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Biomedical subjects

M Fisher

Publications and source records attributed to M Fisher.

At least 235 records · Page 13Linked to original sources
PubMed1996

Abnormalities in weight status, eating attitudes, and eating behaviors among urban high school students: correlations with self-esteem and anxiety.

PURPOSE: The study's objective was to determine the prevalence of abnormalities in weight, eating attitudes, and eating behaviors among an urban teenage population. METHODS: Measures of weight, height, and blood pressure were obtained from 1,001 students attending regularly scheduled physical education classes in a New York City high school the population of which was 66% black and 23% Hispanic. The mean age was 16 years old; 55% were female and 45% were male. Approximately three quarters of the students completed the Eating Attitudes Test (EAT-26), Rosenberg Self-Esteem Scale, Spielberger Trait Anxiety Inventory, and a questionnaire on eating behaviors. RESULTS: By percent ideal body weight (%IBW), 25% of students were obese (>20% above IBW), 18% were overweight, and 5% were underweight. Abnormal EAT scores (>21), were found in 6% of males and 15% of females. Students reported that they had engaged in the following nutritional behaviors at least three times in the past week: eating candy (59%), skipping breakfast (58%), skipping lunch (42%), eating fast foods (28%), and skipping dinner (14%). Self-esteem was high in 60%, medium in 21%, and low in 19%. Mean self-esteem was significantly higher (P < .0001) than established norms. Self-esteem and anxiety were inversely correlated (r = .40, P < .001), and low self-esteem and high anxiety were both associated with high EAT scores (r = .29, P < .001). Self-esteem and anxiety of obese students did not differ from those who were of normal weight. CONCLUSIONS: Among this population of urban high school students there were: (a) a large number of overweight adolescents; (b) a significant subgroup with eating attitudes suggestive of an eating disorder; and (c) high levels of self-esteem and normal levels of anxiety, which were independent of weight status.

Adolescent↗
PubMed1996

Update on adolescent health care in pediatric practice.

PURPOSE: To determine current adolescent health care practices of pediatricians and evaluate whether changes have taken place during the past decade. METHODS: A questionnaire completed by 101 pediatricians in 1985 was abbreviated and adapted by Committee on Youth of Chapter 2, District II of the American Academy of Pediatrics and sent to 1,633 members of the Chapter in June 1993. RESULTS: Forty-three percent of the 436 respondents in 1993 were female, 43% < or = 40 years of age and 53% were in private practice. Most accept new patients > or = 16 years of age (76%), continue to see patients > or = 19 years of age (63%), and interview adolescents without their parents (86%). Although between one-third and two-thirds of respondents report having equipment for gynecologic examinations, most indicate they are "not entirely comfortable" treating adolescent issues and therefore refer to others for management. Between one-quarter and one-half indicate they are "very interested" in learning more about adolescent issues and an additional 40-50% are "somewhat interested." Obstacles to providing adolescent care include: "image as a baby doctor" (65%), fear that parents would object (61%), no separate hours (57%), difficulty in providing confidential care (56%), and difficulty in charging appropriate fees (47%). Females and younger pediatricians are more comfortable with some aspects of gynecologic care and more likely to be satisfied with the adolescent care they are providing. There were few differences between responses in 1993 and 1995. CONCLUSIONS: Few of the pediatricians surveyed provide comprehensive care to adolescent patients. Future policy decisions and medical education must respond to these realities in pediatric practice.

Adolescent↗
PubMed1996

Medical therapy for ischemic stroke.

Therapy for stroke is undergoing major changes. Many of the changes parallel the advances made in the therapy for myocardial infarction. Acute intervention with cytoprotective and thrombolytic agents is undergoing active investigation. Cytoprotective therapy includes drugs that act to prevent cell death during ischemia and reperfusion. These agents include calpain inhibitors, voltage-sensitive calcium- and sodium-channel antagonists, receptor-mediated calcium-channel antagonists [including N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) antagonists], glutamate-synthesis inhibitors, glutamate-release antagonists, gamma-aminobenzoic acid (GABA) antagonists, 5-HT (serotonin) receptor agonists, gangliosides, antioxidants, growth factors, antiapoptotic agents, and antiadhesion molecules. Thrombolysis is effective in myocardial infarction. Thrombolysis is undergoing evaluation in stroke with streptokinase, anisoylated plasminogen streptokinase activator complex (APSAC), tissue plasminogen activator (t-PA; including recombinant t-PA), urokinase, and single-chain urokinase (scu-PA). Both systemic and selective administration are being evaluated. Preventive therapy with both antiplatelet and anticoagulant drugs sheds new light on how best to stratify patients in terms of a risk-benefit ratio. Continuing public education will be essential as stroke therapy advances.

Brain↗
PubMed1996

Male duct ectasia associated with HIV infection.

The incidence of male duct ectasia (periductal mastitis) is extremely rare, only eight cases having been reported. The underlying cause (as in females) is uncertain. Two cases in HIV positive males of recurrent unilateral nipple lesions are reported with histology consistent with duct ectasia. At presentation neither patient had an AIDS defining illness. An impaired immunity secondary to HIV infection may result in an increased susceptibility to repeated nipple infections, and the clinical as well as histological features of duct ectasia. The consideration of HIV infection in future cases of male duct ectasia may be warranted.

Adult↗
PubMed1996

Pneumothorax in AIDS: case reviews and proposed clinical management.

BACKGROUND: Pneumothorax is a not uncommon complication of advanced HIV infection, and may prove difficult to manage in view of its recalcitrant and recurrent nature. In this group where immunosuppression and reduced life expectancy are a feature, standard protocols are often abandoned in favour of a more conservative approach. This is often unsuccessful. METHODS: Patients attending the Department of Genitourinary Medicine, Chelsea and Westminster Hospital who sustained pneumothorax between 1988 and 1992 were identified retrospectively and their notes reviewed. RESULTS: Fifteen patients were identified of whom three had post-procedural pneumothoraces. In the remaining 12 patients, 10 had previously had Pneumocystic carinii pneumonia (PCP), whilst all 12 had some evidence to suggest current PCP (seven proven, five presumptive). In those six patients with a single, unilateral pneumothorax, four were managed successfully with intercostal drainage alone (one patient died early, one required pleurectomy). In those with recurrent pneumothoraces or pneumothoraces that did not respond to prolonged intercostal drainage, failure of medical treatment was judged to have occurred and surgery was performed. Overall, conservative management failed in 7/11 patients. Conversely surgery resulted in resolution in 7/7 with recurrence seen in one individual. Median survival was similar in the two groups. CONCLUSIONS: Pneumothorax in patients with AIDS is associated with a high rate of intercurrent PCP; a low threshold for treating this infection presumptively is indicated. Intercostal drainage was successful in patients with a single, unilateral pneumothorax. However, in patients with recurrent or bilateral pneumothorax extended periods on intercostal drainage were uniformly unsuccessful. Early surgical referral should be considered in this group.

AIDS-Related Opportunistic Infections↗
PubMed1996

Acute and atypical presentations of syringomyelia.

Syringomyelia is characterized by a longitudinal cavity or several cavities in the spinal cord, and syringobulbia demonstrates similar pathology in the brainstem. Both conditions typically present with slowly progressing dissociative sensory deficits as well as upper and lower motor neuron deficits. We recently encountered 3 patients who presented with the rapid onset of such signs and symptoms and had cervical syringes. All 3 patients would have been diagnostic dilemmas had it not been for MRI, which identified a syrinx in each patient, as well as an Arnold-Chiari malformation in 2 of the 3. Syringomyelia and syringobulbia should be considered in the differential diagnosis of patients who have acutely evolving brainstem or cervical spinal cord deficits. MRI is the imaging modality of choice for detecting syringomyelia or syringobulbia presenting atypically.

Adult↗
PubMed1996

Upregulation of basement membrane-degrading metalloproteinase secretion after balloon injury of pig carotid arteries.

Basement membrane-degrading metalloproteinases (gelatinases) appear necessary for vascular smooth muscle cell migration and proliferation in culture and for intimal migration of cells after balloon injury to the rat carotid artery. We investigated in the present study the secretion of gelatinases from pig carotid artery tissue after balloon injury. Segments of injured artery and segments proximal and distal to the area of injury were removed 3, 7, and 21 days after balloon dilatation. Medial explants from these segments were then cultured for 3 days, and the serum-free conditioned media were subjected to gelatin zymography. Production of 72- and 95-kD gelatinases was quantified by densitometry. Balloon-injured segments secreted significantly more 72- and 95-kD gelatinase than did paired distal segments at all time points. Release of both gelatinase activities was increased at 3 and 7 days relative to segments from uninjured arteries but declined again by 21 days after balloon injury. Similar results were found for gelatinase levels in extracts of arterial tissue. Consistent with the protein secretion data, in situ hybridization demonstrated that the mRNAs for both gelatinases were upregulated after balloon injury. Expression was prominent in medial smooth muscle cells, particularly around foci of necrosis, and in neointimal cells 3 and 7 days after balloon injury; 72-kD gelatinase mRNA persisted after 21 days and was prominent in regrown endothelial cells. The upregulation of gelatinase activity paralleled the time course of smooth muscle cell migration and proliferation in this model. We conclude that increased gelatinase production occurs in response to balloon injury and may play a role in permitting migration and proliferation of vascular smooth muscle cells.

Animals↗
PubMed1996

Precipitants of brain infarction. Roles of preceding infection/inflammation and recent psychological stress.

BACKGROUND AND PURPOSE: Antecedent febrile infection and psychological stress are described as predisposing risk factors for brain infarction. We examined the temporal relationship between preceding infection/inflammation and stroke onset as well as the role of recent psychological stress as a potential precipitant for brain infarction. METHODS: In this case-control study, a standardized evaluation including a signs/symptoms-based questionnaire was used to characterize the prevalence and timing of recent prior (< 1 month) infectious and inflammatory syndromes in 37 adults with acute brain infarction, 47 community control subjects, and 34 hospitalized nonstroke neurological patient controls. Recent psychological stress was measured with scales of stressful life events and negative affect. RESULTS: The prevalence of infection/inflammation was significantly higher in the stroke group only within the preceding 1 week compared with either community control subjects (13/37 versus 6/47, P < .02) or hospitalized neurological patient controls (3/34, P < .02). Upper respiratory tract infections constituted the most common type of infection. A substantial proportion of stroke patients with preceding (< 1 week) infection/inflammation (5/13) had no accompanying fever or chills. There were no significant differences between the stroke and control groups in the levels of stressful life events within the prior 1 month or in negative-affect scale scores within the prior 1 week. CONCLUSIONS: Our data suggest that both febrile and nonfebrile infectious/inflammatory syndromes may be a common predisposing risk factor for brain infarction and that the period of increased risk is confined within a brief temporal window of less than 1 week. Results of this study argue against a role for recent psychological stress as a precipitant for cerebral infarction.

Acute Disease↗
PubMed1996

Impairments of the protein C system and fibrinolysis in infection-associated stroke.

BACKGROUND AND PURPOSE: Infection/inflammation appears to be an important predisposing risk factor for brain infarction, but little is known regarding underlying molecular mechanisms. We examined the hypothesis that patients with brain infarction preceded by infection/inflammation within 1 week could be identified by a distinctive procoagulant laboratory profile characterized by abnormalities in the protein C system and endogenous fibrinolysis. METHODS: We performed a case-control study examining the relationship between preceding systemic infectious/inflammatory syndromes and selected immunohematologic variables in 36 patients with acute brain infarction and 81 control subjects (community control subjects [n = 47] and hospitalized nonstroke neurological patient controls [n = 34]). RESULTS: The stroke group had a lower mean level of the circulating antithrombotic enzyme activated protein C (APC) (4.33 +/- 0.34% [log-transformed percentage of control value, mean +/- SD]) than community control subjects (4.51 +/- 0.27%, P < .02) or hospitalized neurological patient controls (4.57 +/- 0.31%, P < .005). The lowest circulating APC levels were found in the stroke group with antecedent infection/inflammation within 1 week preceding index brain infarction (4.23 +/- 0.4%, n = 12). Within the stroke group, circulating APC levels were inversely related to IgG isotype anticardiolipin antibody titers (r = -.55, P < .001). Only the stroke group with infection/inflammation within 1 week had elevated plasma C4b binding protein compared with control subjects (141 +/- 61% versus 112 +/- 44%, P < .05). Stroke patients with antecedent infection/inflammation had a distinctively lower ratio of active tissue plasminogen activator to plasminogen activator inhibitor (0.11 +/- 0.04, n = 9) than other stroke patients (0.19 +/- 0.06, n = 9, P < .01) and control subjects (0.22 +/- 0.16, n = 17, P < .02). CONCLUSIONS: Impairments in the protein C pathway and endogenous fibrinolysis may contribute to the increased risk for brain infarction after recent (< or = 1 week) infection/inflammation. A decrease in the circulating anticoagulant APC may be related to elevated antiphospholipid antibody titers.

Antibodies, Anticardiolipin↗
PubMed1996

Effect of basic fibroblast growth factor on experimental focal ischemia studied by diffusion-weighted and perfusion imaging.

BACKGROUND AND PURPOSE: Basic fibroblast growth factor (bFGF) has documented neuroprotective properties. This study was performed to evaluate the effects of bFGF on infarct size when administered 30 minutes after induction of focal cerebral ischemia in rats. Diffusion-weighted and perfusion MRI were used during the drug infusion. METHODS: We blindly randomized 20 Sprague-Dawley rats to receive either drug (n = 10) or vehicle (n = 10). The animals underwent middle cerebral artery (MCA) occlusion using the suture model. Diffusion-weighted MRI was initiated 30 minutes after induction of ischemia and repeated frequently for 3.5 hours. Drug (45 micrograms/kg per hour) or vehicle (saline) infusion began 30 minutes after MCA occlusion and continued for 3 hours. Perfusion images were made at 25, 90, and 150 minutes after MCA occlusion. The animals were killed after 24 hours of permanent MCA occlusion, and brains were stained with 2,3,5-triphenyltetrazolium chloride (TTC). RESULTS: The TTC-derived, corrected infarct volume postmortem in the bFGF-treated group was significantly smaller than that in controls (126.6 +/- 51.9 versus 180.2 +/- 54.9 mm3, mean +/- SD, P = .038). Diffusion imaging showed essentially equal lesion volumes 3 hours after MCA occlusion (195.4 +/- 61 mm3 in the drug-treated group and 194.4 +/- 65 mm3 in controls). At 4 hours, ischemic lesion size was 182.1 +/- 56.9 mm3 in treated animals and 222.9 +/- 88.7 mm3 in the controls (P = .24, NS). Perfusion imaging did not show a change of cerebral perfusion within ischemic brain regions in the bFGF group during the infusion. No behavioral or physiological side effects were observed. CONCLUSIONS: bFGF is a safe and effective treatment for focal cerebral ischemia in rats. We observed a modest delayed difference of ischemic lesion size in vivo with diffusion MRI. The diffusion-weighted MRI findings suggest a potential delayed therapeutic effect of bFGF, and the perfusion imaging findings imply that the effect is not due to increased blood flow to the ischemic region.

Animals↗
PubMed1996

Regulation of brain capillary endothelial thrombomodulin mRNA expression.

BACKGROUND AND PURPOSE: Endothelial cells regulate hemostasis in part via expression of thrombomodulin, a potent anticoagulant protein. The purpose of this study was to analyze brain capillary endothelial cell expression of thrombomodulin mRNA. METHODS: Bovine brain capillary endothelial cells were grown in a blood-brain barrier model in which endothelial cells form capillary-like structures. In situ hybridization and polymerase chain reaction (PCR) were used to examine thrombomodulin expression. Endothelial cells were then cocultured with astrocytes. We examined both coculture and monoculture preparations for gamma-glutamyl transpeptidase (GGTP), a marker of the blood-brain barrier. We then used quantitative-competitive PCR to compare thrombomodulin expression in endothelial monocultures and astrocyte-endothelial cocultures after 1 and 7 days of culture. RESULTS: Both in situ hybridization and PCR studies demonstrated thrombomodulin mRNA expression by endothelial cells. During 1 week of astrocyte-endothelial coculture, there was (1) progressive association of astrocytes with capillary-like structures and (2) expression of GGTP; endothelial monocultures did not express GGTP. There was no significant difference in thrombomodulin mRNA expression for cocultures versus monocultures after 1 day. After 1 week, however, astrocyte-endothelial cocultures had markedly decreased thrombomodulin mRNA compared with monocultures (9 +/- 2 versus 189 +/- 62 pg/mL; P < .025). This thrombomodulin mRNA decrease thus occurred when elements of the blood-brain barrier phenotype were demonstrable, ie, when astrocyte association with capillary-like structures was maximal and when GGTP was expressed in cocultures. CONCLUSIONS: These findings indicate astrocyte regulation of thrombomodulin mRNA expression in vitro and suggest an important role for the blood-brain barrier in the regulation of thrombomodulin.

Animals↗
PubMed1996

Brain capillary tissue plasminogen activator in a diabetes stroke model.

BACKGROUND AND PURPOSE: Tissue plasminogen activator (TPA) is normally expressed in rat brain capillaries. This study examines the expression of TPA in brain capillaries of diabetic rats in relation to focal ischemic brain injury. METHODS: Diabetes type 1 was induced by streptozotocin for 7 days. Acute hyperglycemia was induced by 50% dextrose. Expression of TPA in brain capillaries was determined by Western blot and reverse transcription-polymerase chain reaction analyses. Focal stroke was produced by 1 hour of reversible middle cerebral artery occlusion. Physiological variables and cerebral blood flow were monitored during occlusion and within 1 hour of reperfusion. Neurological and neuropathologic examinations were performed after 24 hours of reperfusion. RESULTS: All rats developed comparable hyperglycemia (approximately 15 mmol/L). A complete depletion of TPA protein and 6.5-fold decrease in TPA mRNA were found in brain capillaries of diabetic rats, in contrast to normal TPA capillary levels in hyperglycemic rats. The blood flow in the periphery of the ischemic core was significantly reduced during reperfusion by 52% to 62% (P<.001) in diabetic rats and by 23% to 25% (P<.05) in hyperglycemic rats. The neurological score was worsened by 3.2-fold (P<.0003) by diabetes and by 24% by hyperglycemia only. Significant 41% (P<.007) and 29% (P<.05) increases in infarct volume and 163% (P<.007) and 60% increases in edema volume were found in diabetic rats relative to control and hyperglycemic rats, respectively. CONCLUSIONS: Diabetes type 1, but not acute hyperglycemia, produces downregulation of TPA in rat brain capillaries. This TPA reduction is associated with impaired restoration of blood flow after an ischemic insult, poor neurological outcome, and enhanced ischemic brain injury.

Animals↗
PubMed1996

Activated protein C resistance in ischemic stroke not due to factor V arginine506-->glutamine mutation.

BACKGROUND AND PURPOSE: Resistance to activated protein C (APC), a natural plasma anticoagulant, is the most common identifiable risk factor for venous thromboembolic disease. One point mutation in coagulation factor V that renders it APC-resistant is found in >90% of APC-resistant venous thrombosis patients. To determine the prevalence of APC resistance and of this factor V mutation in stroke, we screened a group of ischemic stroke patients. METHODS: Hispanic ischemic stroke patients were screened using two different activated partial thromboplastin time-based assays. One assay using neat patient plasma determined APC resistance, and the other assay using patient plasma diluted into factor V-deficient plasma determined APC-resistant factor V, including the Arg506-->Gln mutation. Results were compared with those in 31 Hispanic control subjects of similar ages. RESULTS: Six of 63 (9.5%) stroke patients had APC resistance compared with none of 31 (0%) control subjects. No patient or control subject had APC-resistant factor V, ie, the factor V Arg506-->Gln mutation. CONCLUSIONS: In Hispanic patients with ischemic stroke, the incidence (approximately 10%) of APC resistance is not caused by the factor V Arg506-->Gln mutation. APC resistance not caused by this factor V mutation may be a risk factor for ischemic stroke in this population.

Arginine↗
PubMed1996

Severe transient hypoglycemia causes reversible change in the apparent diffusion coefficient of water.

BACKGROUND AND PURPOSE: The aim of this study was to determine the effects of temporary severe hypoglycemia on the apparent diffusion coefficient (ADC) acquired by diffusion-weighted MRI of brain water with the use of serial multislice ADC mapping in rats. Severe hypoglycemia reduces the extracellular space volume, as does ischemia. Demonstrating a reduction of ADC with hypoglycemia should increase our understanding of the mechanisms underlying ADC changes in ischemia and other conditions. METHODS: Fasted rats were given regular insulin (15 IU/kg IP). Rats were subjected to 15 minutes (n = 5) and 50 minutes (n = 5) of temporary severe hypoglycemia, causing a transiently isoelectric electroencephalogram (EEG). ADC mapping was performed every 30 seconds beginning at the onset of isoelectricity for 8.5 minutes. ADC maps were also obtained later during the isoelectric EEG period and 10, 20, 30, and 40 minutes after glucose infusion. Control images were obtained from a separate group of animals suffering cardiac arrest (n = 5). RESULTS: Abnormal ADC values were not observed before the onset of cerebral isoelectricity, except for isolated areas in the cortex and periventricular regions. Cortical ADC values globally declined at the onset of EEG isoelectricity. The ADC decline spread to subcortical regions within a few minutes. During the isoelectric period, significant declines of ADC values (27% to 45%) occurred in the entire brain. Glucose infusion normalized most of the ADC changes, even after a 50-minute period of isoelectricity. CONCLUSIONS: ADC mapping during hypoglycemia clearly demonstrates changes likely related to energy depletion. Most of these ADC declines were reversible. Hypoglycemia is a condition known to be associated with shrinkage of the extracellular space. These observations support the hypothesis that ADC reductions observed in ischemia are also related to shifts of water from the extracellular to the intracellular compartment.

Animals↗
PubMed1996

How do members of an interprofessional clinical team adjust to hospice care?

A study was carried out involving interviewing and facilitating a workshop for members of an interprofessional hospice team: nurses, doctors, a physiotherapist, a chaplain and a counsellor. Its aim was to explore how the members adjusted to working with people who are dying and people who are bereaved and whether a developmental model of adjustment from American hospital social work practice could be applied to British interprofessional hospice care. It was found that all participants experienced adjustment to hospice care as a continuous rather than a developmental process with an end point.

Adult↗