Search PubMed⌕ Search

Biomedical subjects

B Levine

Publications and source records attributed to B Levine.

At least 109 records · Page 6Linked to original sources
PubMed1995

Abnormalities of skeletal muscle metabolism during nerve stimulation determined by 31P nuclear magnetic resonance spectroscopy in severe congestive heart failure.

These data confirm the presence of abnormal skeletal muscle metabolic function in patients with chronic heart failure. These changes are independent of patient compliance and central hemodynamic response to conventional exercise, and may explain, in part, the marked decrease in exercise tolerance often observed in patients with chronic severe heart failure. The etiology of these abnormalities of metabolic function and nutritive flow remains uncertain. TNS may prove useful in further elucidation of the peripheral metabolic consequences of chronic heart failure.

Acute Disease↗
PubMed1995

Dissociation of processes underlying spatial s-r compatibility: evidence for the independent influence of what and where.

The process-dissociation procedure was used to estimate the influence of spatial and form-based processing in the Simon task. Subjects made manual (left/right) responses to the direction of arrows (> or <) presented to the left or right of fixation. Manipulating the proportion of incongruent trials (e.g., a right-pointing arrow presented to the left of fixation) affected both the size and direction of the Simon effect. To account for this pattern of data, we compared process estimates based on three possible relationships between spatial and form-based processing: independence, redundancy, and exclusivity. The independence model provided the best account of the data. Most telling was that independent form-based estimates were superior at predicting observed performance on arrows presented at fixation and did so consistently across conditions (r's > .80). The results provide evidence that the form ("what") and spatial location ("where") of a single stimulus can have functionally independent effects on performance. They also indicate the existence of two kinds of automaticity--an associative ("implicit learning") component that reflects prior S-R mappings and a nonassociative component that reflects the correspondence between stimulus and response codes.

Cognition↗
PubMed1995

Concept generation: validation of a test of executive functioning in a normal aging population.

A new test, Concept Generation, was designed to fractionate the processes that underlie sorting performance in an efficient paper-and-pencil format. The test was administered to 60 subjects, aged 18-79. Results indicated age-related deficits for self-initiated concept formation, shifting set, output monitoring, and perseverative tendencies. When cuing was introduced to increase structure, age group differences were attenuated or eliminated. Within the older group, subgroups were identified based upon the nature of their repetitions. The hypothesis that sorting behavior is mediated by executive functions led to correlational analyses between Concept Generation scores and other measures of executive functioning. The pattern of correlations supported the construct validity of the Concept Generation test. In addition to providing preliminary evidence for the usefulness of Concept Generation in executive functioning assessment, the results replicated and extended previous work on executive functioning in older individuals.

Adolescent↗
PubMed1995

Site dependence of postmortem blood methadone concentrations.

A case investigated by the Office of the Chief Medical Examiner, State of Maryland, identified methadone at a heart blood concentration of 2.4 mg/L and a subclavian blood concentration of 0.8 mg/L. Due to these discrepant results, a study was undertaken to determine whether such inconsistencies occurred in other methadone cases. Of the 15 cases studied, only four had heart blood and alternate blood concentrations within 20% of one another. In only 53% of the cases were variations of < 60% observed. The data failed to show a trend where one site was consistently higher or lower than the other site.

Adult↗
PubMed1995

Roles of immunoglobulin valency and the heavy-chain constant domain in antibody-mediated downregulation of Sindbis virus replication in persistently infected neurons.

Clearance of infectious Sindbis virus from neurons is mediated by antibody to the E2 glycoprotein. Properties of the antibody important for downregulation of Sindbis virus replication are unknown. Immunoglobulin isotypes and valency determine many biological properties of antibodies. An immunoglobulin G1 (IgG1) isotype switch mutant and F(ab')2 and Fab fragments of IgG3 monoclonal antibody 209 were prepared and tested for clearance of infectious virus from persistently infected rat dorsal root ganglion neurons in vitro. IgG1, IgG3, and IgG3-derived F(ab')2 fragments were similarly efficacious, while IgG3-derived Fab fragments had no effect on virus replication. Cross-linking of Fab with secondary antibodies restored antiviral activity. Therefore, we found no evidence that IgG subclass plays a role in control of intracellular Sindbis virus replication. However, bivalency appears to be crucial for the ability of E2-specific IgG molecules to mediate clearance of infectious virus from neuron cells, suggesting that cross-linking of E2 molecules is essential.

Animals↗
PubMed1995

Head and neck manifestations of eosinophilia-myalgia syndrome.

Eosinophilia-myalgia syndrome (EMS) is a multisystemic disease that occurs in patients who have consumed products containing L-tryptophan. Prominent features include incapacitating myalgias, arthralgias, neuropathies, and eosinophilia. Despite the frequent association of dysphagia, dyspnea, and the potential for aspiration, the otolaryngology literature is devoid of information on EMS. In order to determine the frequency of otolaryngic symptoms, questionnaires were distributed to patients with EMS in 33 different US states. Among the 28 various head and neck manifestations studied, 70% of EMS patients complained of generalized muscle spasms, 66% xerostomia, 62% dyspnea, and 56% dysphagia. In addition, the epidemiology, clinical presentation, diagnostic criteria, and treatment options are discussed. This paper assesses the frequency of otolaryngic manifestations of EMS, as well as introduces this syndrome to the otolaryngologist-head and neck surgeon. It is important for the otolaryngologist to be aware of EMS and its manifestations and treatments so that patients with this potentially lethal disease can receive appropriate evaluation and expeditious treatment.

Adult↗
PubMed1995

The role of ethanol in heroin deaths.

The purpose of this study was to evaluate the role of ethanol in deaths due to heroin intoxication. Over a 12 month period, all cases investigated by the Office of the Chief Medical Examiner, State of Maryland where a blood screen by Roche Abuscreen radioimmunoassay (RIA) was positive at a cutoff of 100 ng/mL were included in the study. Free morphine was quantitated using the Coat-A-Count RIA and ethanol was quantitated by head space gas chromatography. All presumptive morphine positive cases were confirmed by gas chromatography/mass spectrometry. Seventy of the 119 cases where death was attributed to narcotic or alcohol and narcotic intoxication had blood ethanol concentrations (BAC) greater than or equal to 0.02 g/dL; 48 had BAC > or = 0.10 g/dL. Only 3 of 45 cases where morphine was identified but was unrelated to death had BAC > or = 0.02 g/dL. At all ranges of free morphine concentrations, there was a greater percentage of narcotic deaths when ethanol was present. From the data, we conclude that 1) the use of even small amounts of ethanol with heroin is clearly a risk factor in deaths due to heroin, 2) there are some heroin deaths where no free morphine is identified in the blood. In these deaths, ethanol is unlikely to be present, 3) at blood ethanol concentrations between 0.20 and 0.29 g/dL, the morphine concentrations in heroin deaths increased significantly, 4) at blood ethanol concentrations greater than 0.30 g/dL, morphine became less of a factor than the ethanol in causing death.

Alcoholic Intoxication↗
PubMed1995

Conversion from 2.5 mg to 1.25 mg indapamide in patients with mild to moderate hypertension.

BACKGROUND: Indapamide is an effective antihypertensive drug with diuretic and vasodilating activities. The common starting dose has been 2.5 mg to 5 mg. A lower dose formulation (1.25 mg) is now available. The safety and efficacy of switching patients from indapamide 2.5 mg to indapamide 1.25 mg was evaluated in this randomized, double-blind, multicenter clinical trial. METHODS: Three hundred seventy-eight adult patients with mild to moderate essential hypertension were enrolled in a washout period, during which patients received single-blind placebo for 4 weeks. All 378 patients qualified for the study and received open-label treatment with indapamide 2.5 mg for 8 weeks. Of the 378 patients, 265 responded to indapamide 2.5 mg and were randomized to receive double-blind treatment with either indapamide 1.25 mg (n = 132) or 2.5 mg (n = 133) for 8 weeks. Overall, 245 of the 378 patients who were initially enrolled completed the study. The primary efficacy variable was the number of patients in each treatment group who maintained a supine diastolic blood pressure of < or = 90 mm Hg (treatment success) by the end of the double-blind period (week 16). RESULTS: Treatment with indapamide 1.25 mg once daily was as efficacious as the 2.5-mg once-daily dose. No significant difference was observed for the percentage of patients who achieved treatment success between the patients switched from indapamide 2.5 to 1.25 mg (74%) and the control group maintained on indapamide 2.5 mg (70%). The incidence of drug-related adverse events during the double-blind period was similar between the two treatment groups. The mean change from pretreatment baseline to endpoint in serum potassium was -0.2 mEq/L (-0.2 mmol/L) in the indapamide 1.25 mg treatment group, compared with -0.4 mEq/L (-0.4 mmol/L) in the indapamide 2.5 mg treatment group. CONCLUSIONS: Indapamide 1.25 mg given once daily for 8 weeks was as effective as 2.5 mg once daily in reducing systolic and diastolic blood pressure in patients with mild to moderate hypertension.

Adult↗
PubMed1995

Benzoylecgonine and ecgonine methyl ester concentrations in urine specimens.

The two major urinary metabolites of cocaine are benzoylecgonine (BE) and ecgonine methyl ester (EME). The major advantage of BE screening is that many commercial immunoassays are designed to detect BE. On the other hand, EME is more amenable to gas chromatographic screening. To ascertain the merits of screening BE versus EME for identifying cocaine use, 380 consecutive urine specimens presented to the Office of the Chief Medical Examiner-State of Maryland were tested for BE by EMIT (cutoff 0.3 mg/L) and for EME by gas chromatography-nitrogen-phosphorus detection (cutoff 0.05 mg/L). Each presumptive positive was confirmed by gas chromatography-mass spectrometry. One hundred four specimens tested positive for BE or EME. Ninety three specimens were positive for both BE and EME, seven were positive for BE (cutoff 0.05 mg/L) only and four were positive for EME only. BE concentrations ranged from 0.08-386 mg/L while EME concentrations ranged from 0.06-72 mg/L. The BE concentration was greater than or equal to the EME concentration in 73% of the cases. Using BE as a sole screen, 96% of the cases of cocaine use were identified while EME screening identified 93% of the cases.

Chromatography, Gas↗
PubMed1994

Mefloquine distribution in postmortem cases.

Mefloquine is currently the drug-of-choice for malaria prophylaxis among military personnel. Four active duty military personnel receiving 250 mg mefloquine per week were killed in the line of duty under combat conditions. Samples of blood, bile, liver, kidney, muscle, brain, spleen and lung were submitted to the Division of Forensic Toxicology, Office of the Armed Forces Medical Examiner, for routine toxicologic analysis. Qualitative screening revealed only the presence of ethanol (< 25 mg/dl, probably attributable to postmortem formation) and mefloquine. Quantitation of mefloquine was performed using an HP 5880 gas chromatograph equipped with a nitrogen/phosphorus detector. The column was an HP-5 cross-linked 5% phenyl methyl silicone fused silica capillary column (15 m x 0.25 mm i.d. x 0.25 microns film thickness). The temperature program began at 110 degrees C, was held for 1 min and ramped at 20 degrees C/min to 200 degrees C, held for 1 min and then ramped at 10 degrees C/min to 280 degrees C and held for 10 min. Mefloquine elutes with a relative retention time similar to that of the tricyclic antidepressants. No postmortem data concerning mefloquine concentrations or tissue distribution was available. Quantitated blood concentrations in the presented cases were greater than the expected therapeutic values indicating the possibility of postmortem redistribution of this drug. No mefloquine overdoses were identified in the literature making comparison to the postmortem therapeutic concentrations impossible at this time.

Adult↗
PubMed1994

Intracerebral cytokine mRNA expression during fatal and nonfatal alphavirus encephalitis suggests a predominant type 2 T cell response.

Sindbis virus (SV) causes an acute encephalomyelitis in mice. A T cell-dependent inflammatory response is first detected 3 days after infection and includes T cells, B cells, and macrophages. The cytokines produced locally by intrinsic cells of the brain in response to infection and by infiltrating mononuclear cells and their contributions to outcome of infection have not been identified. Semiquantitative reverse transcriptase-PCR was used to evaluate the expression of mRNAs for IL-1 beta, IL-2, IL-4, IL-6, IL-10, TNF-alpha, leukemia inhibitory factor (LIF), and TGF-beta in the brain during fatal and nonfatal SV encephalitis of immunocompetent BALB/cJ and immunodeficient scid/CB17 mice. IL-1 beta and IL-6 mRNAs were detected in uninfected mice before infection and were up-regulated within 24 h. TGF-beta mRNA was also constitutively expressed in uninfected mice. LIF mRNA was occasionally detected in uninfected mice but increased in amounts only in BALB/cJ not scid mice after infection. TNF-alpha, IL-4, and IL-10 mRNAs were not found in uninfected mice but were induced within 24 h and continued to rise through 7 days after infection with substantially higher levels in BALB/cJ than scid mice. These data suggest that intrinsic brain cells produce IL-1, IL-4, IL-6, IL-10, LIF, and TGF-beta mRNAs in response to viral infection. IFN-gamma and IL-2 mRNAs were detected only in BALB/cJ mice and not until 3 days after infection with the initiation of inflammation. IL-4 and IL-10 mRNAs were more persistent and more easily detectable than IL-2 and IFN-gamma mRNAs. These data suggest a predominant type 2 cytokine response in the brain during SV encephalitis. BALB/cJ mice infected with a neurovirulent strain of SV (NSV), had 100% mortality, whereas NSV-infected scid mice developed persistent nonfatal infection. Inflammation was more intense in NSV-infected mice, however, no substantial differences in cytokine mRNA levels were detected when compared with mice with nonfatal SV infection suggesting that the cytokines measured do not in and of themselves lead to fatal central nervous system disease.

Alphavirus Infections↗
PubMed1994

The effects of alphavirus infection on neurons.

Sindbis virus is an alphavirus that causes encephalitis in mice. The primary target cells for central nervous system infection are neurons. The outcome of neuronal infection is dependent on the age of the mouse at the time of infection (maturity of the neuron) and the strain of virus used for infection (virulence of the virus). Sindbis virus causes neuronal death by inducing apoptosis. As neurons mature, they become resistant to virus-induced apoptosis, resulting in a persistent infection. Host production of antibody to a viral surface glycoprotein acts to downregulate virus replication in the infected neurons by a noncytolytic mechanism and clears infectious virus from the central nervous system. Specific genetic changes in the virus result in more virulent strains that cause severe disease and sometimes death in mature animals. These same genetic alterations also confer the ability to overcome the resistance of neurons to induction of cell death. Therefore, mature neurons infected with virulent viruses do not recover from infection even in the presence of an adequate immune response.

Aging↗
PubMed1994

Age-dependent susceptibility to fatal encephalitis: alphavirus infection of neurons.

Sindbis virus encephalitis in mice provides a model for studying age-dependent susceptibility to acute viral encephalitis. The AR339 strain of SV causes fatal encephalitis in newborn mice, but weanling mice recover uneventfully. Increased virulence for older mice is associated with a single amino acid change from Gln to His at position 55 of the E2 glycoprotein. Weanling mice with normal immune systems clear infectious virus from neurons through an antibody-mediated mechanism. This does not happen in newborn mice because the infected neurons die soon after they are infected. Death in immature neurons, as well as most other mammalian cells infected with Sindbis virus, occurs by induction of apoptosis. This can be prevented by cellular expression of bcl-2, an inhibitor of apoptosis, which is expressed by mature neurons in culture. We conclude that mature neurons are resistant to induction of apoptosis after infection with SV through expression of cellular inhibitors of apoptosis. This provides the opportunity for antibody to clear virus by a noncytolytic mechanism.

Aging↗