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Biomedical subjects

B A Rubin

Publications and source records attributed to B A Rubin.

At least 19 recordsLinked to original sources
PubMed1984

Experimental neuritis induced by a mixture of neural antigens and influenza vaccines. A possible model for Guillain-Barré syndrome.

We describe the development in rats of a possible model for Guillain-Barré syndrome (GBS): experimental neuritis (EN). The clinical symptoms, histopathology and the presence of antibody to nervous tissue are features that EN has in common with both GBS and experimental allergic neuritis (EAN), another GBS model. However, EN may be a more appropriate model than EAN for studying the role of autoimmune reactions in diseases such as GBS, which are triggered by various viruses or antigens, since EN depends on such agents being administered concomitantly with the syngeneic tissue.

Animals↗
PubMed1981

Induction of sister chromatid exchanges in human diploid fibroblasts by mutagens with and without rat liver microsomal activation.

The frequency of sister chromatid exchange (SCE) in WI-38 cells was estimated by the 5-bromodeoxyuridine (BrdUrd)-dye technique after one hour's exposure to cyclophosphamide (CY), N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), 4-nitroquinoline-1-oxide (4NQO), and maleic hydrazide (MH) with and without the addition of rat liver microsomal suspension (S-9) fraction with cofactors (S-9 mix). CY at concentrations from 1 x 10(-5) M to 1 x 10(-3) M with S-9 mix increased the number of SCEs per cell in a dose-dependent manner. Without S-9 mix, CY at concentrations below 1 x 10(-3) M failed to produce more SCEs than the controls. MNNG at 1 x 10(-8) M and 4NQO at 1 x 10(-7) M without S-9 produced significant increases in SCEs per cell. Addition of S-9 during treatment slightly decreased the effects of MNNG and 4NQO in the formation of SCEs. MH was tested at pH 6.4 and pH 7.6. At pH 7.6, MH at 1 x 10(-3)M without S-9 mix inhibited cell multiplication, but did not cause a significant increase of SCEs per cell. There were no interactions between MH (2 x 10(-4) M) and S-9 mix nor between MH and the pH levels tested. These results indicate that in the presence of metabolic activation, SCE formation in human diploid fibroblasts in vitro may be used as a potential assay for mutagenicity.

Biotransformation↗
PubMed1981

Morphological components of herpesvirus. III. Localization of herpes simplex virus type 1 nucleocapsid polypeptides by immune electron microscopy.

Herpes simplex virus type 1 (HSV-1) nucleocapsids were observed in the electron microscope after their reaction with IgG's purified from the sera of rabbits immunized with the individual nucleocapsid polypeptides. The combining sites of NC1, the major capsid protein (mol. wt. 154K), were distributed over the entire capsid surface. This result provides further evidence that NC1 represents the major hexamer constituent. NC2 (mol. wt. 50K) was less widely distributed and appeared to be located at capsid vertices; that antigen may be a constituent of the pentamers or of peripentameric hexamers. One or both of NC3 and NC4 (mol. wt. 40K and 38K) were also located all over the capsid, possibly at positions interior to those of NC1. One or both may represent the intercapsomeric fibrils, hexamer-associated protein or material associated with the pericore. The locations of the other nucleocapsid polypeptides could not be determined.

Capsid↗
PubMed1980

Lincomycin increases synthetic rate and periplasmic pool size for cholera toxin.

Increased enterotoxigenicity of Vibrio cholerae 569B grown with low concentrations of lincomycin, previously described in terms of increased extracellular biological activity (capillary permeability factor and fluid accumulation in ligated rabbit ileal loops), was further characterized. Polyacrylamide gel electrophoresis and single radial immunodiffusion showed that lincomycin-stimulated cells produced increased molar quantities of cholera toxin (CT) both extra- and intracellularly. The intracellular CT was released in comparable amounts by sonication, deoxycholate extraction, and polymyxin B treatment. Polymyxin B release of CT was nearly complete under conditions wherein only 6% of total cellular beta-galactosidase was released, implying a periplasmic pool of CT in stimulated cells. No intracellular choleragenoid (CT subunit B) was found in stimulated cells by polymyxin B release. No proteolysis of 14C-labeled CT was detected after prolonged incubation with sonicated nonstimulated cultures or sonicated concentrated cells. These data support the conclusion that the stimulatory effect of lincomycin involves an increase in the rate of synthesis of the CT molecule, and argue against alternative models involving inhibition of putative normal degradation of CT, increased release of otherwise cell-bound CT, or activation of inactive, or less active, forms of CT.

Cholera Toxin↗
PubMed1980

Immunopharmacologic properties of 1,6-bis[2-(diethylamino)ethoxy]xanthen-9-one dihydrochloride (Wy-15297).

When tested in a series of immunopharmacologic assays, the interferon inducer, WY-15297, was shown to lack activity in early vascular and humoral phases of the inflammatory response, while it was quite effective against the immunologic phase. The profile of activity of Wy-15927 was, however, unlike those previously described for reference antiinflammatory and immunosuppressive drugs and this may represent one of a new class of immunopharmacologic agents capable of selectively modulating the lymphoreticular system.

Animals↗
PubMed1977

Induction of Escherichia coli and Vibrio cholerae enterotoxins by an inhibitor of protein synthesis.

Enterotoxigenic Escherichia coli or Vibrio cholerae 569B (Inaba) grown in the presence of the antibiotic lincomycin, an inhibitor of protein synthesis, produced elevated levels of heat-labile enterotoxin or choleragen, respectively, as assayed by both vascular permeability factor and capacity to elicit fluid accumulation in rabbit ileal loops. This induction of enterotoxin did not reflect either a coupling of lincomycin resistance with increased enterotoxigenicity or an effect of lincomycin on cellular release of enterotoxin, since spontaneously isolated lincomycin-resistant mutants of both E. coli and V. cholerae still required lincomycin for induction, and large increases in E. coli permeability factor activity were found intracellularly as well as extracellularly. After the period of exponential growth, E. coli became refractory to induction by lincomycin, although most of the induced enterotoxin activity appeared only after this period. No increase in copy number of the enterotoxin plasmid in E. coli 711 (P307) was found in induced cells by analysis of deoxyribonucleic acid reassociation kinetics. These and other data suggest that synthesis of enterotoxin, or at least its accumulation, is normally limited by cellular factors whose synthesis is preferentially inhibited by lincomycin. A possible connection between this phenomenon and lincomycin-associated diarrhea is considered.

Animals↗
PubMed1977

Black skin.

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Animals↗
PubMed1976

Activation of Heat-labile Escherichia coli enterotoxin by trypsin.

Trypsin-treated, cell-free filtrates derived from enterotoxigenic Escherichia coli, strain H197 (O78:H11), exhibited a fourfold or greater increase in heat-labile vascular permeability factor activity and a 10-fold or greater increase in the ability to stimulate secretion of growth hormone by cultured rat pituitary cells. In contrast, trypsin-treated filtrates were not different from untreated filtrates in their ability to elicit a secretory response in ligated rabbit intestinal loops. However, incubation of culture filtrate in ligated intestinal loops, or with rabbit intestinal fluid (in vitro), resulted in at least a twofold increase in permeability factor that did not occur in the presence of trypsin inhibitor or with heat-inactivated intestinal fluid. Moreover, trypsin inhibitor could reduce the secretory response to culture filtrate. These findings suggest that activation of heat-labile E. coli enterotoxin by host enzymes may play a role in the development of a full pathogenic effect.

Animals↗
PubMed1976

Morphological components of herpesvirus. II. Preservation of virus during negative staining procedures.

The disruption of envelopes and the fragmentation of capsids of equine herpes-virus type I observed in negatively stained samples were attributed to viral dehydration on carbon films during preparation for electron microscopy. Prior fixation of virus with OSO4 or glutaraldehyde and subsequent application of negative stain before drying minimized envelope disruption and virtually eliminated the occurrence of capsomere sheets and broken capsids. This sample procedure significantly improves electron microscopic evaluation of herpesvirus samples.

Animals↗
PubMed1976

Development of a purified cholera toxoid. III. Refinements in purification of toxin and methods for the determination of residual somatic antigen.

The addition of an ultrafiltration step to the purification procedures previously described for cholera toxin (Rappaport et al., (1974) permitted the preparation of highly purified antigenic toxoids essentially free of somatic antigen(s). The purity of such toxoids is established: (i) by the absence of more than about one part limulus amebocyte lysate (LAL)-positive endotoxin per 10(5) parts toxoid and (ii) by the inability of the toxoids to elicit a significant rise in rabbit vibriocidal antibody. The antigenicity of the toxoids is demonstrated by their ability to produce the same high levels of rabbit serum antitoxin as are produced by comparable toxoids containing small amounts of somatic antigen. The results also indicate that amounts of somatic antigen of the order of less than or equal to 1 mug/100 mug of toxoid do not exert an adjuvant effect on the toxoid, at least with respect to circulating antitoxin. Other data show that, where present, the ability of somatic antigen to elicit vibriocidal antibody is influenced by the immunization schedule employed and that a correlation exists between the LAL-determined endotoxin content of the toxoids and their ability to stimulate vibriocidal antibody. Somatic antigen-free toxoids, purified and tested by the refinements herein described, were prepared for use in the National Institutes of Health sponsored field trials, and data pertaining to their purity and antigenic properties are presented.

Animals↗
PubMed1976

[Localization of the Meler's reaction with ethanol catalase trap in the chain of photosynthetic electron transport].

The common view of photosystem I as the action site of catalase and ethanol at oxygen uptake in chloroplasts are based on indirect data on this reaction. That is why the question on Mehler reaction localization in electron transport chain with ethanolcatalase trap has been investigated anew. It has been demonstrated that oxygen uptake with catalase and ethanol does not decrease in presence of dibromothymoquinone (2,5-dibromo-3-methyl-6 isopropyl-p-benzoquinone--DBTQ) which blocks electron transfer to photosystem I at plastoquinones level. The summation of oxygen uptake activities is observed on the combined action of catalase and ethanol with any of the Mehler reagents functioning in photosystem I (methylviologen,FMN, epinephrine, ferredoxin). Catalase and ethanol in contrast to methylviologen have no effect on photooxidation rate of reduced dichlorphenolindophenol in photosystem I. The quatum yield of oxygen uptake with catalase and ethanol versus wave length of actinic light shows a distinct maximum in the photosystem II absorption area and a "red drop" in the longware area. The obtained data show that the Mehler reaction with catalase and ethanol takes place in photosystem II only.

2,6-Dichloroindophenol↗