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Biomedical subjects

S A Barenberg

Publications and source records attributed to S A Barenberg.

8 recordsLinked to original sources
PubMed1983

Thrombogenesis: effect of molecular motions, surface order, and hydrophobicity of the polymer interface.

The effect and interrelationship between primary and secondary molecular motions, morphological order/disorder, and associated water on thrombogenesis are elucidated using an amorphous hydrophobic polymer of poly[trifluoroethoxy) ( fluoroalkoxy ) phosphazene ], a semicrystalline triblock copolymer of poly[(gamma-benzyl-L-glutamate) (acrylonitrile/butadiene) (gamma-benzyl-L-glutamate)] and a surface cross-linked hydrophilic/hydrophobic(core)/hydrophilic triblock copolymer of poly[(hydroxy propyl glutamine) (gamma-benzyl-L-glutamate) (hydroxy propyl glutamine)]. The thrombogenic response of the polymers indicated that for a semicrystalline polymer an epitaxial model can be employed to correlate and interrelate the ultrastructure morphology, surface chemistry, surface molecular motions, degrees and types of associated bound water and surface/subsurface ion binding to thrombogenesis. Further for an amorphous polymer, of given side chain length and chemistry, the results indicate that there is an initial effect of molecular motions on thrombogenesis, independent of morphological order/disorder and/or associated water.

Animals↗
PubMed1982

Polyphosphazenes: effect of molecular motions on thrombogenesis.

The effect and interrelationship between primary (segmental backbone) and secondary (side chain) molecular motions on thrombogenesis, independent of morphological order/disorder, crystallinity, and/or associated water is elucidated using an amorphous hydrophobic polymer of poly-[(trifluoroethoxy) (fluoroalkoxy)phosphazene] PNF. The results indicate that thrombogenesis for an amorphous hydrophobic polymer is sensitive and dependent on the degrees and types of primary and secondary molecular motions at the polymer interface.

Animals↗
PubMed1982

Membranous glomerulonephritis associated with industrial mercury exposure. Study of pathogenetic mechanisms.

The nephrotoxicity associated with mercury may be manifested as either acute tubular necrosis or an immune complex glomerulonephritis, depending upon the conditions under which the patient is exposed to the metal. Two patients with industrial exposure to mercury developed the nephrotic syndrome due to membranous glomerulonephritis. A multidisciplinary approach was used to define more precisely the pathogenetic mechanisms involved in the production of the glomerular lesion. Although glomeruli were normal by light microscopy, immunohistochemical studies demonstrated confluent finely granular epimembranous deposits of IgG and C3. This distribution was confirmed at the ultrastructural level with immunoelectron microscopy. High resolution elemental analysis of electron dense inclusions in tubular epithelial phagolysosomes demonstrated energy dispersion spectra characteristic of coexisting mercury and selenium. Eluates from the biopsy material were not immunoreactive against normal rat or human kidney. There was no immunoreactivity of epimembranous deposits with antibodies having renal tubular epithelial antigen or urinary uromucoid specificity. These observations suggest that a distinctive immunopathologic lesion is associated with mercury-associated membraneous glomerulonephritis, that the role of the metal itself may only be coincidental, and that the involved antigen remains unknown. Prednisone therapy had no documented persistent beneficial influence upon the level of proteinuria in one patient who has been lost to follow-up. In one patient not treated with steroid therapy, withdrawal of exposure to the metal resulted in disappearance of mercury from body fluids and clinical remission.

Adult↗
PubMed1981

Thrombogenesis: an epitaxial phenomena. I.

A semiempirical epitaxial model has been derived which correlates and interrelates the surface free energy, ultrastructural morphology, surface charge, surface chemistry, and surface molecular motions of a model triblock copolymer to thrombogenesis. This paper addresses the aspect of: (1) ultrastructure order versus disorder, (2) primary and secondary molecular motions, (3) surface and side chain chemistry, (4) thrombogenesis, and (5) the derived epitaxial model based on the above observations. This model can be extrapolated to include and predict the relative thrombogenic responses of various crystalline and semicrystalline polymeric substrates, i.e., aliphatic polyolefins, polyurethanes, and polypeptides.

Animals↗
PubMed1978

Ultrastructural deformation of collagen.

Ultrastructure deformation studies of reconstituted and native rat tail tendon collagen revealed that deformation occurs primarily in the non-staining and presumably non-polar proline rich regions for all ages examined. At low deformation (tension and compression) the deformation occurs somewhat more between the a2 and b1 and b2 and c2 bands than within the rest of the d period. At moderate elongations (greater than 40%), the deformation becomes localized between the c2 and d bands, with subfibrils on the order of 3-15 nm being drawn across the openings between the c2 and d bands. At high elongations (100% or greater) d period splitting occur on a regular basis between the c2 and d bands, along with a retraction of the 64 nm repeat period into 60 nm segments. It is in this deformation region that the effects of molecular slip and the apparent association of the acid mucopolysaccharides can be noted. These results suggest that crosslinking, if increasing as a function of age, does not affect the deformation characteristics of the individual fibrils and that changes with age in mechanical properties should be sought in changes in the fibril size and their interaction with the surrounding matrix.

Aging↗