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Biomedical subjects

M T Medina

Publications and source records attributed to M T Medina.

At least 19 recordsLinked to original sources
PubMed1998

Prevalence of taeniasis and cysticercosis in a population of urban residence in Honduras.

To determine the prevalence of antibodies to Taenia solium and taeniasis in a population of urban residence, an epidemiological study was carried out in a military institution located in Tegucigalpa, the capital city of Honduras. A total of 404 persons were interviewed to collect epidemiological data, investigate antibodies to T. solium cysticercus by the enzyme-linked immunoelectrotransfer blot (EITB) assay and taeniasis by Ritchie's concentration technique. A total of 41 persons that were living at the headquarters and were traveling frequently to their rural hometowns were regarded as rural residents, the remaining 363 persons were considered urban residents. The seroprevalence of antibodies was 22% (9/41) in the rural residents and 15% (54/363) in the urban residents. The overall seroprevalence was 15.6% (63/404). Analyses of risk factors for seropositivity in the urban residents showed that seropositivity was statistically associated with poor household conditions such as raising pigs (odds ratio (OR), 5.39; 95% confidence interval (CI), 1.42-19.50), lack of potable water (OR, 3.66; CI, 1.25-9.94), lack of sanitary toilet (OR, 2.92; CI, 1.35-6.05) and earthen floor (OR, 2.48; CI, 1.28-4.73). Also seropositivity was associated with low academic education (OR, 2.5O; CI, 1.33-4.69) and lack of knowledge about the parasite (OR, 2.39; CI, 1.26-4.49). Out of 328 persons examined for intestinal parasites, two soldiers (0.6%) coming from rural areas were identified as Taenia sp. carriers. T. solium was identified in one case. Although T. solium infections originate and are more prevalent in rural villages, the high seroprevalence found in this study indicates that they can also be found at important levels in urban communities. Migration of tapeworm carriers from rural areas to the city grants the transmission of cysticercosis when poor environmental and social conditions are present.

Adolescent↗
PubMed1998

Childhood absence epilepsy with tonic-clonic seizures and electroencephalogram 3-4-Hz spike and multispike-slow wave complexes: linkage to chromosome 8q24.

Childhood absence epilepsy (CAE), a common form of idiopathic generalized epilepsy, accounts for 5%-15% of childhood epilepsies. To map the chromosomal locus of persisting CAE, we studied the clinical and electroencephalographic traits of 78 members of a five-generation family from Bombay, India. The model-free affected-pedigree member method was used during initial screening with chromosome 6p, 8q, and 1p microsatellites, and only individuals with absence seizures and/or electroencephalogram 3-4-Hz spike- and multispike-slow wave complexes were considered to be affected. Significant P values of .00000-.02 for several markers on 8q were obtained. Two-point linkage analysis, assuming autosomal dominant inheritance with 50% penetrance, yielded a maximum LOD score (Zmax) of 3.6 for D8S502. No other locus in the genome achieved a significant Zmax. For five smaller multiplex families, summed Zmax was 2.4 for D8S537 and 1.7 for D8S1761. Haplotypes composed of the same 8q24 microsatellites segregated with affected members of the large family from India and with all five smaller families. Recombinations positioned the CAE gene in a 3.2-cM interval.

California↗
PubMed1996

Juvenile myoclonic epilepsy in chromosome 6p12-p11: locus heterogeneity and recombinations.

We recently analyzed under homogeneity a large pedigree from Belize with classic juvenile myoclonic epilepsy (JME). After a genome wide search with 146 microsatellites, we obtained significant linkage between chromosome 6p markers, D6S257 and D6S272, and both convulsive and EEG traits of JME. Recombinations in two affected members defined a 40 cM JME region flanked by D6S313 and D6S258. In the present communication, we explored if the same chromosome 6p11 microsatellites also have a role in JME mixed with pyknoleptic absences. We allowed for heterogeneity during linkage analyses. We tested for heterogeneity by the admixture test and looked for more recombinations. D6S272, D6S466, D6S294, and D6S257 were significantly linked (Zmax > 3.5) to the clinical and EEG traits of 22 families, assuming autosomal dominant inheritance with 70% penetrance. Pairwise Zmax were 4.230 for D6S294 (theta m = f at 0.133) and 4.442 for D6S466 (theta m = f at 0.111). Admixture test (H2 vs. H1) was significant (P = 0.0234 for D6S294 and 0.0128 for D6S272) supporting the hypotheses of linkage with heterogeneity. Estimated proportion of linked families, alpha, was 0.50 (95% confidence interval 0.05-0.99) for D6S294 and D6S272. Multipoint analyses and recombinations in three new families narrowed the JME locus to a 7 cM interval flanked by D6S272 and D6S257.

Centromere↗
PubMed1996

Clinical and genetic analysis of a large pedigree with juvenile myoclonic epilepsy.

Juvenile myoclonic epilepsy is a common type of idiopathic generalized epilepsy characterized by myoclonic, generalized tonic-clonic, and in 30% of patients, absence seizures. We studied a three-generation pedigree of 33 members, 10 of whom were clinically affected with juvenile myoclonic epilepsy or presented with subclinical electroencephalographic (EEG) 3.5- to 6.0-Hz diffuse polyspike-wave or spike-wave complexes. Juvenile myoclonic epilepsy and the EEG trait segregated as an autosomal dominant trait with 70% penetrance. Linkage analysis using this model showed significant linkage to four microsatellite markers centromeric to human leukocyte antigen (HLA) in chromosome 6p. Maximum lod scores of 3.43 at theta(m=f)=0.00 for D6S272, D6S466, D6S257, and D6S402 were obtained. Recombinant events in 2 affected members defined the gene region to a 43-cM interval flanked by D6S258 (HLA region) and D6S313 (centromere). Our results in this large family provide evidence that a gene responsible for juvenile myoclonic epilepsy and the subclinical, 3.5- to 6.0-Hz, polyspike-wave or spike-wave EEG pattern is located in chromosome 6p.

Adolescent↗
PubMed1995

Intraepithelial and lamina propria leucocyte subsets in inflammatory bowel disease: an immunohistochemical study of colon and rectal biopsy specimens.

AIMS: To gain new insights into the pathogenesis and differential diagnosis of ulcerative colitis and colonic Crohn's disease. METHODS: Immunohistochemistry for different leucocyte subsets was performed in biopsy specimens of the sigmoid colon and rectum from 55 patients with inflammatory bowel disease and 11 healthy controls. RESULTS: Colonic biopsy specimens from patients with active ulcerative colitis had significantly higher numbers of CD45+ and CD3+ leucocytes compared with those from patients with inactive disease, and higher numbers of total leucocytes and macrophages than those from patients with Crohn's disease. Rectal biopsy specimens from patients with Crohn's disease had greater numbers of intraepithelial leucocytes (CD45, CD3 and CD8 cells) than specimens from patients with active or inactive ulcerative colitis, or from healthy controls. CONCLUSIONS: Because of the phenotypic differences in the inflammatory infiltrate in the mucosa from the sigmoid colon and the rectum, the segment of the intestine to be biopsied should be specified. Assessment of the leucocytic component of the intraepithelial infiltrate in rectal biopsy specimens was more useful than examination of colonic biopsy specimens in the differential diagnosis of ulcerative colitis and Crohn's disease.

Adult↗
PubMed1995

Juvenile myoclonic epilepsy locus in chromosome 6p21.2-p11: linkage to convulsions and electroencephalography trait.

Despite affecting 4 million Americans and 100-200 million persons worldwide, the precise molecular mechanisms of human epilepsies remain unknown. Juvenile myoclonic epilepsy (JME) is the most frequent and, hence, most important form of hereditary grand mal epilepsy. In this epilepsy, electroencephalographic (EEG) 15-30-Hz multispikes produce myoclonic and tonic-clonic convulsions beginning at 8-20 years of age. Moreover, EEG 3.5-6-Hz multispike wave complexes appear in clinically asymptomatic family members. We first studied 38 members of a four-generation LA-Belize family with classical JME but with no pyknoleptic absences. Five living members had JME; four clinically asymptomatic members had EEG multispike wave complexes. Pairwise analysis tightly linked microsatellites centromeric to HLA, namely D6S272 (peak lod score [Zmax] = 3.564-3.560 at male-female recombination [theta m = f] = 0-.001) and D6S257 (Zmax = 3.672-3.6667 at theta m = f = 0-.001), spanning 7 cM, to convulsive seizures and EEG multispike wave complexes. A recombination between D6S276 and D6S273 in one affected member placed the JME locus within or below HLA. Pairwise, multipoint, and recombination analyses in this large family independently proved that a JME gene is located in chromosome 6p, centromeric to HLA. We next screened, with the same chromosome 6p21.2-p11 short tandem-repeat polymorphic markers, seven multiplex pedigrees with classic JME. When lod scores for small multiplex families are added to lod scores of the LA-Belize pedigree, Zmax values for D6S294 and D6S257 are > 7 (theta m = f = .000). Our results prove that in chromosome 6p21.2-p11 an epilepsy locus exists whose phenotype consists of classic JME with convulsions and/or EEG rapid multispike wave complexes.

Brain↗
PubMed1994

Progress in mapping human epilepsy genes.

The chromosomal loci for seven epilepsy genes have been identified in chromosomes 1q, 6p, 8q, 16p, 20q, 21q, and 22q. In 1987, the first epilepsy locus was mapped in a common benign idiopathic generalized epilepsy syndrome, juvenile myoclonic epilepsy (JME). Properdin factor or Bf, human leukocyte antigen (HLA), and DNA markers in the HLA-DQ region were genetically linked to JME and the locus, named EJM1, was assigned to the short arm of chromosome 6. Our latest studies, as well as those by Whitehouse et al., show that not all families with JME have their genetic locus in chromosome 6p, and that childhood absence epilepsy does not map to the same EJM1 locus. Recent results, therefore, favor genetic heterogeneity for JME and for the common idiopathic generalized epilepsies. Heterogeneity also exists in benign familial neonatal convulsions, a rare form of idiopathic generalized epilepsy. Two loci are now recognized; one in chromosome 20q (EBN1) and another in chromosome 8q. Heterogeneity also exists for the broad group of debilitating and often fatal progressive myoclonus epilepsies (PME). The gene locus (EPM1) for both the Baltic and Mediterranean types of PME or Unverricht-Lundborg disease is the same and is located in the long arm of chromosome 21. Lafora type of PME does not map to the same EPM1 locus in chromosome 21. PME can be caused by the juvenile type of Gaucher's disease, which maps to chromosome 1q, by the juvenile type of neuronal ceroid lipofuscinoses (CLN3), which maps to chromosome 16p, and by the "cherry-red-spot-myoclonus" syndrome of Guazzi or sialidosis type I, which has been localized to chromosome 10. A point mutation in the mitochondrial tRNA(Lys) coding gene can also cause PME in children and adults (MERFF).

Chromosome Mapping↗
PubMed1992

Clinical pharmacokinetics of albendazole in patients with brain cysticercosis.

Albendazole pharmacokinetics were studied in eight patients who were receiving albendazole in doses of 15 mg/kg per day for 8 days as treatment of brain cysticercosis. Albendazole was not detected in plasma, but its main metabolite albendazole sulphoxide could be measured. Maximum plasma levels for albendazole sulphoxide ranged from 0.45 to 2.96 micrograms/mL. The half-life of albendazole sulphoxide was between 10 and 15 hours. A double peak was found in three patients. Mean residence time values were from 14 to 20 hours. Plasma levels of albendazole sulphoxide at the steady state showed great intraindividual variability. The results suggest that albendazole can be administered twice daily rather than three times as is currently done.

Administration, Oral↗
PubMed1992

Continuous focal spikes during REM sleep in a case of acquired aphasia (Landau-Kleffner syndrome).

We report a girl 3 years and 6 months old with onset of aphasia at age 3 years and 3 months. There was no evidence of brain damage and there were no seizures. The neuropsychological evaluation showed that the girl tended to be right-handed, that aphasia was global and that other higher cortical functions seemed to be preserved. Isolated spikes and spikes-and-wave were recorded during wake over the right temporal region with rare independent contralateral abnormalities. During polysomnography (PSG), the physiological patterns of sleep were preserved and right temporal epileptiform discharges were significantly increased in all sleep stages. Maximal activation was obtained at sleep onset and during rapid eye movement (REM) sleep periods, when focal abnormalities became continuous and spread contralaterally. Repeat PSGs showed that the activation profile retained this particular trait, although subclinical discharges tended to increase during slow wave sleep (SWS). This pattern of subclinical temporal status epilepticus during REM sleep differs from the characteristic activation profile found in the syndrome of continuous spikes-and-waves during SWS. However, this profile was transient and all epileptiform changes disappeared during clinical recovery at 18 months of follow-up.

Anticonvulsants↗
PubMed1992

Fatty change in the endometrium.

Fatty change of the endometrial stroma is reported for the first time in the literature. This incidental finding further exemplifies the capacity of the endometrial stroma to undergo benign mesenchymal metaplasia.

Adipose Tissue↗
PubMed1990

Dexamethasone increases plasma levels of albendazole.

Therapy of neurocysticercosis with cysticidal drugs is frequently complicated by the exacerbation of symptoms that follows the inflammation triggered by the acute destruction of cysticerci. Treatment of such adverse reactions with dexamethasone is highly effective. However, it has been shown that dexamethasone lowers the plasma levels of praziquantel, thus reducing its cysticidal efficacy. We measured plasma levels of albendazole, another strong cysticidal drug, when dexamethasone was given simultaneously. We found that dexamethasone increased the plasma levels of albendazole by about 50% (P less than 0.002); hence, it seems that cysticercosis and the ensuing inflammation can be treated simultaneously with albendazole and dexamethasone without diminishing the efficacy of the cysticidal drug.

Adult↗
PubMed1990

Plasma and CSF levels of albendazole and praziquantel in patients with neurocysticercosis.

Albendazole or praziquantel were measured in plasma and cerebrospinal fluid (CSF) in 29 patients with neurocysticercosis. Mean levels of albendazole in plasma were 0.918 microgram/ml and in CSF were 0.392 microgram/ml and levels of praziquantel were 1.640 micrograms/ml in plasma and 0.398 microgram/ml in CSF, after doses of 15 and 50 mg/kg, respectively. Drug concentrations in CSF were 43% for albendazole and 24% for praziquantel. The drug levels obtained for both drugs showed ample individual variations that were not related to age, sex, presence of inflammation in the subarachnoid space, or therapeutic effectiveness; such variations seem to be due to individual differences in pharmacokinetics. Both drugs were effective and the doses currently used of each drug seem to be optimal for therapy of neurocysticercosis.

Adolescent↗
PubMed1990

Neurocysticercosis as the main cause of late-onset epilepsy in Mexico.

We studied 100 consecutive Mexican patients with epilepsy that started after the age of 25 years. All patients underwent clinical evaluation, computed tomography, and electroencephalography; additionally, cerebrospinal fluid analysis was performed in 82 of them. Neurocysticercosis or its sequelae were diagnosed in 50 patients (50%); 36 of these patients had partial seizures, 41 had parenchymal calcifications, and 15 had two or more lesions. Our results are in contrast with those of most studies from countries with a low incidence of neurocysticercosis, where brain tumors, cerebrovascular disease, trauma, and alcoholism are the main causes of tardive epilepsy.

Adult↗