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Biomedical subjects

R Eisenberg

Publications and source records attributed to R Eisenberg.

At least 19 recordsLinked to original sources
PubMed1988

Validating the certification process for infection control practice.

Approximately 5 years ago a task analysis was conducted by the Certification Board of Infection Control (CBIC) to describe infection control practice. This task analysis served as the basis for development of the certification examination. This article describes the process used to update and revalidate the original task analysis to ensure the continued validity and job relatedness of the certification process. Using a modified Delphi technique, several panels of representative expert infection control practitioners (ICPs), a total of 29 persons, participated in an iterative process to define the practice dimensions of infection control and to link these practice dimensions to the certification examination. In general, there was a high level of congruence between respondents on the original task analysis and the expert panels, although a few differences in practice were identified among ICPs in extended care facilities and a few new tasks were identified. In addition, a revised content outline for the examination was created by placing clusters of knowledge statements together around common themes.

Certification↗
PubMed1988

Pacemaker implantation in children: a 21-year experience.

Forty-one children, 20 boys and 21 girls, aged 11 days to 19 years (mean 9.9 years) at initial pacemaker implant, were followed 1 to 248 months (mean 90 months). Ten (mean age 8.2 years) were implanted between 1966 and 1972 (Group I), 14 (mean age 9.9 years) between 1973 and 1980 (Group II) and 17 (mean age 10.9 years) from 1981 through April 1988 (Group III). Arrhythmias were congenital complete heart block in 19, postoperative heart block in 15, acquired heart block in 3, sick sinus syndrome in 3, and bradycardia-induced ventricular fibrillation in 1. Twenty-eight of 41 children had a transvenous implant: 40% of Group I, 71% of Group II and 82% of Group III. Thirteen were cephalic, four subclavian and 11 jugular. Generator site was pectoral in 19, abdominal in 12, intrathoracic in one, and retromammary in nine of 12 girls aged 10 years or more at implant. In Groups I, II and III, 5, 14 and 6 had VOO or VVI units; 5, 0 and 8 dual chamber (VAT, VDD and DDD) pacemakers; 0, 0 and 1 AAI; and 0, 0 and 2 rate-modulated (VVIR) units at initial implant. The average interval between pacer-related hospitalizations in Groups I, II and III was 20, 42, and 39 months. Complications included infection in six, hemothorax in one, and impending pacemaker erosion in one. Six patients died, one of pacer infection, four from primary cardiac disease, and one suddenly without apparent reason. Follow-up continues in 31: 14 are employed full-time, three are homemakers, eight are full-time students, and six are active pre-schoolers.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed1986

Primary pulmonary amyloidosis. An unusual case with 14 years' survival.

A 70-year-old woman had nodular lesions and a right hilar infiltrate visible on chest x-ray film. The diagnosis of pulmonary amyloidosis was established by a transbronchial lung biopsy. Over the next 14 years, the patient remained relatively asymptomatic but developed extensive pulmonary involvement. The case illustrates the long and relatively benign course of primary pulmonary amyloidosis.

Aged↗
PubMed1984

Sustained arrhythmias in hypertrophic obstructive cardiomyopathy.

Patients with hypertrophic obstructive cardiomyopathy are subject to syncope and sudden death. Ambulatory monitoring discloses frequent and complex ventricular ectopy in many of these patients, and the occurrence of ventricular tachycardia suggests an increased risk of sudden death. We prospectively evaluated whether induced sustained arrhythmia could explain episodes of cerebral dysfunction in hypertrophic cardiomyopathy. Seven consecutive symptomatic patients (six of whom had an intraventricular gradient of 40 to 130 mm Hg) were subjected to atrial and ventricular stimulation. An electrophysiologic abnormality that would explain the symptoms was identified in every patient: supraventricular tachycardia was present in two, sustained ventricular tachycardia in three, ventricular fibrillation in one, and a prolonged QT interval and dispersion of ventricular refractoriness in one. Antiarrhythmic drugs were selected on the basis of the response to electrophysiologic testing. There has been no recurrence of symptoms in 120 patient-months of follow-up. This experience suggests that arrhythmias are the principal cause of syncope or sudden death in obstructive cardiomyopathy and that electrophysiologic study may be useful in selecting prophylactic therapy.

Adult↗
PubMed1984

Direct demonstration that the abundant 6-kilobase herpes simplex virus type 1 mRNA mapping between 0.23 and 0.27 map units encodes the major capsid protein VP5.

The two partially colinear 6-kilobase (kb) and 1.5-kb mRNAs mapping between 0.23 and 0.27 map units on the herpes simplex virus type 1 genome were precisely located. The 5' end of the 6-kb mRNA was located 28 bases downstream of the sequence ATATATT and was 10 bases to the left of the BamHI site at 0.268. This position is ca. 90 bases to the left of our earlier reported sequence (R. J. Frink, K. G. Draper, and E. K. Wagner, Proc. Natl. Acad. Sci. U.S.A. 78:6139-6143, 1981). We used a polyclonal antibody made against purified herpes simplex virus type 1 VP5 to demonstrate that the 155,000-dalton translation product of the 6-kb mRNA is this capsid protein. The antibody did not react with the 35,000-dalton translation product of the 1.5-kb mRNA. We also confirmed our identification of VP5 as the translation product of the 6-kb mRNA by comparison of tryptic peptides of the in vitro-translated protein and authentic VP5.

Antibodies, Viral↗
PubMed1983

Detailed analysis of the portion of the herpes simplex virus type 1 genome encoding glycoprotein C.

We previously showed that the right third of HindIII fragment L (0.59 to 0.65) of herpes simplex virus type 1 (HSV-1) encodes a family of mRNAs some members of which appear to be related by splicing. In the experiments described in this communication, we determined the nucleotide sequence of the DNA encoding this mRNA family and precisely located the mRNAs associated with this DNA sequence. The major mRNA species is unspliced and encoded by a 2.520-nucleotide region. Just upstream of the 5' end are TATA and CAT box sequences characteristic of HSV-1 promoters. The 3' end maps near a region containing a nominal polyadenylation signal. Three minor species (2,400, 2,200, and 1,900 bases, respectively) appear to share a very short leader sequence with the 5' end of the major mRNA and are then encoded by uninterrupted DNA sequences beginning about 100, 400, and 625 bases downstream of the 5' end of the major unspliced mRNA. These positions map at or very near positions which agree reasonably well with consensus splice acceptor sequences. The fourth mRNA is encoded by a contiguous 730-nucleotide sequence at the 3' end of the major unspliced mRNA and has its 5' end just downstream of recognizable TATA and CAT box sequences. We suggest that this mRNA is controlled by its own promoter. The nucleotide sequence data, in combination with the mRNA localization, demonstrate four potential polypeptides encoded by the region. The largest is 1,569 bases long and defines a 523-amino acid protein with sequence features characteristic of a glycoprotein. This was confirmed to be HSV-1 glycoprotein C by immune precipitation of the in vitro translation product of the major unspliced mRNA, performed with a polyspecific antibody to HSV-1 envelope glycoproteins (anti-env-1 serum), and by comparison of tryptic peptides of this translation product with those of authentic HSV-1 glycoprotein C. Polypeptides encoded by some of the minor species also were tentatively identified.

Base Sequence↗
PubMed1983

Glycopeptides of the type-common glycoprotein gD of herpes simplex virus types 1 and 2.

We have carried out detailed structural studies of the glycopeptides of glycoprotein gD of herpes simplex virus types 1 and 2. We first examined and compared the number of N-asparagine-linked oligosaccharides present in each glycoprotein. We found that treatment of either pgD-1 or pgD-2 with endo-beta-N-acetylglucosaminidase H (Endo H) generated three polypeptides which migrated more rapidly than pgD on gradient sodium dodecyl sulfate-polyacrylamide gels. Two of the faster-migrating polypeptides were labeled with [(3)H]mannose, suggesting that both pgD-1 and pgD-2 contained three N-asparagine-linked oligosaccharides. Second, we characterized the [(3)H]mannose-labeled tryptic peptides of pgD-1 and pgD-2. We found that both glycoproteins contained three tryptic glycopeptides, termed glycopeptides 1, 2, and 3. Gel filtration studies indicated that the molecular weights of these three peptides were approximately 10,000, 3,900, and 1,800, respectively, for both pgD-1 and pgD-2. Three methods were employed to determine the size of the attached oligosaccharides. First, the [(3)H]mannose-labeled glycopeptides were treated with Endo H, and the released oligosaccharide was chromatographed on Bio-Gel P6. The size of this molecule was estimated to be approximately 1,200 daltons. Second, Endo H treatment of [(35)S]methionine-labeled glycopeptide 2 reduced the molecular size of this peptide from approximately 3,900 to approximately 2,400 daltons. Third, glycopeptide 2 isolated from the gD-like molecule formed in the presence of tunicamycin was approximately 2,200 daltons. From these experiments, the size of each N-asparagine-linked oligosaccharide was estimated to be approximately 1,400 to 1,600 daltons. Our experiments indicated that glycopeptides 2 and 3 each contained one N-asparagine-linked oligosaccharide chain. Although glycopeptide 1 was large enough to accommodate more than one oligosaccharide chain, the experiments with Endo H treatment of the glycoprotein indicated that there were only three N-asparagine-linked oligosaccharides present in pgD-1 and pgD-2. Further studies of the tryptic glycopeptides by reverse-phase high-performance liquid chromatography indicated that all of the glycopeptides were hydrophobic in nature. In the case of glycopeptide 2, we observed that when the carbohydrate was not present, the hydrophobicity of the peptide increased. The properties of the tryptic glycopeptides of pgD-1 were compared with the properties predicted from the deduced amino acid sequence of gD-1. The size and amino acid composition compared favorably for glycopeptides 1 and 2. Glycopeptide 3 appeared to be somewhat smaller than would be predicted from the deduced sequence of gD-1. It appears that all three potential glycosylation sites predicted by the amino acid sequence are utilized in gD-1 and that a similar number of glycosylation sites are present in gD-2.

Amino Acids↗
PubMed1983

High-resolution characterization of herpes simplex virus type 1 transcripts encoding alkaline exonuclease and a 50,000-dalton protein tentatively identified as a capsid protein.

Four partially overlapping mRNAs (1.9, 2.3, 3.9, and 4.5 kilobases [kb]) were located between 0.16 and 0.19 map units on the herpes simplex virus type 1 genome. Their direction of transcription was found to be from right to left. The 2.3-kb mRNA was found to be early (beta), whereas the others were late (beta gamma). Partial sequence analysis of the DNA encoding these genes indicated that the promoter for the 2.3-kb mRNA shares structural features with other early (beta) promoters. In vitro translation of hybrid-selected mRNA indicated that among the proteins these mRNAs encode are an 82,000-dalton (d) polypeptide reactive with a monoclonal antibody against herpes simplex virus type 2 alkaline exonuclease and a 50,000-d polypeptide weakly reactive with a polyclonal antibody made against the capsid protein VP19C. Further experiments suggested that the 2.3-kb mRNA encodes the 82,000-d polypeptide, whereas one (or both) of the larger mRNAs encodes the 50,000-d protein. A novel finding was that the 1.9-kb mRNA appears to share part of the translational reading frame for alkaline exonuclease, but any polypeptide it encodes does not react with the monoclonal antibody to this enzyme.

Base Sequence↗
PubMed1982

Measurement of bacterial cell wall in tissues by solid-phase radioimmunoassay: correlation of distribution and persistence with experimental arthritis in rats.

We have developed sensitive and specific solid-phase radioimmunoassays to quantitate the distribution and persistence of bacterial antigen in rats developing arthritis in response to a single injection of streptococcal cell wall material. Three separate assays were specific for either the A polysaccharide (N-acetyl-D-glucosamine), A-variant polysaccharide (polyrhamnose), or peptidoglycan (D-ala-D-ala) moieties of the streptococcal cell wall. Antigen was detected in all tissues surveyed, although the greatest amount was in the liver and spleen. By using three fractions of cell wall separated by size, we have shown that the development of arthritis correlates with the degree of cell wall deposited and persisting in the joints. Further statistical analyses suggested differences in metabolism by different tissues and differential metabolism of different antigenic epitopes in some cases.

Acetylglucosamine↗
PubMed1982

Relationship of complement to experimental arthritis induced in rats with streptococcal cell walls.

Experimental arthritis developed in rats injected intraperitoneally with aqueous suspensions of peptidoglycan-polysaccharide complexes (PG-APS) isolated from group A streptococcal cell walls. Reduction of serum complement by pretreatment with cobra venom factor (COV) reduced acute joint inflammation over the first 3 days following injection of PG-APs. Thereafter, the course of the disease was not different in the COV-treated rats. The serum levels of complement were depressed below detectable levels by 24 hr in rats injected only with cell walls, but rebounded to normal levels or above 3 days after injection. In rats injected with COV before cell walls, the complement levels also increased 3 days after injection of cell walls, in contrast to sustained depressed levels in rat injected only with COV. The correlation between severity of joint inflammation and serum complement levels at day 3 was positive in COV-treated rats. The quantity of cell wall per joint at day 3 correlated with the severity of joint disease. However, COV treatment did not alter the amount of cell wall localized in joint tissue. Therefore, although complement does appear to have a role in early joint inflammation, its effect is not upon the transport of cell wall into joint tissue.

Animals↗
PubMed1978

Symmetry of binding sites of a mouse IgA myeloma protein (MOPC 315).

We have investigated the mechanism of monovalency of the 7S subunit of a mouse IgA myeloma protein (MOPC 315) against a large antigen. This subunit, although it clearly can bind two molecules of a small hapten, fails to precipitate or hemagglutinate the relevant multivalent antigen. In an equilibrium Farr assay, we have shown that the subunit has only one valence for a univalent 40,000 molecular weight antigen (dinitrophenyl-dextran). We have investigated how various levels of affinity labeling quantitatively affect (a) the valence observed in the equilibrium Farr assay against a large antigen, and (b) the binding of the MOPC 315 to an insoluble antigenic matrix. Our results indicate that the Fab regions of the 7S subunit are arranged symmetrically and that the inactivity of one of them toward a large antigen is probably due to steric hindrance caused by the antigen bound to the adjacent site.

Animals↗
PubMed1978

Natural history of nonstenotic, asymptomatic ulcerative lesions of the carotid artery.

To define the natural history of the asymptomatic, nonstenotic, ulcerative lesion involving the carotid artery bifurcation, the arteriograms and clinical course of 67 patients with 72 asymptomatic ulcerative lesions of the carotid artery were reviewed. The angiographic appearance of ulceration was classified into three groups: minimal (group A), large (group B), and compound (group C). Using life-table methods, the clinical course of these patients was compared between groups and was also compared to a nonrandomized surgically treated group of patients with nonstenotic ulcerative lesions in whom operation was performed for hemispheric or monocular symptoms. There were no significant (P greater than .1) differences in mortality, but the differences in stroke incidence was highly significant (P less than .001). The annual stroke rate, averaged over seven years, was 0.4% per year for group A, 1.47% per year for the surgically treated group, and 12.5% per year for groups B and C. The data indicate that group A ulcers have a benign prognosis, in noticeable contrast to group B and C ulcers which incur a high risk for subsequent stroke.

Adult↗
PubMed1977

Thrombotic thrombocytopenic purpura-like syndrome associated with infective endocarditis. A possible immune complex disorder.

A thrombotic thrombocytopenic purpura (TTP)-like syndrome was the chief presenting feature in two patients with infective endocarditis. Clinical and laboratory aberrations of the syndrome were rapidly reversed by specific antimicrobial therapy. Hypocomplementemia and high levels of circulating immune complexes were detected initially in both patients. Because these returned to normal as the TTP syndrome abated, an immunopathologic mechanism may have been operative.

Adult↗