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Biomedical subjects

M Chavez

Publications and source records attributed to M Chavez.

At least 19 recordsLinked to original sources
PubMed2001

Ethnicity, gene flow, and population subdivision in Limón, Costa Rica.

In this paper we examine the effects of ethnicity on the gene flow between two groups living in Limón, Costa Rica. Our main interest is to determine if ethnicity has acted as a barrier to the exchange of genes, and if the groups have remained distinct genetically. We report the admixture estimates, F(st) values, and inbreeding coefficients of the two samples. The data consist of blood samples and surnames obtained from 375 individuals. The subjects' two surnames were analyzed to determine the ethnicity of their parents (individuals carry their father's and mother's first surnames). We used the formula of Crow and Mange ([1965] Eugen Q 12:199-203) to compute F(t), F(n), and F(r) with the surnames. Admixture estimates were computed for both groups using the computer program ADMIX.PAS kindly provided by Jeffrey Long. The estimates for the Hispanic-Limonense group are M1 = 0.5866 European, M2 = 0.3383 Amerindian, and M3 = 0.0751 African ancestry. For the Afro-Limonense group, the admixture estimates indicate M1 = 0.1047 European, M2 = 0.1357 Amerindian, and M3 = 0.7595 African ancestry. The F(st) values are F(st) = 0.00558 for the Hispanic group and F(st) = 0.05137 for the Afro-Limonense group. These F(st) values indicate that the Afro-Limonense group has experienced more genetic drift than has the other group, possibly as a result of its long history of isolation in Costa Rica. Indeed, when plotted along a scaled eigenvector R matrix of Caribbean gene frequencies, the two Limonense groups did not cluster with each other. Thus we conclude that the two ethnic groups have remained distinct breeding populations.

Adult↗
PubMed2001

Intrahepatic hepatitis C virus replication is increased in patients with regular alcohol consumption.

AIMS: To assess clinical significance of liver hepatitis C virus RNA levels and their relationship with epidemiological, biochemical and histological factors. METHODS: A total of 50 patients (mean age 35.5+/-7 years) with biopsy-proven chronic hepatitis C infection were recruited. Risk factors were drug abuse (n=21), transfusion (n=16), other parental routes (n=8; surgery=3, tattooing=5), and idiopathic (n=5). Duration of infection was 16+/-9 years. All patients showed abnormal alanine aminotransferase levels and positive serum hepatitis C virus RNA. Hepatitis C virus genotype was assessed by Inno-Lipa. Liver biopsy was performed for histology and for hepatitis C virus RNA quantification by Amplicor-HCV-Monitor Daily alcohol consumption was recorded on two occasions by anamnesis. Inflammation grade was mild (n=31) or severe (n=19). Fibrosis was early stage (n=42) or advanced (n=8). RESULTS: Mean hepatitis C virus RNA levels were 9.4x10(5)+/-1.5x10(6) copies/microg of total RNA in liver tissue, and 9.1x10(5)+/-1.3x10(6) copies/ml in serum. Viral load in liver was positively correlated with that in serum (r=0.51, p<0.001) and there was a significant relationship between daily alcohol consumption and intrahepatic hepatitis C virus burden (r=0.53; p<0.001). Patients infected with genotype 3a showed lower intrahepatic hepatitis C virus load than patients infected with genotype 1b; albeit without reaching statistical significance (0.49x10(6)+/-0.89x10(6) vs 1.44x10(6)+/-1.9x10(6) copies/microg of total RNA; p=NS). No relationships were observed between liver viral burden and age, risk factor status, duration of infection, ferritin and alanine aminotransferase levels or with grading and staging. CONCLUSIONS: Hepatitis C virus load in serum is a mirror of intrahepatic hepatitis C virus levels. Chronic alcohol consumption enhances intrahepatic hepatitis C virus concentration.

Adult↗
PubMed2000

High-performance liquid chromatography of monoamines on phenyl-bound sorbents using organic free mobile phases.

Tryptophan and its metabolites, 5-hydroxytryptophan, 5-hydroxytryptamine, 5-hydroxyindolacetic acid, as well as dopamine, homovanilic acid and 2,3-dihydroxyphenylacetic acid, were separated on phenyl bound silica gel using isocratic elution with phosphate buffer. The method was successfully transferred to several other phenyl HPLC columns from different manufacturers simply by adjusting the pH of the buffer. The method has been validated by the determination of the level of monoamines in rat hypothalamus.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2000

Characterization and distribution of somatostatin binding sites in goldfish brain.

Somatostatin (SRIF) binding sites were characterized in goldfish brain. Binding of (125)I-[Tyr(11)]-SRIF-14 to a brain membrane preparation was found to be saturable, reversible, and time-, temperature-, and pH-dependent. Binding was also displaceable by different forms of SRIF. Under optimal conditions (22 degrees C, pH 7.2), the equilibrium binding of (125)I-[Tyr(11)]-SRIF-14 to goldfish brain membranes was achieved after 60 min incubation. Analysis of saturable equilibrium binding revealed a one-site model fit with K(a) of 1.3 nM. SRIF-14, mammalian SRIF-28, and salmon SRIF-25 displaced (125)I-[Tyr(11)]-SRIF-14 binding with similar affinity, whereas other neuropeptides, e.g., substance P, were unable to displace (125)I-[Tyr(11)]-SRIF-14. Autoradiography studies demonstrated that (125)I-[Tyr(11)]-SRIF-14 binding sites are found throughout the goldfish brain. A high density of (125)I-[Tyr(11)]-SRIF-14 binding sites was found in the forebrain, including the nucleus preopticus, nucleus preopticus periventricularis, nucleus anterioris periventricularis, nucleus lateralis tuberis, nucleus dorsomedialis thalami, nucleus dorsolateralis thalami, nucleus ventromedialis thalami, and nucleus diffusus lobi inferioris. In midbrain, (125)I-[Tyr(11)]-SRIF-14 binding sites were found in the optic tectum. The facial and vagal lobes and the mesencephalic-cerebellar tract were found to have a high density of binding sites. This study provides the first characterization and distribution of specific binding sites for SRIF in a fish brain.

Animals↗
PubMed1999

APH-1, a POU homeobox gene expressed in the salt gland of the crustacean Artemia franciscana.

We characterized the first POU-homeoprotein in a crustacean (designated APH-1 for Artemia POU-Homeoprotein, EMBL Y15070). The amino acid sequence of the APH-1 POU-domain is identical, except for two residues, to that of the two class III POU proteins Cf1-a (Drosophila) and POU-M1 (Bombyx mori). Southern blot analysis suggests that crustaceans have only one class III POU gene. RT-PCR and whole-mount in situ hybridization show that APH-1 mRNA is present in larvae specifically in the salt gland, an organ which is involved in osmoregulation, and disappears in the adult.

Amino Acid Sequence↗
PubMed1998

Effect of a high-fat diet on food intake and hypothalamic neuropeptide gene expression in streptozotocin diabetes.

Insulin-deficient diabetic rats are markedly hyperphagic when fed a high-carbohydrate (HC) diet, but normophagic when fed a high-fat (HF) diet. When maintained on a HC diet, diabetic rats also exhibit increased gene expression of the orexigenic peptide neuropeptide Y (NPY) in the hypothalamic arcuate nucleus, and reduced expression of the anorectic peptide corticotropin-releasing hormone (CRH) in the paraventricular nucleus, and these changes are hypothesized to contribute to diabetic hyperphagia. In this experiment we assessed whether the normophagia displayed by HF-fed diabetic rats is associated with the opposite profile of NPY and CRH expression. Our results show that relative to diabetic rats on the HC diet, the diabetic rats on the HF diet exhibited significantly reduced caloric intake (-40%), NPY expression in the arcuate nucleus (-27%), and elevated CRH expression in the paraventricular nucleus (+37%). Insulin and corticosterone, which are known to affect hypothalamic NPY and CRH expression, were not different between these two groups, making it unlikely that they can account for the differences in either feeding behavior or hypothalamic peptide expression. There was a small but significant increase in plasma leptin levels in the diabetic animals maintained on the HF, and large differences in parameters associated with elevated fat oxidation. These observations support the hypothesis that the normalization of food intake observed in diabetic rats consuming a HF diet may in part be mediated by reductions in NPY expression and elevations in CRH expression.

Animals↗
PubMed1998

Severe congenital hypopituitarism with low prolactin levels and age-dependent anterior pituitary hypoplasia: a clue to a PIT-1 mutation.

A 20-month-old boy presented with severe congenital growth hormone, thyrotropin, and prolactin deficiencies resulting from a de novo mutation of the PIT-1 gene. This form of congenital hypopituitarism should be suspected if pituitary anatomy is normal, especially if prolactin levels are low and, in boys, if the external genitalia are normal. Pituitary atrophy appears to be an age-dependent phenomenon in this condition.

DNA-Binding Proteins↗
PubMed1998

Chromosomal sublocalization of the transcribed human telomere repeat binding factor 2 gene and comparative mapping in the mouse.

Telomere repeat binding factor 2 (TERF2) is one of two recently cloned mammalian telomere binding protein genes. TERF2 binds as a dimer with high affinity to the double-stranded TTAGGG telomeric repeat through an evolutionarily conserved myb-type DNA binding domain. TERF2 prevents telomere end-to-end fusion and may be important in maintaining genomic stability. We localized the transcribed TERF2 gene to human chromosome 16q22.1, tightly linked to the EST HUM000S343. The mouse Terf2 gene is situated by itself in a newly defined "bin" on chromosome 8 one crossover distal to Psm10 and Sntb2. Human TERF2 and mouse Terf2 are therefore part of a large evolutionarily conserved linkage group comprised of at least 25 known paralogous genes between human chromosome 16q and mouse chromosome 8.

Animals↗
PubMed1997

Insulin in the arcuate nucleus of the hypothalamus reduces fat consumption in rats.

Data are accumulating that insulin acting in the central nervous system is a physiological regulator of food intake and body weight, presumably via its effect in the hypothalamus. The present study investigated whether infusion of a small dose of insulin into two major hypothalamic insulin-binding areas also has an effect on diet selection and behavior. At the beginning of the dark period, rats received local bilateral infusions of 4 microU of insulin or vehicle during 34 min into the arcuate (ARC) or paraventricular (PVN) nucleus of the hypothalamus. Consumption of carbohydrate (C)-, protein (P)-, and fat (F)-enriched food and time spent on certain behaviors (drinking, resting, grooming, rearing, exploring/sniffing) were assessed during the first nocturnal hour. In addition, 21-h diet selection was assessed. The percentage contribution of macronutrients (C/P/F) to total energy content of the C-, P-, and F-enriched diets was 71.9/17.2/10.9, 45.8/43.4/10.8, and 47.1/17.5/35.4, respectively. During the first hour, infusion of insulin into the PVN increased grooming behavior compared to infusion of the vehicle. Although infusion of insulin had no effect on diet selection during the first hour, insulin infused in the ARC caused a reduction in F-enriched food consumption and total intake of F (as a macronutrient) over the 21-h period without altering total food intake. Infusion of a higher dose of insulin (10 microU) into the third ventricle had no effect on any of the assessed parameters. The data are explained to indicate that insulin (being an indicator of a positive energy balance) adjusts body weight homeostasis by modulating the preference for fat, at least at the level of the ARC, but not at the PVN.

Animals↗
PubMed1997

Organization and expression of human telomere repeat binding factor genes.

The ends of mammalian chromosomes terminate in structures called telomeres. Recently a human telomere repeat binding factor (TRF1) that binds the vertebrate TTAGGG telomeric repeat in situ was isolated by Chong et al. (1). TRF1 regulates telomere length (2), which is often altered in cancer cells. To understand their genetic organization, TRF1 genes were localized to human chromosomes 13cen, 21cen, and Xq13 by analysis of human monochromosomal hybrids, and by fluorescent in situ hybridization. We also confirmed the recent localization of a human TRF1 gene to chromosome 8, and provide evidence that this locus is alternatively spliced. In contrast to the TRF1 genes on chromosomes 8 and X, the chromosomes 13 and 21 TRF1 genes contained a 60 bp deletion in the coding region. The results suggest that two distinct forms of TRF1 are expressed and that the TRF1 gene family includes at least three pseudogenes whose dispersal in the human genome may have occurred via cDNA intermediates.

Alternative Splicing↗
PubMed1997

Adrenalectomy increases sensitivity to central insulin.

When infused into the third ventricle of rats, insulin dose-dependently reduces food intake and body weight, with doses of 1 mU/day and lower being ineffective. Because corticosterone functionally antagonizes many of insulin's peripheral actions, and because corticosterone acts in the brain to enable hyperphagia under some conditions, a subthreshold dose of insulin (1 mU/day), or its saline vehicle, was infused into the third ventricle of adrenalectomized (ADX) and sham-ADX male Long-Evans rats. Sham-ADX rats that received insulin or saline had no significant change of food intake or body weight over a 2-week interval. Likewise, saline-infused ADX were unaffected. In contrast, ADX rats receiving insulin had a significant reduction of food intake and body weight. These results suggest that the absence of circulating glucocorticoids increases the brain's sensitivity to insulin, and that insulin in the brain acts to lower food intake and body weight via a glucocorticoid-sensitive mechanism.

Adrenalectomy↗
PubMed1997

Electrical remodeling of the human atrium: similar effects in patients with chronic atrial fibrillation and atrial flutter.

OBJECTIVES: This study sought to determine whether chronic atrial fibrillation (AF) and atrial flutter in patients lead to electrical remodeling of the human atrial myocardium, manifested by an abnormal relation between atrial cycle length and action potential duration (APD). BACKGROUND: Experimental studies in goats and isolated human atrial tissue have shown that prolonged AF leads to persistent shortening of atrial refractoriness, a phenomenon referred to as electrical remodeling and which helps to explain why AF begets AF. Direct data on human in situ myocardium are still lacking. METHODS: Using monophasic action potential recordings at two right atrial sites simultaneously, we determined in 7 patients with chronic AF and 13 with chronic atrial flutter (3 weeks to 3 years in duration) the relation between paced cycle length and APD at 90% repolarization (APD90) 15 to 30 min after conversion to sinus rhythm. APD90 was measured during regularly paced cycle lengths (250 to 800 ms) to determine the steady state cycle length relation and during extrastimulus intervals (from 800 ms to refractoriness) at a basic cycle length of 600 ms to determine electrical restitution curves. The same pacing protocols and measurements were performed in nine control patients with sinus rhythm and no overt atrial disease. RESULTS: In control patients, steady state APD90 increased steadily with increases in cycle length from 250 to 800 ms, reaching a maximal value of 325 +/- 41 ms (mean +/- SD) at a cycle length of 800 ms. In patients with cardioversion from atrial flutter or AF, the steady state cycle length-APD90 relation was shifted downward and flattened at cycle lengths >400 ms, reaching only 219 +/- 44 and 245 +/- 39 ms, respectively, at the 800-ms cycle length (p < 0.005 vs. control). The early time course of electrical restitution (200- to 300-ms extrastimulus intervals) was similar between all three groups, but at extrastimulus intervals >350 ms, APD90 was shorter in both the AF and atrial flutter groups than in the control group (p < 0.05). There were no significant differences between patients with cardioversion from atrial flutter and those with cardioversion from AF. APD90 at a steady state cycle length of 600 ms showed no significant correlation with the duration of previous AF or atrial flutter. CONCLUSIONS: AF and atrial flutter lead to marked, quantitatively similar decreases in the right atrial APD during steady state pacing and extrastimulation a considerable time after cardioversion. These data confirm that both AF and atrial flutter lead to electrical remodeling in the human atrium, with a preponderance at longer cycle lengths. It may be prudent to abort both types of arrhythmias early to prevent electrical remodeling.

Action Potentials↗
PubMed1997

Chemical lesion of visceral afferents causes transient overconsumption of unfamiliar high-fat diets in rats.

Because it is commonly assumed that the major role of visceral afferents in food intake control is to terminate meals by carrying negative-feedback signals to the brain, we hypothesized that overconsumption should occur in rats with chemically lesioned visceral afferents if they were presented with an unfamiliar diet. Adult male Sprague-Dawley (SD) rats were treated with multiple doses of capsaicin or vehicle as a control. Five weeks later, a series of 3-h feeding tests after 24-h deprivation was carried out, first with chow and then with either a solid (vegetable shortening) or liquid (Ensure) unfamiliar high-fat diet. Both groups consumed similar amounts of their powdered chow maintenance diet, but capsaicin-treated rats consumed at least 50% more of either high-fat diet than vehicle controls (P < 0.01) at the beginning of the first trial. During second and third trials with the now-familiar high-fat diet, intake was no longer significantly different between the two groups, suggesting rapid engagement of redundant control mechanisms. These results support a role of capsaicin-sensitive visceral afferents in providing negative feedback for early meal termination during the ingestion of unfamiliar diets.

Afferent Pathways↗
PubMed1997

Liposome encapsulation attenuates hemoglobin-induced vasoconstriction in rabbit arterial segments.

Free hemoglobin (Hb) induces a potent vasoconstrictor response that may limit its therapeutic application as a red blood cell replacement. We have investigated whether encapsulation of stroma-free Hb (SFHb) or cross-linked Hb (alpha alpha-Hb) in liposomes modulates Hb vasoactivity in isolated blood vessels. Relaxation of rabbit thoracic vessels was measured before and after exposure to acellular SFHb, alpha alpha-Hb, and liposome-encapsulated SFHb or alpha alpha-Hb. SFHb and alpha alpha-Hb caused significant inhibition of carbachol-induced relaxation at 0.5 mg/dl, whereas encapsulation inhibited vessel relaxation at 30- to 60-fold higher Hb concentrations. The contractile response of rabbit ear arterial segments to electrical stimulation in the presence of acellular alpha alpha-Hb resulted in a 150% increase (EC150) in contractile amplitude at 0.23 mg/dl, whereas the EC150 for encapsulated alpha alpha-Hb was 13.7 mg/dl. Mechanistic studies of the vasoconstrictor activity of Hb demonstrated that acellular alpha alpha-Hb had no effect on norepinephrine release in the rabbit ear artery. In addition, neither acellular nor encapsulated alpha alpha-Hb preparations inhibited endothelial nitric oxide (NO) synthase activity isolated from bovine pulmonary artery. However, inhibition of vessel relaxation by acellular or encapsulated alpha alpha-Hb was reversed by the NO donor S-nitrosylpenacillamine, implicating Hb-NO binding as a possible mechanism for the vasoconstrictor response. In vitro stopped-flow kinetic studies of Hb-NO binding showed similar rates of reaction for conversion of oxyhemoglobin to methemoglobin (metHb; < 2 ms), followed by rapid conversion of metHb to NO-Hb (300 ms) for both acellular and encapsulated alpha alpha-Hb, demonstrating that liposome encapsulation does not retard NO-Hb binding. The attenuated vasoactivity of encapsulated Hb may, therefore, result from the limited access of encapsulated Hb to NO imposed by the physical size of the liposome and reduced penetration of Hb across the vascular endothelium.

Animals↗
PubMed1997

Comparisons of noninvasive bone mineral measurements in assessing age-related loss, fracture discrimination, and diagnostic classification.

The purpose of this study was to examine the commonly available methods of noninvasively assessing bone mineral status across three defined female populations to examine their interrelationships, compare their respective abilities to reflect age- and menopause-related bone loss, discriminate osteoporotic fractures, and classify patients diagnostically. A total of 47 healthy premenopausal (age 33 +/- 7 years), 41 healthy postmenopausal (age 64 +/- 9 years), and 36 osteoporotic postmenopausal (age 70 +/- 6 years) women were examined with the following techniques: (1) quantitative computed tomography of the L1-L4 lumbar spine for trabecular (QCT TRAB BMD) and integral (QCT INTG BMD) bone mineral density (BMD); (2) dual X-ray absorptiometry of the L1-L4 posterior-anterior (DXA PA BMD) and L2-L4 lateral (DXA LAT BMD) lumbar spine, of the femoral neck (DXA NECK BMD) and trochanter (DXA TROC BMD), and of the ultradistal radius (DXA UD BMD) for integral BMD; (3) peripheral QCT of the distal radius for trabecular BMD (pQCT TRAB BMD) and cortical bone mineral content (BMC) (pQCT CORT BMC); (4) two radiographic absorptiometric techniques of the metacarpal (RA METC BMD) and phalanges (RA PHAL BMD) for integral BMD; and (5) two quantitative ultrasound devices (QUS) of the calcaneus for speed of sound (SOS CALC) and broadband ultrasound attenuation (BUA CALC). In general, correlations ranged from (r = 0.10-0.93) among different sites and techniques. We found that pQCT TRAB BMD correlated poorly (r < or = 0.46) with all other measurements except DXA UD BMD (r = 0.62,p < or = 0.0001) and RA PHAL BMD (r = 0.52, p < or = 0.0001). The strongest correlation across techniques was between QCT INT BMD and DXA LAT BMD (r = 0.87, p < or = 0.0001), and the weakest correlation within a technique was between pQCT TRAB BMD and pQCT CORT BMC (r = 0.25,p < or = 0.05). Techniques showing the highest correlations with age in the healthy groups also showed the greatest differences among groups. They also showed the best discrimination (as measured by the odds ratios) for the distinction between healthy postmenopausal and osteoporotic postmenopausal groups based on age-adjusted logistic regression analysis. For each anatomic site, the techniques providing the best results were: (1) spine, QCT TRAB BMD (annual loss, -1.2% [healthy premenopausal and healthy postmenopausal]); Student's t-value [not the T score], 5.4 [healthy postmenopausal vs. osteoporotic postmenopausal]; odds ratio, 43 [age-adjusted logistic regression for healthy postmenopausal vs. osteoporotic postmenopausal]); (2) hip, DXA TROC BMD (-0.46; 3.5; 2.2); (3) radius, DXA UD BMD (-0.44; 3.3; 1.9) and pQCT, CORT BMC (-0.72; 2.9; 1.7); (4) hand, RA PHAL (-0.51; 3.6; 2.0); and (5) calcaneus, SOS (-0.09; 3.4; 2.1) and BUA (-0.52; 2.6; 1.7). Despite these performance trends, the differences among sites and techniques were statistically insignificant (p > 0.05) using age-adjusted receiver operating characteristic (ROC) curve analysis. Nevertheless, kappa score analysis (using -2.0 T score as the cut-off value for osteopenia and -2.5 T score for osteoporosis) showed that in general the diagnostic agreement among these measurements in classifying women as osteopenic or osteoporotic was poor, with kappa scores averaging about 0.4 (exceptions were QCT TRAB/INTG BMD, DXA LAT BMD, and RA PHAL BMD, with kappa scores ranging from 0.63 to 0.89). Often different patients were estimated at risk by using different measurement sites or techniques.

Absorptiometry, Photon↗