Biomedical subjects

N Vincent

Publications and source records attributed to N Vincent.

At least 19 recordsLinked to original sources

PubMed2001

Treatment preference and patient satisfaction in chronic insomnia.

STUDY OBJECTIVES: The purposes of this study were to examine treatment preference and satisfaction with group treatment in individual with chronic insomnia. DESIGN: Correlational. SETTING: The study was conducted in an outpatient hospital setting. PATIENTS OR PARTICIPANTS: Participants were 43 adult volunteers from the community. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Prior to treatment, participants were presented with descriptions of behavioral and pharmacological treatment for the problem of insomnia and asked to rate the acceptability, presumed effectiveness, and presumed side-effects of treatment. A sub-sample of these individuals (n = 37) participated in a 6-week cognitive behavioral treatment group for insomnia. Sleep diary and questionnaire data were collected prior to and following treatment. Results showed that cognitive-behavioral therapy was significantly preferred over pharmacological therapy at pre-treatment and that more favorable assessments of cognitive-behavioral therapy at pre-treatment were associated with better adherence but not improved outcome. Of treatment techniques, participants least liked sleep restriction and most liked sleep hygiene. Results indicated that more favorable ratings of the usefulness of sleep restriction were associated with improvements in sleep efficiency, sleep-related impairment, and quality of life. CONCLUSIONS: Implications of these findings are that patient preference is important to assess prior to treating insomnia and that more work may be needed to increase patients' awareness of the benefits of sleep restriction.

Adult↗

PubMed2001

Anxiety sensitivity: predictor of sleep-related impairment and medication use in chronic insomnia.

The relationship between anxiety sensitivity and sleep was investigated in a sample of 53 adults with chronic insomnia. Using hierarchical regression analyses, and after controlling for the propensity to worry and the presence of psychiatric comorbidity, results showed that anxiety sensitivity reliably improved the prediction of sleep-related impairment and frequency of hypnotic medication use, but not actual sleep disturbance. Specifically, fear of cognitive dyscontrol was associated with greater sleep-related impairment. There was a trend towards fear of physical distress predicting more frequent medication use. Implications of these findings for the treatment of insomnia are discussed and suggestions for future research are made.

Adult↗

PubMed2001

14 years of therapeutic plasma exchange in France.

The French Registry for plasma exchange (PE) was set up in 1985. For 14 years it has allowed analysis of the techniques used along with the indications and complications. Recent analysis shows a slight fall in activity as some studies have ended, while the neurological disorders remain the most frequent indications for PE. The important changes observed over the years are the increased use of the centrifugation technique, the development of plasma and whole blood treatment and plasma substitution using a mixture of albumin and pentastarch. The French Registry for PE is the largest such database which, along with the Canadian Registry for therapeutic hemapheresis, allows both retrospective and prospective studies.

Anticoagulants↗

PubMed1999

Treatment preference in hypochondriasis.

Promising cognitive-behavioral and medication treatments for hypochondriasis are in the early stages of evaluation. Little is known about the treatment preferences and opinions of individuals seeking help for this problem. In this exploratory study, 23 volunteers from the community with a DSM-IV diagnosis of hypochondriasis were recruited through a newspaper advertisement. Participants were presented with a survey which included balanced descriptions of both a medication and a cognitive-behavioral treatment for intense illness concerns (hypochondriasis). The brief descriptions of the treatments discussed the time commitment required as well as the major advantages and disadvantages of each. Results showed that, relative to medication treatment, cognitive-behavioral treatment was predicted to be more effective in both the short and long terms and was rated as more acceptable. Psychological treatment was indicated as the first choice by 74% of respondents, medication by 4%, and 22% indicated an equal preference. Forty-eight percent of respondents would only accept the psychological treatment.

Adult↗

PubMed1998

Presence of a gene encoding choline sulfatase in Sinorhizobium meliloti bet operon: choline-O-sulfate is metabolized into glycine betaine.

Glycine betaine is a potent osmoprotectant accumulated by Sinorhizobium meliloti to cope with osmotic stress. The biosynthesis of glycine betaine from choline is encoded by an operon of four genes, betICBA, as determined by sequence and mutant analysis. The betI and betC genes are separated by an intergenic region containing a 130-bp mosaic element that also is present between the betB and betA genes. In addition to the genes encoding a presumed regulatory protein (betI), the betaine aldehyde dehydrogenase (betB), and the choline dehydrogenase (betA) enzymes also found in Escherichia coli, a new gene (betC) was identified as encoding a choline sulfatase catalyzing the conversion of choline-O-sulfate and, at a lower rate, phosphorylcholine, into choline. Choline sulfatase activity was absent from betC but not from betB mutants and was shown to be induced indifferently by choline or choline-O-sulfate as were the other enzymes of the pathway. Unlike what has been shown in other bacteria and plants, choline-O-sulfate is not used as an osmoprotectant per se in S. meliloti, but is metabolized into glycine betaine. S. meliloti also can use this compound as the sole carbon, nitrogen, and sulfur source for growth and that depends on a functional bet locus. In conclusion, choline-O-sulfate and phosphorylcholine, which are found in higher plants and fungi, appear to be substrates for glycine betaine biosynthesis in S. meliloti.

Amino Acid Sequence↗

PubMed1998

Distribution of phosphate-activated glutaminase isozymes in the chicken: absence from liver but presence of high activity in pectoralis muscle.

The distribution of glutaminase expression in a uricotelic species, the chicken, has been examined using cDNA probes to the rat isozymes. The results suggest that chickens do not possess a glutaminase isozyme equivalent to the liver-type isozyme of mammalian liver. Measurements of enzymic activity also showed very low glutaminase activity in chicken liver. Extra-hepatic tissues in the chicken do express a glutaminase isozyme mRNA which is detected by rat kidney-type glutaminase cDNA. The abundance of this mRNA was highest in kidney and breast muscle and relatively abundant in brain, spleen and adipose tissue. Chicken small intestine expressed relatively low levels of the mRNA. The high level of glutaminase mRNA in chicken pectoralis muscle was accompanied by high glutaminase enzymic activity. In contrast, in mixed leg muscle glutaminase mRNA was barely detectable by Northern blot and glutaminase activity was relatively low. Starvation for 48 h resulted in a slight decrease in the activity of glutaminase in pectoralis muscle, but a large decrease in the relative abundance of the mRNA. The results suggest that in the chicken, hepatic glutamine hydrolysis is not quantitatively important, but skeletal muscle may be a major site of glutamine catabolism.

Animals↗

PubMed1997

Rat hepatic glutaminase: identification of the full coding sequence and characterization of a functional promoter.

Glutamine catabolism in mammalian liver is catalysed by a unique isoenzyme of phosphate-activated glutaminase. The full coding and 5' untranslated sequence for rat hepatic glutaminase was isolated by screening lambda ZAP cDNA libraries and a Charon 4a rat genomic library. The sequence produces a mRNA 2225 nt in length, encoding a polypeptide of 535 amino acid residues with a calculated molecular mass of 59.2 kDa. The deduced amino acid sequence of rat liver glutaminase shows 86% similarity to that of rat kidney glutaminase and 65% similarity to a putative glutaminase from Caenorhabditis elegans. A genomic clone to rat liver glutaminase was isolated that contains 3.5 kb of the gene and 7.5 kb of the 5' flanking region. The 1 kb immediately upstream of the hepatic glutaminase gene (from -1022 to +48) showed functional promoter activity in HepG2 hepatoma cells. This promoter region did not respond to treatment with cAMP, but was highly responsive (10-fold stimulation) to the synthetic glucocorticoid dexamethasone. Subsequent 5' deletion analysis indicated that the promoter region between -103 and +48 was sufficient for basal promoter activity. This region does not contain an identifiable TATA element, indicating that transcription of the glutaminase gene is driven by a TATA-less promoter. The region responsive to glucocorticoids was mapped to -252 to -103 relative to the transcription start site.

Amino Acid Sequence↗

PubMed1997

Robot nurses.

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Ethics, Nursing↗

PubMed1996

The geometric structure, construction, and interpretation of path-following (trail-making) tests.

Diagnostic comparisons of performance on parts A and B of the Trail Making Test (TMT) assume that path structure in the two parts is equivalent but that task complexity is greater for B. The two parts are shown to differ with respect to length and angular variability. However, measures of fractal dimension show no difference in structural complexity between paths A and B. This analysis suggests a principled method for generating alternative pathways, varying in complexity, and opens the way for a systematic study of path-following. It also suggests that path-following may be interpretable within a general approach, in which perceptual, linguistic, reasoning and motor processes are seen as related through different groups of geometric transformations.

Adult↗

PubMed1994

Transcriptional control of rat hepatic glutaminase expression by dietary protein level and starvation.

Mammalian liver possesses a unique isozyme of phosphate-activated glutaminase that is subject to long-term regulation. In rats during starvation or after consumption of diets containing high amounts of protein (60%), hepatic glutaminase activity was 100% higher than in rats fed a 20% protein diet. Conversely, rats fed low protein diets (0 and 5%) had lower hepatic glutaminase activity when compared with rats fed the 20% protein diet. Differences in activity with different dietary protein levels were not due to differences in the amount of food consumed. The relative abundance of mRNA encoding hepatic glutaminase was lower in rats fed 0% protein and higher in those starved or fed 60% protein diet when compared with rats fed the 20% protein diet. The mRNA elongation assay in hepatic nuclei isolated from these animals demonstrated that the rate of transcription of the glutaminase gene was also different in rats starved or fed different levels of dietary protein. Overall, the results indicate that differences in hepatic glutaminase activity in rats starved or fed different levels of protein are mainly due to differences in the rate of transcription of the gene. In this way the regulation of hepatic glutaminase expression is similar to that seen for other enzymes involved in hepatic amino acid catabolism but differs markedly from that of renal glutaminase, in which changes in transcription rate are not observed and alterations of mRNA turnover are the principle mechanism of long-term regulation.

Animals↗

PubMed1994

Adenovirus-mediated transfer of a human dystrophin gene to skeletal muscle of mdx mouse.

Due to their quiescent nature and spatial complexity, many target tissues for gene therapy will require novel strategies. An alternative to ex vivo gene transfer, providing many technical advantages and possibly allowing sufficient transfer of the therapeutic gene, is direct in vivo delivery of the vehicle. For a favorable outcome, this procedure is dependent on a high-titer vector, fully competent before post-mitotic cells. In view of the restrictions with the use of retroviruses, we investigated the potentials of adenovirus. Adenoviruses have as primary targets of infection the differentiated epithelial cell. The large DNA genome of the virus hints to a large cloning capacity. Furthermore, the wild type adenovirus has been largely used in man as a vaccine against adenovirus-induced respiratory disease. Taken together, the biological characteristics of adenovirus and the precedent of administration to humans are suggestive of adenovirus-based gene therapy for diseases involving a variety of quiescent tissues. The use of a replication-defective adenovirus carrying a gene encoding a nuclearly-targeted beta-galactosidase Ad.RSV beta gal demonstrated that replication-defective adenovirus offers an efficient means to transfer a gene for extended periods of time in the liver, muscle, lung and brain (1-6).

Adenoviridae↗

PubMed1993

Efficient adenovirus-mediated transfer of a human minidystrophin gene to skeletal muscle of mdx mice.

Duchenne progressive muscular dystrophy is a lethal and common X-linked genetic disease caused by the absence of dystrophin, a 427K protein encoded by a 14 kilobase transcript. Two approaches have been proposed to correct the dystrophin deficiency in muscle. The first, myoblast transfer therapy, uses cells from normal donors, whereas the second involves direct intramuscular injection of recombinant plasmids expressing dystrophin. Adenovirus is an efficient vector for in vivo expression of various foreign genes. It has recently been demonstrated that a recombinant adenovirus expressing the lac-Z reporter gene can infect stably many mouse tissues, particularly muscle and heart. We have tested the ability of a recombinant adenovirus, containing a 6.3 kilobase pair Becker-like dystrophin complementary DNA driven by the Rous sarcoma virus promoter to direct the expression of a 'minidystrophin' in infected 293 cells and C2 myoblasts, and in the mdx mouse, after intramuscular injection. We report here that in vivo, we have obtained a sarcolemmal immunostaining in up to 50% of fibres of the injected muscle.

Adenoviridae↗

PubMed1993

A simple model for alanine metabolism in isolated rat hepatocytes.

A simple model describing reactions of alanine metabolism in isolated hepatocytes from fasted rats is proposed and applied to radioactive data obtained in experiments in which L-[1-14C]-, L-[2-14C]-, L-[3-14C]-, and L-[U-14C]alanine as well as L-alanine plus NaH14CO3 were used as substrates in parallel. Measurements of the rates of incorporation of the label into glucose and CO2 and of accumulation of [1-14C]pyruvate, [1-14C]lactate, [1-14C]alanine and [1-14C]glutamate plus [1-14C]glutamine from the different substrates used allows to calculate flux of alanine carbon through the various metabolic steps taken into account in the model. The validity of this model is indicated by the agreement found between calculations and measurement of the 14CO2 released from [1-14C]alanine as well as between the values of flux through pyruvate carboxylase calculated in two different ways. It is shown that the oxaloacetate synthesized by pyruvate carboxylase enters into the Krebs cycle and into the pathway of phosphoenolpyruvate synthesis in about equal proportions and that about 40% of the oxaloacetate synthesized as a result of alanine metabolism is derived from the Krebs cycle operation. These results, together with the conclusion that flux of alanine carbon through pyruvate dehydrogenase is negligible, are in agreement with known characteristics of hepatic alanine metabolism in the fasted state and, therefore, provide further evidence for the validity of the model proposed in the present study.

Alanine↗

PubMed1993

Long-term correction of mouse dystrophic degeneration by adenovirus-mediated transfer of a minidystrophin gene.

Duchene muscular dystrophy (DMD) is a fatal progressive X-linked muscle disorder, caused by mutations in the dystrophin gene. We have investigated adenovirus-mediated transfer of a dystrophin minigene in a mutant mouse lacking dystrophin, the mdx mouse. We report here that six months after a single intramuscular injection of a recombinant adenovirus containing a human dystrophin minigene, a large number of dystrophin-positive fibres are still detected in the injected muscles. Moreover, although the minigene encodes a truncated protein, its expression is able to protect the fibres efficiently against the degeneration process that affects the dystrophin-deficient mdx myofibres.

Adenoviridae↗

PubMed1993

Congenital longitudinal deficiency of the fibula (fibular hemimelia). Parental refusal of amputation.

Fibular hemimelia with significant limb-length inequality is usually best treated with foot ablation and prosthetic fitting. Parents tend to be reluctant to agree to allow their child's foot to be amputated at an early age, especially when the foot is near normal and the limb length is not grossly abnormal. Experience with some families of children with fibular hemimelia who initially refused amputation of the affected limb prompted a retrospective review of the treatment experience with these children. Twenty-four children with 36 affected limbs were treated during the last three decades. Amputation of the foot was performed for 16 limbs in 12 of the 24 patients. The 12 patients whose limbs were not amputated were reviewed in detail. Six of these children were advised to have an amputation, but their families refused to consent. These children were managed by specially designed prostheses to incorporate their foot deformity and limb-length inequality. Four patients required subsequent corrective surgical procedures in an attempt to stabilize the feet or lengthen the limb. To facilitate treatment decisions for both the clinic team as well as the involved families, the authors propose a more practical classification of fibular hemimelia.

Abnormalities, Multiple↗

PubMed1992

Glycine, a new regulator of glutamine metabolism in isolated rat-liver cells.

Glycine (0.1-10 mM) caused a dose-dependent increase in the removal of 5 mM [1-14C]glutamine by isolated rat-liver cells; at low concentrations of glycine, an increase in the formation of 14CO2, urea and glucose from glutamine occurred. At 2-10 mM, glycine also caused an accumulation of ammonia, a well-established activator of glutaminase (E.C. 3.5.1.2) and, at concentrations found in the presence of glutamine plus glycine, ammonia stimulated glutamine removal. The inhibition of urea synthesis from glutamine observed with 10 mM glycine was relieved by the addition of ornithine, suggesting that this inhibition occurred by reducing the availability of ornithine for the ornithine transcarbamoylase reaction. The metabolism of glycine as sole substrate led to a small increase in the accumulation of ammonia. Glycine did not alter hepatic glutaminase activity but swelling of rat hepatocytes, a factor considered to stimulate glutamine metabolism, was observed in the presence of glycine (1 mM). It is concluded that stimulation by glycine of hepatic utilization of glutamine is mediated by the accumulation of ammonia arising from both glycine and glutamine metabolism and by hepatocyte osmotic swelling secondary to glycine transport.

Ammonia↗

PubMed1992

Distal transcript of the dystrophin gene initiated from an alternative first exon and encoding a 75-kDa protein widely distributed in nonmuscle tissues.

A transcript generated by the distal part of the Duchenne Muscular Dystrophy (DMD) gene was initially detected in cells where the full size 14-kilobase (kb) messenger RNA is not found at a significant level. This transcript, approximately 4.5 kb long, corresponds to the cysteine-rich and carboxyl-terminal domains of dystrophin. It begins with a novel 80- to 100-nucleotide exon containing an ATG start site for a new coding sequence of 17 nucleotides in-frame with the consecutive dystrophin cDNA sequence from exon 63. This result suggests the existence of a third promoter that would be localized about 8 kilobases upstream from exon 63 of the DMD gene. The distal transcript is widely distributed but is absent in adult skeletal and myometrial muscle. It is much more abundant in fetal tissues. With an antibody directed against the dystrophin carboxyl terminus, the protein corresponding to this transcript was detected as a 70- to 75-kDa entity on Western blots. It was found in all tissues analyzed except in skeletal muscle. It was not found in lymphoblastoid cells from a Duchenne patient with a complete deletion of the dystrophin gene. The role and subcellular localization of this protein is not known. It may explain extramuscular symptoms exhibited by some Duchenne patients.

Animals↗

PubMed1992

Release and fixation of CO2 by guinea-pig kidney tubules metabolizing aspartate.

1. The metabolism of L-[U-14C]aspartate, L-[1-14C]aspartate and L-[4-14C]aspartate was studied in isolated guinea-pig kidney tubules. 2. Oxidation of C-1 plus that of C-4 of aspartate accounted for 90-92% of the CO2 released from aspartate, whereas oxidation of the inner carbon atoms of aspartate (which occurs beyond the 2-oxoglutarate dehydrogenase step) represented only 8-10% of aspartate carbon oxidation. 3. The formation of [1-14C]glutamine and [1-14C]glutamate from [1-14C]aspartate and [4-14C]aspartate indicated that about one-third of the oxaloacetate synthesized from aspartate underwent randomization at the level of fumarate. 4. With [U-14C]aspartate as substrate, the percentage of the C-1 of glutamate and glutamine found radiolabelled after 60 min of incubation was 92.7% and 47.5% in the absence and the presence of bicarbonate respectively. 5. That CO2 fixation occurred at high rates in the presence of bicarbonate was demonstrated by incubating tubules with aspartate plus [14C]bicarbonate; under this condition, the label fixed was found in C-1 of glutamate, glutamine and aspartate, as well as in C-4 of aspartate, demonstrating not only randomization of aspartate carbon but also aspartate resynthesis secondary to oxaloacetate cycling via phosphoenolpyruvate carboxykinase, pyruvate kinase and pyruvate carboxylase. 6. The importance of CO2 fixation in glutamine synthesis from aspartate is discussed in relation to the possible role of the guinea-pig kidney in systemic acid-base regulation in vivo.

Acetazolamide↗