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Biomedical subjects

B Rubin

Publications and source records attributed to B Rubin.

At least 37 records · Page 2Linked to original sources
PubMed2000

Montmorillonite-phenyltrimethylammonium yields environmentally improved formulations of hydrophobic herbicides.

This study aimed to design formulations of hydrophobic herbicides, alachlor and metolachlor, by adsorbing them on the clay mineral montmorillonite preadsorbed by the small organic cation phenyltrimethylammonium (PTMA). An adsorption model that considers electrostatics and specific binding and the possibility of cation adsorption above the cation exchange capacity (CEC) could explain and yield predictions for PTMA adsorption in the presence of NaCl concentrations from 0 to 500 mM. Adsorption of alachlor and metolachlor from aqueous solution on a clay mineral preadsorbed by PTMA was determined by GC and modeled by Langmuir equation. Herbicide interactions with the organoclay were studied by Fourier transform infrared spectroscopy. Leaching of herbicides was determined by a bioassay using a column technique and Setaria viridis as a test plant. The adsorbed amounts of alachlor and metolachlor on montmorillonite preadsorbed by PTMA at a loading of 0. 5 mol/kg (Mont-PTMA0.5) were higher than at a loading up to the CEC, that is, 0.8 mol/kg, and were higher than those obtained by using several other organic cations. Herbicide formulations based on Mont-PTMA0.5 yielded the largest shifts of the infrared peaks of the herbicides. These formulations based on Mont-PTMA0.5 gave slower release and showed improved weed control in comparison with formulations based on other organoclays. These formulations maintained herbicidal activity in the topsoil and yielded the most significant reduction in herbicide leaching.

Adsorption↗
PubMed2000

Organo-clay formulations of the hydrophobic herbicide norflurazon yield reduced leaching.

The study aimed to reduce leaching of the hydrophobic herbicide norflurazon (4-chloro-5-methylamino-2-(alpha,alpha, alpha)-trifluoro-m-tolylpyridazin-3-(2H)-one) by adsorbing it on clays or organo-clays. The surface of the clay mineral montmorillonite was modified from hydrophilic to hydrophobic by preadsorbing it with organic cations, of which thioflavin-T (TFT) at a loading corresponding to (5)/(8) of the cation-exchange capacity of the clay mineral yielded the highest affinity of adsorption of norflurazon. Pillared clay (PC) used without organic cations exhibited enhanced affinity for norflurazon adsorption, much higher than that of montmorillonite or sepiolite. Fourier transform infrared (FTIR) results showed interactions between aromatic moieties of preadsorbed TFT and the herbicide. Stronger interaction of the herbicide with a clay mineral or organo-clay corresponded to its slower release. Formulations prepared on the basis of montmorillonite-TFT and PC were more effective in reducing herbicide leaching in soil columns in comparison to the commercial formulation, whereas the herbicidal efficiencies were comparable.

Aluminum Silicates↗
PubMed2000

Photostabilization of the herbicide norflurazon by using organoclays.

Photostable formulations of the herbicide norflurazon [4-chloro-5-(methylamino)-2-(alpha,alpha, alpha-trifluoro-m-tolyl)pyridazin-3-(2H)-one] were achieved by adsorbing it on pillared clay or on montmorillonite preadsorbed with the organic cation thioflavin T (TFT). Diffuse reflectance Fourier transform infrared spectra showed the existence of strong interactions between the aromatic moieties of preadsorbed TFT and the herbicide, particularly after irradiation. The photostabilization of norflurazon obtained with TFT-clay was mainly due to energy transfer from the herbicide to the organic cation via pi-pi interactions. An additional mechanism is the lower production of radicals from the clay when the clay mineral surface is covered with the organic cation. These radicals are responsible for the enhanced photodegradation observed when norflurazon was irradiated in the presence of untreated montmorillonite.

Aluminum Silicates↗
PubMed2000

Dissection of the role of CD3gamma chains in profound but reversible T-cell receptor down-regulation.

T-lymphocyte activity in the immune system is regulated by the quantity of surface membrane T-cell antigen receptors (TCR). The amount of surface-bound TCR is dependent on the rate of [1] biosynthesis, assembly and intracellular transport of the individual chains composing the TCR/CD3 complex and [2] the internalization and recycling of the receptors. The TCR-ligand interaction augments receptor internalization. In the present paper, we have studied short- and long-term down-regulation of TCR/CD3 complexes with monoclonal anti-TCR/CD3 antibodies, and attempted to determine which component(s) of the TCR/CD3 complex are responsible for these two phenomena. Our data indicate that short- and long-term down-regulation is mediated by different mechanisms, and that the extracellular and/or transmembrane regions of CD3gamma molecules appear to play an important role in chronic TCR/CD3 down-regulation and subsequent deficient re-expression. These results may have important implications for the understanding of induction of T-cell tolerance or anergy.

Antibodies, Monoclonal↗
PubMed2000

A new monoclonal anti-CD3epsilon antibody reactive on paraffin sections.

We generated a new monoclonal antibody (MAb), F7.2.38, by immunizing mice with CD3varepsilongammadelta/CD3omega complexes purified from human T-cells by OKT3 MAb-Sepharose affinity chromatography. Immunoprecipitation experiments and Western blotting analysis showed that MAb F7.2.38 recognized the CD3varepsilon chain in CD3varepsilon cDNA-transfected FOX B-cells and in various T-cell lines. Using flow cytometry on permeabilized or intact cells, the epitope was found to be located in the cytoplasmic tail of the CD3varepsilon chain. Immunohistochemical staining on paraffin-embedded sections showed that the reactivity of MAb F7.2.38 was comparable to that of the commercially available anti-CD3varepsilon polyclonal antibody. Of the 52 well-characterized T-cell lymphomas, 41 were positive for F7. 2.38 (79%), whereas all 37 B-cell lymphomas and 69 non-lymphoid tumors were unreactive. This new anti-CD3varepsilon antibody would be particularly useful for phenotyping T-cell lymphomas on routinely processed paraffin-embedded tissue sections.

Animals↗
PubMed1999

Conformational and biochemical differences in the TCR.CD3 complex of CD8(+) versus CD4(+) mature lymphocytes revealed in the absence of CD3gamma.

Mature CD4(+) and CD8(+) T lymphocytes are believed to build and express essentially identical surface alphabeta T-cell receptor-CD3 (TCR.CD3) complexes. However, TCR.CD3 expression has been shown to be more impaired in CD8(+) cells than in CD4(+) cells when CD3gamma is absent in humans or mice. We have addressed this paradox by performing a detailed phenotypical and biochemical analysis of the TCR.CD3 complex in human CD3gamma-deficient CD8(+) and CD4(+) T cells. The results indicated that the membrane TCR.CD3 complex of CD8(+) T lymphocytes was conformationally different from that of CD4(+) lymphocytes in the absence of CD3gamma. In addition, CD8(+), but not CD4(+), CD3gamma-deficient T lymphocytes were shown to contain abnormally glycosylated TCRbeta proteins, together with a smaller, abnormal TCR chain (probably incompletely processed TCRalpha). These results suggest the existence of hitherto unrecognized biochemical differences between mature CD4(+) and CD8(+) T lymphocytes in the intracellular control of alphabetaTCR. CD3 assembly, maturation, or transport that are revealed when CD3gamma is absent. Such lineage-specific differences may be important in receptor-coreceptor interactions during antigen recognition.

Blotting, Northern↗
PubMed1999

Prediction of early-onset asthma in genetically at-risk children.

The W.T. Grant Foundation Asthma Risk Study was designed to prospectively examine children who were considered at a genetically increased risk for the development of asthma. The respective contributions of 11 potential risk factors, both environmental and biological, were assessed in order to determine their relative roles in affecting the early onset of asthma. This is a report of an inception cohort of children born to asthmatic mothers and followed for a 3-year period. All 150 families were recruited from the general community and living within 2 h of the National Jewish Center for Immunology and Respiratory Medicine (Denver, CO). Mothers in the index risk sample had been previously diagnosed with asthma and were recruited during their pregnancy through physician referrals and media solicitation. The index sample of 150 families was 92% Caucasian and predominantly middle class. The mean age of mothers was 29.3 years, and of fathers, 31.1 years. The main outcome was the determination of the early onset of asthma and its association with quantified risk factors. By age 3 years, 14 of the 150 children had developed asthma. Frequent illness, IgE levels at age 6 months, parenting difficulties, and early eczema were significantly associated with the onset of asthma (P = 0.003, P = 0.006, P = 0.01, and P = 0.03, respectively). Only frequent illness, elevated serum IgE levels, and parenting difficulties entered a predictive model where they were independently related to the development of asthma.

Age of Onset↗
PubMed1999

Counseling youth in tobacco-use prevention: determinants of clinician compliance.

OBJECTIVE: The rate and determinants of tobacco prevention and cessation counseling to youth were examined for orthodontists participating in a controlled trial to decrease the incidence of tobacco use among adolescents. METHODS: A cross-sectional interview design in private practice offices throughout Southern California was used. The survey was completed with 126 (82%) orthodontists. Clinicians randomly assigned to the experimental group (N = 77) received a 1.5 h workshop, anti-tobacco materials, reimbursement for provision of anti-tobacco prescriptions, and quarterly checkup visits. Control group clinicians (N = 77) did not receive training, materials, or visits. RESULTS: Experimental group clinicians talked to more adolescent nonsmokers about never beginning tobacco use than did control group clinicians (P < 0.05). Experimental group clinicians talked to more adolescent tobacco users than did control group clinicians; however, the difference was not statistically significant. Content and determinants of counseling were affected by participation in the intervention. CONCLUSIONS: Though training and support increased prevention and cessation counseling, absolute rates remained less than optimal. Social learning factors were associated with prevention and cessation counseling.

Adolescent↗
PubMed1999

Molecular mechanisms in the TCR (TCR alpha beta-CD3 delta epsilon, gamma epsilon) interaction with zeta 2 homodimers: clues from a 'phenotypic revertant' clone.

The association between the TCRalphabeta-CD3gammaepsilondeltaepsilon hexamers and zeta2 homodimers in the endoplasmic reticulum (ER) constitutes a key step in TCR assembly and export to the T cell surface. Incompletely assembled TCR-CD3 complexes are degraded in the ER or the lysosomes. A previously described Jurkat variant (J79) has a mutation at position 195 on the TCR Calpha domain causing a phenylalanine to valine exchange. This results in a lack of association between TCRalphabeta-CD3gammaepsilondeltaepsilon hexamers and zeta2 homodimers. Two main hypotheses could explain this phenomenon in J79 cells: TCR-CD3 hexamers may be incapable of interacting with zeta2 due to a structural change in the TCR Calpha region; alternatively, TCR-CD3 hexamers may be incapable of interacting with zeta2 due to factors unrelated to either molecular complex. In order to assess these two possibilities, the TCR-CD3 membrane-negative J79 cells were treated with ethylmethylsulfonate and clones positive for TCR membrane expression were isolated. The characterization of the J79r58 phenotypic revertant cell line is the subject of this study. The main question was to assess the reason for the TCR re-expression. The TCR on J79r58 cells appears qualitatively and functionally equivalent to wild-type TCR complexes. Nucleotide sequence analysis confirmed the presence of the original mutation in the TCR Calpha region but failed to detect compensatory mutations in alpha, beta, gamma, delta, epsilon or zeta chains. Thus, mutated J79-TCR-CD3 complexes can interact with zeta2 homodimers. Possible mechanisms for the unsuccessful TCR-CD3 interaction with zeta2 homodimers are presented and discussed.

Cell Membrane↗
PubMed1998

Kawasaki disease: a dangerous acute childhood illness.

Kawasaki disease is an acute febrile illness most commonly seen in children under the age of 5. It is characterized by fever, rash, cervical lymphadenopathy, bilateral nonexudative conjunctivitis, oropharyngeal mucosal changes, and erythema of the hands and feet followed by desquamation. However, a child with Kawasaki disease may not exhibit all of these symptoms. The disease resembles many other childhood illnesses, such as measles and scarlet fever, and misdiagnosis is common. Left untreated, Kawasaki disease has potential life-threatening consequences; 20% to 25% of children develop coronary artery aneurysms as a result. Although no specific laboratory tests exist that identify Kawasaki disease definitively, there are clinical and laboratory findings that guide diagnosis and treatment. Treatment includes the hospitalization of the child and subsequent administration of high doses of aspirin and intravenous immunoglobulin. With recovery, aspirin doses are reduced and the child may be monitored at home with outpatient follow-up. It is imperative that the health care provider be aware of the symptoms of Kawasaki disease in order to make the diagnosis and treat the child before cardiac sequelae ensue.

Child, Preschool↗
PubMed1997

T cell receptor alpha-chain tail is required for protein kinase C-mediated down-regulation, but not for signaling.

Antigen stimulation through the T cell receptor (TCR) induces phosphorylation of the associated CD3 gamma delta epsilon- and zeta-chain cytoplasmic tails. These events lead to the induction of the intracellular signaling pathways with concomitant receptor down-regulation. The TCR is down-regulated from the cell surface by the activation of protein kinase, C (PKC) and subsequent serine phosphorylation of the CD3 gamma-chain. We report here that the TCR alpha-chain cytoplasmic tail is also necessary for PKC-mediated internalization of the TCR complex. The requirement for the TCR alpha-chain cytoplasmic tail is specific for internalization of the TCR complex, since down-regulation of CD4 is still intact in hybridoma cells expressing a tailless TCR alpha-chain. The absence of TCR internalization directly correlates with defective PKC-mediated phosphorylation of the CD3 gamma-chain. Despite deficient PKC-mediated TCR down-regulation, the tailless alpha beta TCR still transduces antigenic signals resulting in the production of interleukin-2. Although the TCR tails are not obviously required for signal transduction, the TCR alpha-tail may serve as a targeting domain for PKC-mediated down-regulation of the TCR complex.

Amino Acid Sequence↗
PubMed1997

Mutation in splicing consensus sequences causes lack of TCR membrane expression due to exon excision.

T-cell antigen receptor (TCR) membrane-negative T-cell mutants can be divided into two groups: 1) those which lack one of the six TCR polypeptides and 2) those which contain a mutated TCR chain. The present experiments reveal a new mechanism for the development of TCR membrane-negative T-cell variants: mutations in splicing consensus motifs causing excision or misreading of an entire exon (exon 3 of the TCRAC or TCRBC genes). C27.15 cells transcribe a TCR alpha chain consisting of TCRAVJCexon1Cexon2-encoded amino acids plus six new amino acids. The assembly defect seems to be that the truncated alpha chain does not interact with CD3 delta molecules; consequently, no TCR alphabeta/CD3 deltaepsilongammaepsilon complexes are formed. E6.E12 cells transcribe a TCR beta chain composed of TCRBVDJCexon1Cexon2-encoded amino acids plus twenty-seven new amino acids, which seem not to form a transmembrane region. The truncated beta chain does associate with CD3 gammaepsilon heterodimers, yet no TCR alphabeta/CD3 deltaepsilongammaepsilon complexes are made. This may be due either to low assembly of TCR beta/CD3 gammaepsilon trimers or to lack of access of the mutated TCR beta/CD3 gammaepsilon trimers to the TCR alpha/CD3 deltaepsilon compartment in the endoplasmic reticulum.

Amino Acid Sequence↗
PubMed1997

Differential cytosolic tail dependence and intracellular fate of T-cell receptors internalized upon activation with superantigen or phorbol ester.

Activation of T lymphocytes by T-cell receptor (TCR) ligands such as peptide/MHC complexes, superantigens or anti-TCR mAbs, or by pharmacological activators of protein kinase C such as phorbol esters, results in the internalization and cell surface downregulation of TCRs. We investigated the role of internalization motifs located in the cytosolic region of CD3 gamma in the internalization of TCR complexes induced by enterotoxin superantigens, anti-TCR mAbs or phorbol esters. To this end, a series of CD3 gamma mutants were expressed in a CD3 gamma-deficient variant of the human T-cell line Jurkat. We found that serine126 and the di-leucine motif (Leu131-Leu132) are required for phorbol-ester-induced TCR downregulation, but they are not necessary for enterotoxin superantigen or antibody-induced TCR downregulation. Moreover, the tyrosine-based motifs (residues 138 to 141 and 149 to 152) are not required either for phorbol aster or for superantigen or antibody-induced TCR downregulation. Confocal microscopy analysis reveals that TCR complexes accumulate in an early endocytic/recycling compartment upon activation of cells with phorbol esters, whereas TCRs internalized upon activation with superantigen or anti-TCR mAbs are routed to lysosomes. Consistent with this intracellular localization, TCRs internalized in response to phorbol ester are not degraded and can be reexpressed on the cell surface. In contrast, TCRs internalized upon superantigen activation are degraded.

Antibodies, Monoclonal↗
PubMed1997

Expression and signal transduction of T-cell antigen receptor (TCR)/CD3 complexes on fresh or in vitro expanded T lymphocytes from patients with Hodgkin's and non-Hodgkin's lymphomas.

T-cell responses against soluble antigens, alloantigens and mitogens are frequently diminished in patients with certain types of cancer. In the present study, the authors investigated possible mechanisms for the partial T-cell immunodeficiency in patients with Hodgkin's or non-Hodgkin's lymphomas. It was found that T-cells from lymphoma patients had significantly reduced proliferative responses to EBV-transformed B-cell lines and to anti-TCR/CD3 MoAb; a 30-50% reduction of cells expressing membrane T-cell receptor (TCR) complexes; and a significantly reduced signal transduction function. Long-term in vitro culture conditions were developed to expand T cells in TCR/CD3-dependent or TCR/CD3-independent manners. With such methods, it was found that the decreased T-cell responses in patients with Hodgkin's and non-Hodgkin's lymphomas appeared to be an intrinsic T-cell defect (not at the antigen presenting cell level), and the T-cell responses could be recovered after only a few days in culture. Thus, it is suggested that the T-cell response-defect in Hodgkin or non-Hodgkin lymphoma patients is a reversible phenomenon, dependent on the patient's tumour-bearing environment.

B-Lymphocytes↗
PubMed1997

The interchain disulfide bond between TCR alpha beta heterodimers on human T cells is not required for TCR-CD3 membrane expression and signal transduction.

In the present paper, it was attempted to define the amino acids or regions on TCR beta molecules that determine the TCR alpha-TCR beta interaction. Sequence studies on HBP-ALL variant cells with an intrinsic deficiency in TCR alpha beta dimer formation elucidated a conserved amino acid motif in the TCR-C beta beta-strand E, = Y(C)(L)(S)SRLR(V)(S)(A); this motif seems to represent one interaction area for the TCR alpha-TCR beta interaction. In addition, amino acids in the connecting peptide may be shaped in a precise structure (by the interactions with CD3 molecules?) involved in TCR alpha-TCR beta dimerization. This result was supported by the finding that the interchain disulfide bond between TCR alpha and beta chains is not required for membrane expression or transmembrane signal transduction of TCR alpha beta-CD3 complexes. Finally, comparative results from two membrane TCR-CD3-negative Jurkat variants R4.9 and E6.E12 suggest that TCR-C beta exon 1- and 2-encoded amino acids are important for the TCR beta-CD3 gamma epsilon association.

Amino Acid Sequence↗
PubMed1997

A comparison of zopiclone and propiomazine as hypnotics in outpatients: a multicentre, double-blind, randomized, parallel-group comparison of zopiclone and propiomazine in insomniacs.

In a double-blind, parallel-group study of 135 patients with a mean age of 60 years, zopiclone 5 mg was compared with propiomazine 25 mg. The patients rated their sleep in a diary. There were statistically significant differences in favour of zopiclone for nine out of 13 variables measuring subjective sleep quality and quantity. Concerning side-effects, bad taste was reported more frequently in the zopiclone group and restless legs in the propiomazine group.

Adult↗
PubMed1996

Defective interactions between TCR chains and CD3 heterodimers prevent membrane expression of TCR-alpha beta in human T cells.

The human TCR complex is composed of two clonotypic polypeptide chains, TCR-alpha and TCR-beta (or TCR-gamma and TCR-delta) associated with CD3 gamma-, delta-, and epsilon-chains and zeta 2 homodimers. All six polypeptide chains are indispensable for TCR membrane expression and signaling function. In the present paper is described the analysis of a new TCR membrane-negative Jurkat T cell variant: E6.R3. The defect in this variant bears on the interaction between TCR and CD3 chains. E6.R3 cells have deleted three nucleotides in the TCR-alpha transmembrane (TM) region, which consequently lacks a leucine. This defect causes 1) lack of association between TCR alpha-chains and CD delta epsilon heterodimers; 2) lack of formation of disulphide-linked, fully glycosylated TCR-alpha beta heterodimers; and 3) lack of interaction between TCR-alpha beta/CD3 complexes and zeta-chains. Despite these defective interactions, TCR alpha-chains appear to become fully glycosylated, i.e., they are not retained in the endoplasmic reticulum but are further processed in the Golgi apparatus without such interactions. The defect may be due to the observation that in the E6.R3 TCR alpha- chains TM region, the two charged amino acids are situated on the same side of the alpha-helix; these two amino acids are exposed on opposite faces of the TM alpha-helix in normal TCR alpha-chains, possibly allowing TCR alpha-chains to interact with both CD3 delta- and CD3 epsilon-chains. Further possible consequences of the leucine deletion in the E6.R3 TCR-alpha TM region are discussed.

Amino Acid Sequence↗