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Biomedical subjects

N Moore

Publications and source records attributed to N Moore.

At least 73 records · Page 4Linked to original sources

Thoracic outlet syndromes and magnetic resonance imaging.

The thoracic outlet syndromes encompass the diverse clinical entities affecting the branchial plexus or subclavian artery including cervical ribs or bands. Thoracic outlet syndrome are often difficult to diagnose on existing clinical and electrophysiological criteria and new diagnostic methods are necessary. This study reports our experience with magnetic resonance imaging (MRI) of the brachial plexus in 20 patients with suspected thoracic outlet syndrome. The distribution of pain and sensory disturbance varied widely, weakness and wasting usually affected C8/T1 innervated muscles, and electrophysiology showed combinations of reduced sensory nerve action potentials from the fourth and fifth digits, and prolonged F-responses or tendon reflex latencies. The MRI study was interpreted blind. Deviation of the brachial plexus was recorded in 19 out of the 24 symptomatic sides (sensitivity 79%). Absence of distortion was correctly identified in 14 out of 16 asymptomatic sides (specificity 87.5%). The false positive rate was 9.5%. Magnetic resonance imaging demonstrated all seven cervical ribs visible on plain cervical spine radiographs. Magnetic resonance imaging also showed a band-like structure extending from the C7 transverse process in 25 out of 33 sides; similar structures were detected in three out of 18 sides in control subjects. These MRI bands often underlay the brachial plexus distortion observed in our patients. We also observed instances of plexus distortion by post-traumatic callus of the first rib, and by a hypertrophied serratus anterior muscle. If they did not demonstrate a cervical rib, plain cervical spine radiographs had no value in predicting brachial plexus distortion. We believe MRI to be of potential value in the diagnosis of thoracic outlet syndrome by: (i) demonstrating deviation or distortion of nerves or blood vessels; (ii) suggesting the presence of radiographically invisible bands; (iii) disclosing other causes of thoracic outlet syndrome apart from ribs or bands.

Adult↗

Mortality studies in the long-term evaluation of treatment of alcoholics.

Mortality studies demonstrate that, in all the Countries evaluated, alcoholics die twenty years earlier than expected. Causes of death vary according to drinking patterns. Though mortality data seem crude, they can detect changes due to clinical intervention. Alcoholism studies should benefit by improvement of research methodologies as already applied to other chronic diseases.

Alcoholism↗

[Mechanical adaptation of muscular arteries to acute increase of blood pressure in man. Contribution of the measurement of arterial wall thickness].

Although it was usually admitted that hypertension is associated with a reduction in conduit artery compliance and distensibility, recent experiments using newly developed high precision echo-tracking devices allowing simultaneous, non-invasive measurements of blood pressure and arterial diameter have suggested that compliance and distensibility, when calculated at equal transmural pressure, could indeed be maintained, or even increased, in hypertensive subjects. Such a maintained arterial compliance could be explained best by a decrease in wall stress despite the increase in arterial blood pressure, through either an increase in wall thickness or a decrease in arterial wall elastic modulus. Thus, the goal of the present study was to assess the role of the changes in these determinants of vessel compliance in the arterial response to an acute increase in arterial pressure in 7 healthy volunteers. Arterial pressure (AP, Finapress) as well as right radial artery internal diameter and wall thickness (Echo-Tracking, NIUS 2, Asulab) were measured continuously before and after a 2 min cold pressor test (CPT). The following parameters were then calculated at fixed (105 mmHg) pressure from the pressure/diameter curve: compliance (mm2/mmHg) and distensibility (mmHg-1) mid-wall stress (dynes/cm2) and incremental elastic modulus (dynes/cm2). During CPT, mean AP increased (from 83 +/- 4 to 106 +/- 8 mmHg; p < 0.01), compliance distensibility; and mean internal diameter (mm) decreased, mean wall thickness (mm) increased, whereas wall stress and elastic modulus remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

A low molecular weight heparin decreases plasma aldosterone in patients with primary hyperaldosteronism.

Four patients with primary hyperaldosteronism were treated with nadroparin 4100 or 6150 antiXa IU daily for 4 days. Plasma and urine sodium and potassium, and plasma aldosterone and renin were monitored before, during and after the study. After four days of treatment, and for the following two days, plasma aldosterone was decreased (by a mean of 49% on Day 6), and urinary Na/K was increased (3.7-fold). The direction of the changes was reversed on Day 8. The study has confirmed the effect of low molecular weight heparin on aldosterone, and makes it unlikely that it is related to inhibition of angiotensin II stimulation in these patients, as renin could not be detected in their plasma.

Aged↗

Influence of rifampin on the pharmacokinetics of pefloxacin.

Pefloxacin and rifampin are frequently associated in the antibiotic therapy of deep-seated, and especially bone-located, infections. The influence of rifampin, a potent drug metabolism enzyme inducer, on the pharmacokinetics of pefloxacin was studied in a randomized crossover trial involving eight young healthy male volunteers. Every volunteer received either pefloxacin alone (period A) or pefloxacin after a 10-day induction by rifampin (period B) given as a 900 mg daily oral dose, and both periods were separated by a 3-week washout period. During both periods, pefloxacin was given during 3 days as a 400 mg b.i.d. oral dose (six doses) followed by a 400 mg intravenous dose on the fourth day. The kinetics of pefloxacin are significantly influenced by rifampin: The minimum (12-hour) plasma concentration, area under the concentration-time curve, and elimination half-life decreased respectively from 4.26 +/- 1.57 to 2.70 +/- 1.00 mg/L, 78.91 +/- 22.82 to 57.81 +/- 16.69 mg.hr/L, 14.46 +/- 3.46 to 10.08 +/- 2.44 hours (p less than 0.05). The renal clearance of pefloxacin was unchanged, but the plasma clearance increased from 94.04 +/- 39.04 to 126.82 +/- 47.36 ml/min (p less than 0.05). The plasma clearance of N-demethyl and N-oxide metabolites were similar for both periods, but the cumulative renal excretion (0 to 96 hours) decreased significantly (p less than 0.01) for period B versus period A. This definite but moderate inductive effect of rifampin on the pharmacokinetics of pefloxacin does not suggest a dose modification of pefloxacin in therapeutic association with rifampin, but pefloxacin assay in plasma seems to be advisable.

Adult↗

Liver glutathione and cytochrome P450 activity in experimental infection: study of the relative effects of infectious stress and malnutrition.

OBJECTIVE: To study the effects of infection and malnutrition on liver glutathione and cytochrome P450 (P450) in rats. DESIGN: Controlled experimental groups (12 groups). ANIMALS: Adult male Sprague-Dawley rats. INTERVENTIONS: Experimental endocarditis, pyelonephritis, or peritonitis were caused. Controls included free-fed rats and sham-operated rats, pair-fed to infected animals. Infection was verified by tissue culture. Rats were killed 3 days (acute infection) or 10 days (chronic infection, except endocarditis) after the induction of infection. RESULTS: Sham rats had lower liver weights, liver/body weight, and liver glutathione values than controls. Infected rats had larger liver weights and liver/body weight ratios and liver glutathione content than shams, and larger liver/body weight ratios than controls (acute infection). Infected rats had lower P450 values than both shams and controls. CONCLUSION: The malnutrition associated with infection caused decreased liver weight and glutathione content. Infection increased the liver weight, and liver glutathione content, but caused severe reduction in liver P450. If the same finding is true in infected patients, it could have consequences for the management of such patients.

Animals↗