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J Eldridge

Publications and source records attributed to J Eldridge.

At least 37 records · Page 2Linked to original sources
PubMed1991

The Drosophila homologue of vertebrate myogenic-determination genes encodes a transiently expressed nuclear protein marking primary myogenic cells.

We have isolated a cDNA clone, called Dmyd for Drosophila myogenic-determination gene, that encodes a protein with structural and functional characteristics similar to the members of the vertebrate MyoD family. Dmyd clone encodes a polypeptide of 332 amino acids with 82% identity to MyoD in the 41 amino acids of the putative helix-loop-helix region and 100% identity in the 13 amino acids of the basic domain proposed to contain the essential recognition code for muscle-specific gene activation. Low-stringency hybridizations indicate that Dmyd is not a member of a multigene family similar to MyoD in vertebrates. Dmyd is a nuclear protein in Drosophila, consistent with its role as a nuclear-gene regulatory factor, and is proposed to be a transiently expressed marker for muscle founder cells. We have used an 8-kilobase promoter fragment from the gene, which contains the first 55 amino acids of the Dmyd protein, joined to lacZ, to follow myogenic precursor cells into muscle fibers with antibodies to beta-galactosidase and to Dmyd. Unlike the myogenic factors in vertebrate muscle cells, Dmyd appears to be expressed at a much lower level in differentiated Drosophila muscles, so Dmyd cannot be followed continuously as a muscle marker. This fact is reflected in the loss of Dmyd RNA expression in 12- to 24-hr embryos, a major period of early myogenesis, as well as in the undetectable level of the nuclear antigen in primary cultures of embryonic and adult Drosophila muscle.

Age Factors↗
PubMed1991

Serological evidence of infection with Helicobacter pylori may predict gastrointestinal intolerance to non-steroidal anti-inflammatory drug (NSAID) treatment in rheumatoid arthritis.

Specific circulating antibodies to the spiral gastric organism, Helicobacter pylori (HP) were detectable in 43% of 68 patients with rheumatoid arthritis by complement fixation test (CFT) and enzyme-linked immunosorbent assay (ELISA), a frequency comparable with that of a normal, age-matched population. Presence of these antibodies correlated strongly with a previous history of peptic ulcer disease (PUD) and to the severity of NSAID-related dyspeptic symptoms, the latter often leading to multiple drug intolerance. This contrasts with short term, prospective NSAID toxicity data, which show little relationship between ulceration and HP carriage. This result suggests, however, that HP may have a definite role in the pathogenesis of symptomatic PUD associated with more chronic NSAID usage, and may have important implications for ulcer prophylaxis in these patients.

Adult↗
PubMed1990

Transgenic rearranged T cell receptor gene inhibits lymphadenopathy and accumulation of CD4-CD8-B220+ T cells in lpr/lpr mice.

The lpr gene in homozygous form induces development of CD4-CD8-B220+ T cells and lymphadenopathy in MRL and C57BL/6 mice. Although the propensity for excessive production of T cells is related to an intrinsic T cell defect, a thymus is also required because neonatal thymectomy eliminates lymphadenopathy. Recent evidence suggests that excessive production and release of autoreactive T cells from the thymus of lpr/lpr mice might lead to downregulation of CD4 and CD8 as a "fail safe" tolerance mechanism that occurs during late thymic or post-thymic development. To test this hypothesis, T cell receptor (TCR) transgenic mice that produce large numbers of immature thymocytes recognizing the H-2Db and male H-Y antigens were backcrossed with C57BL/6-lpr/lpr mice and MRL-lpr/lpr mice. It was predicted that Db male lpr/lpr mice would produce large numbers of autoreactive T cells during early thymic development that would lead to an accelerated lymphoproliferative disease. In contrast, Db female lpr/lpr mice would produce large numbers of Db H-Y-reactive T cells, but might not develop lymphadenopathy because the male H-Y antigen would not be present. Unexpectedly, there was complete elimination of lymphadenopathy in both male and female TCR transgenic lpr/lpr mice. The elimination of lymphadenopathy was not due to a failure of thymic maturation since the thymus of H-2Db female lpr/lpr mice contained nearly normal numbers of mature thymocytes. Elimination of lymphadenopathy was also not due to a lack of autoreactive T cells in the peripheral lymph nodes (LN) since there was an increased syngeneic mixed lymphocyte proliferative response of LNT cells from transgenic lpr/lpr compared with +/+ mice in vitro. Hypergammaglobulinemia and autoantibody production in the transgenic lpr/lpr was present at levels comparable with or higher than control nontransgenic lpr/lpr mice, suggesting a dissociation of autoantibody production from the lymphoproliferative disease in the TCR transgenic mice. Conversely, the development of lymphadenopathy and production of CD4-CD8-B220+ T cells appear to be intimately linked, as both were completely eliminated in T cells expressing the transgenic TCR. We propose that lymphoproliferation and production of CD4-CD8-6B2+ T cells in lpr/lpr mice is related to decreased expression of the TCR, and providing the T cells with a rearranged TCR transgene overcomes this defect.

Animals↗
PubMed1989

An avian muscle factor related to MyoD1 activates muscle-specific promoters in nonmuscle cells of different germ-layer origin and in BrdU-treated myoblasts.

We isolated the cDNA encoding a myogenic factor expressed in embryonic chick breast muscle by virtue of its weak hybridization to the mouse MyoD1 clone. Nucleotide sequence analysis and amino acid comparison define this clone, CMD1, as encoding a protein similar to mouse MyoD1. CMD1 encodes a polypeptide smaller than MyoD1, 298 versus 318 amino acids, respectively, and is 80% concordant by amino acid sequence overall. The basic and myc domains required for myogenic conversion of mouse 10T1/2 'fibroblasts' to myoblasts with MyoD1 are completely conserved in CMD1. CMD1 is just as efficient as the mouse homolog in myogenic conversion of 10T1/2 cells and coactivates the endogenous mouse MyoD1 gene in the process. The efficiency of myoblast conversion depends on the levels of CMD1 expression and suggests that the cellular concentration of CMD1 plays a role in the onset of myogenesis. Transient expression of CMD1 in a variety of nonmuscle cells from different germ-layer origins activates both cotransfected muscle-specific promoters and, in some cases, endogenous muscle-specific genes. 5-Bromodeoxyuridine (BrdU) treatment of chicken and mouse myoblasts reduces the expression of CMD1 and MyoD1, respectively, and may explain how this thymidine analog inhibits myogenesis and the activity of transfected muscle-specific promoters in BrdU-treated myoblasts. Transient expression of CMD1 in BrdU-treated myoblasts reactivates cotransfected muscle-specific promoters. CMD1 activates muscle-specific promoters in cotransfections regardless of cell type, whereas 'housekeeping' or constitutive promoters can be activated moderately, unaffected, or repressed, depending on the promoter and cell background. The rate and degree of myogenic conversion may be more restricted by cell phenotype than by germ-layer origin.

Amino Acid Sequence↗
PubMed1989

Antipneumococcal effects of C-reactive protein and monoclonal antibodies to pneumococcal cell wall and capsular antigens.

Antibodies to pneumococcal capsular polysaccharides are well known for their ability to protect against pneumococcal infection. Recent studies indicate that antibodies to cell wall antigens, including pneumococcal surface protein A and the phosphocholine (PC) determinant of teichoic acids as well as human C-reactive protein (which also binds to PC), can protect mice against pneumococcal infection. In the present study we compared the protective effects of these agents as measured by mouse protection, the blood bactericidal assay, and clearance of pneumococci from the blood and peritoneal cavity. Our findings extend previous results indicating that human C-reactive protein and antibodies to noncapsular antigens are generally less protective than anticapsular antibodies. The new results obtained indicate the following: (i) mouse protection studies with intraperitoneal and intravenous infections provide very similar results; (ii) monoclonal immunoglobulin G2a (IgG2a) antibodies to PC, like IgG1, IgG2b, and IgG3 antibodies to PC, are highly protective against pneumococcal infection in mice; (iii) human antibody to PC is able to protect against pneumococcal infection in mice; (iv) antibodies to PspA are effective at mediating blood and peritoneal clearance of pneumococci; (v) complement is required for the in vivo protective effects of both IgG and IgM antibodies to PC; (vi) IgG1, IgG2b, and IgG3 anti-PC antibodies all mediate complement-dependent lysis of PC-conjugated erythrocytes; and (vii) antibodies and human C-reactive proteins that are reactive with capsular antigens but not cell wall antigens are able to mediate significant antibacterial activity in the blood bactericidal assay.

Animals↗
PubMed1988

Further evidence of von Willebrand factor involvement in thrombotic thrombocytopenia purpura.

Fourteen patients diagnosed as having thrombotic thrombocytopenia purpura (TTP) were studied. Those who survived have been followed during a 1 to 7 year period. The clinical diagnosis was based on changing neurological findings, thrombocytopenia and evidence of microangiopathic hemolytic anemia. Laboratory tests included the determination of von Willebrand factor antigen (VWF:Ag), ristocetin cofactor (RiCof) and the electrophoretic mobility of von Willebrand factor (CIE VWF:Ag). The ratio of RiCof to VWF:Ag was then calculated. Control individuals included healthy subjects and patients with thrombocytopenia of several etiologies. Statistical differences between the values of RiCof, the ratio of RiCof:VWF:Ag and the CIE of VWF:Ag were found for samples comparing active disease and remission phase. The recovery from thrombocytopenia paralleled the correction of abnormal parameters. Similarly, significant differences were found when above parameters were compared between thrombocytopenia of TTP with other thrombocytopenic states. We suggest that these abnormal tests could be useful in distinguishing TTP from other disorders, and may have prognostic significance in patients already diagnosed as having TTP.

Adolescent↗
PubMed1987

Aerobic responses to low level exercise testing following an acute myocardial infarction.

Thirty-four patients who had recently sustained an acute myocardial infarction performed low-level exercise testing with analysis of expired gas 7.1 +/- 2.6 days after the event. They were classified as finishers (F) and nonfinishers (NF) of the low-level protocol. The ejection fraction in the NF was 39 +/- 14% vs 56 +/- 17% in the F (p less than 0.01), and the NF had 2.6 +/- 0.8 vessels stenosed vs 1.8 +/- 0.9 vessels stenosed in the F (p less than .05). Ten normal subjects also performed the exercise test. At the same workload, patients with recent myocardial infarction had significantly lower oxygen consumption (NF less than F), significantly higher minute ventilation (NF greater than F), ventilatory equivalent for oxygen (NF greater than F), and higher respiratory exchange ratio (NF greater than F) than did normal subjects. The heart rate responses were higher in the post infarction patients than in normal subjects. The oxygen pulse was significantly lower in the cardiac patients compared to normals. These findings suggest that during the early recovery phase from an acute myocardial infarction, patients, particularly the NF, utilize less oxygen at submaximal work loads than do normal subjects. This suggests that in these patients part of the energy requirements for exercise are met anaerobically. This could be due to abnormal extraction of oxygen by the working muscles or as a result of poor delivery of oxygen due to abnormal left ventricular function.

Exercise Test↗
PubMed1987

Gastritis and gastric campylobacter-like organisms in patients without peptic ulcer.

Gastric biopsy specimens were obtained from 83 patients without peptic ulcer disease and analysed histologically. Culture and serological studies were done on the last 64 patients. The patients were divided into two age groups (young and old groups.) In 34 patients with chronic superficial gastritis, gastric campylobacter-like organisms (GLCO) were identified histologically in 91% and grown on culture in 88%: antibody to GCLO was detected in 81%. No age-related difference in the prevalence of the organism was demonstrated. In the 23 patients with atrophic gastritis (all elderly), presence of the organisms appeared to be related to the presence of an inflammatory cell infiltrate into the gastric mucosa. These figures for the prevalence of the organism in this selected group of patients are similar to those reported in previous studies of unselected patients which included those with peptic ulcer. This suggests that GCLO is unlikely to be causally related to peptic ulcer.

Adult↗
PubMed1986

Antibody to the gastric campylobacter-like organism ("Campylobacter pyloridis")--clinical correlations and distribution in the normal population.

Different cellular proteins of the gastric campylobacter-like organism (GCLO) were shown to be immunogenic for man. Antibodies to GCLO were detected in sera by both complement fixation and enzyme-linked immunoabsorbent assay. Antibody was found in 133 (52%) of 254 patients attending for gastroscopy. There was a high correlation between presence of antibody and a positive GCLO culture from the gastric mucus. Patients with normal endoscopic appearances, duodenal ulcer, duodenitis and oesophagitis had similar prevalences (c. 50%) of antibody. Only patients with endoscopically visible gastritis or gastric ulcer had a higher frequency (c. 80%) of antibody. In a normal population, antibody was uncommon in individuals less than 20 years old, but the prevalence of antibody increased (to c. 50%) with age. There was little evidence to support an important pathological role for GCLO in disorders of the upper gastrointestinal tract, although the possibility that it may be a co-factor in the pathogenesis of gastric ulcer cannot be excluded.

Adolescent↗
PubMed1985

Nucleotide sequence of the chicken cardiac alpha actin gene: absence of strong homologies in the promoter and 3'-untranslated regions with the skeletal alpha actin sequence.

The entire nucleotide sequence of the chicken cardiac alpha-actin (CC alpha A) gene has been determined. This is the first complete sequence of a cardiac actin gene that includes the promoter region, cap site, all the introns, and the polyadenylation site. The gene contains six introns, five of which interrupt the coding region at amino acids (aa) 41, 150, 204, 267, and 327. The first intron is in the 5'-noncoding region and is 438 bp in length. The CC alpha A gene encodes an mRNA of approx. 1400 bp with 5'- and 3'-untranslated region of 59 and 184 nucleotides (nt), respectively. Like the chicken skeletal alpha-actin gene, the CC alpha A gene has the codon for the aa cysteine between the initiator ATG and the codon for the N-terminal aspartic acid residue of the mature protein. There are no strong homologies (less than 13 consecutive nt) in the promoter or 3'-untranslated regions between the CC alpha A and chicken skeletal alpha-actin genes even though both are expressed in skeletal muscle during development. However, the 3'-untranslated region of the CC alpha A gene demonstrates significant sequence homology (76% over a 200-nt region) with the same region in the partial sequence of the human cardiac gene. The conservation of these sequence homologies between identical isoforms rather than the different alpha actin genes suggests these conserved regions may have a role in regulation rather than tissue-specific expression, as previously proposed.

Actins↗
PubMed1984

Campylobacter like organisms on the gastric mucosa: culture, histological, and serological studies.

Biopsy samples were taken from the gastric mucosa of 50 patients attending a gastroscopy clinic; blood was also taken for serological studies. A campylobacter like organism was grown from 31 patients (62%) and the organism was seen in sections from 27 biopsies. Antibody was found in 31 patients by complement fixation and in 27 by bacterial agglutination. There were strong positive correlations between the presence of the organism, detectable antibody, and histological gastritis. Antibody to the campylobacter like organism was comparatively uncommon in patients without gastritis and in samples from blood donors and antenatal patients.

Adult↗
PubMed1981

Serological studies in two outbreaks of Campylobacter jejuni infection.

Two outbreaks of campylobacter enteritis in residential student populations are described. In the first outbreak, 34 of 240 students in one hall of residence became ill over the course of 4 or 5 days. A single serotype of C. jejuni was isolated from sample of faeces. Sera collected demonstrated that the students had little pre-existing antibody and antibody responses were demonstrated in those who were infected. About 30% of students with serological evidence for infection with C. jejuni did not have gastro-intestinal symptoms. In the second outbreak, 77 of 300 agricultural students developed symptoms over a period of 3 weeks. Unpasteurized milk was the source of infection. Two serotypes of C. jejuni were isolated from faeces. Antibody responses were detected to both these serotypes and to another serotype, suggesting the presence of at least 3 serotypes in the milk. Bactericidal antibody consistent with recent infection was found in all students with symptoms and in 63% of students in the absence of symptoms, indicating the possible development of immunity. The high prevalence of antibody in these students was correlated with the habitual consumption of unpasteurized milk.

Adult↗