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Biomedical subjects

M Rodriguez

Publications and source records attributed to M Rodriguez.

At least 127 records · Page 7Linked to original sources
PubMed2000

Effect of a low calcium dialysate on parathyroid hormone secretion in diabetic patients on maintenance hemodialysis.

Diabetic patients on maintenance dialysis often are characterized by a relative parathyroid hormone (PTH) deficiency and a form of renal osteodystrophy with low bone turnover known as adynamic bone. The goal of the present study was to determine whether a reduction in the dialysate calcium concentration would increase the predialysis (basal) PTH and maximal PTH level. Thirty-three diabetic maintenance hemodialysis patients with basal PTH values less than 300 pg/ml were randomized to be dialyzed with either a regular (3.0 mEq/liter or 3.5 mEq/liter, group I) or low (2.25 mEq/liter or 2.5 mEq/liter, group II) calcium dialysate for 1 year. At baseline and after 6 months and 12 months of study, low (1 mEq/liter) and high (4 mEq/liter) calcium dialysis studies were performed to determine parathyroid function. At baseline, basal (I, 126+/-20 vs. II, 108+/-19 pg/ml) and maximal (I, 269 pg/ml+/-40 pg/ml vs. II, 342 pg/ml+/-65 pg/ml) PTH levels were not different. By 6 months, basal (I, 98+/-18 vs. II, 200+/-34 pg/ml, p = 0.02) and maximal (I, 276 pg/ml+/-37 pg/ml vs. II, 529 pg/ml+/-115 pg/ml; p = 0.05) PTH levels were greater in group II. Repeated measures analysis of variance (ANOVA) of the 20 patients who completed the entire 12-month study showed that only in group II patients were basal PTH (p = 0.01), maximal PTH (p = 0.01), and the basal/maximal PTH ratio (p = 0.03) different; by post hoc test, each was greater (p < 0.05) at 6 months and 12 months than at baseline. When study values at 0, 6, and 12 months in all patients were combined, an inverse correlation was present between basal calcium and both the basal/maximal PTH ratio (r = -0.59; p < 0.001) and the basal PTH (r = -0.60; p < 0.001). In conclusion, in diabetic hemodialysis patients with a relative PTH deficiency (1) the use of a low calcium dialysate increases basal and maximal PTH levels, (2) the increased secretory capacity (maximal PTH) during treatment with a low calcium dialysate suggests the possibility of enhanced parathyroid gland growth, and (3) the inverse correlation between basal calcium and both the basal/maximal PTH ratio and the basal PTH suggests that the steady-state PTH level is largely determined by the prevailing serum calcium concentration.

Calcium↗
PubMed2000

Concurrence of inflammatory bowel disease and multiple sclerosis.

OBJECTIVES: To quantify the coexistence of inflammatory bowel disease (IBD) and multiple sclerosis (MS) and to characterize the diseases when they coexist. PATIENTS AND METHODS: In this retrospective study of medical records spanning 1950 through 1995, the diagnoses of Crohn disease (CD), ulcerative colitis (UC), and MS were based on review of inpatient and outpatient records by a gastroenterologist and a neurologist. RESULTS: We identified 4 residents of Olmsted County, Minnesota, with IBD (3 UC, 1 CD) who had concurrent, clinically definite MS; all had mild neurologic disease with little disability. These comprised 1% of the IBD and 1.8% of the MS cohort. The CD patient had undergone terminal ileal resection; of the UC patients, 2 had pancolitis, and 1 had proctosigmoiditis. The observed prevalence of MS at onset of IBD was 3.7 times the expected (95% confidence interval, 0.8-10.8). We also reviewed the records of 32 referral patients with both diagnoses. Disability from MS was moderate at median follow-up of 8.5 years. By 15 years, ambulation was impaired in most patients. Neurologic disability was similar between patients with CD and UC. CONCLUSIONS: Concurrence of the 2 diseases was greater than expected. Although MS and IBD may share common predisposing factors, not enough information is available to speculate about possible mechanisms.

Adolescent↗
PubMed2000

Common trisomy mosaicism diagnosed in amniocytes involving chromosomes 13, 18, 20 and 21: karyotype-phenotype correlations.

Karyotype-phenotype correlations of common trisomy mosaicism prenatally diagnosed via amniocentesis was reviewed in 305 new cases from a collaboration of North American cytogenetic laboratories. Abnormal outcome was noted in 10/25 (40%) cases of 47,+13/46, 17/31 (54%) cases of 47,+18/46, 10/152 (6.5%) cases of 47,+20/46, and in 49/97 (50%) cases of 47,+21/46 mosaicism. Risk of abnormal outcome in pregnancies with less than 50% trisomic cells and greater than 50% trisomic cells were: 26% (4/15) versus 60% (6/10) for 47,+13/46, 52% (11/21) versus 75% (6/8) for 47,+18/46, 4.5% (6/132) versus 20% (4/20) 47,+20/46, and 45% (27/60) versus 59% (22/37) for 47,+21/46. Phenotypically normal liveborns were observed with mean trisomic cell lines of 9.3% for 47,+13/46, 8.6% for 47,+18/46, 27% for 47, +20/46, and 17% for 47,+21/46. Cytogenetic confirmation rates were 46% (6/13 cases) for 47,+13/46 mosaicism, 66% (8/12 cases) for 47, +18/46, 10% (10/97 cases) for 47,+20/46, and 44% (24/54 cases) for 47,+21/46. There were higher confirmation rates in pregnancies with abnormal versus normal outcome: 50% versus 44% for 47,+13/46 mosaicism, 100% versus 33% for 47,+18/46, 66% versus 7% for 47, +20/46, and 55% versus 40% for 47,+21/46. Repeat amniocentesis is not helpful in predicting clinical outcome. It may be considered when there is insufficient number of cells or cultures to establish a diagnosis. Fetal blood sampling may have a role in mosaic trisomy 13, 18, and 21 as the risk for abnormal outcome increases with positive confirmation: 1/5 (20%) normal cases versus 5/8 (62%) abnormal cases. High resolution ultrasound examination(s) is recommended for clinical correlation and to facilitate genetic counselling.

Abnormalities, Multiple↗
PubMed2000

Pathophysiology of levodopa-induced dyskinesias in Parkinson's disease: problems with the current model.

The anatomical and physiological basis of levodopa-induced dyskinesias (LIDs) in patients with Parkinson's disease (PD) is reviewed in the light of the current model for the organization of the basal ganglia. This model, which was developed in the late 1980s, works relatively well in explaining the motor features of PD but, for example, it does not account for why tremor, rigidity, bradykinesia, gait dysfunction and postural instability present to differing degrees in different patients, and may respond differently to levodopa treatment or surgical procedures. Recent information suggests that LIDs develop as a consequence of pulsatile stimulation of dopamine receptors, with consequent dysregulation of genes and proteins in downstream neurons resulting in changes in neuronal firing patterns. A modified model of the basal ganglia in PD patients with LID is proposed, which incorporates more recent clinical and experimental data.

Basal Ganglia↗
PubMed2000

Biphasic and regionally-restricted chemokine expression in the central nervous system in the Theiler's virus model of multiple sclerosis.

Intracerebral infection of susceptible strains of mice with Theiler's murine encephalomyelitis virus (TMEV) induces a biphasic disease characterized by acute polioencephalitis followed by chronic demyelination and viral persistence in the spinal cord white matter. There has been limited study of soluble mediators responsible for the initial recruitment of inflammatory cells into the gray matter, and the secondary influx into the white matter during infection with TMEV. We used sensitive and specific RT - PCR/dot blot hybridization assays to quantitate the relative levels of chemokine mRNA in the brains and spinal cords during the acute and chronic phases of TMEV infection in mice susceptible (B10.M, H-2f) and resistant (B10, H-2b) to virus-induced demyelination. TMEV infection resulted in robust expression of mRNA for IP-10, RANTES, and MCP-1, but not GRO-alpha, in brains and spinal cords in both strains of mice within 5 days. By day 21, virus was cleared, inflammation reduced, and expression of all three chemokines subsided to baseline levels in the brains and spinal cords of resistant mice, and the brains of susceptible mice. Chemokine expression was also reduced in the spinal cords of susceptible mice, corresponding to a shift in TMEV replication from the gray to the white matter. During the chronic, demyelinating phase of infection, there was a resurgence in IP-10, RANTES, and MCP-1 mRNA in spinal cords of susceptible B10.M mice. This study demonstrates the coordinated regulation and regionally restricted expression of chemokines in a biphasic disease of the central nervous system and provides greater understanding of the mechanism by which inflammation is established and maintained in the CNS.

Acute Disease↗
PubMed2000

The evolution and origin of motor complications in Parkinson's disease.

Levodopa is the major symptomatic therapy for Parkinson's disease (PD), having revolutionized the treatment of PD and provided benefit to virtually all patients. However, after 5-10 years of treatment, levodopa therapy is complicated by the development of motor complications, which include dyskinesia and motor fluctuations. The initial long duration response to a dose of levodopa becomes progressively shorter, and periods in which the patient responds to the drug become complicated by involuntary dyskinetic movements. Thus, patients may cycle between "on" periods that are complicated by dyskinesia and "off" periods in which they are severely parkinsonian. As a consequence they may experience profound disability despite the fact that levodopa remains an effective anti-parkinson agent throughout the course of the disease. In this article we review the various motor complications associated with the treatment of PD and present current concepts on the origin of these problems.

Humans↗
PubMed2000

Antibody-mediated remyelination: relevance to multiple sclerosis.

Intravenous immunoglobulin (IVIG) is widely used for treatment of autoimmune neurological disorders and is currently in clinical trials as a therapy for multiple sclerosis. We have previously demonstrated that certain mouse monoclonal antibodies of the IgM isotype, promote significant remyelination when administered to mice with chronic Theiler's murine encephalomyelitis virus-induced demyelinating disease. These IgM antibodies bind to antigens expressed on oligodendrocytes. We now demonstrate that polyclonal human IgG (IVIG) and polyclonal human IgM also promote remyelination in this system. Although both polyclonal human IgG and IgM promote remyelination, IgM is more potent. Polyclonal human IgM also differs from human IgG in its ability to bind strongly to antigens expressed in the CNS and by oligodendrocytes. We propose that polyclonal IgG and polyclonal IgM may function to promote remyelination by different mechanisms. IVIG may function based on its immunomodulatory activity, while the activity of IgM is critically dependent upon its reactivity with CNS antigens. This possibility has clear relevance to the use of antibodies as a therapy for multiple sclerosis, suggesting that combined treatment with antibodies exerting immunomodulatory activity, in concert with antibodies that function through direct binding to CNS antigens, may synergize to enhance the efficacy of the therapy.

Animals↗
PubMed2000

Pathophysiologic basis of surgery for Parkinson's disease.

Dopamine depletion induces a series of changes in the basal ganglia motor circuit that underlie the origin of the cardinal features of Parkinson's disease. It has now been established that hyperactivity of the subthalamic nucleus (STN) is an essential feature of the parkinsonian state. This leads to increased excitatory driving onto the globus pallidum internum (GPi) and substantia nigra reticulata (SNr) which, in turn, overinhibits the motor projections to the thalamus and brainstem. The STN and GPi have become the preferred targets for surgery to treat PD. In keeping with the classic pathophysiologic model, physiologic and neuroimaging studies in patients have shown that lesioning or functional blockades (by deep brain stimulation, or DBS) of these nuclei increased cortical activation, in parallel with clinical improvements of bradykinesia. Neuronal recording during surgery has also shown tremor-related activity in both the STN and GPi. However, the pathophysiologic model of the basal ganglia needs further refinement to provide a more detailed explanation of the origin of both tremor and rigidity in Parkinson's disease and to explain the antidyskinetic effect of surgery of the GPi and STN.

Basal Ganglia↗
PubMed1999

Quantitation of spinal cord demyelination, remyelination, atrophy, and axonal loss in a model of progressive neurologic injury.

Spinal cord pathology, such as demyelination and axonal loss, is a common feature in multiple models of central nervous system (CNS) injury and disease. Development of methods to quantify spinal cord pathology objectively would aid studies designed to establish mechanisms of damage, correlate pathology with neurologic function, and assess therapeutic interventions. In this study, we describe sensitive methods to objectively quantify spinal cord demyelination, remyelination, atrophy, and axonal loss following the initiation of a progressive inflammatory demyelinating disease with Theiler's murine encephalomyelitis virus (TMEV). Spinal cord demyelination, remyelination, and atrophy were quantified from representative 1-microm-thick cross sections embedded in Araldite plastic using interactive image analysis. In addition, this study demonstrates novel, automated methodology to quantify axonal loss from areas of normal-appearing white matter, as a measure of secondary axonal injury following demyelination. These morphologic methods, which are applicable to various models of CNS injury, provide an innovative way to assess the benefits of therapeutic agents, to determine mechanisms of spinal cord damage, or to establish a correlation with sensitive measures of neurologic function. J. Neurosci Res 58:492-504.

Animals↗
PubMed1999

Gender differences in p53 mutational status in small cell lung cancer.

Mutations in the p53 tumor suppressor gene have been demonstrated to be one of the most frequent genetic abnormalities in human cancers. Previous studies have shown that the frequency of p53 mutations is significantly higher in small cell lung cancer than in non-small cell lung cancer. However, this conclusion was based in large part on data derived from tumor cell lines and from studies with relatively small sample sizes and biased gender populations. To determine the mutational frequency in the p53 tumor suppressor gene and a potential difference in gender, we analyzed primary small cell lung cancer tumors from 65 patients (37 males and 28 females) for p53 mutations between exons 5 and 9. Mutations were found in 37 of 65 tumors (57%) within the region of p53 analyzed. Interestingly, none of the tumors from females contained more than one mutation, whereas four of the tumors from males contained more than one mutation. The most common mutation in this population was an adenosine-to-guanine transition (27%), followed by guanine-to-thymidine transversion (17%) and guanine-to-adenosine transition (12%). The gender difference in p53 mutational rate identified in this study suggests that a higher proportion of female tumors may develop through pathways not involving p53 mutations.

Adult↗
PubMed1999

Cloning and characterization of the 5' flanking region of the human uncoupling protein 3 (UCP3) gene.

Uncoupling protein 3 (UCP3), a member of the UCP family, mainly expressed in skeletal muscle could be responsible for thermogenesis in humans. Since little is known about its regulation, we studied the 5' flanking region of the human UCP3 (hUCP3) gene, which potentially contains the promoter sequences. We report the hUCP3 transcription initiation on a G located 764 nucleotides upstream the A contained in the first translated codon. Therefore, hUCP3 first exon has 669 bases of untranslated sequence. We also report the cloning and sequencing of seven kilobases from the gene 5' end and analyze the features of the potential proximal promoter. The MyoD family binding motif, called E-box, is the most abundant on this region. Other muscle-specific motives present in the potential proximal promoter include a MEF2 site as well as binding sequences for ubiquitous factors such as GC box and two CAAT boxes. Additionally, three putative peroxisome proliferator and one thyroid hormone response elements (PPRE and TRE, respectively) are found, which suggest a potential role for the peroxisome proliferator-activated receptor (PPAR) and thyroid hormone in human UCP3 gene expression. The description of the promoter region of the UCP3 gene will facilitate the elucidation of its transcriptional control.

Base Sequence↗
PubMed1999

Improvement of myelopathy in Sjögren's syndrome with chlorambucil and prednisone therapy.

The authors present a patient with Sjögren's syndrome with a fluctuating and then progressive myelopathic syndrome, and optic nerve involvement. Treatment with chlorambucil and prednisone improved the patient's function from being wheelchair bound to walking unaided. Spinal MRI showed multiple, extensive intraparenchymal areas of abnormal T2-weighted signal intensity, gadolinium enhancement, and cord swelling, which also improved during the period of treatment.

Adult↗
PubMed1999

A simulation study of the effects of acaricides and vaccination on Boophilus cattle-tick populations.

This paper describes a simulation model to evaluate different control strategies for Boophilus microplus. The model combines a dynamic life-history module for tick-population dynamics with other modules for vaccination, sterile-hybrid larval release and use of acaricide dipping vats. The tick life-history module considers the cattle's nutritional level and allows for distribution of ticks by age at all stages of growth. Appropriately, the model was sensitive to host resistance and to host-nutritional status. The validity of the life-history module--as well as that of the vaccination and acaricide dipping--vats modules--was demonstrated by comparing simulated and real data for several geographical locations in Cuba and Brazil. Optimum tick-control strategies for the first year of vaccination were designed and the effect of long-term vaccination on tick population was also studied.

Animals↗
PubMed1999

A Theiler's virus alternatively initiated protein inhibits the generation of H-2K-restricted virus-specific cytotoxicity.

In susceptible mouse strains, the wild-type Daniel's (wt-DA) strain of Theiler's murine encephalomyelitis virus induces a persistent central nervous system (CNS) infection with chronic demyelination. The virus is cleared from resistant mice with no resulting demyelination. We characterized the role of the DA L* protein in late demyelination and persistent infection. The DA genome has two alternative reading frames, encoding the virus polyprotein and L*, respectively. The mutant virus DAL*-1 fails to synthesize L* and does not persist in the CNS of wt-DA-susceptible SJL/J or B10.S mice. Since class I-restricted cytotoxicity has been shown to determine resistance to virus persistence and demyelination in this model, virus-specific cytotoxicity in the CNS of DA-resistant (B6 or B10) and -susceptible (SJL/J and B10.S) mice during the acute stage of DA and DAL*-1 infection was characterized. Following intracerebral inoculation with DAL*-1, virus-specific Db- and Kb-restricted CTLs were demonstrated in the CNS of resistant B10 mice, whereas only Db-restricted CTL were found in wt-DA-inoculated mice. CTLs specific to wt-DA or DAL*-1 recognized class I-presented peptides from either of the viruses. Of particular interest, Ks-restricted virus-specific cytotoxicity-restricted CTLs were identified in the CNS of susceptible SJL/J (H-2s) and B10.S (H-2s) mice inoculated with DAL*-1. In contrast, no virus-specific CTLs were identified in the CNS of SJL/J and B10.S mice inoculated with wt-DA. We propose that L* inhibits the generation of H-2K-restricted virus-specific cytotoxicity in the CNS, permitting a persistent infection in susceptible strains, with subsequent inflammatory demyelination in the CNS similar to that in human multiple sclerosis.

Alternative Splicing↗
PubMed1999

A randomized trial of plasma exchange in acute central nervous system inflammatory demyelinating disease.

There are no established treatments for patients with acute, severe neurological deficits caused by multiple sclerosis or other inflammatory demyelinating diseases of the central nervous system who fail to recover after treatment with high-dose corticosteroids. We conducted a randomized, sham-controlled, double-masked study of plasma exchange without concomitant immunosuppressive treatment in patients with recently acquired, severe neurological deficits resulting from attacks of inflammatory demyelinating disease, who failed to recover after treatment with intravenous corticosteroids. Patients who did not achieve moderate or greater improvement after the first treatment phase crossed over to the opposite treatment. Moderate or greater improvement in neurological disability occurred during 8 of 19 (42.1%) courses of active treatment compared with 1 of 17 (5.9%) courses of sham treatment. The primary analysis was positive. Improvement occurred early in the course of treatment, and was sustained on follow-up. However, 4 of the patients who responded to the active treatment experienced new attacks of demyelinating disease during 6 months of follow-up. Moderate or greater improvement occurred during follow-up in only 2 of 13 patients who failed to improve during the treatment phase. Plasma exchange leads to functionally important neurological recovery in an important proportion of severely disabled patients with acute attacks of idiopathic inflammatory demyelinating disease.

Adult↗