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M Day

Publications and source records attributed to M Day.

At least 37 records · Page 2Linked to original sources
PubMed1998

Protein structures.

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Computer Communication Networks↗
PubMed1998

Role of anticardiolipin antibodies in young persons with migraine and transient focal neurologic events: a prospective study.

Anticardiolipin antibodies (aCL) are a risk factor for cerebral ischemia. In migraine, the association is controversial, with widely varying results in different small series. The controversy in part may be due to the inherent difficulty in distinguishing the transient focal neurologic events (TFNE) of migraine from TIA. To assess the frequency of aCL in migraine, we prospectively evaluated consecutive adults under 60 years of age with migraine without aura and with recent TFNE (<24-hour duration) clinically suggestive of either migraine with aura or TIA. We concomitantly enrolled persons with no CNS disease. Each person was interviewed and had blood drawn for solid-phase ELISA with IgG and IgM aCL isotyping. Neuroradiologic studies were reviewed. Patients with TFNE were followed every 6 months for the duration of the 3-year study. The frequency of aCL positivity (IgG >20, IgG >40, IgM >7.5) for the 645 patients with TFNE (8.8, 3.1, 4.2%), the 518 persons in the TFNE subgroup with migraine with aura (8.9, 3.3, 4.1%), the 497 persons with migraine without aura (7.0, 2.0, 3.6%), and the 366 control subjects (9.3, 3.6, 3.9%) did not differ significantly between groups. In TFNE patients with elevated aCL titer, the association was positive with diabetes mellitus, TFNE duration <15 minutes, and diplopia and was negative with hemiparesis, tinnitus, and family history of stroke. Findings on imaging consistent with cerebral ischemia were more frequent in aCL-positive persons. The short-term risk of stroke was uniformly low. In young persons, aCL is not associated with migraine or with TFNE, although diabetes mellitus, negative family history of stroke, and brief duration of symptoms (including diplopia) may predict immunoreactivity. Imaging studies suggest an ischemic etiology of TFNE in this cohort.

Adolescent↗
PubMed1998

Specificity, isotype, and titer distribution of anticardiolipin antibodies in CNS diseases.

BACKGROUND AND PURPOSE: There is an association between anticardiolipin antibodies (aCL) and ischemic stroke. There are, however, also occasional reports linking aCL with other CNS diseases (OND), particularly with multiple sclerosis (MS). Hence, we studied the specificity of aCL for ischemic stroke. METHODS: Prospective, consecutively identified patients evaluated for aCL (immunoglobulin G [IgG] and immunoglobulin M [IgM] isotypes) were divided into two groups: ischemic stroke (first ever) and OND (stroke-free subjects affected by OND). RESULTS: The ischemic stroke group (n = 300) and the OND (n = 149) differed in the following risk factors: age (64 +/- 14 versus 58 +/- 15 years; p < 0.001) and proportions of African Americans (67% versus 29%; p < 0.001); current cigarette smoker (26% versus 17%; p = 0.028); hypertensive (69% versus 34%; p < 0.001); diabetic (18% versus 7%; p = 0.001); history of angina (16% versus 8%; p = 0.015) or myocardial infarction (15% versus 3%; p < 0.001). There were higher rates of aCL positivity (26% versus 17%; p = 0.050), IgG-aCL > 10 GPL (23% versus 11%; p = 0.003) or IgG aCL > 20 GPL (12% versus 4%; p = 0.012) among the stroke group than among the OND group. No differences in IgG-aCL positivity were found between the MS group and the rest of the OND group but the MS patients had a higher rate of IgM-aCL positivity than the other OND patients. CONCLUSION: IgG-aCL positivity does not appear to be a marker for CNS disease generally but of ischemic stroke.

Antibodies, Anticardiolipin↗
PubMed1996

Expression of normal and mutant huntingtin in the developing brain.

Huntington's disease (HD) is caused by a genetic mutation that results in a polyglutamine expansion in huntingtin. The time course of neuronal loss in the HD striatum and other affected brain regions before the onset of symptoms is unknown. To determine the potential influence of huntingtin on brain development, we examined its expression in the developing mouse and in human control and HD brain. By Western blot, huntingtin was detected throughout the adult mouse brain and at all stages of embryonic and postnatal brain development. The protein increased significantly between postnatal day 7 (P7) and P15, which marks a period of active neuronal differentiation and enhanced sensitivity to excitotoxic injury in the rodent striatum. Immunoreactivity was found in neurons throughout the brain and localized mostly to the somatodendritic cytoplasm and to axons in fiber bundles. Staining was variable in different groups of neurons and within the same cell population. In developing brain, huntingtin was limited primarily to neuronal perikarya. Increased immunoreactivity in large neurons followed the gradient of neurogenesis and appeared in the basal forebrain and brainstem by embryonic days 15-17, in regions of cortex by P0-P1, and in the striatum by P7. In human brain at midgestation (19-21 weeks), huntingtin was detected in all regions. The brain of a 10-week-old infant with the expanded HD allele expressed a higher molecular weight mutant form of huntingtin at levels comparable to those of the wild-type protein. Thus, mutant huntingtin is expressed before neuronal maturation is complete. Results suggest that huntingtin has an important constitutive role in neurons during brain development, that heterogeneity in neuronal expression of the protein is developmentally regulated, and that the intraneuronal distribution of huntingtin increases in parallel with neuronal maturation. The presence of mutant huntingtin in the immature HD brain raises the possibility that neurons may be affected during brain development and possibly in the postnatal period when vulnerability to excitotoxic injury is at its peak.

Animals↗
PubMed1996

Cardiac and arterial interactions in end-stage renal disease.

Although cardiac hypertrophy is a frequent complication of end-stage renal disease (ESRD), relatively little is known about large arterial geometry and function in vivo in these patients, and the relationship between arterial changes and cardiac hypertrophy is unknown. Common carotid artery (CCA) intima-media thickness and internal diameter and left ventricular geometry and function were determined by ultrasound imaging in 70 uncomplicated ESRD patients and in 50 age-, sex-, and blood pressure-matched controls. Arterial distensibility and compliance were determined from simultaneously recorded CCA diameter and stroke changes in diameter and CCA pressure waveforms, obtained by applanation tonometry, and also by the measurement of carotid-femoral pulse wave velocity. Compared with control subjects, ESRD patients had greater left ventricular diameter (P < 0.01), wall thicknesses and mass (P < 0.001), increased CCA diameter (6.25 +/- 0.87 vs. 5.55 +/- 0.65 mm; P < 0.001), larger CCA intima-media thickness (777 +/- 115 vs. 678 +/- 105 microns; P < 0.001) and intima-media cross-sectional area (17.5 +/- 4.5 vs. 13.4 +/- 3.3 mm2; P < 0.001). In uremic patients, arterial hypertrophy was associated with decreased CCA distensibility (17.8 +/- 8.8 vs. 24.0 +/- 12.7 kPa-1.10(-3); P < 0.001) and compliance (5.15 +/- 2 vs. 6.0 +/- 2.5 m2.kPa-1.10(-7); P < 0.05), accelerated carotid-femoral pulse wave velocity (1055 +/- 290 vs. 957 +/- 180 cm/seconds; P < 0.001), early return and increased effect of arterial wave reflections (20.5 +/- 15.4 vs. 9.2 +/- 18.4%; P < 0.001). The latter phenomenons were responsible for increased pulsatile pressure load in CCA (58.3 +/- 21 vs. 48 +/- 17 mm Hg; P < 0.01) and were associated with a decreased subendocardial viability index (157 +/- 31 vs. 173 +/- 30%; P < 0.001). The CCA diameter was correlated with the left ventricular diameter (P < 0.01), and a significant correlations existed between CCA wall thickness or CCA intima-media cross-sectional area and left ventricular wall thicknesses and/or left ventricular mass (P < 0.01). In multivariate analysis, these relationships were independent regarding age, sex, blood pressure and body surface area. The present study documents parallel cardiac and vascular adaptation in ESRD, and demonstrates the potential contribution of structural and functional large artery alterations to the pathogenesis of left ventricular hypertrophy and functional alterations.

Adult↗
PubMed1995

Feasibility study of N-of-1 trials with blood pressure self-monitoring in hypertension.

The objective of this study was to assess individual responses to antihypertensive treatment by N-of-1 trials using blood pressure self-monitoring in 79 patients of both sexes referred to a hypertension clinic. Thirty-five patients who remained untreated (study 1) and 44 N-of-1 trial participants (study 2) were consecutively selected if their clinic blood pressure was between 160/95 and 220/115 mm Hg and there were no hypertensive complications. Blood pressure was measured daily at home for 21 days (three consecutive measures, morning and evening). Each N-of-1 trial was a single-blind treatment consisting of two successive 10-day treatment pairs, each pair comprising 5 days of placebo followed by 5 days of 20 mg enalapril once daily in the morning. Study 1 showed no significant blood pressure regression toward the mean over 20 days and justified the choice of 5-day treatment periods in study 2. In study 2, blood pressure fell significantly 12 hours after the first administration of enalapril and rose within 24 hours of the end of the 5-day active treatment period. Using evening blood pressure values (12 hours after enalapril intake) from the first treatment pair, 33 patients were classified as responders (diastolic blood pressure fall > or = mm Hg). In 16 of these 33 patients, the fall in blood pressure above 6 mm Hg was not maintained in the morning, 24 hours after drug intake. Response reproducibility was tested by comparison with the second treatment pair: the observed agreement was only 0.71 (chance-corrected agreement: 0.34) when defined according to both evening and morning values.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Self-measurement of blood pressure at home to evaluate drug effects by the trough: peak ratio.

AIM: Studies were carried out to assess (1) the statistical and clinical meaning of the trough:peak ratio and (2) the value of self-measurement of blood pressure at home in monitoring the duration of action of antihypertensive drugs in individual patients and in groups of patients. PATIENTS AND METHODS: Data from previous single-blind trials in 44 individual patients were reanalysed. The trough:peak ratio was calculated from mean blood pressure values. RESULTS: There are two major limitations in using this method. (1) Estimates of the trough:peak ratio are biased by the inclusion of non-responders. These patients have the usual random variations in blood pressure, and small differences can result in a spuriously high trough:peak ratio which may lead to an overestimate of the actual ratio. (2) The standard deviation of the trough:peak ratio is large; for a given mean trough:peak ratio some patients have the required 24-h drug cover, whereas others do not. The large standard deviation is partly a result of statistical problems, since four different blood pressure values are used to calculate the ratio. It is therefore essential to increase the precision of the measurement to decrease the standard deviation. CONCLUSIONS: Self-measurement of blood pressure at home might be a useful and inexpensive way of estimating the trough:peak ratio. As repeated measurements of blood pressure can be carried out at home under standardized conditions, this method increases the precision of each measurement. It is possible, therefore, to calculate individual trough:peak ratios and the drug regimen (once or twice a day) can be individualized.

Antihypertensive Agents↗
PubMed1993

Plasmid replication and maintenance in binary fissile microorganisms.

The mechanisms of nonconjugative plasmid replication (in the single cell) and maintenance (at the population level) are of concern to the microbiologist and to the genetic engineer who wishes to exploit their ability to express cloned genes. This article concentrates mainly on Escherichia coli as the host organism and examines the mechanisms by which both naturally occurring and genetically engineered plasmids persist in populations during periods of growth. Additional strategies to ensure high yields of recombinant product are briefly considered.

Cell Division↗
PubMed1993

Self blood pressure measurement at home.

Forty-six untreated patients measured their blood pressure at home for three weeks using an A and D, UA 751 automatic device, and were examined three times at the outpatient clinic. Home blood pressure was significantly lower than clinic blood pressure, even at the third visit when the correlations between clinic and home values were the most significant. The differences between clinic and home values had a gaussian distribution. The variance analysis of home blood pressure values showed that 67% of the variance was attributable to the between-subject component, 2% to the day effect, 15% to the time of the day effect and 16% to the residual (the measurement error). The standard deviation of the difference between two five-day periods of self blood pressure monitoring at home (5.4 and 4.1 mm Hg) was much lower than what has been reported for clinic measurements or 24-hour ambulatory monitoring.

Adult↗
PubMed1992

Autosomal dominant polycystic kidney disease with primary hyperaldosteronism.

We report three cases of primary aldosteronism associated with autosomal dominant polycystic kidney disease. The diagnosis of primary hyperaldosteronism was based on the presence of hypokalaemia with excessive urinary potassium excretion and/or the characteristic hormonal changes. Renal function impairment due to autosomal dominant polycystic kidney disease could mask hypokalaemia. The interpretation of adrenal imagery may be hindered by adjacent renal cysts. In one case an adrenal adenoma was detected and surgically removed, with only partial correction of the blood pressure. This could be explained by the persisting underlying autosomal dominant polycystic kidney disease. We conclude that in a hypertensive patient with polycystic kidney disease, extrarenal causes of hypertension may be present.

Adult↗
PubMed1992

[Treatment of hypertension in diabetes: threshold of intervention and therapeutic options].

Early screening for hypertension in diabetic patients and for glycoregulation abnormalities in hypertensives is justified by the additive cardiovascular risks when hypertension and diabetes co-exist and by the accelerated development of diabetic nephropathy and retinopathy if hypertension co-exists. In insulin-dependent diabetes, hypertension is generally preceded by microalbuminuria, known to be reduced by angiotensin converting enzyme inhibitors. The requirement for nephropathy prevention and the hemodynamic and/or tissular effects of this therapeutic class could justify their use at a blood pressure level less than that conventionally considered hypertensive. This strategy must be confirmed by prospective trials, already underway, evaluating the nephroprotective efficacy of this therapy. In non-insulin-dependent diabetes, hypertension is often present before the diabetes is diagnosed and antihypertensive therapy, especially thiazide diuretics, could play a demasking or favorizing role. The optimal blood pressure level to which these patients at high renal and coronary risk should be lowered still has to be determined. A prospective study, comparing the effects of strict (treated diastolic blood pressure less than 80 mmHg) and less strict (treated diastolic blood pressure between 90 and 100 mmHg) hypertensive control on coronary event prevention in essential hypertension, is in progress and will have important implications for hypertension treatment in diabetics. Appropriate treatment of other risk factors, such as hyperlipidaemia and smoking, contributes to coronary and renal prevention in all diabetic hypertensives.

Albuminuria↗