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Biomedical subjects

A Fuks

Publications and source records attributed to A Fuks.

At least 55 records · Page 3Linked to original sources
PubMed1988

Effect of trauma to the primary incisors on the alignment of their permanent successors in Israelis.

117 children who had experienced trauma to their primary incisors were re-examined in their transitional or permanent dentition stage. The control group consisted of 174 children with a corresponding dental developmental age. All the children were examined clinically and the intra- and interarch relations of the anterior segments were recorded. The prevalence of patients with at least one malposed incisor was higher in the trauma group. Trauma to the primary dentition was found to be a contributing factor affecting the alignment of the permanent successors. Early loss of the primary incisors did not cause loss of space in most of the cases; however, it was associated with malposition of their permanent successors. Lack of eruption guidance or the direct effect of the injury on the position of the developing bud could be considered as contributing etiologic factors. There was a very low prevalence of more serious malocclusion features, like impaction, in the trauma group.

Child↗
PubMed1988

Association of susceptibility to spontaneous diabetes in rat with genes of major histocompatibility complex.

This study was designed to map the diabetes susceptibility gene(s) associated with the rat major histocompatibility complex (MHC) RT1. We have crossed spontaneously diabetic male rats bearing the recombinant RT1r8 haplotype with female rats of the AC1.1r4 congenic strain. Three diabetic rats were determined to be homozygous for the r4 haplotype by serotyping. The absence of recombination within the MHC was confirmed by inspection of restriction-fragment-length patterns of the diabetic animals and the parental strains. In conjunction with previous breeding studies, this study maps the diabetes susceptibility gene to the right of the RT1-A locus and to the left of the RT1-C locus. A low incidence of diabetes in the F2 (4.5%) emphasizes the multifactorial nature of the susceptibility. The presence of depressed responsiveness of peripheral blood lymphocytes to concanavalin A stimulation increases the prevalence of the overt disease. An unusual feature of the diabetic syndrome in this study is the sparse or absent pancreatic lymphocytic inflammatory response, with true insulitis being a rare finding.

Animals↗
PubMed1988

IDDM in BB rats. Enhanced MHC class I heavy-chain gene expression in pancreatic islets.

Modulation in major histocompatibility complex (MHC) gene expression correlates with the inflammatory reactions that occur during graft rejection and autoimmune disease. We analyzed the expression of class I and II MHC genes in the pancreatic islets of prediabetic and newly diabetic BB rats by immunohistochemistry of tissue sections and Northern blotting of RNA extracted from isolated islets. We show that enhanced levels of MHC class I heavy-chain RNA are present in pancreatic islets before overt inflammation and the onset of insulin-dependent diabetes mellitus (IDDM) in the spontaneously diabetic BB rat. Immunohistochemical analysis revealed enhanced class I antigen expression throughout the pancreatic islets of newly diabetic animals but no induction of class II antigen on endocrine cells within the islet. Varying degrees of inflammatory infiltrate were observed in the sections exhibiting enhanced class I antigen expression or in nearby serial sections. Southern blot analysis revealed no restriction-fragment-length polymorphism or amplification of the endogenous class I heavy-chain genes compared with those of seroidentical disease-resistant Wistar-Furth rats. I-A alpha and I-E alpha hybridizing RNA appeared de novo before overt diabetes, although concomitantly with T-lymphocyte-receptor beta-chain and interferon-gamma gene hybridizing RNA and after MHC class I heavy-chain RNA enhancement was observed. These data indicate the possibility that enhanced class I heavy-chain gene expression plays a role in the progression of IDDM.

Animals↗
PubMed1987

Isolation and characterization of full-length functional cDNA clones for human carcinoembryonic antigen.

Carcinoembryonic antigen (CEA) expression is perhaps the most prevalent of phenotypic changes observed in human cancer cells. The molecular genetic basis of this phenomenon, however, is completely unknown. Twenty-seven CEA cDNA clones were isolated from a human colon adenocarcinoma cell line. Most of these clones are full length and consist of a number (usually three) of surprisingly similar long (534 base pairs) repeats between a 5' end of 520 base pairs and a 3' end with three different termination points. The predicted translation product of these clones consists of a processed signal sequence of 34 amino acids, an amino-terminal sequence of 107 amino acids, which includes the known terminal amino acid sequence of CEA, three repeated domains of 178 amino acids each, and a membrane-anchoring domain of 27 amino acids, giving a total of 702 amino acids and a molecular weight of 72,813 for the mature protein. The repeated domains have conserved features, including the first 67 amino acids at their N termini and the presence of four cysteine residues. Comparisons with the amino acid sequences of other proteins reveals homology of the repeats with various members of the immunoglobulin supergene family, particularly the human T-cell receptor gamma chain. CEA cDNA clones in the SP-65 vector were shown to produce transcripts in vitro which could be translated in vitro to yield a protein of molecular weight 73,000 which in turn could be precipitated with CEA-specific antibodies. CEA cDNA clones were also inserted into an animal cell expression vector and introduced by transfection into mammalian cell lines. These transfectants produced a CEA-immunoprecipitable glycoprotein which could be visualized by immunofluorescence on the cell surface.

Adenocarcinoma↗
PubMed1987

Autopolymerized versus light-polymerized fissure sealant.

This study found that 31 months after placement of a sealant, no significant difference was seen in the clinical performance and retention between the visible light-polymerized and autopolymerized materials. Practitioners can use either material without compromising efficacy.

Chemical Phenomena↗
PubMed1987

Major histocompatibility complex restriction of T-lymphocyte responses to islet cell antigens in IDDM rats.

BBUF rats, derived from BB rats, spontaneously develop a form of insulin-dependent diabetes mellitus (IDDM) associated with infiltration of the islets of Langerhans by lymphocytes (insulitis). BBUF rats bear the RT1u major histocompatibility complex (MHC) haplotype that we have shown to be necessary for the expression of this form of IDDM. A T-lymphocyte line obtained from the pancreas of a diabetic rat (UPCC.5) and three T-lymphocyte hybridomas derived by fusing T-lymphocytes of BBUF rats (MUS1.2, MUS1.13, and MUP3.21) respond to islet cell antigens in an MHC-restricted way. UPCC.5 responds to a combination of islet cell antigens (ICAg) and antigen-presenting cells by proliferation, whereas the T-hybridoma responses are detected on the basis of IL-2 production in a similar assay. This study reveals that an antiserum against mu-haplotype MHC antigens or a monoclonal antibody against the product of the D class II subregion of the rat MHC could inhibit ICAg recognition. A monoclonal antibody against the product of the B class II MHC subregion of the rat was not inhibitory. These results suggest that RT1.D antigens (analogous to human DR and mouse I-E) restrict islet cell recognition in this rat model of spontaneous IDDM.

Animals↗
PubMed1987

Reticuloendothelial system Fc receptor function in systemic lupus erythematosus: effect of decreased sensitization on clearance of autologous erythrocytes.

Recent reports of reticuloendothelial system Fc receptor function using anti-Rh(D) coated red blood cells (RBC) provide conflicting data regarding the degree of abnormality in systemic lupus erythematosus (SLE). The effect of different sensitizing doses of anti-Rh(D) on Fc receptor function was evaluated in 10 controls and 9 patients with SLE (5 with renal disease, 4 without) using 1 microgram anti-Rh(D) (6,700 molecules anti-Rh(D)/RBC by saturation analysis) and 0.125 microgram anti-Rh(D) (1,100 molecules/RBC). At the lower sensitizing dose the sensitivity of the assay was significantly increased. To correctly interpret the significance of studies of Fc receptor function from different centers, it is necessary to know the exact sensitizing doses used for each study.

Adult↗
PubMed1986

Insulin-dependent diabetes mellitus is associated with genes that map to the right of the class I RT1.A locus of the major histocompatibility complex of the rat.

Previous studies have demonstrated that the presence of at least one u-haplotype of the rat major histocompatibility complex (MHC), RT1, is a necessary but not sufficient condition for the development of overt diabetes mellitus. The present studies were undertaken to determine which portion of the RT1 gene complex is necessary for the occurrence of diabetes. We crossed hooded diabetic rats (RT1.AuBuDu) with PVGr8 rats (RT1.AaBuDu). F1 animals were mated to give 82 F2 animals and backcrossed with the hooded diabetics to produce 41 backcross animals. Diabetes occurred in animals with all three possible RT1.A genotypes. The diabetes was similar to that seen in BB rats and in hybrid strains developed from them. An immunoregulatory defect was marked by decreased percentage of peripheral blood lymphocytes staining with w3/25 monoclonal antibody, by an increased percentage of peripheral blood lymphocytes binding a mouse ascites control protein, and by decreased responsiveness of peripheral blood lymphocytes to stimulation by concanavalin A. We conclude that the u-allele of the class I A-locus gene product is not necessary for susceptibility to the development of diabetes in the rat. Therefore, either genes coding for the class II products of the u-haplotype or genes in linkage disequilibrium with these genes and mapping to the right of the A locus provide the permissive condition. Furthermore, the data suggest, but do not prove, that the u-haplotype derived from a strain remote from the BB rat can confer this susceptibility to the development of diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Epitopes of carcinoembryonic antigen defined by monoclonal antibodies prepared from mice immunized with purified carcinoembryonic antigen or HCT-8R cells.

A library of 18 monoclonal antibodies (MAbs) reactive with purified carcinoembryonic antigen (CEA) has been prepared. The specificity of these MAbs was tested and they have been separated into nine subgroups, each recognizing a different region of the CEA molecule. Seven MAbs from four of the groups also react with the nonspecific cross-reacting antigen. Some of the MAbs are directed against conformational determinants: three of the MAb groups bind poorly to sodium dodecyl sulfate-treated CEA, while five of the groups are not reactive with reduced and alkylated CEA. Three of the groups react with purified CEA but not with the cell surface CEA of HCT-8R cells, while the other groups react with both forms. The MAbs were tested for binding to fragments of CEA obtained by chemical cleavage and the groups of MAbs were found to react with different subsets of such fragments.

Antibodies, Monoclonal↗
PubMed1986

Characterization of monoclonal antibodies to carcinoembryonic antigen with increased tumor specificity.

Nine monoclonal antibodies reacting with carcinoembryonic antigen (CEA) were produced after immunization of mice with either purified CEA or a CEA-producing human cell line. Their specificities were assessed by immunohistochemistry on tissue sections of neoplastic and nonneoplastic lesions. These monoclonal antibodies have different patterns of tissue reactivity. Two of them, D14 and B18, were found to have a high degree of specificity for colonic carcinoma and did not react with formalin-fixed paraffin-embedded sections of normal colon with standardized staining conditions. Most cases of noncolonic adenocarcinomas and normal epithelial structures were not stained by these two monoclonal antibodies. The specificity of the monoclonal antibodies was further investigated immunochemically using intact, reduced, and alkylated or chemically fragmented CEA. Liquid phase radioimmunoassays and antibody competition immunoenzymatic assays confirmed that the antibodies recognize different epitopes of CEA. These data support the concept of CEA heterogeneity and the reactivity of the D14 and B18 monoclonal antibodies with colonic adenocarcinomas indicates that they are useful immunohistochemical probes.

Animals↗
PubMed1986

Genetics of the spontaneous diabetic syndrome. Interaction of MHC and non-MHC-associated factors.

The occurrence of the spontaneous insulin-dependent diabetic syndrome in the rat is the result of several genetic susceptibilities. There is a requirement for the u haplotype of the rat major histocompatibility complex (MHC), RT1. More specifically this requirement is for genes mapping to the right of the RT1 A locus, which codes for class I products. Furthermore, u haplotypes from inbred strains other than the BB rat can provide this permissive u haplotype. Diabetes occurs in animals with either one or two u haplotype and the diabetic syndrome is similar in its characteristics. In addition to the requirement for the MHC genes, there are abnormalities of the immune system of the various diabetes-prone strains, which are present in animals that develop overt disease. These abnormalities segregate independently of the RT1 and interaction between the susceptibilities is necessary for the manifestation of the complete clinical syndrome.

Alleles↗
PubMed1985

Impaired Kupffer cell function precedes development of secondary amyloidosis.

It has been demonstrated previously that the acute phase reactant, serum amyloid A (SAA), is subject to degradation by surface membrane-associated proteinases of peripheral blood monocytes. However, monocytes obtained from the blood of patients with amyloidosis degraded SAA incompletely, leaving a cleavage product that, biochemically and immunologically, resembled the amyloid protein A (AA) deposited in their tissues. To investigate the role of fixed macrophages in amyloidogenesis and to establish more definitively that amyloid deposition is attributable to faulty processing of the precursor protein rather than aberrant synthesis, secondary amyloidosis was induced in C57BL/6J mice by serial injections of casein. Kupffer cells (KC) were isolated from livers of mice that had received 0, 8, 13, 18, and greater than 30 injections of the stimulant. The cells were cultured with SAA for 4, 8, and 18 h and then subjected to electron microscopy and enzyme analyses. The medium was analyzed by SDS-PAGE to determine the amount of residual SAA and/or the appearance of AA. KC of healthy animals degraded SAA completely whereas KC of stimulated mice showed increasing amounts of residual SAA and the appearance of the AA cleavage product. The AA peptide appeared in KC cultures early during the course of casein injections and before any amyloid could be demonstrated in the organs of the stimulated mice. The addition of KC isolated from healthy mice to cultures that had produced AA eliminated the abnormal peptide. The results, indicate that defective KC function precedes amyloidosis. The abnormal AA cleavage product formed by such cells is still susceptible to hydrolysis by normal cells. In addition, ultrastructural evidence is presented that suggests that KC may also play a role in fibrillogenesis of the AA protein.

Amyloidosis↗
PubMed1985

Eruption of rootless teeth in congenital renal disease.

Eruption of rootless mandibular premolars and other dental defects in a girl suffering from congenital kidney disease are described. The successful management of these excessively mobile teeth allowed them to develop roots of sufficient length. Hypotheses of tooth emergence are viewed in the light of these rootless eruptions.

Bicuspid↗
PubMed1985

Plasma membrane orientation of simian virus 40 T antigen in three transformed cell lines mapped with monoclonal antibodies.

Simian virus 40 large T antigen transforms cells from several species. Recent studies show that it is present on the cell surface. As in other tumor virus systems, this may be important for transformation. We have used a radioimmunoassay to map antigenic determinants on living and formaldehyde-fixed transformed cells with six different monoclonal antibodies to T antigen. Nonrelevant monoclonal antibodies of the same subclasses served as controls. With the transformed mouse line SVT2, antibody PAb 101, which reacts with the C-terminal region of T antigen, and PAb 1700, which is directed against an internal region of T, reacted with both formaldehyde-fixed and living cells. Antibodies PAb 402 (C terminus) and 419 (N terminus) reacted only with living cells, their determinants being destroyed upon formaldehyde fixation. Antibodies PAb 405 (C terminus) and 100 (internal) fail to react on either fixed or living cells. Similar results were obtained on the simian virus 40-transformed human line SV80 and the fixed hamster line CHLwt23, although all antibodies failed to react with living CHLwt23 cells. The data suggest that T antigen is inserted into the plasma membrane of transformed cells in a specific, nonrandom manner, with the C and N termini exposed on the cell surface and the midportion either buried in the lipid bilayer, hidden by the tertiary structure of T antigen, or masked by a post-translational modification such as fatty acid acylation.

Animals↗