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Biomedical subjects

E Vela

Publications and source records attributed to E Vela.

At least 19 recordsLinked to original sources
PubMed2006

The enigma of hypertensive ESRD: observations on incidence and trends in 18 European, Canadian, and Asian-Pacific populations, 1998 to 2002.

BACKGROUND: Despite improved treatment of hypertension and decreasing rates of stroke and coronary heart disease, the reported incidence of hypertensive end-stage renal disease (ESRD) increased during the 1990s. However, bias, particularly from variations in acceptance into ESRD treatment (ascertainment) and diagnosis (classification), has been a major source of error when comparing ESRD incidences or estimating trends. METHODS: Age-standardized rates were calculated in persons aged 30 to 44, 45 to 64, and 65 to 74 years for 15 countries or regions (separately for the Europid and non-Europid populations of Canada, Australia, and New Zealand), and temporal trends were estimated by means of Poisson regression. For 10 countries or regions, population-based estimates of mean systolic blood pressures and prevalences of hypertension were extracted from published sources. RESULTS: Hypertensive ESRD, comprising ESRD attributed to essential hypertension or renal artery occlusion, was least common in Finland, non-Aboriginal Australians, and non-Polynesian New Zealanders; intermediate in most European and Canadian populations; and most common in Aboriginal Australians and New Zealand Maori and Pacific Island people. Rates correlated with the incidence of all other nondiabetic ESRD, but not with diabetic ESRD or community rates of hypertension. Between 1998 and 2002, hypertensive ESRD did not increase in Northwestern Europe or non-Aboriginal Canadians, although it did so in Australia. CONCLUSION: Despite the likelihood of classification bias, the probability remains of significant variation in incidence of hypertensive ESRD within the group of Europid populations. These between-population differences are not explained by community rates of hypertension or ascertainment bias.

Aged↗
PubMed2006

Rarity of JC virus DNA sequences and early proteins in human gliomas and medulloblastomas: the controversial role of JC virus in human neurooncogenesis.

JC virus (JCV), the agent of progressive multifocal leucoencephalopathy (PML), exerts an oncogenic effect in several laboratory animal models. Moreover, JCV genomic DNA and early viral protein T-antigen have been detected in various types of human central nervous system (CNS) neoplasms. To further explore this association we have studied paraffin-embedded brain biopsy tissue from 60 neoplasms (55 gliomas and five medulloblastomas) and 15 reactive gliosis cases for the presence of JCV DNA sequences and proteins. Four post mortem cases of HIV-associated PML were used as positive controls. Samples were assessed by polymerase chain reaction (PCR) amplification of early (large T antigen) and late (virion protein 3) sequences and immunohistochemistry (IHC) with both PAb 2024 and anti-SV40 large T antigen monoclonal antibodies. Five cases (three neoplasms and two reactive gliosis instances) showed low viral DNA levels when PCR-tested for VP3 or large T, while no case was immunoreactive for any of the two antibodies used. The four PML cases yielded positive results with both PCR and IHC. Additionally, IHC with both antibodies was applied to a tissue micro-array including 109 CNS tumours and 21 reactive gliosis samples. No immunoreactivity was detected in any of these tissue micro-array samples. The rarity of JCV DNA sequences and early proteins in our brain tumours enriches the controversy over the role of JCV in human neurooncogenesis, whose clarification is in need of further molecular and epidemiologic studies.

Adult↗
PubMed2005

Obesity in renal transplantation: analysis of 2691 patients.

OBJECTIVE: Obesity is a cardiovascular risk factor in renal transplantation (RT). The objective of this study was to analyze the prevalence of post-RT obesity and risk factors associated with its development. PATIENTS AND METHODS: The study included all patients with a functioning renal transplant on December 31, 2003, who were residents of Catalonia, aged older than 14 years and who underwent transplantation between 1990 and 2003 (n = 2793); 102 patients (3.7%) were excluded due to lack of data for 1 or more study variables. Mean age was 53 +/- 14 years (range, 15-83) (61% men). Mean transplant duration was 63.0 +/- 44.5 months (range, 0-168). The chi-square test was used to compare proportions, analysis of variance (ANOVA) to compare mean values, and logistic regression to study risk factors for post-RT obesity. All data were taken from the Renal Registry of Catalonia (RMRC). RESULTS: Among RT patients, 38% were overweight (body mass index [BMI], 25-29.9 kg/m(2)) and 16% were obese (BMI >30). Prevalence of obesity was higher in women (21% vs 13%; P < .0001). Age was associated with obesity in RT patients aged 45-64 (20%) and 65-74 (18%) with respect to the group aged 15-44 years (9%) or >74 years (13%) (P < .0001). A total of 26% of patients who were normal weight before RT (BMI, 20-24.9) became overweight post-RT and 6% developed obesity (P < .0001). Among patients who were overweight pre-RT, 68% persisted with post-RT excess weight and 16% progressed to obesity (P < .0001). In the multivariate study, significant risk factors for developing post-RT obesity included the following: female (relative risk [RR], 2.46; P < .0001), age (45-64 years; RR, 2.36; P < .0001; and 65-74 years; RR, 2.23; P = .002), high blood pressure (RR, 1.44; P = .03), duration of transplant (RR, 1.06; P < .0001), cardiomyopathy (RR, 1.51; P = .007), and, particularly, the presence of excess weight (RR, 2.69; P < .0001) and pre-RT obesity (RR, 59.02; P < .0001). CONCLUSIONS: There is a high prevalence of post-RT excess weight and obesity. Adequate control of cardiovascular risk in renal transplant recipients should also include strict measures to prevent and treat obesity.

Adolescent↗
PubMed2003

CblE type of homocystinuria: mild clinical phenotype in two patients homozygous for a novel mutation in the MTRR gene.

Patients with the cblE type of homocystinuria usually present with megaloblastic anaemia, feeding difficulties, developmental delay and cerebral atrophy. We present a 14-year-old Spanish girl (patient 1) and a 10-year-old Portuguese boy (patient 2) with cblE disease and mild clinical phenotype. The main clinical feature in both patients was persistent megaloblastic anaemia observed at 3 years and at 2 months of age, respectively. Diagnosis was made at the ages of 9 and 7 years, respectively, owing to persistent macrocytosis despite cobalamin treatment. Plasma total homocysteine values at diagnosis were 91 micromol/L and 44 micromol/L, respectively, in the absence of methylmalonic aciduria. Neurological and neurophysiological examinations were normal except for two small lesions on brain MRI suggestive of ischaemia and slight abnormalities in somatosensitive evoked potentials. Enzymatic analysis, complementation studies and clearly reduced production of methylcobalamin from 57Co-labelled cyanocobalamin indicated functional methionine synthase reductase deficiency due to the cblE defect. Genetic analysis confirmed that both patients are homozygous for a novel mutation c.1361C>T in the methionine synthase reductase gene leading to a replacement of serine by leucine (S454L) in a highly conserved FAD-binding domain. We propose that homozygosity for this novel mutation may be associated with a mild phenotype, although its long-term deleterious neurological consequences remain possible. Furthermore, we propose that even in the absence of apparent neurological involvement, total homocysteine should be investigated in patients with resistant megaloblastic anaemia to detect possible mild forms of the cblE type of homocystinuria.

Adolescent↗
PubMed2001

Environmental context-dependent memory: a review and meta-analysis.

To address questions about human memory's dependence on the coincidental environmental contexts in which events occur, we review studies of incidental environmental context-dependent memory in humans and report a meta-analysis. Our theoretical approach to the issue stems from Glenberg's (1997) contention that introspective thought (e.g., remembering, conceptualizing) requires cognitive resources normally used to represent the immediate environment. We propose that if tasks encourage processing of noncontextual information (i.e., introspective thought) at input and/or at test, then both learning and memory will be less dependent on the ambient environmental contexts in which those activities occur. The meta-analysis showed that across all studies, environmental context effects were reliable, and furthermore, that the use of noncontextual cues during learning (overshadowing) and at test (outshining), as well as mental reinstatement of appropriate context cues at test, all reduce the effect of environmental manipulations. We conclude that environmental context-dependent memory effects are less likely to occur under conditions in which the immediate environment is likely to be suppressed.

Association Learning↗
PubMed2000

Mechanisms of CD26/dipeptidyl peptidase IV cytokine-dependent regulation on human activated lymphocytes.

Among the cellular pathways activated by IL-12, we had previously found that both the percentage and intensity of CD26(+)cells in the PHA-stimulated T cells increased when IL-12 was present (independently of its CD4 or CD8 phenotype). Now, we examined the molecular mechanisms of this IL-12-mediated effect. The IL-12 regulation pathway is dependent of de novo protein synthesis and independent of cytokine secretion. Our results show two transcripts for CD26 in PBMC for the first time and no regulation by ILs at this level. Furthermore, secretion of the serum forms of CD26/DPPIV were not affected by IL-12. Interestingly, assays with neutralizing mAbs against TNF-alpha suggest that this cytokine negatively modulates CD26 expression. The fact that translation and probably translocation of CD26 toward the cell surface can be regulated by IL-12 and TNF-alpha reveals new aspects about the control of this T(H1)marker.

Cells, Cultured↗
PubMed2000

Thioredoxin, a putative oncogene product, is overexpressed in gastric carcinoma and associated with increased proliferation and increased cell survival.

Human thioredoxin is a putative oncogene that may confer both a growth and survival advantage to tumor cells. Overexpressed thioredoxin mRNA has been found in both primary human lung and colorectal cancers. To determine the intratumor distribution and amount of thioredoxin protein in human primary carcinomas, we developed an immunohistochemical assay for thioredoxin in paraffin-embedded tissue. We then studied 10 patients with primary high-risk gastric carcinoma. To further relate thioredoxin protein overexpression to cell death and survival, we used a paraffin-based in situ end-labeling (ISEL) assay. To delineate proliferation, we used the nuclear proliferation antigen detected by Ki-67. In this survey, we found that thioredoxin was localized to tumor cells and overexpressed compared with normal gastric mucosa in 8 of 10 gastric carcinomas. The thioredoxin was found at high levels in 5 of the 8 overexpressing carcinomas. The overexpression of thioredoxin was typically found in both a nuclear and cytoplasmic location in the neoplastic cells. There was a significant positive correlation (P = .0061) with cancer cell proliferation measured by Ki-67. There was a significant negative correlation (P = .0001) with DNA damage measured by the ISEL assay, suggesting decreased apoptosis and increased carcinoma cell survival. Thus, human primary gastric tumors that are highly expressive of thioredoxin have both a higher proliferative rate and a higher survival rate than tumors that do not express thioredoxin. With these newly developed assays in hand, it is now feasible to question whether this thioredoxin-related combined growth and survival advantage translates into poor clinical outcome.

Adenocarcinoma↗