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Biomedical subjects

P B Baker

Publications and source records attributed to P B Baker.

At least 37 records · Page 2Linked to original sources
PubMed1995

Interinstitutional comparison of bladder carcinoma surgical pathology report adequacy. A College of American Pathologists Q-Probes Study of 7234 bladder biopsies and curettings in 268 institutions.

Participants in the 1992 College of American Pathologists' Q-Probes Study of bladder carcinoma surgical report adequacy evaluated 7234 bladder biopsies and curettings from 268 institutions. In over 98% of the cases evaluated, the histologic type was stated. In over 95%, the histologic grade was stated where appropriate. Of the 7234 cases studied, 2149 (29.7%) were invasive, 4498 (62.2%) were noninvasive, and invasiveness (presence or absence of invasion) was not stated for 587 (8.1%). For invasive carcinomas, there was definitive assessment for the presence or absence of muscularis propria in 1145 (53.3%) of 2149 cases, and in 67 (3.1%) of 2149 cases no muscle or muscularis was present. For noninvasive carcinomas, there was a definitive evaluation of the muscularis propria (presence or absence) in 1349 (30%) of 4498 cases.

Biopsy↗
PubMed1995

Delusional infestation. The interface of delusions and hallucinations.

Delusional infestation represents a unique subtype of the delusional disorder category. This article presents the phenomenology, etiology, and treatment of delusional infestation. This article also reviews historical and theoretical attempts to distinguish tactile sensory phenomena as either hallucinations or delusions.

Delusions↗
PubMed1995

Fulminant hepatic failure associated with etodolac use.

Etodolac is a new pyranocarboxylic acid nonsteroidal anti-inflammatory agent with a unique chemical structure indicated for use in patients with painful musculoskeletal disorders and rheumatoid disease. Hepatotoxicity, in the form of reversible elevations in transaminases or bilirubin, occurs rarely. We present the first reported case of fulminant hepatic failure related to etodolac.

Aged↗
PubMed1994

A gene defect that causes conduction system disease and dilated cardiomyopathy maps to chromosome 1p1-1q1.

Longitudinal evaluation of a seven generation kindred with an inherited conduction system defect and dilated cardiomyopathy demonstrated autosomal dominant transmission of a progressive disorder that both perturbs atrioventricular conduction and depresses cardiac contractility. To elucidate the molecular genetic basis for this disorder, a genome-wide linkage analysis was performed. Polymorphic loci near the centromere of chromosome 1 demonstrated linkage to the disease locus (maximum multipoint lod score = 13.2 in the interval between D1S305 and D1S176). Based on the disease phenotype and map location we speculate that gap junction protein connexin 40 is a candidate for mutations that result in conduction system disease and dilated cardiomyopathy.

Adult↗
PubMed1994

Identification of a heroin esterase in Rhodococcus sp. strain H1.

A strain of a Rhodococcus sp. (termed H1) capable of utilizing heroin as its sole carbon and energy source was isolated by selective enrichment. An inducible heroin esterase was partially purified and shown to catalyze the hydrolysis of both of the acetylester groups of heroin. The enzyme displays optimum activity at pH 8.5 and appears to be a trimer of identical subunits with an M(r) or 39,000 and a native M(r) of 120,000.

Acetylesterase↗
PubMed1992

Effects of verapamil on the acute toxicity of doxorubicin in vivo.

BACKGROUND: Studies indicating that verapamil substantially enhances doxorubicin levels in certain drug-resistant tumor cells have led to the use of verapamil in combination with doxorubicin in animal and clinical studies of multidrug-resistant tumors. These studies have shown this drug combination to be associated with severe toxic effects. It is important to determine whether verapamil modulates the dose-limiting and potentially lethal cardiotoxicity of doxorubicin and to elucidate possible mechanisms. PURPOSE: The aims of this study were to evaluate the in vivo effects of verapamil on (a) doxorubicin-stimulated cardiac lipid peroxidation and cardiac damage, (b) doxorubicin-induced animal mortality, and (c) biodistribution of doxorubicin to the heart. METHODS: Male (BALB/c x DBA/2)F1 mice were treated with a high dose of doxorubicin (15 mg/kg, injected intraperitoneally), verapamil (25 mg/kg, injected intraperitoneally), or combinations of the two. Lipid peroxidation was determined using the 2-thiobarbituric acid assay for malonaldehyde. Light microscopy was used for histopathologic examination of cardiac tissue. A fluorometric assay procedure was employed to determine doxorubicin levels in the heart. RESULTS: Verapamil was an effective inhibitor of peroxidative damage to myocardial lipids following a high dose of doxorubicin (15 mg/kg, injected intraperitoneally). However, mice treated with verapamil and doxorubicin had a lower survival rate and a higher initial peak concentration of doxorubicin in the heart than those treated with doxorubicin alone. They also demonstrated a higher incidence and severity of degenerative changes in cardiac tissue. CONCLUSIONS: Our findings suggest that verapamil effectively inhibits doxorubicin-mediated lipid peroxidation in vivo but that cardiac lipid peroxidation is not the major limiting mechanism underlying doxorubicin-induced toxicity. A possible explanation for the excess mortality and cardiac injury in mice treated with verapamil plus doxorubicin is that verapamil alters the pharmacokinetics of doxorubicin. IMPLICATIONS: Further studies are necessary for development of safer protocols and/or drug combinations to treat multidrug-resistant tumors. We are currently studying treatment of tumor-bearing animals with a cumulative dosage regimen of doxorubicin in the presence and absence of verapamil.

Animals↗
PubMed1989

Physical chemical evidence of structural weakness in coronary arterial calcification.

Physical-chemical properties of calcified human coronary arteries were obtained through 857 electron probe microanalyses of samples of endarterectomy tissue from 12 patients and by X-ray and electron diffraction from separate samples. The calcific phase exhibited a weight percentage calcium to phosphorus ratio of 2.5 (SEM 0.15), a density of 2.95 (0.02) g.cm-3, and a crystalline unit cell volume of 530 (0.5) A3, or 53 (0.05) nm3. The phase has been characterised as a phosphorus deficient dahllite variant of apatite in which the crystal structure has been weakened by the incorporation of water molecules and tetrahedral hydroxyl groups in isomorphic substitution conforming with the McConnell-type defect. Isomorphic substitution within the apatitic cell appears sufficient to suggest that the crystal structure of the mineral deposit is weakened to the extent that means might be sought to attack the early formation of the pathological deposition.

Apatites↗
PubMed1988

Hyperthermia, hypertension, hypertonia, and coma in a massive thioridazine overdose.

This report characterizes an atypical presentation of a thioridazine overdose. Clinical manifestations included wide Q.R.S. complex, hyperthermia, hypertension, hypertonia, and coma. Plasma catecholamine levels were markedly elevated. The patient was treated with dantrolene sodium and supportive care. The patient's condition improved over time, with questionable response to dantrolene sodium. Supportive care was the mainstay of treatment.

Acute Disease↗
PubMed1988

Floppy mitral valve chordae tendineae: histopathologic alterations.

Pathologic studies of floppy or myxomatous mitral valves have focused primarily on changes in the valve cusps, with little attention given to the chordae tendineae. In a systematic study of the histopathology of floppy mitral valve chordae tendineae, 128 nonruptured chordae from 8 severely regurgitant floppy mitral valves were compared to 152 chordae from 10 normal control mitral valves and to 152 chordae from 8 control mitral valves with severe regurgitation due to ischemic heart disease. Collagen alterations were observed in 2% of normal mitral valve chordae and 3% of control regurgitant mitral valve chordae compared to 38% of floppy mitral valve chordae. Moderate or severe acid mucopolysaccharide accumulation was observed in 2% of normal mitral valve chordae and 3% of control regurgitant mitral valve chordae compared to 39% of floppy mitral valve chordae. Nonuniform histopathologic alterations, rare in normal and control regurgitant mitral valve chordae tendineae, were frequent in floppy mitral valve chordae tendineae (p less than 0.001). Histopathologic alterations provide the basis for abnormal physical properties previously demonstrated in floppy mitral valve chordae tendineae and may predispose to chordal elongation and rupture.

Aged↗
PubMed1987

Regional myocyte hypertrophy and increased interstitial myocardial fibrosis in hypertrophic cardiomyopathy.

The purpose of this study was to determine if the thickened cardiac walls of patients with hypertrophic cardiomyopathy (HC) are due to increased size or number of myocytes or increased amounts of fibrous tissue. Eight patients, aged 18 to 42 years, who died from complications of HC and 8 age-matched control subjects without heart disease were studied. A 1.5-cm3 block of tissue was removed from the left ventricular free wall, right ventricular free wall and ventricular septum (VS). Each region of each wall was evaluated for fibrous tissue by point counting; cell diameter was measured using an ocular micrometer disc. Cell layers were counted across the walls. The results revealed that increased cell size, cell layers and fibrous tissue are characteristic of HC, but only in the VS are all 3 significantly increased. The fibrous tissue was most extensive in the VS (19 +/- 9%), but it was more extensive than in the control subjects in all 3 walls. Cell diameters were largest in the layers closest to the left ventricular cavity.

Adult↗
PubMed1987

Morphologic and functional characteristics of the heart in Friedreich's ataxia.

The purpose of this study was to characterize the heart in patients with Friedreich's ataxia by two-dimensional echocardiography, systolic time intervals, and heart biopsy. Ten patients with Friedreich's ataxia (seven females and three males, age 15 +/- 7 years) were compared with 10 age-matched normal subjects (five males and five females, age 16 +/- 7 years). The mean systolic blood pressure in the patients with Friedreich's ataxia was lower (114 +/- 9 mm Hg) than that in the control subjects (122 +/- 8 mm Hg; p less than 0.05); diastolic blood pressures were the same. The heart rate in the patients with Friedreich's ataxia (102 +/- 17 beats/minute) was greater than that in the control subjects (76 +/- 12 beats/minute; p less than 0.001). The interventricular septal wall thickness was much greater in Friedreich's ataxia (13 +/- 2 versus 8 +/- 1 mm, p less than 0.001) as was the posterior wall thickness (13 +/- 3 versus 8 +/- 1 mm, p less than 0.001). The left ventricular end-diastolic diameter was smaller in Friedreich's ataxia (35 +/- 6 mm versus 47 +/- 6 mm; p less than 0.01), and the fractional change of the left ventricular minor axis with systole was greater in Friedreich's ataxia (40 +/- 9 percent versus 33 +/- 5 percent; p less than 0.05). An 11th patient with Friedreich's ataxia (age 33) had clinical heart failure, but his course was complicated by alcohol abuse. Heart biopsy in three patients with Friedreich's ataxia demonstrated myocyte hypertrophy (21.5 +/- 2.0 microns diameter; normal, 14 to 17 microns) and increased fibrosis (16 +/- 9 percent; normal, less than 5 percent). Thus, heart disease in Friedreich's ataxia is characterized by myocyte hypertrophy, interstitial fibrosis, increased left ventricular wall thickness, decreased left ventricular cavity size, sinus tachycardia, and normal systolic function. Further biochemical analysis of tissues may lead to the link of the neurologic and cardiac diseases and eventually to more effective therapy of this condition.

Adolescent↗
PubMed1986

Extent of myocardial fibrosis and cellular hypertrophy in dilated cardiomyopathy.

The distribution of fibrosis and cellular hypertrophy was studied in the hearts of patients with dilated cardiomyopathy (DC). Transmural sections were removed from the left and right ventricular free walls and the ventricular septum of 9 patients with heart failure and 6 control subjects. These sections were stained with hematoxylin-eosin (to determine cell size) and trichrome (to determine percent fibrosis). The sections were separated into equal areas from epicardium to endocardium in the free walls and right to left across the septum. Percent fibrosis was greater in patients with DC (20 +/- 4%) than control subjects (4 +/- 1%, p = 0.0001). A pattern of increasing fibrosis in the left ventricular free wall from epicardium (14 +/- 6%) to endocardium (22 +/- 9%, p less than 0.05) was documented. Fibrosis was greater on the left (21 +/- 12%) than the right (15 +/- 6%, p less than 0.05) side of the septum. No pattern was evident in the right ventricular free wall or in the control group. Myocardial cell diameter was greater in the heart failure group (22 +/- 5 micron) than the control group (17 +/- 2 micron, p less than 0.05), but no pattern of hypertrophy across the walls was seen. The increased fibrosis, the pattern of fibrosis and the increased cell diameter in patients with DC help to characterize DC.

Adult↗
PubMed1986

Value of endomyocardial biopsy.

The role of endomyocardial biopsy may be restricted to the diagnosis of myocarditis. On the other hand, a broad utilization of the biopsy technique may be championed by those who believe that the light and electron microscopic characteristics of the tissue are important and that the biochemical features of the tissue may hold important clues to the diagnosis and therapy of dilated cardiomyopathy. The popularity of endomyocardial biopsy arises from the ease and safety of the procedure. Light microscopy of the tissue is useful not only to diagnose myocarditis but also to discover infiltrative cardiomyopathies and to characterize the dilated cardiomyopathies by the amount of fibrosis and cellular hypertrophy. Electron microscopy supplies more detailed information on the myofibrils, nuclei, tubular structures, mitochondria, glycogen, and lipofuscin. At present, these data are clinically applicable only to the anthracycline cardiomyopathies. On an investigational basis, subcellular characteristics may help us better understand the etiology and pathogenesis of dilated cardiomyopathy. The greatest promise lies in the biochemical assessment of tissue, which may uncover single or multiple biochemical abnormalities in heart failure. Although the clinical usefulness of endomyocardial biopsy is quite restricted at present, its future looks quite promising.

Amyloid↗
PubMed1986

Dissecting hematoma (aneurysm) of coronary arteries.

Isolated dissecting hematoma (aneurysm) of a coronary artery is a rare occurrence that often results in myocardial infarction and sudden death. A case of dissecting hematoma involving the left main, left anterior descending, and left circumflex coronary arteries is described in a patient who had received vigorous closed-chest cardiac resuscitation. This is believed to be the first reported case of coronary artery dissection caused by epicardial trauma from closed-chest cardiac resuscitation. This case demonstrates that dissecting hematoma of the coronary artery can be a complication of cardiac resuscitation.

Aged↗
PubMed1986

Vivax malaria.

Malaria occurs in the United States infrequently and is found exclusively among immigrants and travelers returning from areas where the disease is endemic. Cases of acute relapses of Plasmodium vivax infection can present to the emergency department. Patients are often immigrants from developing countries who were symptom-free in this country for weeks or months preceding their illness. The clinical presentation and current treatment of malaria are reviewed. Malarial infection may become apparent months after leaving endemic areas despite adherence to prophylactic regimens. The disease usually responds to appropriate drug therapy with rapid and often dramatic results, but it can be fatal if unrecognized.

Acute Disease↗
PubMed1986

Aging of the human myocardium: a histologic study based upon endomyocardial biopsy.

This study assesses the effect of aging on human myocardial morphology. Fifteen patients, ranging in age from 28 to 75 with normal cardiac history, physical examination and noninvasive tests of left ventricular function, underwent right ventricular endomyocardial biopsy prior to cancer chemotherapy. Cell diameter, nuclear area and fibrosis were quantified by light microscopy. Semiquantitative methods of electron microscopy were used to grade lipofuscin deposition, tubular dilation, myofibrillar loss, folding of discs and lipid deposition. The results demonstrated that myocardial cell diameter correlated directly with age (r = 0.73, p less than 0.01) and systolic blood pressure (r = 0.51, p less than 0.05). Nuclear area (r = 0.76, p less than 0.01) and folded discs (r = 0.53, p less than 0.05), two signs of increased protein production also correlated with age. Lipid deposition (r = 0.40), tubular dilation (r = 0.31) and lipofuscin deposition (r = 0.20) increased with, but did not correlate significantly with age. Lipid deposition (r = 0.56, p less than 0.05) and tubular dilation (r = 0.43, p less than 0.05) did correlate with cell diameter. Thus, the aging myocardium is characterized by increased cell size and some degenerative changes.

Adult↗