Biomedical subjects

L M Silverman

Publications and source records attributed to L M Silverman.

83 records · Page 5Linked to original sources

PubMed1977

Electrophoretic patterns for serum glycoproteins reflect the presence of human breast cancer.

We describe a group of glycoproteins that are synthesized and released by human breast tumors maintained in organ culture and similar glycoproteins released by a human breast carcinoma cell line (BT-20). The electrophoretic mobility of these glycoproteins on cellulose acetate is consistent with increased glycoprotein-staining material present in the alpha2- to beta-globulin region of serum glycoprotein electropherograms from patients with breast cancer. Moreover, after mastectomy, this glycoprotein material in serum decreases to concentrations seen in a control population of patients with benign breast lesions. Patients with proven metastatic breast cancer have patterns reflecting their clinical status: those who respond to treatment have glycoprotein electropherograms similar to the group of patients with benign breast lesions, while those who do not have increased amounts of alpha2- beta-glycoprotein. We believe serum glycoprotein measurements in breast-cancer patients reflect the presence of glycoproteins that are released by the malignant cells and enter the circulation.

Breast Neoplasms↗

PubMed1976

Imipramine-serotonin induced myopathy.

Imipramine and serotonin (5-HT) were used to produce a myopathy in rats. Imipramine was used to stimulate a defect in transport of 5-HT observed in the platelets of Duchenne's dystrophy patients. The most effective dosage schedule was imipramine, 10 mg per kilogram, for 7 days followed by 5-HT, 100 mg per kilogram, 6 hours after the final imipramine dose. A single series of injections produced focal groups of necrotic and regenerating muscle fibers. In some rats, multiple series of injections resulted in a chronic myopathy with a predilection for proximal muscles, particularly quadriceps. In addition to skeletal muscle lesions, focal areas of myocardial damage were seen. The affected rats had a marked elevation of plasma creatine phosphokinase (including MB isoenzyme), serum glutamic oxaloacetic transaminase, and lactic dehydrogenase. Femoral nerve section did not affect the development of muscle lesions.

Animals↗

PubMed1976

Significance of creatine phosphokinase isoenzymes in Duchenne dystrophy.

Study of creatine phosphokinase (CPK) isoenzymes using a quantitative column chromatographic technique showed that there was a significant difference in serum MB isoenzyme activity between patients with Duchenne muscular dystrophy (42 mU per milliter) and those with other kinds of neuromuscular diseases (8 mU per milliter). In the Duchenne patients, the serum MB isoenzyme activity did not correlate with clinical cardiac disease. Furthermore, skeletal muscle damage produced in the rat by aortic ligation and 5-hydroxytryptamine resulted in significant elevations of plasma MB isoenzyme activty. These studies suggest that the serum MB isoenzyme activity in the Duchenne muscular dystrophy patients is probably arising from skeletal, not cardiac muscle and may reflect a distinct pathogenesis from other kinds of neuromuscular disorders.

Animals↗

PubMed1976

Sarcolemmal membrane changes related to enzyme release in the imipramine/serotonin experimental animal model.

We report specific findings in the imipramine/serotonin animal model that are consistent with sarcolemmal membrane alterations. Among these findings are cytoplasmic enzyme release, diminished uptake of alpha-aminoisobutyrate (an amino acid analog), decreased oxygen consumption in isolated rat diaphragm, and ribosuria. Furthermore, we describe for the first time the release of the MB isoenzyme of creatine kinase from a source other than cardiac tissue; that is, isolated diaphragms from imipramine/serotonin-treated animals release increased amounts of MB isoenzyme as compared to diaphragms from control animals. We believe the similarities between this animal model and the human disease (Duchenne muscular dystrophy) support a genetically determined generalized membrane abnormality in the pathogenesis of this form of muscular dystrophy.

Adenosine Triphosphatases↗

PubMedDate not supplied

Cerebrospinal fluid analysis in human immunodeficiency virus infection.

Cerebrospinal fluid (CSF) analytes were evaluated in 59 human immunodeficiency virus (HIV+) individuals to assess neurological involvement. Glucose, total protein, cell counts, p24 antigen, CSF: serum albumin/IgG ratios, and oligoclonal bands were measured. Eighty percent of samples showed abnormalities in one or more analyte. In some patients samples, these abnormalities could mimic those of secondary opportunistic infection when none was present. The presence of oligoclonal banding in CSF (31 percent) and disturbances in CSF: serum albumin/IgG ratio (30 percent) were related to decreases in serum CD4+ lymphocytes. Disturbances in CSF: Serum albumin/IgG ratio were also related to severity of non-neurological HIV disease staging. Cerebrospinal fluid oligoclonal bands were distinct from that found in serum in the same subjects. Since immune complexes between immunoglobulins and enzymes are observed in these same patients, these oligoclonal bands may result in artifactually elevated enzyme results secondary to decreased clearance leading to erroneous clinical decisions. There was no significant relationship between any abnormalities and the presence of neurologic disease as established by a wide variety of other studies. It is important to recognize the limits of CSF interpretation in this patient group.

AIDS-Related Complex↗

PubMedDate not supplied

Whether no means no.

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Acquired Immunodeficiency Syndrome↗

PubMedDate not supplied

Review of serum lipids and apolipoproteins in risk-assessment of coronary heart disease.

Coronary heart disease (CHD), the leading cause of death in the western world, is multifactorial in nature. Abnormal lipoprotein levels are among the risk factors that cause atherosclerosis and, therefore, have been used as biochemical markers in assessing risk of developing CHD. The measurement of serum cholesterol, lipoprotein cholesterol, and apolipoproteins accurately and reliably has been hampered with technical difficulties. In addition, the interpretation of these tests and the determination of their clinical values have been challenging for both physicians and laboratory scientists. This article addresses and reviews the major current analytical and clinical concerns in the testing of lipids as well as the prevention and treatment of CHD.

Adult↗

PubMedDate not supplied

Cerebrospinal fluid and plasma apolipoproteins in patients with multiple sclerosis.

Apolipoprotein (apo) E is synthesized by cells of the central and peripheral nervous systems, and its synthesis and secretion in the peripheral nervous systems, and its synthesis and secretion in the peripheral nervous system of animals are greatly stimulated following Wallerian degeneration. It has been suggested that apo E functions in the metabolism of myelin lipids, but its physiologic role in nervous tissue has not been elucidated. To determine if apo E might play a role in demyelinating neuropathy, the concentrations were examined of apos E and A-1 in the cerebrospinal fluid (CSF) and plasma of patients with multiple sclerosis during clinical remission, and in patients with no neurologic disease. Serum and CSF albumin concentrations were measured to account for the possible influences of serum apo E concentration and/or altered blood-brain barrier permeability on the CSF apo E pool. A CSF index for apo E and apo A-1 was calculated in the same manner presently used for calculation of immunoglobulin G (IgG) production in the nervous system of patients with multiple sclerosis (MS). The results showed that the concentrations of apo E, apo Al, and albumin in the CSF of the MS patients were not significantly altered. The concentration of apo E in the serum, however, was significantly (p less than 0.001) decreased by 44 percent in the MS patients. The difference was relatively specific for serum apo E because the serum apo Al and albumin concentrations were unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMedDate not supplied

Bidding for donors.

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Autopsy↗

PubMedDate not supplied

Creatine kinase elevations in marathon runners: relationship to training and competition.

Elevation of creatine kinase (CK) in serum after exertion is a reliable marker of skeletal muscle injury. Limited data exist on CK levels in conditioned athletes after endurance training and competition. Serum CK was measured by a kinetic UV method (normal < 100 U/L) in 15 long distance runners before (pre-race), 24 hours after (post-race) and four weeks following (post-race) the 1979 Boston Marathon. CK levels were elevated throughout the study. Mean values for all runners and for those finishing before and after three hours and 30 minutes are as follows: Post-race CK was significantly elevated among the ten faster as compared to the five slower runners (p = 0.025). Elevations of creatine kinase drawn 24 hours post-marathon are inversely related to finishing times among the runners tested.

Adult↗

PubMedDate not supplied

In situ amplification: detection of target sequences in whole tissues.

Using the polymerase chain reaction (PCR) specific gene target sequences can be routinely amplified from isolated nucleic acids. However, this does not allow the investigator the option of correlating the presence of amplified product with cellular localization. When PCR is performed in situ and coupled with either a direct or indirect method of detecting amplified product, a powerful investigative tool exists. Owing to variability in results, the features of in situ PCR which are most likely to contribute to these effects are described. Also described is an amplification chamber for localized in situ amplification (LISA) which utilizes tissue culture cloning rings and allows for the amplification of gene target sequences in specific regions of paraffin-embedded tissue sections.

Animals↗