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Biomedical subjects

A Arroyo

Publications and source records attributed to A Arroyo.

At least 19 recordsLinked to original sources
PubMed1999

[Development of Escherichia coli strands resistant to quinolones in stools of patients with liver cirrhosis submitted to selective bowel decontamination].

BACKGROUND: Selective intestinal decontamination (SID) with norfloxacin in patients with cirrhosis may promote the development of quinolone-resistant (QR) gram-negative bacteria in stools. It is not known wether this fact may become a predisposing factor for the development of infections due to these bacteria. MATERIAL AND METHODS: We designed a prospective study to evaluate the incidence of Escherichia coli in stools at admission in patients with cirrhosis that had previously received norfloxacin as primary or secondary prophylaxis of spontaneous bacterial peritonitis (SBP) (group I, n = 28) vs those who did not (group II, n = 55). RESULTS: QR strains of E. coli were observed in 37.5 and in 1.47% of patients from groups I and II, respectively (p < 0.001). During admission, 36 patients underwent norfloxacin prophylaxis (group III), and 40 did not (group IV). Eleven patients from group III and one patient from group IV showed QR E. coli in stools. We observed 5 bacterial infections in group III and 14 in group IV (p = 0.0039). No patient with QR E. coli in stools developed infections due to this bacteria. CONCLUSION: The incidence of QR E. coli in stools of patients with cirrhosis is significantly increased in patients previously treated with prophylactic norfloxacin. However, this fact seems not to be associated with an increment in the prevalence of QR E. coli infections.

Aged↗
PubMed1999

Protective role of ubiquinone in vitamin E and selenium-deficient plasma membranes.

We have studied the effects of dietary depletion of vitamin E and selenium on endogenous ubiquinone-dependent antioxidant system. Deficiency induced an increase in both coenzyme Q9 and Q10 in liver tissue, reaching a maximum between 4 and 7 weeks of deficient diet consumption. Cytochrome b5 reductase polypeptide was also enriched in membranes after 5 weeks of deficient diet consumption. Substantial DT-diaphorase activity was found in deficient, but not in control plasma membranes. Deficient membranes were very sensitive to lipid peroxidation, although a great protection was observed after incubation with NAD(P)H. Our results show that liver cells can boost endogenous ubiquinone-dependent protective mechanisms in response to deficiency in vitamin E and selenium.

Animals↗
PubMed1999

Development of quinolone-resistant strains of Escherichia coli in stools of patients with cirrhosis undergoing norfloxacin prophylaxis: clinical consequences.

BACKGROUND/AIM: Norfloxacin prophylaxis decreases the incidence of bacterial infections in high-risk cirrhotic patients, but may promote the development of quinolone-resistant gram-negative bacteria in stools, and eventually lead to infections due to these bacteria. The aim of the study was to evaluate the prevalence of quinolone-resistant strains of E. coli in stools on admission, and the characteristics of any nosocomial infections. METHODS: Eighty-three consecutively hospitalized cirrhotic patients were included in this prospective study. The presence of quinolone-resistant strains of E. coli in stools on admission, and the characteristics of any nosocomial infections were recorded. RESULTS: Fourteen out of 83 patients (16.8%) showed quinolone-resistant E. coli in stools (Group I), and 69 did not (Group II). Thirteen out of 14 from Group I (92.8%) and 17/69 (24.6) from Group II had received primary or secondary prophylaxis with norfloxacin (p<0.001). During hospitalization, 12/12 (100%) of patients from Group I and 25/66 (37.8%) of patients from Group II underwent norfloxacin prophylaxis. Three bacterial infections in patients from Group I, 3 from Group II patients receiving norfloxacin and 16 from Group II patients not receiving norfloxacin were recorded (p<0.05). No infections due to quinolone-resistant E. coli were observed in patients colonized with these bacteria. Treatment with norfloxacin induced the development of quinolone-resistant E. coli in 6/14 (42.8%) patients in a mean time of 18.5+/-9.8 days. CONCLUSIONS: The development of quinolone-resistant strains of E. coli is significantly associated with previous administration of norfloxacin prophylaxis. However, in our series this fact is not associated with an increased incidence of quinolone-resistant E. coli or other gram-negative infections.

Aged↗
PubMed1999

The insulin-like growth factor system in the GT1-7 GnRH neuronal cell line.

Evidence suggests that insulin-like growth factors (IGFs; IGF-I and IGF-II) are involved in the regulation of reproductive function including the development of the gonadotropin-releasing hormone (GnRH) neuronal system and the modulation of GnRH secretory activities. To further characterize the regulatory role of the IGF system on GnRH neuronal function, we have examined the gene expression of IGF-I, IGF-II, IGF-I receptor (IGF-IR), and IGF-binding proteins (IGFBPs) in a GnRH neuronal cell line (GT1-7 cells). The relative effects of IGFs and insulin on GnRH secretion by these cells was also investigated. RT-PCR analysis demonstrated IGF-I, IGF-II and IGF-IR mRNAs in GT1-7 cells. The mRNAs for IGFBP-2, -3, -4, -5 and -6 but not IGFBP-1 were also detected. Immunoreactive protein bands for IGFBP-2, -4 and -5 but not for other IGFBPs were demonstrated by Western blot with IGFBP-5 appearing to be the most abundant IGFBP secreted by GT1-7 cells. IGFBP-5 production by GT1-7 cells was stimulated by both IGF-I and IGF-II in a dose-dependent manner with approximately equal potency, whereas insulin caused no significant effect. GnRH secretion by GT1-7 cells treated with IGF-I or IGF-II but not insulin showed an increase (80-100%) at 2 h of treatment followed by a decrease (46%) at 6 h that continued up to 24 h. We conclude that the expression of IGFs, IGF-IR and IGFBPs and their interactions in the regulation of GnRH secretion by GT1-7 cells as demonstrated by our study provide a basis for an autocrine regulatory role for the IGF system in GnRH neuronal secretory activities.

Animals↗
PubMed1999

Bioflavonoid effects on the mitochondrial respiratory electron transport chain and cytochrome c redox state.

The polyphenolic structure common to flavonoids enables them to donate electrons and exert antioxidant activity. Since the mitochondrial electron transport chain consists of a series of redox intermediates, the effect of flavonoids in a complex mixture of polyphenols, as well as related pure flavonoids, was evaluated on the rat liver mitochondrial electron transport chain. A French maritime pine bark extract (PBE), a complex mixture of polyphenols and related pure flavonoids, was able to reduce cytochrome c reversibly, possibly by donation of electrons to the iron of the heme group; the donated electrons can be utilized by cytochrome c oxidase. Among single flavonoids tested, (-)-epicatechin gallate had the greatest ability to reduce cytochrome c. In addition, PBE competitively inhibited electron chain activity in both whole mitochondria and submitochondrial particles. A 3.5-fold increase in the apparent Km value for succinate was calculated from reciprocal plots. Among the flavonoids tested, taxifolin and (-)-epicatechin gallate showed minor inhibitory effects, while (+/-)-catechin and (+)-epicatechin were ineffective. Activities of NADH-ubiquinone, succinate-ubiquinone, and ubiquinol-cytochrome c reductases were inhibited by low concentrations of PBE to a similar extent. However, inhibition of cytochrome c oxidase activity required 4-fold higher PBE concentrations. These results suggest that flavonoids reduce cytochrome c and that PBE inhibits electron transport chain activity mainly through NADH-ubiquinone, succinate-ubiquinone, and ubiquinol-cytochrome c reductases.

Animals↗
PubMed1998

Plasma membrane NADH-coenzyme Q0 reductase generates semiquinone radicals and recycles vitamin E homologue in a superoxide-dependent reaction.

We investigated the ability of plasma membrane CoQ reductase (PMQR) purified from pig liver to reduce phenoxyl radicals of a vitamin E homologue, Trolox. We report that NADH-driven one-electron reduction of CoQ0 catalyzed by PMQR produced CoQ0 semiquinone radical and CoQoH2. These in turn, recycle vitamin E homologue, Trolox, via reducing its phenoxyl radical. A significant part of NADH/PMQR-catalyzed reduction of CoQ0 (and Trolox recycling) was superoxide-dependent. Overall, our results demonstrate that PMQR in the model system used can act as an antioxidant enzyme that recycles water-soluble homologues of coenzyme Q and vitamin E.

Animals↗
PubMed1998

Vitamin E and selenium deficiency induces expression of the ubiquinone-dependent antioxidant system at the plasma membrane.

We have used a model of dietary deficiency that leads to a chronic oxidative stress to evaluate responses that are adaptations invoked to boost cellular defense systems. Long-Evans hooded rats were fed with a diet lacking vitamin E (E) and selenium (Se) for 7 wk from weaning leading to animals deficient in both nutrients (-E -Se). In the absence of an electron donor, liver plasma membranes from these rats were more sensitive to lipid peroxidation, although they contained 40% greater amounts of ubiquinone than the plasma membranes from rats consuming diets with sufficient vitamin E and Se (+E +Se). The incubation of plasma membranes with NAD(P)H resulted in protection against peroxidation, and this effect was more pronounced in -E -Se membranes. Deficiency was accompanied by a twofold increase in redox activities associated with trans plasma membrane electron transport such as ubiquinone reductase and ascorbate free radical reductase. Staining with a polyclonal antibody against pig liver cytochrome b5 reductase, which acts as one ubiquinone reductase in the plasma membrane, showed an increased expression of the enzyme in membranes from -E -Se rats. Little DT-diaphorase activity was measured in +E +Se plasma membranes, but this activity was dramatically increased in -E -Se plasma membranes. No such increase was found in liver cytosols, which contained elevated activity of calcium-independent phospholipase A2. Thus, ubiquinone-dependent antioxidant protection in +E +Se plasma membranes is based primarily on NADH-cytochrome b5 reductase, whereas additional protection needed in -E -Se plasma membranes is supported by the increase of ubiquinone levels, increased expression of the cytochrome b5 reductase, and translocation of soluble DT-diaphorase to the plasma membrane. Our results indicate that, in the absence of vitamin E and Se, enhancement of ubiquinone-dependent reductase systems can fulfill the membrane antioxidant protection.

Animals↗
PubMed1998

Pericardial fluid postmortem: Comparative study of natural and violent deaths.

Thanatochemistry is an increasingly important ancillary procedure in forensic practice. Alterations are known to take place in biochemical components during the postmortem period, particularly in the blood, and both research results and their interpretation have been the object of some controversy. For that reason, emphasis has been placed on the examination of fluids that are neither altered nor contaminated as rapidly as blood after death. This study tested the hypothesis that pericardial fluid (PF) may be a suitable medium for biochemical analysis in corpses. The study sought to determine concentrations of urea, creatinine, glucose, creatinine kinase 2, proteins, calcium, sodium, and potassium, in the pericardial fluid of corpses. The study sample was divided into two groups, natural deaths and violent deaths. Intergroup results were compared, using Mann-Whitney's U test for paired data. No significant differences were obtained between the natural death and violent death groups for the parameters studied, with the exception of urea (p < .05). Further studies are required to compare these results and create the possibility for new conclusions.

Autopsy↗
PubMed1997

Role of cytochrome b5 reductase on the antioxidant function of coenzyme Q in the plasma membrane.

Cytochrome b5 reductase purified from liver plasma membrane reduces coenzyme Q (CoQ) in reconstituted liposomes in the absence of cytochrome b5. Both CoQ and its reductase are responsible for the reduction of the ascorbate free radical at the cell surface. Thus, NADH-CoQ reductase represents a partial reaction of NADH-AFR reductase in the plasma membrane. Cytochrome b5 reductase maintains CoQ and ascorbate in their reduced state to support antioxidations. Reduced CoQ prevents lipid peroxidation in liposomes and plasma membranes. Also, oxidized CoQ can prevent lipid peroxidations in the presence of cytochrome b5 reductase and NADH. Addition of CoQ to intact cells prevents serum withdrawal-induced lipid peroxidation and apoptosis. The prevention of apoptosis by CoQ is independent of the bcl-2 protein content in the cell. Antioxidants that act at the plasma membrane as CoQ and ascorbate would represent a first barrier to protect lipids from oxidative stress and subsequent apoptosis. Cytochrome b5 reductase is then an enzyme leading this function at the plasma membrane. These data support the idea that when the plasma membrane barrier fails, bcl-2 protein would be required to prevent cell death.

Animals↗
PubMed1997

Vinorelbine as neoadjuvant chemotherapy in advanced cervical carcinoma.

PURPOSE: To evaluate the efficacy and toxicity of vinorelbine (VNB) as single-agent neoadjuvant chemotherapy in advanced cervical carcinoma (ACC). PATIENTS AND METHODS: Between December 1993 and October 1995, 43 untreated patients with stages IIB to IVA squamous cell cervical cancer were entered onto this study. Forty-two patients are assessable for response and 43 for toxicity. The median age was 46 years (range, 28 to 65). Distribution by stages (International Federation of Gynecology and Obstetrics [FIGO]) was as follows: IIB, 18 patients; IIIA, one; IIIB, 19; and IVA, five. Therapy consisted of VNB 30 mg/m2 by 20-minute intravenous (IV) infusion repeated weekly for 12 injections and followed by radical surgery if feasible or definitive radiotherapy. Both staging and response assessment were performed by a multidisciplinary team. RESULTS: One patient was considered not assessable for response. A total of 493 cycles of therapy were administered and objective remissions were observed in 19 of 42 patients (45%; 95% confidence interval, 30% to 60%). Two patients (5%) had a complete response (CR) and 17 (40%) a partial response (PR); no change (NC) was observed in 16 (38%) and progressive disease (PD) in seven (17%). Six of 19 patients (32%) who achieved objective responses (ORs) underwent surgery. The median time to failure and median survival time have not been reached yet. There were no therapy-related deaths. The dose-limiting toxicity was myelosuppression. Leukopenia occurred in 35 patients (81%) and was grade 3 or 4 in seven (17%). Twelve patients (28%) developed peripheral neuropathy, while myalgias occurred in 10 (23%). Constipation was observed in nine patients (21%), one with a prolonged ileum. Phlebitis was recorded in 18 patients (41%). In contrast, emesis and mucositis were rarely observed. No patient developed alopecia grade 3. By the end of the twelfth course of treatment, the average received dose-intensity was 85.4% of that projected. CONCLUSION: VNB is an active drug against ACC with moderate toxicity. Its activity is among the highest reported for single agents. Further evaluation in association with other agents is clearly justified.

Adult↗
PubMed1997

Inappropriate gonadotropin secretion in polycystic ovary syndrome: influence of adiposity.

In recent years, there has been uncertainty concerning the association of inappropriate gonadotropin secretion (high LH and normal FSH) and the polycystic ovary syndrome (PCOS). In the present study, we ascertained the influence of body composition on LH pulsatile parameters in 33 PCOS and 32 normal cycling (NC) women across a wide range of body mass index (BMI, 19-42 kg/m2). Twenty four-hour pulsatile parameters for serum LH (10-min sampling) and pituitary gonadotropin responses to i.v. bolus GnRH (10 micrograms) were evaluated. Fasting (0800 h) FSH and steroid hormone concentrations and 24-h mean insulin levels were determined. Insulin sensitivity (SI) was assessed by rapid i.v. glucose tolerance test in a subset of 28 PCOS and 29 NC subjects. Our results showed that BMI, an indicator of relative adiposity, had a significant negative impact on 24-h mean LH pulse amplitude (r = -0.63, P < 0.001) and the peak increment of LH in response to GnRH stimulation (r = -0.41; P = 0.02) for PCOS but not NC women. In contrast, 24-h LH pulse frequency was uniformly increased (40%) in PCOS as compared with NC women independent of BMI. In PCOS women, the blunting of pulse amplitude with increasing BMI resulted in a decline in 24-h mean LH levels (r = -0.63, P < 0.001) and the ratio of LH/FSH (r = -0.44, P = 0.02) not seen in NC. With BMI < 30 kg/m2, 24-h mean LH values for PCOS women were greater than the normal range for NC in 95% (18/19) of cases, whereas 24-h LH levels failed to discriminate PCOS from NC women in 43% (6/14) of obese (BMI > 30 kg/m2) PCOS women. Thus, the diagnostic value of LH determinations is retained for PCOS women with BMI < 30 kg/m2. For screening purposes, the mean of two LH values in samples collected at 30-min intervals was found to have a discriminatory power equal to that of the 24-h mean. These findings suggest that 1) BMI negatively influences LH pulse amplitude in PCOS women principally by an effect at the pituitary level; 2) accelerated LH pulse frequency in PCOS women is not influenced by BMI and represents a basic component of hypothalamic dysfunction in PCOS women; and 3) BMI does not influence gonadotropin secretion in normal cycling women. Thus assessments of basal LH levels and the LH/FSH ratio in hyperandrogenic anovulatory women are clinically meaningful when BMI is taken into account. Investigations to define the factor(s) that link adiposity and the attenuation of LH pulse amplitude in PCOS women would add further understanding of this complex neuroendocrine-metabolic disorder.

17-alpha-Hydroxyprogesterone↗
PubMed1997

DMPS-arsenic challenge test. I: Increased urinary excretion of monomethylarsonic acid in humans given dimercaptopropane sulfonate.

The purpose of the present study was to evaluate in a novel manner the arsenic exposure of humans living in two towns in Northeastern Chile. Residents of one town drink water containing 593 microg As/l. Those in the control town drink water containing 21 microg As/l. Our hypothesis was that the administration of the chelating agent, 2,3-dimercaptopropane-1-sulfonic acid, Na salt (DMPS, DIMAVAL) would increase the urinary excretion of arsenic, alter the urinary profile of arsenic species and thus result in a better indication of the body load of arsenic and a better biomarker for arsenic exposure. The method used to evaluate these subjects was to give them 300 mg DMPS by mouth, after an overnight fast, and collect urine at specified time periods. The urine samples were analyzed for inorganic arsenic, monomethylarsonic acid (MMA), dimethylarsinic acid (DMA) and total arsenic by hydride generation and atomic absorption spectrophotometry. The results indicated that: 1) During the 2-hr period after DMPS administration, MMA represented 42%, inorganic As, 20 to 22% and DMA, 37 to 38% of the total urinary arsenic. The usual range of the MMA percentage in human urine has been 10 to 20%. The % MMA increased almost equally for both the arsenic-exposed and control subjects. 2) The exposed subjects had a greater urinary excretion of total arsenic, before and after DMPS administration, than the control subjects. 3) Although buccal cells were obtained only from a few subjects, the prevalence of mononucleated buccal cells, an indication of genotoxicity, was 5-fold greater for those who consumed drinking water with the higher arsenic content than among control subjects. Our conclusions are that 1) DMPS has a highly specific effect in humans on MMA metabolism and/or urinary excretion; 2) the human body stores substantial amounts of arsenic; and 3) the urinary arsenic concentration after DMPS administration may be more indicative of the body burden of arsenic because it was greater than that found before DMPS was given.

Adult↗
PubMed1996

Congenital factor VII deficiency in a patient with an abdominal aortic aneurysm.

A patient with congenital factor VII deficiency underwent surgery for an inflammatory abdominal aortic aneurysm. No references in the literature have been found on the management of this coagulation defect in patients who require vascular surgery. We present one such case, with special reference to the perioperative management of factor VII replacement therapy.

Aged↗
PubMed1996

Ifosfamide and cisplatin as neoadjuvant chemotherapy for advanced cervical carcinoma.

A phase II trial was performed to evaluate the efficacy and toxicity of a combination of cisplatin (CDDP) and ifosfamide (IFX) as neoadjuvant chemotherapy in advanced cervical carcinoma (ACC). Between August 1991 and September 1993, 57 untreated patients with stages IIB to IVA were entered into this study. Median age was 44 years (range, 25 to 74 years). The distribution by stages (International Federation of Gynecology and Obstetrics) was as follows: IIB, 31 patients; IIIB, 21 patients; and IVA, 5 patients. Therapy consisted of IFX 2000 mg/m(2) 1-h i.v. infusion days 1 to 3; mesna 400 mg/m(2) i.v. bolus at hours 0 and 4, and 800 mg p.o. at hour 8; and CDDP 100 mg/m(2) on day 3. Cycles were repeated every 28 days for a total of three courses. Both staging and response assessment were performed by a multidisciplinary team. An objective response was observed in 30 of 56 patients (54%; 95% confidence interval, 41 to 67%). Four patients (7%) had a complete response (CR) and 26(46%) had a partial response (PR). Patients with CR or operable PR underwent surgery, otherwise received definitive radiotherapy. Toxicity was mild to moderate. There were no toxicity related deaths. These results indicate that IFX/CDDP is an active combination for ACC with mild toxicity. The results of phase III studies that evaluate the real impact of neoadjuvant chemotherapy are awaited.

Adult↗
PubMed1996

Parents' evaluations of wheezing in their children with asthma.

OBJECTIVE: Wheezing is a widely used physical sign of asthma that physicians assess in evaluation of their asthmatic patients. It may be possible to teach the parents to recognize it and to assess its severity so as to help them make better informed judgment in monitoring their children with asthma. STUDY DESIGN: Parents were taught to recognize wheezing by placing their ear over the chest and in front of the open mouth of their child. One session lasting a few minutes was sufficient for teaching. Subsequently, the parent and a physician evaluated the child independently for the presence and the severity of wheezing categorized as easily, barely, and none detected, and results were compared. Severity of wheezing was also compared with peak expiratory flow rate (PEFR) whenever possible. RESULTS: Six hundred thirty-six observations were made in 89 parent-child pairs. Wheezing was detected by the physician in 64% of examinations and by the parents in 56% (p < 0.001 by chi 2). When the physician heard the wheezing easily on 240 occasions, the parents also heard it in 99%. When the physician heard the wheezing barely on 170 occasions, the parents heard it only on 68% of the time. Mean PEFR was 55% predicted when the parents heard the wheezing easily, 75% when heard barely, and 93% when not heard (the difference is significant, p < 0.001 by analysis of variance). CONCLUSIONS: Parents can be taught to detect wheezing in their child with considerable accuracy when it is easily detectable to a physician. Such skills should be helpful to the parents in monitoring their child with asthma and in deciding when to increase medications and when to seek emergency care.

Adolescent↗