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Biomedical subjects

P Henry

Publications and source records attributed to P Henry.

At least 73 records · Page 4Linked to original sources
PubMed1996

[The combination of oral lysine-acetylsalicylate and metoclopramide compared with oral sumatriptan in the treatment of migraine attacks. A randomized, double-blind, placebo-controlled clinical trial].

A combination of lysine acetylsalicylate (equivalent to 900 mg aspirin) and 10 mg metoclopramide (LAS + MTC) was compared with oral sumatriptan (100 mg) and placebo in 421 patients with migraine in a randomized, double-blind, clinical trial. LAS + MTC was as effective as sumatriptan with a decrease in headache from severe or moderate to mild or none in 57% and 53%, respectively, for the first migraine attack treated, the primary efficacy parameter. Both treatments were better than placebo (success rate 24%, p < 0.001). LAS + MTC was better tolerated than sumatriptan (adverse events in 18% and 28%, respectively, p < 0.05).

Administration, Oral↗
PubMed1996

[Street pathology].

Diseases of the homeless do not constitute a nosological list. Their nature depends rather on the conditions in which the homeless live, making them susceptible to various classical diseases. Many of these disorders have otherwise become infrequent and of little concern. The "medieval" nature and intrication of these diseases should not prejudice rational diagnosis and treatment, which in the end is rather simple. The homeless live alone. This solitude if often the factor that determines management decisions of the physician.

Diagnosis↗
PubMed1996

Protein kinase C inhibition of cloned inward rectifier (HRK1/KIR2.3) K+ channels expressed in Xenopus oocytes.

1. The effect of protein kinase activators on cloned inward rectifier channels expressed in Xenopus oocytes was examined using a two-electrode voltage clamp. PKA activators caused no change in KIR1.1, KIR2.1, or KIR2.3 current. The PKC activators phorbol 12-myristate 14-acetate (PMA) and phorbol 12, 13-dibutyrate (PDBu) inhibited KIR2.3 currents, but not KIR2.1 or KIR1.1 current. This inhibition was blocked by staurosporine. An inactive phorbol ester, 4 alpha-phorbol 12, 13-didecanoate (4 alpha-PDD), had no effect on KIR2.3. 2. Upon changing solution from 2 to 98 microM K+, KIR2.3 but not KIR1.1 or KIR2.1 currents typically 'ran down' over 5 min to 60-80% of maximum amplitude. Rundown occurred even if PMA was applied before changing to high [K+] solution, indicating that rundown was independent of PKC activity. Rundown was evoked by substituting NMG+ for Na+, showing that it results from low [Na+] and not from high [K+]. 3. These results suggest that KIR2.3, but not KIR1.1 or KIR2.1, is subject to regulation, both by PKC activation and as a consequence of low [Na+]o. The difference in secondary regulation may account for specific responses to PKC stimulation of tissues expressing otherwise nearly identical KIR channels.

Animals↗
PubMed1996

WW domains of Nedd4 bind to the proline-rich PY motifs in the epithelial Na+ channel deleted in Liddle's syndrome.

The amiloride-sensitive epithelial sodium channel (ENaC) plays a major role in sodium transport in kidney and other epithelia, and in regulating blood pressure. The channel is composed of three subunits (alphabetagamma) each containing two proline-rich sequences (P1 and P2) at its C-terminus. The P2 regions in human beta and gammaENaC, identical to the rat betagammarENaC, were recently shown to be deleted in patients with Liddle's syndrome (a hereditary form of hypertension), leading to hyperactivation of the channel. Using a yeast two-hybrid screen, we have now identified the rat homologue of Nedd4 (rNedd4) as the binding partner for the P2 regions of beta and gammarENaC. rNedd4 contains a Ca2+ lipid binding (CaLB or C2) domain, three WW domains and a ubiquitin ligase (Hect) domain. Our yeast two-hybrid and in vitro binding studies revealed that the rNedd4-WW domains mediate this association by binding to the P2 regions, which include the PY motifs (XPPXY) of either betarENaC (PPPNY) or gammarENaC (PPPRY). SH3 domains were unable to bind these sequences. Moreover, mutations to Ala of Pro616 or Tyr618 within the betarENaC P2 sequence (to PPANY or PPPNA, respectively), recently described in Liddle's patients, led to abrogation of rNedd4-WW binding. Nedd4-WW domains also bound to the proline-rich C-terminus (containing the sequence PPPAY) of alpharENaC, and endogenous Nedd4 co-immunoprecipitated with alpharENaC expressed in MDCK cells. These results demonstrate that the WW domains of rNedd4 bind to the PY motifs deleted from beta or gammaENaC in Liddle's syndrome patients, and suggest that Nedd4 may be a regulator (suppressor) of the epithelial Na+ channel.

Amino Acid Sequence↗
PubMed1996

[Mechanisms of atrial fibrillation. Recent progress and therapeutic implications].

Atrial fibrillation is usually due to multiple microreentry circuits. However, in some cases, the initial arrhythmia inducing the atrial fibrillation may be an abnormal automatism, or a macroreentry. The initial abnormalities may induce a desynchronization due to multiple macroreentry circuits. The main factors of atrial vulnerability are intraatrial conduction disturbances and changes in refractory periods. Critical mass and effects of autonomic nervous system may also play a role. Shortened refractory periods and decreased conduction velocity imply a short wavelength and an important arrhythmogenic risk. On the other hand, the longer the duration of atrial fibrillation, the more refractory periods will shorten and the more atrium will become vulnerable: atrial fibrillation tends to beget atrial fibrillation because of an electrophysiologic remodelage. In some cases atrial fibrillation, if its duration is long and if its rate is high, may be responsible for the development of a tachycardiomyopathy. The knowledge of atrial fibrillation mechanism may have interesting therapeutic implications such as resynchronization of the atria by stimulation or ablation, for example in the approaches comparable to the maze operation.

Arrhythmias, Cardiac↗
PubMed1996

Effects of central dopaminergic stimulation by apomorphine on swallowing disorders in Parkinson's disease.

Swallowing disorders are common in Parkinson's disease but are of obscure and complex nature and pathophysiology. The effect of central dopaminergic stimulation on disordered swallowing is not well known. We studied the effects of apomorphine (in combination with domperidone) on buccolinguofacial motoricity and on various swallowing stages by using videofluoroscopy in eight patients with dysphagia. Swallowing abnormalities more frequently encountered were vallecular stasis (n = 7), fragmentation of the bolus (n = 7), and buccal stagnation of the bolus. Apomorphine improved vallecular stasis and fragmentation in about half the cases and improved buccal stagnation in all cases. Direct laryngeal penetration was found in three cases and improved in two of them. The total swallowing duration was improved by apomorphine in a subset of patients (n = 5). This improvement correlated with an improvement of the buccolinguofacial motoricity and was combined with an improvement of pharyngeal transit time. Thus central dopaminergic stimulation by apomorphine improved swallowing in a subgroup of patients, mainly in its early stages.

Aged↗
PubMed1996

Pain in multiple system atrophy.

Pain is a recognized feature of idiopathic Parkinson's disease (IPD) but has never been studied in multiple system atrophy (MSA), the commonest cause of atypical parkinsonism. We retrospectively analysed histories of pain in 100 consecutive cases of clinically probable MSA. Details were obtained from the medical records of 100 patients with MSA, comprising 82 with the striatonigral degeneration (SND) type and 18 with the olivopontocerebellar atrophy (OPCA) type of MSA. Pain was reported in 47% of the MSA patients. It was classified as rheumatic in 64% of MSA patients reporting pain, sensory in 28%, dystonic in 21%, and levodopa-related in 16%, mostly related to off-period or diphasic dystonias. There was a mixed pain syndrome in 19% of these patients. Pain was significantly more commonly reported by females (P = 0.02), and by patients with levodopa-induced dyskinesias (P = 0.02). No other clinical feature differentiated MSA patients who reported pain from those who did not. The mean delay between disease onset and onset of pain was 2.9 years, but pain was reported at the time of, or before, disease onset in about 30% of patients. The overall prevalence of pain in MSA was similar to that reported in IPD, but the distribution of pain categories was different.

Adult↗
PubMed1996

MIG ACCESS: a population-based, nationwide, comparative survey of access to care in migraine in France.

A national control-matched survey was conducted in France to evaluate the access of migraineurs to health care. A validated IHS criteria-based diagnostic procedure for screening was conducted in adults drawn from a sample of 6,000 households. A group of 650 subjects fulfilling the IHS criteria for migraine were matched by sex, age and activity status with a group of non-headache, non-migraine controls. Response rates were 87% and 82% for the migraineurs and the controls, respectively. The comparability of the groups was demonstrated by the absence of statistical differences between either respondents versus non-respondents or migraineurs versus controls for sex, age and occupation. The 3-month prevalence of migraine was estimated at 13% (95% CI: 12-14). The health care consumption of migraineurs was not higher than that of the controls. Migraineurs rarely consult for headaches and seem to content themselves with their routine analgesic treatment. They believe, however, that improvement in their condition is possible and discuss this with their physicians. This ambivalent attitude mainly reflects a fatalistic outlet which may constitute the major obstacle of an improved management of migraine.

Adolescent↗
PubMed1996

Method for quantitation of low-abundance nerve growth factor mRNA expression in human nervous tissue using competitive reverse transcription polymerase chain reaction.

Nerve growth factor (NGF) is a polypeptide hormone important for the development, function, and survival of neurons. NGF is an important target for investigation because of its potential therapeutic importance in neurological diseases and injury, yet its low level of expression in nervous tissue makes it difficult to measure. We report here the development of a quantitative assay for human NGF mRNA, using competitive reverse transcription polymerase chain reaction (cRT-PCR), with mouse submandibular gland mRNA as an internal standard. Exhibiting high homology to the human transcript, mouse NGF mRNA is co-amplified with the human NGF transcript through both the reverse transcription and PCR steps using identical primers and conditions. Products are distinguished by a convenient unique restriction site in the mouse transcript. Phosphorimage detection and quantitation of radiolabeled product provides femtogram sensitivity. Generation of a standard curve from a dilution series of mouse mRNA allows the amount of co-amplified human NGF mRNA transcripts to be determined. We demonstrate the amplification and quantitation of human NGF mRNA from 175-350 nanograms of poly(A)+mRNA from human frontal and parietal cortex. This technique is ideal for rapid detection and quantitation of low-abundance NGF mRNA from limited amounts of tissue.

Animals↗
PubMed1996

Adenosine A1 stimulation activates delta-protein kinase C in rat ventricular myocytes.

By making use of immunoblotting and immunocytochemical analysis, we explored whether stimulation of adenosine A1 receptors would promote the activation of delta-protein kinase C (delta-PKC) immunolabeled with a polyclonal antibody. Immunoblot analysis of Triton X-100-soluble cell membrane and cytosolic fractions revealed the presence of a specific 75-kD band reactive to the delta-PKC polyclonal antibody. In freshly isolated rat cardiac myocytes, 28% of the total immunoreactive delta-PKC was associated with the membrane fraction, whereas 72% was associated with the soluble fraction. Under stimulation with the tumor-promoting phorbol 12-myristate 13-acetate (PMA, 50 nmol/L) used as a positive control, delta-PKC translocated to the cell membrane, with the membrane fraction representing 88% and the cytosolic fraction representing 12% of the total immunoreactive delta-PKC. Transverse optical sections performed with confocal laser microscopy showed that immunostaining with anti-delta-PKC antibody was distributed in the cytosol membrane under PMA stimulation. In the membrane fraction of cells pretreated with adenosine (100 mumol/L) or with the adenosine A1 agonist (--)-N6-(2-phenylisopropyl)-adenosine (R-PIA, 1 mumol/L), the 75-kD band corresponding to delta-PKC increased by 57% and 66%, respectively, when compared with nonstimulated cells processed under the same experimental conditions. In cells exposed to either of the purine agonists, specific fluorescence staining decorated the cell membrane, a pattern that was not observed in control cells. Activation of membrane delta-PKC produced either by adenosine itself or by its analogue R-PIA was fully antagonized by the specific A1 antagonist 8-cyclopentyl-1,3-dipropylxanthine (1 mumol/L). From these data, we conclude that adenosine A1 stimulation activates delta-PKC in freshly isolated rat ventricular myocytes.

Adenosine↗
PubMed1996

Perceived problem-solving and vocational identity: implication for nontraditional premedical students.

The purpose of this study was to examine the relationship between vocational identity and self-appraised problem solving. A total of 86 students enrolled in a special program took the Vocational Identity subscale of My Vocational Situation and the Problem Solving Inventory one week apart. Pearson product-moment correlations indicated a relationship between personal problem-solving appraisal and vocational identity, suggesting the inventories assess one construct. Implications for intervention strategies for the present population are discussed.

Adult↗
PubMed1996

Effects of U-74389G, a novel 21-aminosteroid, on small intestinal ischemia and reperfusion injury in horses.

OBJECTIVE: To determine the effects of the 21-aminosteroid, U-74389G, on reperfusion of the equine jejunum, using total (TVO) and partial (PVO) vascular occlusion during the ischemic period. DESIGN: TVO: 16 healthy horses were randomly allotted to 3 groups-4 horses received the vehicle alone, 6 horses received a low dosage (3 mg/kg o body weight), and 6 horses a high dosage (10 mg/kg) of U-7438G. PVO: 10 healthy horses were randomly allotted to 2 groups--5 horses received the vehicle alone, and 5 horses received the low dosage (3 mg/kg) of U-74389G. PROCEDURES: TVO was induced for 1 hour followed by 2 hours of reperfusion. During PVO, blood flow was reduced to 20% of baseline for 2 hours, followed by 2 hours of reperfusion. For both models, either the vehicle alone or the drug was given 15 minutes prior to reperfusion. Samples were obtained before, during, and after ischemia for determination of myeloperoxidase (MPO) activity, malondealdehyde (MDA) concentration, concentration of conjugated dienes (PVO experiment only), and morphometric analysis. RESULTS: TVO: tissue concentration of MDA and MPO activity were not altered in any group by ischemia or reperfusion. During ischemia, mucosal volume and surface area were reduced. After reperfusion, no further reduction occurred. After initial decrease in submucosal volume during ischemia, there was a significant increase after reperfusion in the vehicle-only group (P < 0.05). PVO: there were no alterations in the concentration of either MDA or conjugated dienes. There was significant increase in the activity of MPO during ischemia and reperfusion (P < 0.05). These effects were similar for the vehicle-only and drug groups. During ischemia, there was a significant decrease in mucosal surface area and volume (P < 0.05), that was continued during reperfusion for the vehicle-only (P < 0.05). Submucosal volume increased during ischemia and reperfusion. CONCLUSIONS AND CLINICAL RELEVANCE: Reduced blood flow during ischemia (PVO group) caused continued loss in mucosal volume and surface area during reperfusion. At the dosage given, the 21-aminosteroid, U-74389G, was not effective in preventing continued reduction in mucosal volume and surface area after restoration of blood supply in the horses subjected to reduced blood flow.

Animals↗
PubMed1996

Acute simulated ischaemia produces both inhibition and activation of K+ currents in isolated ventricular myocytes.

OBJECTIVE: The aim was to investigate the effects of acute ischaemia on cardiac repolarizing K+ currents. METHODS: We developed a model of acute ischaemia in isolated rat ventricular myocytes transiently surrounded with a mineral oil droplet. During ischaemic challenges, we recorded intracellular pH using the fluorescent probe seminaphthorhodafluor-1 (SNARF-1) and whole-cell K+ currents using the patch-clamp technique. RESULTS: Decrease in intracellular pH (pH1) during simulated ischaemia was dependent upon the extracellular proton buffer used (pH1 decreased from 7.44 +/- 0.02 to 7.16 +/- 0.04 in a Hepes-buffered medium and from 7.08 +/- 0.04 to 6.56 +/- 0.07 with bicarbonate buffer). In Hepes, action potential duration initially lengthened and then shortened under the effects of ischaemia. Initial action potential duration lengthening was concomitant with a block of the inward rectifier K+ current, whereas late shortening corresponded with the activation of the ATP-sensitive K+ current. Similar changes occurred in bicarbonate buffer although with different amplitudes and kinetics. Patch-clamp experiments also showed inhibition of the transient outward K+ current. Brief transient episodes of ischaemia activated ATP-sensitive K+ current in only 20% of control cells (n = 21) but in 100% of cells treated with 15 microM cromakalim (n = 9). CONCLUSIONS: (i) Simulated ischaemia produces complex effects on repolarizing K+ currents including both inhibition and activation; (ii) cromakalim accelerates activation of ATP-sensitive K+ current during simulated ischaemia.

Action Potentials↗
PubMed1995

The effectiveness of combined oral lysine acetylsalicylate and metoclopramide compared with oral sumatriptan for migraine.

Aspirin is commonly used to treat migraine attacks, although sumatriptan, a much more expensive treatment, is also effective. We compared a combination of lysine acetylsalicylate (equivalent to 900 mg aspirin) and 10 mg metoclopramide (LAS+MTC) with oral sumatriptan (100 mg) and placebo in 421 patients with migraine. LAS+MTC was as effective as sumatriptan with a decrease of headache from severe or moderate to mild or none of 57% and 53%, respectively, for the first migraine attack treated. Both treatments were better than placebo (success rate 24%, p < 0.0001). LAS+MTC was significantly more effective in the treatment of nausea than sumatriptan (p < 0.0001) and was better tolerated (adverse events in 18% and 28%, respectively, p < 0.05). LAS+MTC is as effective as sumatriptan in the treatment of migraine attacks. It is also much cheaper.

Administration, Oral↗
PubMed1995

[Efficacy and tolerance of an effervescent aspirin-metoclopramide combination in the treatment of a migraine attack. Randomized double-blind study using a placebo].

OBJECTIVES: A double blind, randomized, multicenter, parallel group study was carried out to compare the efficacy and tolerance of aspirin 900 mg-metoclopramide 10 mg effervescent association (AAM) with those of placebo in the treatment of acute migraine attack. All patients were selected according to the International Headache Society criteria. METHODS: A total of 303 out-patients with an acute migraine attack were treated orally with either AAM (n = 152) or placebo (n = 151). RESULTS: The aspirin-metoclopramide association was significantly more effective than placebo at relieving headache (principal criterion) within 2 h of treatment (54.3% versus 25.9% : p < 0.001), producing entire resolution of acute migraine attack (14.2% versus 5.3% : p = 0.017), reducing the percentage of patients requiring rescue medication (44.3% versus 63.2% : p = 0.001) and increasing the percentage of patients able to resume their usual activities (44.1% versus 22.1% : p = 0.003). AAM also provided more frequent relief from associated symptoms as compared with placebo (37.4% versus 22.1% : p = 0.006). The therapeutic efficacy was rated as good or excellent by 39.7% of patients in the AAM group compared with 20.7% in the placebo group (p < 0.001). Moreover 64.2% of AAM treated patients said they would be prepared to take the treatment again compared with 46.4% who received placebo (p < 0.001). The percentage of patients reporting adverse events was not different between the two treatments (20.4% AAM versus 18.5% placebo : p = 0.684). The most commonly reported symptoms were gastro-intestinal disorders. Similar number of gastralgia occurred with AAM (n = 4) and placebo (n = 3). CONCLUSION: It is concluded that the aspirin-metoclopramide association may be used as a first intention treatment of acute migraine attack in out-patients.

Administration, Oral↗
PubMed1995

Dementia of frontal lobe type due to adult polyglucosan body disease.

We describe a patient with adult polyglucosan body disease (APBD) who presented with a dementia of frontal lobe type (FLD), with a neurogenic bladder but no symptoms of sensory motor peripheral neuropathy. Diagnosis was made from a cerebral biopsy specimen which showed an accumulation of intra-axonal polyglucosan bodies in the central nervous system. This case differs from the usual presentation, in which gait disturbance is the main symptom and diagnosis is possible by sural nerve biopsy. Little is known about the neuropsychological pattern of APBD dementia but FLD has not previously been described. APBD is a heterogeneous clinical entity of unknown cause. This diagnosis must be considered in elderly patients with dementia.

Aged↗