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Biomedical subjects

C Fisch

Publications and source records attributed to C Fisch.

At least 19 recordsLinked to original sources
PubMed2005

C-reactive protein mediates CD11b expression in monocytes through the non-receptor tyrosine kinase, Syk, and calcium mobilization but not through cytosolic peroxides.

OBJECTIVE: C-Reactive protein (CRP) can modulate integrin surface expression on monocytes following Fcgamma receptor engagement. We have investigated the signal transduction events causing this phenotypic alteration. METHODS: CRP-induced signalling events were examined in THP-1 and primary monocytes, measuring Syk phosphorylation by Western blotting, intracellular Ca(2+) ([Ca(2+)](i)) by Indo-1 fluorescence and surface expression of CD11b by flow cytometry. Cytosolic peroxides were determined by DCF fluorescence. RESULTS: CRP induced phosphorylation of Syk and an increase in [Ca(2+)](i) both of which were inhibitable by the Syk specific antagonist, piceatannol. Piceatannol also inhibited the CRP-induced increase in surface CD11b. In addition, pre-treatment of primary monoytes with the Ca(2+) mobiliser, thapsigargin, increased CD11b expression; this effect was accentuated in the presence of CRP but was abolished in the presence of the [Ca(2+)](i) chelator, BAPTA. CRP also increased cytosolic peroxide levels; this effect was attenuated by antioxidants (ascorbate, alpha-tocopherol), expression of surface CD11b not being inhibited by antioxidants alone. CONCLUSION: CRP induces CD11b expression in monocytes through a peroxide independent pathway involving both Syk phosphorylation and [Ca(2+)](i) release.

Antioxidants↗
PubMed2001

Induction of labour with a viable infant: a randomised clinical trial comparing intravaginal misoprostol and intravaginal dinoprostone.

OBJECTIVE: To compare the efficacy and safety of vaginal misoprostol (50 microg) with vaginal dinoprostone. DESIGN: Double-blind randomised trial. SETTING: Obstetrics Department, Poissy Hospital, France. PARTICIPANTS: 370 patients with medical indications for induction of labour. OUTCOME MEASURES: Vaginal deliveries within 24 hours, as well as time to vaginal deliveries, caesarean rates, costs, and fetal, neonatal and maternal condition. RESULTS: Compared with vaginal dinoprostone, vaginal misoprostol resulted in greater efficacy in several areas: vaginal delivery within 24 hours; time to vaginal delivery; and vaginal delivery within 12 hours. There was a non-significant increase in the caesarean section rate for fetal distress in the misoprostol group, but fewer caesarean sections for failed induction. Fetal tolerance was similar in the two groups, although significantly more neonates had a cord pH <7.20 and (non-significantly) none had meconium stained amniotic fluid in the misoprostol group. The incidence of poor neonatal outcome was similar in both groups. Subgroup analysis by indication for induction showed that the higher rates of arterial cord pH <7.20 and of meconium-stained amniotic fluid with misoprostol persisted only in possible fetal compromise. Poor neonatal outcome was less frequent in the misoprostol group in cases of induction for non-fetal indications. CONCLUSIONS: Vaginal misoprostol resulted in successful and earlier induction of labour more often than dinoprostone, but the safety of misoprostol raises some concern in potentially compromised infants. Misoprostol should be preferred to dinoprostone in cases of induction for non-fetal indications.

Administration, Intravaginal↗
PubMed2000

Centennial of the string galvanometer and the electrocardiogram.

This article is a review of the history of the string galvanometer and of the electrocardiogram (ECG) on the occasion of the centennial of the instrument. Einthoven most likely developed the string galvanometer prior to 1901, the date of the first publication. The galvanometer made electrocardiography practical creating a new branch of medicine and even a new industry. In 1791 Galvani, in 1842 Mateucci and in 1855 Kolliker and Muller recorded, using the nerve muscle preparation, contraction of injured muscle, contraction of muscle when laid across a beating heart, and occasionally two contractions. In 1872 Lippmann introduced the capillary manometer. Using the capillary manometer Waller recorded for the first time from body surface voltage changes generated by the heart. Einthoven and Lewis dominated the early years of electrocardiography. The former made his contributions by 1913 while Lewis continued the studies of arrhythmias until 1920. The period following 1920 was influenced largely by Wilson. None did as much to advance ECG knowledge as did Wilson. The interest shifted to the theory of the ECG, abnormalities of wave form and of ECG leads. A major contribution of the ECG is in evaluation of ischemic heart disease and cardiac arrhythmias. Issues facing electrocardiography in the year 2000 include a shortage of experienced electrocardiographers, the advent of new noninvasive procedures and, paradoxically, wide acceptance of the ECG by the medical profession. The role of the computer in analysis of the clinical ECG is limited. The technique, while reasonably reliable for analysis of the normal tracing and some ECG waveforms, has serious limitations when applied to arrhythmias. The early hopes for "stand-alone" programs are yet to be realized.

Cardiology↗
PubMed1999

Accelerated coronary reperfusion through the use of rapid bedside cardiac markers--case reports.

Each year, acute myocardial infarctions (AMI) account for more than half a million deaths in the United States. Complicating treatment of AMI is the difficulty in accurately diagnosing the event, for patients have nondiagnostic electrocardiograms (ECG) more than 50% of the time. In this population, cardiac markers are essential to confirm the diagnosis. The new bedside cardiac markers, which use eight drops of whole blood and require 15 minutes to be read negative, make it possible to shorten time needed to diagnose AMI. One hundred twenty-seven consecutive patients presented to the emergency department complaining of atypical chest pain. All had ECGs that were nondiagnostic for myocardial infarction. Serial cardiac markers were performed: myoglobin, troponin I, rapid myoglobin, and rapid troponin I. One hundred eighteen patients with negative serial cardiac markers had exercise treadmill tests in the emergency department. Nine patients with positive serial cardiac markers received emergent primary angioplasty. Six of the nine patients were treated based on the positive results of the rapid bedside cardiac markers. A 100% correlation existed between the quantitative serum results and the rapid bedside markers. With the availability of rapid bedside assays, dependency on the laboratory can be minimized, since quantitative cardiac markers require at least 1 hour of turnaround time. Rapidly and correctly diagnosing AMIs in patients with ECGs nondiagnostic for AMI has always been a dilemma. Rapid bedside assays enable the physician to accurately diagnose myocardial infarction and safely decrease the time in evaluating chest pain, thus maximizing the benefits of early reperfusion.

Adult↗
PubMed1999

Retropharyngeal abscesses: a clinical and radiologic correlation.

OBJECTIVE: This study evaluates the efficacy at our centre of the lateral neck x-ray and the computed tomography (CT) scan in differentiating retropharyngeal cellulitis from abscess in retropharyngeal space inflammatory process. METHOD: We reviewed the medical records of 37 patients with the diagnosis of retropharyngeal abscess or cellulitis hospitalized at the Centre Universitaire de Santé de l'Estrie in Sherbrooke between 1986 and 1997. Patients with a positive drainage at surgery were considered as retropharyngeal abscess and the rest as cellulitis. We measured the sensitivity, specificity, and positive and negative predictive values for the lateral neck x-ray and CT scan. Demographic and clinical data were also extracted for each patient. RESULTS: Twenty-five patients were classified as retropharyngeal cellulitis and only six patients as retropharyngeal abscess, although 13 patients went to the operating room for drainage. Results for the sensitivity and specificity were 80% and 100% for the lateral neck x-ray and 100% and 45% for the CT scan. Positive and negative predictive values for lateral neck x-ray were 100% and 94%, respectively. Forty percent and 100% were the values calculated for the CT scan. Clinical data were consistent with what has been reported in the literature. CONCLUSION: CT scan is helpful in the management of retropharyngeal abscess but has limits in differentiating cellulitis and abscess. Lateral neck x-ray was found to be very specific when the air sign was present.

Cellulitis↗
PubMed1997

Electrocardiographic manifestations of dual atrioventricular node conduction during sinus rhythm.

OBJECTIVES: The objective of this study was to correlate electrocardiographic (ECG) PR interval changes during normal sinus rhythm with recent observations regarding the anatomy and physiology of the dual, slow and fast atrioventricular (AV) pathways. BACKGROUND: The least common manifestation of dual AV conduction is an abrupt PR interval change in the setting of sinus rhythm. Whereas isolated cases of this phenomenon have been reported, the relatively large series we have collected makes it possible to correlate the ECG findings with the anatomy, composition and electrophysiology of the dual AV pathways. METHODS: The ECGs of 21 patients with sinus rhythm and PR interval changes consistent with dual AV node physiology were studied. Observations include duration of the short and long PR intervals, the difference between the two and the events responsible for the PR interval change. RESULTS: Eighteen of the 21 ECGs exhibited an abrupt and persistent PR interval change. Two of the other three ECGs manifested PR interval alternans, with slow and fast pathway, and a Wenckebach type I AV block; in the third ECG, findings compatible with simultaneous conduction along both pathways in response to a single stimulus were noted. Events responsible for the PR change included atrial premature complexes, atrial tachycardia, interpolated ventricular premature complexes and interpolated junctional premature complexes. In two the PR interval change appeared during a regular sinus rhythm. CONCLUSIONS: The behavior of the PR interval is consistent with dual AV conduction. The PR interval duration hypothesized to represent slow pathway conduction is in keeping with the calculated anatomic length of the slow pathway. The Wenckebach type I block in the slow and fast pathways, as well as the altered conduction time in the slow pathway parallel with changing sinus rate, is evidence that the pathway is influenced by autonomic (?parasympathetic) innervation, supporting the premise that the pathways contain AV node-like tissue.

Arrhythmias, Cardiac↗
PubMed1996

Cell-generated nitric oxide inactivates rat hepatocyte mitochondria in vitro but reacts with hemoglobin in vivo.

BACKGROUND & AIMS: Nitric oxide forms inactive iron-nitrosyl complexes within hepatic mitochondria in vitro. However, when formed in vivo, NO might react instead with hemoglobin. The aim of this study was to compare the effects of cell-derived NO on rat hepatocyte mitochondria in vitro and in vivo. METHODS: First, hepatocytes were cultured in vitro for 24 hours under a porous membrane supporting macrophages that were stimulated by endotoxin. Second, hepatic macrophage hyperplasia was induced in vivo by preadministration of killed Corynebacterium parvum; 7 days later, rats received endotoxin and were killed after 6 hours. Third, mitochondria were exposed to sodium nitroprusside in vitro, washed, mixed with blood, and recovered. RESULTS: Iron-nitrosyl complexes and hepatocyte mitochondrial dysfunction were observed in the in vitro model and prevented by an NO synthase inhibitor. In the in vivo model, however, despite a 130-fold increase in plasma nitrate levels and formation of hemoglobin-NO complexes in blood, no iron-nitrosyl complex was detected in hepatic mitochondria, and hepatic mitochondrial function was not impaired. In the third model, mitochondria lost preformed iron-nitrosyl complexes when exposed to blood. CONCLUSIONS: Although NO reacts with hepatocyte mitochondria in vitro, in vivo it reacts with sinusoidal hemoglobin without detectable impairment of hepatic mitochondrial function.

Animals↗
PubMed1995

Effects of female sex hormones on mitochondria: possible role in acute fatty liver of pregnancy.

Acute fatty liver of pregnancy occurs in some women. As other cases of microvesicular steatosis are due to impaired mitochondrial oxidation of fatty acids, we investigated the effects of female sex hormones on liver mitochondria in female mice. Three hours after administration of both estradiol (36 mumol/kg) and progesterone (150 mumol/kg), the in vitro beta-oxidation of [U-14C]palmitic acid and the activity of the tricarboxylic acid cycle decreased 49 and 54%, whereas the in vivo oxidation of [U-14C]palmitic acid decreased 38%. One week of treatment with both sex hormones produced ultrastructural lesions of mitochondria, decreased the recovery of mitochondrial proteins by 34%, increased state 4 respiration by 54-77%, and decreased the activities per gram of liver of several enzymes involved in the activation, mitochondrial uptake, and oxidation of fatty acids by 34-54%. We conclude that female sex hormones have deleterious effects on liver mitochondria and suggest that these effects, together with other factors, may contribute to the development of acute fatty liver of pregnancy in some women.

Acute Disease↗
PubMed1994

Toxicity of the antiandrogen flutamide in isolated rat hepatocytes.

The hepatotoxicity of flutamide, an antiandrogen that produces hepatitis in some human recipients, was studied in isolated rat hepatocytes. Flutamide (1 mM) led to the covalent binding of reactive electrophilic metabolites to male rat hepatocyte proteins. It decreased the reduced glutathione (GSH)/glutathione disulfide ratio and total protein thiols. This was associated with an early increase in phosphorylase a activity (a Ca(++)-dependent enzyme) and a decrease in cytoskeleton-associated protein thiols, the formation of plasma membrane blebs, the release of lactate dehydrogenase (LDH) and a loss of cell viability. Both covalent binding and LDH release were decreased by piperonyl butoxide (an inhibitor of cytochrome P450) and increased by dexamethasone pretreatment (which induces cytochrome P450 3A). The toxicity was increased by beta-naphthoflavone (which induces cytochrome P450 1A). Hepatocytes from female rats (which lack cytochrome P450 3A2) exhibited lower covalent binding and lower LDH release. The addition of cystine (a GSH precursor) increased hepatocellular GSH and decreased LDH release in male hepatocytes. The administration of a diet deficient in sulfur-containing amino acids had the opposite effects; it produced toxicity with 100 microM flutamide. Flutamide (50 microM) markedly inhibited respiration (mainly at the level of complex I) in isolated male rat liver mitochondria and flutamide (1 mM) decreased ATP levels in isolated male rat hepatocytes. It was concluded that flutamide is toxic to rat hepatocytes as a result of the cytochrome P450 (3A and also 1A)-mediated formation of electrophilic metabolites, whose damaging effects are further aggravated by the inhibitory effect of flutamide on mitochondrial respiration and ATP formation.

Adenosine Triphosphate↗
PubMed1994

Inhibition by nilutamide of the mitochondrial respiratory chain and ATP formation. Possible contribution to the adverse effects of this antiandrogen.

The effects of nilutamide on the mitochondrial respiratory chain were investigated in rats. In isolated mitochondria, nilutamide (100 microM) inhibited respiration that was supported by substrates feeding electrons into complex I of the respiratory chain but did not inhibit respiration that was supported by substrates donating electrons to complexes II, III or IV. Inhibition of complex I occurred without any lag time. In submitochondrial particles, nilutamide (100 microM) decreased both oxygen consumption mediated by NADH and the oxidation of NADH; addition of superoxide dismutase and catalase did not alleviate inhibition. There was no electron spin resonance evidence for detectable mitochondrial formation of the nilutamide nitro anion free radical by submitochondrial particles or for the formation of iron-nitrosyl complexes with mitochondrial Fe-S clusters in isolated hepatocytes. Severe inhibition of complex I by nilutamide (500 microM) led to upstream inhibition of fatty acid beta-oxidation. Nilutamide (100 microM) decreased the mitochondrial membrane potential and ATP formation in mitochondria energized by malate plus glutamate. In hepatocytes incubated without glucose, nilutamide (500 microM) led to an early (2 hr) drop in cellular ATP and early (4 hr) toxicity. With 5 mM glucose, however, ATP was not decreased and toxicity was mild at these early times. It was concluded that nilutamide itself inhibited the mitochondrial respiratory chain at the level of complex I and decreased ATP in hepatocytes incubated without glucose, which resulted in early toxicity. In the presence of glucose, ATP was not depleted at early times and delayed toxicity was probably the result of an oxidative stress (as previously reported).

Adenosine Triphosphate↗