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C Rodriguez

Publications and source records attributed to C Rodriguez.

At least 91 records · Page 5Linked to original sources
PubMed1999

Pancreas ultrastructural alterations in mice inoculated with Tityus discrepans (Buthidae) venom.

The symptoms of scorpionic envenomation in mice appear almost immediately after intraperitoneal injection and are manifested by great agitation, hair bristling, accelerated respiration, salivation and lacrimation, vomits and diarrhoea. In this work we intend to correlate those clinical manifestations appearing in response to the toxic aggression by Tityus discrepans venom, to the cellular or subcellular alterations produced in the mouse pancreas, probably similar to those damages found in envenomed humans. To evaluate pancreas subcellular response to Tityus discrepans venom, male C57/Bl adult mice were randomised into two groups: envenomed were intraperitoneally injected (hypochondrial left region) at a dose of 5 mg/Kg weight and controls received saline solution. Samples after preparation were studied in a Hitachi-300 transmission electron microscope. The most relevant ultrastructural changes in pancreatic tissues were an increase in the nuclear heterochromatin, with a corresponding decrease of euchromatin. In the cytoplasm, rough endoplasmic reticulum exhibited zones of oedema, losing its organised aspect. The secretion granules presented smaller electron density and variability in dimensions. At higher magnification a nucleus with picnotic appearance, with indentation of its perinuclear cistern was observed. There was a mitochondrial degeneration, with destruction of the mitochondrial matrix and autophagic vacuoles in its interior. At 48 h the lesions became intensified, with an evident increase in the intercellular spaces.

Animals↗
PubMed1998

Zinc is essential for binding of p56(lck) to CD4 and CD8alpha.

Binding of the protein tyrosine kinase p56(lck) to T-cell co-receptors CD4 and CD8alpha is necessary for T-lymphocyte development and activation. Association of p56(lck) with CD4 requires two conserved cysteine residues in the cytosolic domain of CD4 and two in the amino terminus of p56(lck), consistent with the notion that these four residues coordinate a single metal atom (1-5). Here we demonstrate that Zn2+ is essential for complex formation. In an in vitro binding reaction, Zn2+ mediates p56(lck) association with a glutathione S-transferase (GST) fusion protein containing the cytosolic domains of CD4 or CD8alpha; no other metals tested support binding. Treatment of preformed GST-CD4.p56(lck) dimers with the Zn2+ chelators 1,10-O-phenanthroline or 8-hydroxyquinoline-5-sulfonic acid results in dissociation of GST-CD4 from p56(lck), consistent with the finding of Huse et al. (5) that Zn2+ is contained within similar complexes. Furthermore, we show that, within live cells, CD4.p56(lck) and CD8alpha.p56(lck) interactions occur in a zinc-dependent fashion. Specifically, pretreatment of the human Jurkat T-cell line with membrane permeable zinc chelators disrupts CD4.p56(lck) complexes, and treatment of COS cells co-expressing CD8alpha and p56(lck) with such chelators likewise leads to dissociation of CD8alpha.p56(lck) complexes. CD4. p56(lck) and CD8alpha.p56(lck) represent the first examples of intracellular proteins that require zinc as a bridge for heterodimerization.

Animals↗
PubMed1998

Occupation and breast cancer mortality in a prospective cohort of US women.

The authors examined the association between main lifetime occupation and subsequent breast cancer mortality in a large prospective study of US adults. After 9 years of follow-up, 1,780 cases of fatal breast cancer were observed among 563,395 women who were cancer-free at interview in 1982. Main lifetime occupation was derived based on self-reports of current and former occupational titles and was classified into 14 broad occupational groups and 16 more narrowly defined occupational titles. Results from Cox proportional hazards models, adjusted for breast cancer risk factors, revealed little variability in breast cancer mortality by occupation. Two significant associations were observed: In comparison with housewives, women in "administrative support, including clerical" occupations were at a small increased risk (rate ratio (RR) = 1.14, 95% confidence interval (CI) 1.01-1.31), and an increased risk was seen for "executives" (RR = 1.93, 95% CI 1.03-3.62), based on 10 breast cancer deaths. No significant increases in risk were observed for teachers and librarians (RR = 0.89), nurses (RR = 0.84), managers (RR = 0.89), or women employed in sales (RR = 0.88) or service (RR = 0.84) occupations. When analyses were limited to women who had worked in their occupation for 10 or more years, the results for each occupational title were virtually unchanged. These results offer little support for an association between occupation and breast cancer mortality in general or for particular occupational titles, including teachers and nurses.

Adult↗
PubMed1998

Family history score as a predictor of breast cancer mortality: prospective data from the Cancer Prevention Study II, United States, 1982-1991.

A consistent predictor of a woman's risk for breast cancer is a family history of the disease. Most studies of family history and breast cancer have used the number of affected relatives in the family to calculate relative risk, but they have not considered the heterogeneity of the familial risk for breast cancer in a systematic way. With the use of data from a large prospective mortality study of US adults, the authors compared simple classification of family history of breast cancer (yes/no) to the method of using a quantitative family history score method, which takes into account the effects of family structure, age, and birth cohort as predictors of breast cancer mortality. After 9 years of follow-up, 1,428 cases of fatal breast cancer were observed among 453,073 women with complete information on number and age of siblings and family history. With the use of the family history score, about one-third of women with a positive family history of breast cancer were at no higher risk for breast cancer mortality than those without a family history of the disease. As a quantitative measure of relative risk for each family, family history score gave a better fit to the data, and it provided an incremental improvement of predictive accuracy of developing fatal breast cancer. Family history score can also be used as a categorical variable to stratify families. This allows researchers to focus on which risk groups would benefit from conducting further genetic analysis and to test the effects of genetic factors, environmental exposure, and gene-environment interactions on the etiology of the development of breast cancer.

Adult↗
PubMed1998

Long-term expression of differentiated functions in hepatocytes cultured in three-dimensional collagen matrix.

Hepatocytes entrapped in collagen gel and cultured in serum-free conditions survived longer than cells cultured on plastic (5 days vs. 3 weeks), showed fewer signs of early cell senescence (no increase in c-fos oncoprotein expression), and maintained the expression of differentiated hepatic metabolic functions over a longer period of time. Cells cultured in collagen gels retained their ability to respond to hormones. The insulin-stimulated glycogen synthesis rate remained fairly constant during 18 days in culture (between 5.4 +/- 0.37 and 9 +/- 2.7 nmol glucose/h/microg DNA). Collagen-cultured hepatocytes recovered glycogen stores to levels similar to those found in liver, or in hepatocytes isolated from fed rats. Urea synthesis from ammonia remained stable for more than 2 weeks (average value, 23 +/- 4 nmol urea/h/microg DNA). The rate of albumin synthesis in collagen-entrapped cells was maintained above the day-1 level during 18 days in culture. Cells showed high levels of glutathione (GSH) (1,278 +/- 152 pmol/microg DNA). Biotransformation activities CYP4501A1, CYP4502A2, CYP4502B1, and CYP4503A1 remained fairly stable in collagen-cultured hepatocytes. CYP4502E1 and CYP4502C11 decreased but were still measurable after 18 days. After 4 days in culture, GST activity returned to levels observed in isolated hepatocytes. In contrast with plastic cultures, cells responded to CYP450 inducers (methylcholanthrene for CYP4501A1, CYP4501A2, and glutathione-transferase, and ethanol for CYP4502E1) for more than 2 weeks. CYP4501A1, CYP4501A2, and glutathione-transferase A2 (GST A2) induction was preceded by an increase in specific mRNA, while the effects on CYP4502E1 seemed to be at a posttranslational level. Analysis of the expression of relevant hepatic genes by reverse Northern and semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) revealed that culturing hepatocytes in collagen gels results in a sustained higher expression of key liver transcription factor genes DBP, C/EBP-alpha and -beta, and HNF-1 and -4, as well as specific liver enzyme genes (phosphoenol pyryvate carboxykinase, and carbamoylphosphate-synthetase I).

Animals↗
PubMed1998

Increased peroxidation and reduced antioxidant enzyme activity in Alzheimer's disease.

The overall peroxidation activity in brain tissue by region from patients with Alzheimer's disease (AD) and age-matched controls was determined employing the thiobarbituric acid-reactive substances (TBARS) assay, a measure of lipid peroxidation, followed by a determination the activities of the antioxidant enzymes Cu/Zn superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT), in the frontal, temporal, and cerebellar cortex of 10 AD and 9 control brains. The level of TBARS was elevated in all regions, with particular statistical significance in the temporal cortex when compared to age-matched controls. SOD activity was significantly decreased in AD frontal and AD temporal cortex, while catalase activity was significantly decreased in AD temporal cortex. There was no significant difference in GSH-Px activity found in any of the regions examined. This study supports the theory that in AD the brain is affected by increased oxidative stress which, when combined with a decrease in SOD activity, produces oxidative alterations, seen most significantly in temporal cortex in AD, where the pathophysiologic changes are most severe.

Acatalasia↗
PubMed1998

Short-wave cone signal in the red-green detection mechanism.

Previous work shows that the red-green (RG) detection mechanism is highly sensitive, responding to equal and opposite long-wave (L) and middle-wave (M) cone contrast signals. This mechanism mediates red-green hue judgements under many conditions. We show that the RG detection mechanism also receives a weak input from the short-wave (S) cones that supports the L signal and equally opposes M. This was demonstrated with a pedestal paradigm, in which weak S cone flicker facilitates discrimination and detection of red-green flicker. Also, a near-threshold +S cone flash facilitates detection of red flashes and inhibits green flashes, and a near-threshold -S cone flash facilitates detection of green flashes and inhibits red flashes. The S contrast weight in RG is small relative to the L and M contrast weights. However, a comparison of our results with other studies suggests that the strength of the absolute S cone contrast contribution to the RG detection mechanism is 1/4 to 1/3 the strength of the S contribution to the blue-yellow (BY) detection mechanism. Thus, the S weight in RG is a significant fraction of the S weight in BY. This has important implications for the 'cardinal' color mechanisms, for it predicts that for detection or discrimination, the mechanisms limiting performance do not lie on orthogonal M-L and S axes within the equiluminant color plane.

Color Perception↗
PubMed1998

Warthin tumor. A new hypothesis concerning its development.

OBJECTIVE: Warthin tumor is the second most common benign parenchymal salivary neoplasm. The purpose of this study was to evaluate the histopathologic features of Warthin tumor to determine whether a developmental pattern could be identified. STUDY DESIGN: Seventy-nine Warthin tumors in 63 patients (62 male and 1 female; average age, 58.62 years) were examined. All cases were histopathologically classified and morphometrically analyzed with an Optomax system to measure the proportions of lymphoid tissue and cystic cavities. RESULTS: The predominantly epithelial type (21% of all cases) of Warthin tumor was associated with a mean patient age at diagnosis of 53 years, a mean evolution time of 2.8 months, an average size of 1 cm, and a mean lymphoid component of 10%. In the case of the classical type (61% of all cases), the mean patient age at diagnosis was 58 years, the mean evolution time 9 months, the average size 2.4 cm, and the mean lymphoid component 40%. For the predominantly lymphoid type (18% of all cases), these values were, respectively, 62 years, 11 months, 2.8 cm, and 74%. The mean size of the classical and lymphoid tumors (79% of the Warthin tumors) was significantly greater (p < 0.0001) than the mean size of the epithelial type (21% of the Warthin tumors). A positive correlation between tumor size and evolution time was found. CONCLUSION: Our results suggest that the Warthin tumor initially develops as an adenomatous epithelial proliferation followed by lymphocytic infiltration.

Adenolymphoma↗
PubMed1998

Diabetes mellitus and pancreatic cancer mortality in a prospective cohort of United States adults.

OBJECTIVES: Diabetes mellitus and pancreatic cancer are known to be associated, but it is not known whether diabetes is a true risk factor, preceding development of the cancer, or if it is an early manifestation of the cancer. To address this uncertainty, we examined the association of pancreatic cancer mortality and reported diabetes of at least one year's duration in a large, prospective study of United States adults. The vast majority of diabetes in this cohort is likely to be non-insulin-dependent diabetes. METHODS: After 12 years of follow-up, 2,953 deaths from pancreatic cancer were observed in a cohort of 1,089,586 men and women who were cancer-free at study entry in 1982. Cox proportional hazards models, adjusted for age, race, smoking, family history of pancreatic cancer, body mass index (wt/ht2), and education, were used to assess associations. RESULTS: A history of diabetes was significantly related to pancreatic cancer mortality in both men (rate ratio [RR] = 1.49, 95 percent confidence interval [CI] = 1.25-1.77) and women (RR = 1.51, CI = 1.24-1.85). However, the strength of the association varied over the follow-up period. The death rate from pancreatic cancer was twice as high in diabetics as in non-diabetics during the second and third years of follow-up (adjusted RR = 2.05, CI = 1.56-2.69) but only about 40 percent higher in years nine to 12 (adjusted RR = 1.38, CI = 1.08-1.77). CONCLUSIONS: The small but persistent increased risk of death from pancreatic cancer, seen even when the diagnosis of diabetes preceded death by many years, supports the hypothesis that diabetes may be a true, albeit modest, risk factor for pancreatic cancer.

Adult↗
PubMed1998

Infertility and risk of fatal ovarian cancer in a prospective cohort of US women.

OBJECTIVES: It is difficult to separate the possible role of fertility drugs from underlying infertility as risk factors for ovarian cancer. The present study examined the relationship between self-reported infertility and death from ovarian cancer among married women unlikely to have been exposured to fertility drugs. METHODS: Women were selected for study from the 676,526 female participants in Cancer Prevention Study II (CPS-II). After twelve years of follow-up, 797 deaths from ovarian cancer were observed among women with no prior history of cancer or hysterectomy and 40 years of age or older in 1967 when ovulatory stimulants were approved in the United States. Cox proportional hazards modeling was used to compute rate ratios (RRs) and to adjust for other potential risk factors. RESULTS: Overall, self-reported infertility was not significantly associated with ovarian cancer mortality (adjusted rate ratio (RR) = 1.1, 95 percent confidence interval (CI) = 0.9-1.3). Ovarian cancer death rates among nulligravid women with self-reported infertility, however, were 40 percent higher than for nulligravid women who never tried to become pregnant (RR = 1.4, 95 percent CI = 0.9-2.4). Multigravid women who reported infertility problems were not at increased risk. CONCLUSIONS: These results suggest that infertility itself, without concomitant exposure to fertility drugs, may increase risk of fatal ovarian cancer among nulligravid women.

Adult↗
PubMed1998

Melatonin prevents apoptosis induced by 6-hydroxydopamine in neuronal cells: implications for Parkinson's disease.

It was recently reported that low doses of 6-hydroxydopamine (6-OHDA) induce apoptosis of naive (undifferentiated) and neuronal (differentiated) PC12 cells, and this system has been proposed as an adequate experimental model for the study of Parkinson's disease. The mechanism by which this neurotoxin damages cells is via the production of free radicals. Given that the neurohormone melatonin has been reported 1) to be a highly effective endogenous free radical scavenger, 2) to increase the mRNA levels and the activity of several antioxidant enzymes, and 3) to inhibit apoptosis in other tissues, we have studied the ability of melatonin to prevent the programmed cell death induced by 6-OHDA in PC12 cells. We found that melatonin prevents the apoptosis caused by 6-OHDA in naive and neuronal PC12 cells as estimated by 1) cell viability assays, 2) counting of the number of apoptotic cells, and 3) analysis and quantification of DNA fragmentation. Exploration of the mechanisms used by melatonin to reduce programmed cell death revealed that this chemical mediator prevents the 6-OHDA induced reduction of mRNAs for several antioxidant enzymes. The possibility that melatonin utilized additional mechanisms to prevent apoptosis of these cells is also discussed. Since this endogenous agent has no known side effects and readily crosses the blood-brain-barrier, we consider melatonin to have a high clinical potential in the treatment of Parkinson's disease and possibly other neurodegenerative diseases, although more research on the mechanisms is yet to be done.

Animals↗
PubMed1998

C-reactive protein serum level is a valuable and simple prognostic marker in non Hodgkin's lymphoma.

Interleukin-6 plays a central role in normal B-cell maturation and in proliferation of some B-cell malignancies including multiple myeloma and some non Hodgkin's lymphomas (NHL). Furthermore, this cytokine also plays a major role in acute phase response by mediating synthesis of acute phase proteins such as C-reactive protein (CRP). In order to evaluate the exact role of CRP serum level as a simple prognostic factor, we analyzed CRP and IL-6 serum levels in 39 patients with NHL. Eleven patients had low grade NHL, 15 intermediate grade NHL, and 13 high grade NHL. Thirty percent of the patients presented detectable IL-6 serum levels (mean+/-SD: 33.6+/-95.2 U/ml, range: 0 to 500). Increased serum CRP levels were found in 42% of the patients with a mean of 29.2+/-41.97 mg/l] (range: 0 to 129). Thirty seven patients were studied for both markers. Three groups of patients were determined. One with low IL-6 and CRP serum levels (N=21), a second with high level of both markers (N=10), and the third with high serum CRP levels alone (N = 5). Only one patient had high level of serum IL-6 with no detectable CRP. The correlation of serum IL-6 and CRP levels with patient survival was investigated. Median survival in the group with low IL-6 level was not reached. 67% of patients of this group were still alive at 32 months from diagnosis. The group of patients with detectable IL-6 had a median of survival of 12 months (p<0.025). The survival of patients with a CRP<10 mg/l was not reached. 75% of patients survive at 32 months from diagnosis, whereas the group with higher CRP level reached a median survival at 8.5 months (p<0.009). As expected, on univariate analysis, there is a significant relationship between CRP and IL-6 levels (p<0.00017), and CRP levels and B symptoms (p<0.001). Furthermore there is a significant relationship between CRP and LDH levels (p<0.042).These results indicated that CRP may be considered as a valuable and easy prognostic biomarker of NHL.

Biomarkers, Tumor↗
PubMed1997

Inequalities in income and long-term disability in Spain: analysis of recent hypotheses using cross sectional study based on individual data.

OBJECTIVE: To compare the relation between inequalities in long-term disability and income in the 17 regions of Spain. DESIGN: Data were taken from the survey on impairments, disabilities, and handicaps that was carried out in Spain in 1986. For each region the inequality in long-term disability associated with income was calculated as the odds ratio associated with reducing monthly household income by 10,000 pesetas (about Ponds 50) (estimate of effect of inequality of income) and the odds ratio for the inequality in long-term disability between those at the bottom and those at the top of the income hierarchy (relative index of inequality). MAIN OUTCOME MEASURE: Prevalence of long-term disability. RESULTS: Five of the eight regions where lowering income had a greater effect on long-term disability were among those with the lowest income per head, while six of the remaining nine regions where the effect was smaller were among those with the highest income per head. Three regions with the highest estimate of relative index of inequality had the highest estimate of effect, and another three regions with the lowest estimate of relative index of inequality had the lowest estimate of effect. In contrast, the relative position of the remaining 11 regions varied from one measure to another. CONCLUSIONS: These results support the theory that additional increments in material wellbeing have a negligible effect on health in countries with high socioeconomic development. However, inequality in income distribution did not determine inequality in health between those at the bottom and those at the top of the income hierarchy in many Spanish regions.

Cost of Illness↗
PubMed1997

Mapping of DNA amplifications at 15 chromosomal localizations in 1875 breast tumors: definition of phenotypic groups.

DNA amplification is frequent in breast cancer and has been associated with specific clinicopathological parameters and/or worsened course of the disease. In the present work, we were interested in further defining the association linking the occurrence of DNA amplification to the emergence of specific breast tumor phenotype. To this aim, we studied by Southern blotting a total of 1875 breast tumor DNAs with 26 probes mapping at 15 distinct chromosomal localizations. Of the 26 loci tested, 11 loci showed elevated levels of amplification, 9 loci showed occasional and/or low level of DNA copy number increase, and 6 loci showed very rare or no variation. This allowed us to define six amplified domains mapping at 8p12, 8q24, 11q13, 12q13, 17q12, and 20q13.2, respectively. Over 60% of the tumors analyzed presented at least one amplification at one of these localizations. Amplifications often covered large regions of DNA and bore complex patterns involving coamplification of several colocalized markers. Statistical analysis revealed correlations associating DNA amplification with breast tumor phenotype, as well as sets of preferential coamplifications. Based on these correlations, we defined three subsets of breast cancer according to their patterns of DNA amplification. The first subset (group A) was organized around the amplifications at 11q13 and/or 8p12 and was predominantly composed of estrogen receptor-positive tumors and presented a large proportion of lobular cancers. The second subset (group B) was organized around the amplifications of ERBB2 and/or MYC. These tumors were mostly estrogen receptor-negative and of the ductal invasive type. The third subset (group C) corresponded to tumors in which no amplification was detected in the present screen. Tumors in this group were largely diploid and of low histopathological grading.

Adult↗
PubMed1997

Analysis of prognostic factors and patterns of failure in dogs with malignant oral tumors treated with megavoltage irradiation.

OBJECTIVE: To determine quality and duration of progression-free survival (PFS) time in dogs with malignant oral tumors after definitive megavoltage irradiation, to analyze prognostic factors for PFS time and patterns of failure, and to analyze the influence of tumor recurrence and development of metastasis on survival. DESIGN: Prospective clinical trial. ANIMALS: 105 dogs with squamous cell carcinoma, fibrosarcoma, or malignant melanoma of the oral cavity without evidence of metastasis. PROCEDURE: Dogs were treated with 48 Gy over 4 weeks on an alternate-day schedule of 4 Gy/fraction. Multivariate analysis was done by use of Cox's regression model to determine significant prognostic factors and by use of a competing risk model to determine the differential effects of prognostic factors on type of, and time to, failure. In 8% of the dogs, severe acute radiation reactions in the final week of treatment resulted in treatment discontinuation. In 7.6% of the dogs, chronic radiation reactions, including bone necrosis and fistula formation, developed. RESULTS: Prognostic factors that independently affected PFS time were histologic type and tumor T stage. Histologic type significantly influenced pattern of failure, but not time to failure, whereas clinical stage significantly influenced time to failure, but not type of failure. CLINICAL IMPLICATIONS: Irradiation was a safe and effective treatment of malignant oral tumors. Because the local efficacy of radiation was influenced only by tumor size, early treatment of oral tumors should improve the prognosis. In dogs without tumor recurrence, systemic metastases, rather than regional metastases, limited long-term survival after radiation therapy.

Animals↗