cells is still unclear. These may be derived from either undifferentiated progenitor cells or, in part from mature oligodendrocytes, that have escaped destruction during lesional activity. Complete remyelination of plaques is possible, leading to the formation of 'shadow plaques'. No reliable data are available at present on the frequency of remyelination in different forms of MS. However, most studies agree that remyelination is especially prominent at the early stages of the disease, whereas it is sparse after several years of disease duration. In addition, very little remyelination is found in cases of primary progressive MS.

Brain↗
PubMed1997

Treatment of putative immune-mediated and idiopathic cervical dystonia with intravenous methylprednisolone.

A young pregnant woman developed a persistent dystonic head tremor a few days after Rho (D) immune globulin administration; further deterioration occurred after a second administration of Rh(o) (D) immune globulin with the development of marked retrocollis. This persisted and she was treated 2 months later with a 5-day course of intravenous (1 g daily) methylprednisolone (IVMP) with resolution of her condition. We proceeded to treat similarly the next four patients with idiopathic cervical dystonia who were seen in our practice and who had current symptoms of less than 6 months duration. One also experienced persistent resolution and another had a marked, but transient, improvement after each of two separate courses of IVMP. The other two patients did not have improvement. This suggests a possible autoimmune pathogenesis for a limited subset of cervical dystonia. However, identifying which cases of recent-onset cervical dystonia will respond to IVMP therapy has yet to be determined.

Adult↗
PubMed1997

Risk factors for developing multiple sclerosis after childhood optic neuritis.

We reviewed the records of all children (younger than 16 years of age) who presented with a diagnosis of optic neuritis (ON) identified through the comprehensive records-linkage system at the Mayo Clinic and identified 94 cases between 1950 and 1988 with a documented history of idiopathic ON. Detailed follow-up information was available on 79 patients, with a median length of follow-up of 19.4 years. Life-table analysis showed that 13% of the 79 patients with isolated ON had progressed to clinically or laboratory-supported definite multiple sclerosis (MS) by 10 years of follow-up, 19% by 20 years, 22% by 30 years, and 26% by 40 years. Gender, age, funduscopic findings, visual acuity, or family history of either ON or MS did not predict the development of MS. The presence of bilateral sequential or recurrent ON increased the risk of developing MS (p = 0.002; hazard ratio = 5.09), whereas the presence of infection within 2 weeks before the onset of ON decreased the risk of developing MS (p = 0.060; hazard ratio = 0.24). This study of childhood ON supports the lower risk of recurrence and progression to MS compared with adults.

Adolescent↗
PubMed1997

Nuclear localization of I kappa B alpha promotes active transport of NF-kappa B from the nucleus to the cytoplasm.

I kappa B alpha tightly regulates the transcriptional activity of NF-kappa B by retaining it in the cytoplasm in an inactive form. In the present work, we report that I kappa B alpha, when expressed in the nuclear compartment, not only abrogates NF-kappa B/DNA interactions and NF-kappa B-dependent transcription, but also transports NF-kappa B back to the cytoplasm. This function of I kappa B alpha is insured by a nuclear export sequence located in the C-terminal domain of I kappa B alpha and homologous to the previously described export signal found in HIV-1 Rev protein as well as in PKI (the inhibitor of the catalytic subunit of protein kinase A). Thus, inhibition of NF-kappa B/DNA binding and the consecutive efficient nuclear export of the transcription factor of I kappa B alpha could represent an important mechanism for the control of the expression of NF-kappa B-dependent genes.

Amino Acid Sequence↗
PubMed1997

Evidence for both abnormal set point of PTH stimulation by calcium and adaptation to serum calcium in hemodialysis patients with hyperparathyroidism.

In vitro studies of parathyroid glands removed from dialysis patients with secondary hyperparathyroidism and hypercalcemia have demonstrated the presence of an increased set point of parathyroid hormone (PTH) stimulation by calcium (set point [PTHstim]), suggesting an intrinsic abnormality of the hyperplastic parathyroid cell. However, clinical studies on dialysis patients have not observed a correlation between the set point (PTHstim) and the magnitude of hyperparathyroidism. In the present study, 58 hemodialysis patients with moderate to severe hyperparathyroidism (mean PTH 780 +/- 377 pg/ml) were evaluated both before and after calcitriol treatment to establish the relationship among PTH, serum calcium, and the set point (PTHstim) and to determine whether changes in the serum calcium, as induced by calcitriol treatment, modified these relationships. Calcitriol treatment decreased serum PTH levels and increased the serum calcium and the setpoint (PTHstim); however, the increase in serum calcium was greater than the increase in the setpoint (PTHstim). Before treatment with calcitriol, the correlation between the set point (PTHstim) and the serum calcium was r = 0.82, p < 0.001, and between the set point (PTHstim) and PTH was r = 0.39, p = 0.002. After treatment with calcitriol, the correlation between the set point (PTHstim) and the serum calcium remained significant (r = 0.70, p < 0.001), but the correlation between the set point (PTHstim) and PTH was no longer significant (r = 0.09); moreover, a significant correlation was present between the change in the set point (PTHstim) and the change in serum calcium that resulted from calcitriol treatment (r = 0.73, p < 0.001). The correlation between the residual values (deviation from the regression line) of the set point (PTHstim), derived from the correlation between PTH and the set point (PTHstim), and serum calcium was r = 0.77, p < 0.001 before calcitriol and r = 0.72, p < 0.001 after calcitriol. In conclusion, the set point (PTHstim) increased after a sustained increase in the serum calcium, suggesting an adaptation of the set point to the existing serum calcium; the increase in serum calcium resulting from calcitriol treatment was greater than the increase in the set point (PTHstim); the set point (PTHstim) was greater in hemodialysis patients with higher serum PTH levels; and the correlation between PTH and the set point (PTHstim) may be obscured because the serum calcium directly modifies the set point (PTHstim).

Adaptation, Physiological↗
PubMed1997

[18F] FDG PET in gastric non-Hodgkin's lymphoma.

The possibility of using [18F] FDG PET for assessment of tumor extension in primary gastric non-Hodgkin's lymphoma (NHL) was studied in 8 patients (6 high-grade and 2 low-grade, one of the MALT type) and in a control group of 7 patients (5 patients with NHL without clinical signs of gastric involvement, 1 patient with NHL and benign gastric ulcer and 1 patient with adenocarcinoma of the stomach). All patients with gastric NHL and the two with benign gastric ulcer and adenocarcinoma, respectively, underwent endoscopy including multiple biopsies for histopathological diagnosis. All patients with high-grade and one of the two with low-grade NHL and the patient with adenocarcinoma displayed high gastric uptake of [18F] FDG corresponding to the pathological findings at endoscopy and/or CT. No pathological tracer uptake was seen in the patient with low-grade gastric NHL of the MALT type. In 6/8 patients with gastric NHL, [18F] FDG PET demonstrated larger tumor extension in the stomach than was found at endoscopy, and there was high tracer uptake in the stomach in two patients who were evaluated as normal on CT. [18F] FDG PET correctly excluded gastric NHL in the patient with a benign gastric ulcer and in the patients with NHL without clinical signs of gastric involvement. Although the experience is as yet limited, [18F] FDG PET affords a novel possibility for evaluation of gastric NHL and would seem valuable as a complement to endoscopy and CT in selected patients, where the technique can yield additional information decisive for the choice of therapy.

Aged↗