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1.  Binding of beta-lactam antibiotics to penicillin-binding proteins of Staphylococcus aureus and Streptococcus faecalis: relation to antibacterial activity. 
The binding of 14 structurally diverse beta-lactam antibiotics to penicillin-binding proteins of Staphylococcus aureus and Streptococcus faecalis was studied, and the results were examined in the context of the antibacterial activity of the compounds. Penicillin-binding proteins 1 (molecular weight, 87,000) and 3 (molecular weight, 75,000) of S. aureus and penicillin-binding proteins 1 (molecular weight, 105,000) and 3 (molecular weight, 79,000) of S. faecalis bound beta-lactam antibiotics at concentrations comparable to minimum inhibitory concentrations and might therefore be essential. The low affinity of S. faecalis penicillin-binding proteins, relative to that of S. aureus penicillin-binding proteins, toward most beta-lactam antibiotics is probably responsible for the resistance of the former organism to most of these compounds.
PMCID: PMC284100  PMID: 6778388
2.  Penicillin-binding proteins in bacteria. 
The penicilllin-binding proteins (PBPs) of several gram-positive and gram-negative bacteria have been examined. The results indicate that: (i) PBPs are membrane proteins with molecular weights ranging from 40,000 to 120,000. When extracted with Triton X-100 from sonicated cells, they appear to fall into two patterns: one found in rods and the other in spheres. A major difference is in the low-molecular-weight component, which is usually the major PBP in bacilli but a minor one in cocci. (ii) There is a wide variation in both the number and the amount of PBPs in different bacteria, and taxonomically related bacteria tend to have similar PBP patterns. These patterns often correlate with the affinity of PBPs for penicillin and other beta-lactam antibiotics. (iii) The low-molecular-weight component usually releases penicillin spontaneously with a half-life of 10 min or less. Most, but not all, PBPs release bound penicillin in the presence of neutral hydroxylamine (0.2 to 0.8 M).
PMCID: PMC283955  PMID: 7416741
3.  Effects of human complement component 1 inactivator on neutrophil chemotaxis and chemotactic deactivation. 
Infection and Immunity  1980;28(3):700-707.
This study was undertaken to ascertain the relationship between complement-derived chemotactic factors and complement component 1 inactivator (C1INA) enhancement of neutrophil chemotaxis. Studies were also designed to determine whether the C1s- reactive or binding site on C1INA was functional in altering chemotactic responsiveness of neutrophilic leukocyes. Chemotaxis was assessed by determining cell migration in micropore filters. C1INA was found to enhance the chemotactic response to zymosan-activated plasma, C5a, and N-formyl-L-methionyl-L-phenylalanine and to bring the response of chemotactically deactivated cells to normal. In contrast, C1INA inhibited the chemotactic response to trypsin and EAC4oxy2-activated C3. Complexes of C1INA and C1s- failed to mediate the usual C1INA-enhanced response. Artificially produced C5-deficient plasma, when treated with zymosan, failed to support chemotaxis or to produce chemotactic deactivation. C1INA was without effect when this activated plasma was used as a source of chemotactic factors. We conclude from these data that C1INA enhancement of neutrophil chemotaxis to activated plasma is associated with C5-derived chemotactic fragments. The effects of C1INA are apparently related to the C1s- reactive or binding site(s) on the C1INA molecule. We suggest that C1INA may play a homeostatic role in neutrophil chemotaxis.
PMCID: PMC551007  PMID: 7399690
4.  12-O-Tetradecanoyl-Phorbol-13-Acetate Release of Glycosyltransferases from Human Blood Cells 
Journal of Clinical Investigation  1980;65(6):1365-1371.
The mononuclear cells separated from human blood by Ficoll-Hypaque centrifugation contained and released sialyltransferase, galactosyltransferase, and fucosyltransferase. Granulocytes contained and released lesser amounts of glycosyltransferases, whereas platelets released more fucosyltransferase than sialyltransferase or galactosyltransferase. When mononuclear cells were incubated with 12-O-tetradecanoyl-phorbol-13-acetate (TPA), the release of these three glycosyltransferases increased two- to six-fold, and cell suspension glycosyltransferase activities decreased 10-50%. Mononuclear cells were fractionated into lymphocytes and monocytes using baby hamster kidney cells microexudate-coated flasks. TPA stimulated the release of glycosyltransferases from lymphocytes but not from monocytes. The release of glycosyltransferases by TPA-treated mononuclear cells was not further stimulated by reincubation with TPA and was not affected by puromycin, cAMP, or cGMP. Concanavalin A, a mitogenic stimulator of lymphocytes, also stimulated the release of glycosyltransferases from mononuclear cells, but to a lesser extent. TPA did not stimulate the release of 5′-nucleotidase or decrease its activity on the cell pellet. Triton X-100 (0.2%) stimulated the release of glycosyltransferases to the same extent as TPA, but also caused the release of 5′-nucleotidase. [3H]TPA bound specifically and reversibly to mononuclear cells. The possible relationship between glycosyltransferase release and TPA effect on the plasma membrane is discussed.
PMCID: PMC371474  PMID: 6447709
5.  The Role of Payment Source in Differentiating Nursing Home Residents, Services, and Payments 
Health Care Financing Review  1980;2(1):51-61.
In 1976, it cost $10.6 billion to care for the over one million nursing home residents in the U.S. (Gibson et al, 1977). While public and private sources spent almost equal amounts, it is widely believed that differences exist between public and private patients in terms of need for institutionalization, services received, and rates of payment for care. This paper presents a descriptive analysis of data from a national probability survey, the 1976 Survey of Institutionalized Persons (SIP), and examines variations associated with source of payment for institutionalized long-term care.
PMCID: PMC4191149  PMID: 10309257
6.  Animal models of primary myocardial diseases. 
Feline and canine cardiomyopathies (primary myocardial diseases) were reviewed and divided into three groups based on the clinical, hemodynamic, angiocardiographic, and pathologic findings: (1) feline and canine hypertrophic cardiomyopathy, (2) feline and canine congestive (dilated) cardiomyopathy, and (3) feline restrictive cardiomyopathy. All three groups consisted predominantly of mature adult male cats and dogs. Cardiomyopathy in the hamster and turkey was also reviewed. The most common presenting signs were dyspnea and/or thromboembolism in the cat, systolic murmurs with gallop rhythms on auscultation, cardiomegaly with (groups 1 and 3) or without (group 2) pulmonary edema, abnormal electrocardiograms, elevated left ventricular end-diastolic pressures, and angiocardiographic evidence of mitral regurgitation with left ventricular concentric hypertrophy (group 1), left ventricular dilatation (group 2), or midventricular stenosis (group 3). Some cats in groups 1 and 3 also had evidence of left ventricular outflow obstruction. The principal pathologic findings in all of the cats and dogs were left atrial dilation, hypertrophy, increased septal:left ventricular free wall thickness ratio with disorganization of cardiac muscle cells (group 1); dilatation of the four chambers with degeneration of cardiac muscle cells (group 2); and extensive endocardial fibrosis and adhesion of the left ventricle (group 3). Aortic thromboembolism was commonly observed in the cats of all three groups. These clinical and pathologic findings indicate that cardiomyopathy in the cat or dog is similar to the three forms of cardiomyopathy in humans (hypertrophic, congestive, and restrictive).
PMCID: PMC2595887  PMID: 6447412

Results 1-6 (6)