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Biomedical subjects

V Bernard

Publications and source records attributed to V Bernard.

At least 37 records · Page 2Linked to original sources
PubMed1996

Chromatin diminution in nematodes.

The process of chromatin diminution in Parascaris and Ascaris is a developmentally controlled genome rearrangement, which results in quantitative and qualitative differences in DNA content between germ line and somatic cells. Chromatin diminution involves chromosomal breakage, new telomere formation and DNA degradation. The programmed elimination of chromatin in presomatic cells might serve as an alternative way of gene regulation. We put forward a new hypothesis of how an ancient partial genome duplication and chromatin diminution may have served to maintain the genetic balance in somatic cells and simultaneously endowed the germ line cells with a selective advantage.

Animals↗
PubMed1996

Glial cell line-derived neurotrophic factor (GDNF) gene expression in the human brain: a post mortem in situ hybridization study with special reference to Parkinson's disease.

Glial cell line-derived neurotrophic factor (GDNF) is a potent neurotrophic factor for dopaminergic neurons. Since dopaminergic neurons degenerate in Parkinson's disease, this factor is a potential therapeutical tool that may save dopaminergic neurons during the pathological process. Moreover, a reduced GDNF expression may be involved in the pathophysiology of the disease. In this study, we tested whether altered GDNF production may participate in the mechanism of cell death in this disease. GDNF gene expression was analyzed by in situ hybridization using riboprobes corresponding to a sequence of the exon 2 human GDNF gene. Experiments were performed on tissue sections of the mesencephalon and the striatum from 8 patients with Parkinson's disease and 6 control subjects matched for age at death and for post mortem delay. No labelling was observed in either group of patients. This absence of detectable expression could not be attributed to methodological problems as a positive staining was observed using the same probes for sections of astroglioma biopsies from human adults and for sections of a newborn infant brain obtained at post-mortem. These data suggest that GDNF is probably expressed at a very low level in the adult human brain and its involvement in the pathophysiology of Parkinson's disease remains to be demonstrated. GDNF may represent a powerful new therapeutic agent for Parkinson's disease, however.

Aged↗
PubMed1996

Peri-articular injection of tenoxicam for painful shoulders: a double-blind, placebo controlled trial.

Eighty out-patients (50 F, 30 M), aged 58 +/- 12 years (range: 26-84) and weighing 72 +/- 10 kg (range: 50-97), presenting with an acute or subacute (< 3 months) episode of rotator cuff tendinitis without (n = 28) or with movement restriction (n = 52) of the shoulder and having a pain intensity of at least 4 on VAS for pain at rest or on active movement, were treated at random and in double blind conditions for 1 to 4 weeks with 1 weekly periarticular anterior injection of tenoxicam 20 mg or placebo. Tenoxicam treated patients improved more than placebo-injected patients in a statistically highly significant manner with regard to clinical index, pain on VAS during active movement and at rest, active mobility (degrees), pain or pressure and clinical global impression (assessed by investigator and patient). There was a nonsignificant opinion that placebo treated patients consumed more rescue medication. Safety assessments were not significantly better in the placebo-treated patients through local tolerability tended to be better in that group. These results indicate that tenoxicam 20 mg injected locally is effective in alleviating pain and in improving shoulder mobility in patients with a painful shoulder episode and suggest that such a treatment is safe and well tolerated. Local injection of tenoxicam seems to be a promising new treatment of acute, painful, local inflammatory processes in Rheumatology, Orthopaedics, Physical Medicine and Sports Medicine. Further studies in other pathologies are warranted.

Adult↗
PubMed1996

Phenotype of striatal cells expressing c-Fos following amphetamine treatment of rats with intrastriatal dopaminergic grafts.

Activation of the nigrostriatal dopaminergic system by psychostimulants such as amphetamine increases c-Fos expression in the striatum, mostly in the striatonigral substance P-ergic pathway. This effect is greatly reduced in the neostriatum deprived of dopaminergic afferents. Dopaminergic grafts implanted into the denervated neostriatum restore the reactivity of the striatum to amphetamine. However, the number of striatal neurons expressing c-Fos is greatly increased in the graft-bearing striatum compared with the normal striatum. We examined whether this increase in the number of c-Fos-expressing neurons corresponds to the recruitment of a new neuron population, or whether it reflects an increase in the proportion of substance P-ergic neurons exhibiting activation of c-Fos. Adult rats received a unilateral 6-hydroxydopamine lesion of the ascending dopaminergic mesotelencephalic pathway, and a suspension of embryonic mesencephalic neurons was subsequently implanted into the denervated neostriatum. Three months after implantation, animals were injected with d-amphetamine (5 mg/kg) and killed 2 h later. In the first experiment, striatal sections were processed to visualize both c-Fos protein, by immunohistochemistry, and preproenkephalin A or substance P, by in situ hybridization. In the second experiment, c-Fos and neuropeptide Y were visualized on the same sections. In addition, some sections incubated with anti-c-Fos antibody were counterstained with toluidine blue in order to determine whether cholinergic neurons were expressing c-Fos following amphetamine treatment. The density of neurons expressing c-Fos following amphetamine treatment was three-fold higher in the graft-bearing striata than in the striata of control animals. Approximately 75% of the c-Fos expressing cells were substance P-ergic in control animals whereas 6% were enkephalinergic and only a few were neuropeptide Y-ergic or cholinergic. Similar proportions were found in the graft-bearing striatum, signifying that the pattern of activation of c-fos following amphetamine administration is not changed by the graft. Thus, the increased expression of c-Fos predominantly reflects a graft-induced increase in the proportion of neurons expressing c-Fos within the same population of neurons which normally expresses c-Fos in the striatum, i.e. the striatonigral substance P-ergic neurons; there is no recruitment of a new neuronal population. This increased activation of the striatonigral substance P-ergic pathway may underlie the abnormal behavioural reactions brought about by amphetamine-induced stimulation of the implanted dopaminergic neurons.

Amphetamine↗
PubMed1995

Anatomical analysis of the neurons expressing the acetylcholinesterase gene in the rat brain, with special reference to the striatum.

The localization of the neurons expressing the acetylcholinesterase gene in the rat central nervous system was studied by in situ hybridization. The striatal and nigral neurons containing acetylcholinesterase messenger RNA were especially identified. Acetylcholinesterase messenger RNA was detected in numerous areas of the central nervous system, including cholinergic areas, like striatum, nucleus basalis of Meynert, septum and diagonal band of Broca, but also non-cholinergic areas, like the cerebral cortex, the hippocampus, the cerebellum and the raphe dorsalis. In the striatum, 75% of the neurons expressing the acetylcholinesterase gene were identified as cholinergic neurons and 25% as somatostatin-producing neurons. All dopaminergic neurons of the substantia nigra pars compacta and ventral tegmental area were demonstrated to express the acetylcholinesterase gene. Our results suggest that several neuronal populations could contribute to the presence of acetylcholinesterase in the striatum: the striatal cholinergic and somatostatin-containing interneurons, the nigral dopaminergic neurons and other neurons that may be the corticostriatal, thalamostriatal and raphe-striatal neurons. This demonstrates that, especially in the striatum, acetylcholinesterase is not a specific marker of the cholinergic neurons. The diversity of the origins of striatal acetylcholinesterase suggests a multiplicity of functions for this enzyme: besides its cholinolytic actions, it may also possibly play a non-cholinolytic role in neuromodulation.

Acetylcholinesterase↗
PubMed1995

Chronic treatment with dizocilpine maleate increases the number of striatal neurons expressing the D2 receptor gene.

N-methyl-D-aspartate antagonists have been proposed as potential therapeutic agents in different neurological diseases, including Parkinson's disease. The effects of gene expression of a chronic treatment with the non-competitive N-methyl-D-aspartate antagonist, dizocilpine maleate (0.8 mg/kg day, per os for 50 days) were analysed in rat striata. Using quantitative in situ hybridization, we measured the messenger RNA expression of the genes encoding D1, D2 dopamine receptors, N-methyl-D-aspartate receptor 1 subunit of N-methyl-D-aspartate receptor, preproenkephalin A and substance P. Chronic treatment with dizocilpine maleate induced a moderate but significant increase in messenger RNA of the N-methyl-D-aspartate receptor 1 subunit in the striatum and the adjacent cortex, suggesting an action of dizocilpine maleate in these two regions. This treatment did not induce any change in D1 receptor, preproenkephalin A or substance P messenger RNA content in the striatum, whereas D2 receptor messenger RNA was increased in the striatum of treated rats. Microscopic analysis revealed that it was the number of medium-sized neurons expressing D2 receptor messenger RNA that was significantly enhanced, while the mean amount of message per cell remained unchanged. These results demonstrate that glutamate via N-methyl-D-aspartate receptors, regulates the D2 receptor gene in striatal neurons. A chronic treatment with dizocilpine maleate increases the number of striatal neurons expressing the D2 receptor gene, suggesting a recruiting phenomenon.

Animals↗
PubMed1994

Ribosomal heterogeneity from chromatin diminution in Ascaris lumbricoides.

The genome of Ascaris lumbricoides encodes both germline- and soma-specific proteins homologous to the eukaryotic small ribosomal protein (Rp) S19. The two Ascaris homologs differ by 24 amino acid substitutions and are both components of the small ribosomal subunits. In oocytes, the germline RpS19 homolog (RpS19G) predominates. During chromatin diminution, however, the gene is eliminated from all presomatic cells, and RpS19G is replaced by the product of the somatic gene (RpS19S). Chromatin diminution in A. lumbricoides causes a change in the protein composition of ribosomes during development and represents an alternative means of gene regulation.

Amino Acid Sequence↗
PubMed1994

Extremely stable transcripts may compensate for the elimination of the gene fert-1 from all Ascaris lumbricoides somatic cells.

The single-copy gene fert-1 becomes eliminated from all somatic cells during the process of chromatin diminution in Ascaris lumbricoides var. suum. By using Northern blot and in situ hybridization techniques, we have analyzed its rather unusual expression pattern. Different splicing and 3' end formation events generate in a developmentally regulated manner various poly(A)+ and poly(A)- fert-1 RNA species. The lack of any significant open reading frame in most of its RNA products indicates that fert-1 may function as structural RNA rather than encoding a protein. Fert-1 transcripts are produced in the precursors of the gametes, but degraded at the time of meiosis and not passed on to the zygote. Embryonic transcription of fert-1 sets in as soon as the female nucleus has completed its meiosis. Our data thus demonstrate that the Ascaris transcription apparatus is active prior to the general onset of zygotic transcription, which we think takes place in the four- to six-cell-stage embryos. Upon elimination of fert-1 gene from the somatic cells, most of its transcripts disappear. Two short fert-1 RNA products, however, are stably maintained throughout development until the second larval stage, which is more than 1 month after the elimination of their coding sequences. Possible functions of fert-1 are discussed.

Amino Acid Sequence↗
PubMed1994

[Choice of the mode of stimulation after ablation of the bundle of His. Experience based on a retrospective survey of 192 patients].

A retrospective study of 192 patients centered on the outcome of supraventricular arrhythmias after catheter ablation of the atrioventricular junction provided some useful information concerning the choice of pacing mode in these patients. With the exception of atrioventricular bloc after ablation of the rapid nodal pathway where simple DDD pacing is adequate, rate adaptive pacing would seem to be essential. The VVIR mode should be the mode of choice in atrial flutter, permanent atrial fibrillation, poorly controlled atrial fibrillation and paroxysmal atrial fibrillation of elderly subjects (over 70 years) and/or of male sex, and/or complicating advanced cardiac disease (valvular, ischaemic or primary). The DDDR mode (with an algorithm to prevent endless loop tachycardia) is the mode of choice in sinus node dysfunction and/or in young patients (under 60), and/or females and/or in idiopathic arrhythmias and/or when retrograde VA conduction persists. When the pacemaker is replaced, the indication should be reviewed with respect to the outcome of the arrhythmia, which underlines the value of accurate implanted Holter systems.

Aged↗
PubMed1993

Fos immunoreactivity after stimulation or inhibition of muscarinic receptors indicates anatomical specificity for cholinergic control of striatal efferent neurons and cortical neurons in the rat.

Cholinergic neurons play a major role in the control of striatal activity via muscarinic receptors. The action of acetylcholine also appears to be dependent on the striosome-matrix compartmentalization of the striatum. This study was designed to find out whether modification of acetylcholine tone activates neurons in the striatum and forebrain of the rat. We looked for the appearance of immunoreactivity to Fos, a regulatory protein that is thought to convert synaptic signals into changes in gene expression. Pharmacological manipulation of muscarinic receptors was found to induce specific patterns of Fos immunoreactivity in distinct neuronal populations of the forebrain, including the striatum. Oxotremorine, a non-selective muscarinic agonist, induced Fos immunoreactivity in the striatum with a large predominance in striosomes (mostly in enkephalinergic neurons), in layers 4 and 6 of the cortex, and also in the piriform cortex and septum. The muscarinic agonist pilocarpine had an identical effect in the cortex, but the striosomal prevalence was less clear-cut than that observed after oxotremorine. Treatment with dopamine-depleting agents (6-hydroxydopamine or reserpine) and inhibitors of glutamate and opiate receptor (MK-801 and naloxone respectively) had no effect on the action of oxotremorine. This suggests that the induction of Fos provoked by oxotremorine does not involve dopamine, glutamate or opiates. Atropine, a non-specific muscarinic antagonist, also induced Fos immunoreactivity in the striatum but with matrix predominance (mostly in substance P neurons), as well as in the cingulate cortex, and the olfactory tubercle. Scopolamine, a muscarinic antagonist, induced Fos in both striosomal and matrix compartments in the striatum.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗