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Biomedical subjects

A Quintanilla

Publications and source records attributed to A Quintanilla.

At least 19 recordsLinked to original sources
PubMed2004

Evolution of toxicity upon wet catalytic oxidation of phenol.

This work reports on the evolution of the toxicity of phenol-containing simulated wastewater upon catalytic wet oxidation with a commercial copper-based catalyst (Engelhard Cu-0203T). The results of the study show that this catalyst enhances detoxification, in addition to its effect on the oxidation rate. The EC50 values of the intermediates identified throughout the oxidation route of phenol have been determined and used to predict the evolution of toxicity upon oxidation. The predicted values have been compared with the ones measured directly from the aqueous solution during the oxidation process. To learn about the evolution of toxicity through out the routes of phenol oxidation, experiments have been performed with simulated wastewaters containing separately phenol, catechol, and hydroquinone as original pollutants. The significant increase of toxicity observed during the early stages of phenol oxidation is not directly related to the development of the brown color that derives mainly from catechol oxidation. This increase of toxicity is caused by the formation of hydroquinone and p-benzoquinone as intermediates, the former showing the highest toxicity. Furthermore, synergistic effects, giving rise to a significant increase of toxicity, have been observed. These effects derive from the interactions among copper leached from the catalyst and catechol, hydroquinone, and p-benzoquinone and demand that close attention be paid to this potential problem in catalytic wet oxidation.

Catalysis↗
PubMed2002

Environmental transformation of the Bilbao estuary, N. Spain: microfaunal and geochemical proxies in the recent sedimentary record.

The distribution and abundance of benthic foraminifera and a range of elements have been analysed in six long cores (up to 10 m long) from the Bilbao estuary, N. Spain, to document environmental transformation of this estuarine ecosystem and to determine sediment contamination levels. Three different environmental zones could be distinguished in the recent sedimentary record based on its microfaunal and geochemical contents. Initially, a pre-industrial zone containing very abundant and diverse foraminiferal assemblages together with baseline metal levels. Secondly, an older industrial zone exhibiting co-existence of abundant and diverse foraminiferal assemblages with high concentrations of metals. Finally, a younger industrial zone with extreme concentrations of metals and barren of indigenous foraminifera. This environmental transformation has been caused by the discharge of untreated domestic and industrial effluents during the last 150 years. The occurrence of foraminifera in the two industrial zones and along the estuary is not related to defined levels of metals, and this seems to confirm oxygen limitation as the key factor to explain complete estuarine defaunation during deposition of the younger industrial zone (period 1950-2000). Effectiveness of current regeneration schemes could be assessed using microfaunal and geochemical proxies as environmental quality indicators.

Animals↗
PubMed1998

Changes in chromosomal localization of heterochromatin-binding proteins during the cell cycle in Drosophila.

We examined the heterochromatic binding of GAGA factor and proliferation disrupter (Prod) proteins during the cell cycle in Drosophila melanogaster and sibling species. GAGA factor binding to the brownDominant AG-rich satellite sequence insertion was seen at metaphase, however, no binding of GAGA factor to AG-rich sequences was observed at interphase in polytene or diploid nuclei. Comparable mitosis-specific binding was found for Prod protein to its target satellite in pericentric heterochromatin. At interphase, these proteins bind numerous dispersed sites in euchromatin, indicating that they move from euchromatin to heterochromatin and back every cell cycle. The presence of Prod in heterochromatin for a longer portion of the cell cycle than GAGA factor suggests that they cycle between euchromatin and heterochromatin independently. We propose that movement of GAGA factor and Prod from high affinity sites in euchromatin occurs upon condensation of metaphase chromosomes. Upon decondensation, GAGA factor and Prod shift from low affinity sites within satellite DNA back to euchromatic sites as a self-assembly process.

Adenine↗
PubMed1997

Biological characterization of Drosophila Rapgap1, a GTPase activating protein for Rap1.

The activity of Ras family proteins is modulated in vivo by the function of GTPase activating proteins, which increase their intrinsic rate of GTP hydrolysis. We have isolated cDNAs encoding a GAP for the Drosophila Rap1 GTPase. Drosophila Rapgap1 encodes an 850-amino acid protein with a central region that displays substantial sequence similarity to human RapGAP. This domain, when expressed in Escherichia coli, potently stimulates Rap1 GTPase activity in vitro. Unlike Rap1, which is ubiquitously expressed, Rapgap1 expression is highly restricted. Rapgap1 is expressed at high levels in the developing photoreceptor cells and in the optic lobe. Rapgap1 mRNA is also localized in the pole plasm in an oskar-dependent manner. Although mutations that completely abolish Rapgap1 function display no obvious phenotypic abnormalities, overexpression of Rapgap1 induces a rough eye phenotype that is exacerbated by reducing Rap1 gene dosage. Thus, Rapgap1 can function as a negative regulator of Rap1-mediated signaling in vivo.

Amino Acid Sequence↗
PubMed1995

Characterization of rho GTPase family homologues in Drosophila melanogaster: overexpressing Rho1 in retinal cells causes a late developmental defect.

The rho family of GTPases has been implicated in regulating changes in cell morphology in response to extracellular signals. We have cloned three widely expressed members of this family from Drosophila melanogaster; a rho homologue (Rho1) and two rac homologues (Rac1 and Rac2). Flies harbouring a Rho1 transgene that is specifically expressed in the eye exhibit a dramatic dose dependent disruption of normal eye development. Flies bearing at least two copies of the transgene display a severe rough eye phenotype characterized by missing secondary and tertiary pigment cells, a substantial reduction in the number of photoreceptor cells and a grossly abnormal morphology of the rhabdomeres. Cell fate determination in the imaginal disc occurs normally and abnormalities become manifest late in pupariation, coincident with the phase when the cells undergo major morphological changes. This phenotype is modified by mutations at several other loci that have been implicated in signal transduction, but not by mutations in ras pathway components.

Amino Acid Sequence↗
PubMed1993

Behaviour of platelets and beta-thromboglobulin.

Platelet count, platelet aggregation responses, and plasma beta-thromboglobulin were assessed before and at intervals during each study dialysis. As expected, modest thrombocytopenia was observed following treatment with all dialysers, but Filtral showed the least effect. Concordantly, modest increases in plasma beta-thromboglobulin were observed with all devices except Filtral (caveat: the device also seems to adsorb beta-thromboglobulin). Interpatient variability was more striking for platelet aggregation responses, and made it difficult to discern patterns; however, aggregation in response to ADP was augmented during haemodialysis with the Filtral device, and blunted when the G120 M was employed. Differences between hollow-fibre and parallel plate devices with the same membrane material suggest that membrane geometry, manufacturing residues, membrane support, or potting materials may also contribute to platelet activation.

Adenosine Diphosphate↗
PubMed1992

Renal handling of enalaprilat.

Most converting enzyme inhibitors share a predominantly renal dual elimination pathway consisting of glomerular filtration and tubular secretion. Since enalaprilat has two functional acidic groups, it is likely that it may be secreted via the proximal tubule organic acid system and, thus, its clearances would exceed that of glomerular filtration rate markers. We therefore examined the renal clearance of enalaprilat in normal volunteers and compared it with simultaneously measured inulin and creatinine clearances to explore the contribution of tubular secretion to the renal elimination of the drug. Twelve healthy male subjects with an age range of 24 to 58 years (mean +/- SE, 33.1 +/- 2.8) were studied. They had representative height (178.6 +/- 1.99 cm) and weight (73.3 +/- 2.1 kg) and had normal renal function as judged by blood urea nitrogen (BUN) (6 +/- 0.3 mmol/L [17 +/- 0.8 mg/dL]), plasma creatinine (88 +/- 3 mumol/L [1.0 +/- 0.03 mg/dL]), and creatinine clearance determined by a prestudy 24-hour urine collection (123.2 +/- 6.2 mL/min). Results are as follows: mean creatinine clearance, 2.12 mL/s (127 mL/min); mean inulin clearance, 119.1 ml/min mean creatinine clearance/inulin clearance, 1.07 mean enalaprilat protein binding, 37.9% unbound enalaprilat clearance, 222.4 ml/min; and the mean fractional enalaprilat clearances were: enalaprilat clearance/creatinine clearance, 1.72 (P less than 0.05, difference from 1.0); enalaprilat clearance/inulin clearance, 1.85, (P less than 0.05, difference from 1.0). Our results demonstrate that the clearance of free enalaprilat exceeds that of inulin and creatinine, suggesting that elimination of the drug proceeds through two complementary pathways, namely glomerular filtration and tubular secretion.

Adult↗
PubMed1991

The hepatocellular thyroid status of uremic rats estimated from the abundances of thyroid hormone-dependent nucleoplasmic proteins.

Although the serum thyroxine (T4) and triiodothyronine (T3) concentrations of uremic rats are commensurate with moderate hypothyroidism, their thyroid status at the tissue level remains controversial. To help establish the hepatocellular thyroid status of uremic rats, a novel tissue marker (nuclear protein abundances) was evaluated in uremic rats (U), hypothyroid rats (H), and hypothyroid uremic rats (HU). Uremia was established by five-sixths nephrectomy. Moderate hypothyroidism was established by partial thyroidectomy or by provision of drinking water supplemented with propylthiouracil and T4. Normal rats (N) and pair-fed, sham-operated rats (1 to 3 weeks after surgery) served as controls. Animals were killed 1 to 5 weeks postoperatively. The following values were obtained 5 weeks after surgery, at which time the total and free serum T4 and T3 levels of the hypothyroid rats (H) were equivalent to those of the uremic rats (U). Total T4 (micrograms/dL +/- 1 SD): N, 5.4 +/- 1.7; H, 2.2 +/- 0.5; U, 1.9 +/- 1.5; HU, 0.5 +/- 0.0. Free T4 (ng/dL +/- 1 SD): N, 535 +/- 165; H, 126 +/- 37; U, 135 +/- 89; HU, 26 +/- 1. Total T3 (ng/dL +/- 1 SD): N, 63 +/- 20; H, 39 +/- 14; U, 38 +/- 18; HU, 13 +/- 4. Free T3 (ng/dL +/- 1 SD): N, 7.83 +/- 3.00; H, 3.87 +/- 1.05; U, 3.47 +/- 1.73; HU, 0.94 +/- 0.47. Hepatocellular thyroid status was estimated from the relative abundances of two nucleoplasmic proteins on polyacrylamide gel electrophoregrams.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

The effects of postoperative factors on serum thyroid hormones and rat liver nuclear 3,5,3'-triiodothyronine receptor concentrations in surgical models of uremia and regenerating liver.

We have determined the individual effects of postoperative fasting, surgical/anesthetic factors, acute uremia (AU), and regenerating liver (RL) on nucleoplasmic (NP; 0.15 M KCl-extractable) and chromatin-bound (CB; 0.4 M KCl-extractable) rat liver T3 receptors. AU and RL rats were studied 24 h after bilateral nephrectomy (blood urea nitrogen, 128 +/- 13 mg/dl) or two thirds hepatectomy, respectively. The effects of postoperative fasting were assessed by comparison of normal rats (N) with control rats (N6) pair-fed to match the caloric intake of the AU and RL rats. Surgical/anesthetic effects were determined by comparison of N6 rats with sham-operated pair-fed rats (S6). The effects of AU or RL were obtained by comparison with S6 controls. Changes in mean body weight attributable to fasting (N6-N), surgical/anesthetic effects (S6-N6), acute uremia (AU-S6), and regenerating liver (RL-S6) were: -17.3 (P less than 0.001), -4.0 (P = NS), -4.5 (P less than 0.05), and -1.0 g/24 h (P = NS), respectively. Changes in mean serum T4 (N, 5.3 +/- 1.3 micrograms/dl) were: -1.0 (P = NS), -0.6 (P = NS), -0.9 (P less than 0.05), and -1.0 micrograms/dl (P less than 0.05), respectively. Changes in mean serum T3 (N, 53 +/- 23 ng/dl) were: -8 (P = NS), -18 (P less than 0.05), -10 (P = NS), and -14 ng/dl (P less than 0.05), respectively. The NP and CB receptor pools of the AU and RL rats were not significantly different from those of age-matched N rats (NP, 25 +/- 5 fmol/mg DNA; CB, 405 +/- 134 fmol/mg DNA). Chronically uremic (CU) rats 2 weeks after five sixths nephrectomy (blood urea nitrogen, 36 +/- 2 mg/dl) did not exhibit significant change in their extractable receptor pools. Complete starvation for 24 h (NO) or 72 h (NOO) generally resulted in marked reductions in receptor concentrations compared to those in age-matched N rats fed ad libitum: NP pool (N, 31 +/- 17 fmol/mg DNA): NO-N, -40% (P = NS); NOO-N, -59% (P less than 0.01); CB pool (N, 303 +/- 105 fmol/mg DNA): NO-N, -19% (P less than 0.05); NOO-N, -41% (P less than 0.001). These studies indicate that severe AU, moderate CU, and LR have relatively little effect on solubilized rat liver nuclear receptor concentrations. In contrast, complete starvation is a potent depressant of both nuclear receptor pools. In the surgical models of AU and LR, postoperative fasting was the primary cause of weight loss.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1983

Kinetic analysis of D-xylose absorption in normal subjects and in patients with chronic renal failure.

D-Xylose kinetics were studied in 12 normal subjects and in nine patients with chronic renal failure requiring dialysis (five hemodialysis and four peritoneal dialysis). None of the study subjects had demonstrable gastrointestinal disease. Doses of D-xylose were given intravenously (10 gm) and orally (25 gm) on different nondialysis days in order to determine the distribution and elimination kinetics and the absolute bioavailability of this compound. Our findings were as follows. (1) The nonrenal clearance of D-xylose is markedly reduced in chronic renal failure patients (43.3 vs. 90.9 ml/min, p less than 0.002). (2) D-Xylose is less completely absorbed in patients with chronic renal failure than in normal subjects (48.6% vs. 69.4%, p less than 0.01). (3) The absorption rate of D-xylose is slower in these patients than in normal subjects (0.555 hr-1 vs. 1.03 hr-1, p less than 0.05). (4) The absorption rate is positively correlated with the extent of D-xylose absorption (r = 0.49, p = 0.03). (5) Although peak D-xylose concentrations measured 1 hr after oral administration are well correlated with the extent of D-xylose absorption in normal subjects and in functionally anephric patients (r = 0.59, p less than 0.01), formal kinetic study is required to determine D-xylose bioavailability precisely because of the large variability in peak serum D-xylose concentrations and in the time required to reach these peak concentrations.

Adult↗
PubMed1981

Comparison of antihypertensive effects of captopril and propranolol in essential hypertension.

The antihypertensive effects of the oral converting enzyme inhibitor captopril and of propranolol were evaluated in a single-blind trial of 12 weeks in 19 ambulatory men with moderated essential hypertension (supine diastolic blood pressure [DPB], 100 to 120 mm Hg after receiving placebo for two weeks) whose sodium intake was unrestricted. The captopril group included 12 patients and the propranolol group seven. After the initial dose-finding period of four weeks, supine DBP was significantly reduced in eight patients receiving captopril and in four of the patients receiving propranolol. In these patients DBP decreased throughout the following eight weeks. In the remaining patients from each group, DBP was not reduced by either drug given alone at maximum allowable dosages during dose-finding periods, nor by combined administration in following weeks. No adverse side effects attributable to captopril were noted, except in one patient in whom proteinuria developed after seven weeks. Captopril has potential value in the treatment of moderate essential hypertension.

Adult↗
PubMed1981

Hemodialysis vs. peritoneal dialysis: results of a 3-year prospective controlled study.

A prospective comparison of peritoneal dialysis to hemodialysis was undertaken to identify advantages and disadvantages of either treatment relative to the other. Hematologic, biochemical, lipid, and neurobehavioral parameters were followed. Careful controls were imposed to assure that the treatment groups were comparable. Patients on peritoneal dialysis proved to have more normal concentrations of BUN, hemoglobin, potassium, bicarbonate, and high-density lipoproteins. Hemodialysis patients had more normal concentrations of albumin, total protein, and calcium. Hypertriglyceridemia was only minimally greater in peritoneal patients. Neurobehavioral results documented multiple abnormalities in both. The profile of results obtained provides preliminary criteria for selecting either form of dialysis for a particular patient.

Adult↗
PubMed1981

Long-term treatment of hypertension with methyldopa. IV. Duration of methyldopa therapy.

Methyldopa was administered for an average of 3 years to 435 patients with essential hypertension who were included in this retrospective survey. In 73% of patients, methyldopa was added to prior diuretic therapy, and in 19%, methyldopa and a diuretic were started concurrently. The remaining patients (8%) started treatment with methyldopa alone. After the initiation of methyldopa administration, a diuretic and/or additional antihypertensive agent(s) was included in the treatment regimen of 167 (38%) of the 435 patients. Treatment was interrupted in 147 patients - 14 (3%) because of lack of response, 73 (17%) with adverse effects, and 60 (14%) because of other or unknown reasons. Two-thirds of the patients treated had been receiving methyldopa continuously up to the time these data were collected in early 1979.

Adolescent↗
PubMed1980

Effect of mannitol on acute amphotericin B nephrotoxicity.

This study was undertaken to examine the value of mannitol as protection against the acute nephrotoxicity of amphotericin B under controlled conditions in a reproducible model of toxicity in the dog. Eleven dogs received amphotericin B, 2.5 mg x kg-1 b. wt. by i.v. infusion over a 4-h period. Six dogs were treated with mannitol, 6.25 g, i.v. every hour and five served as controls. Urinary volume (V), inulin clearance (CIn), p-aminohippurate clearance (CPAH), and Na excretion (UNaV) were measured every hour throughout the experiment. Although a higher urinary output was maintained in mannitol-treated dogs, a progressive decline in renal function was observed in treated and in control dogs. During the 4th h, mannitol-treated dogs showed higher CIn (37.4 vs. 19.7 ml x min-1 and CPAH (95 vs. 54 ml x min-1 than controls. However, statistically the differences were barely significant. The results fail to show that mannitol offers a definite protection against amphotericin B nephrotoxicity.

Amphotericin B↗
PubMed1980

Glucose metabolism in uremia.

Formation of CO2 from uniformly labeled 14C-glucose was measured in liver slices from uremic and normal rats. Both CO2 formation and lactate concentration were decreased in the uremic liver slices suggesting an inhibition of glucose oxidation. In addition, a net loss of glucose from the medium in the uremic preparation and a net gain in the normal controls suggested that there was increased nonoxidative utilization in the uremic liver. Such changes could not be explained by differences in glucose availability consequent to alterations in glycogen degradation. The most likely explanation is diversion of glucose into other biosynthetic pathways such as the synthesis of amino acids. In this regard, synthesis of glutamine appeared to be enhanced in uremia. Thus, products of carbohydrate metabolism may provide a potential mechanism for disposition of ammonia and synthesis of amino acids in uremia.

Animals↗