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Biomedical subjects

C H Barton

Publications and source records attributed to C H Barton.

13 recordsLinked to original sources
PubMed1992

Plasma concentration and urinary excretion of erythropoietin in adult nephrotic syndrome.

PURPOSE: Nephrotic syndrome (NS) is associated with a significant alteration of protein metabolism. While lowering the plasma concentrations of certain proteins, the disease often raises the level of certain other proteins. The current study was undertaken to determine the effect of NS on erythropoietin (EPO) metabolism. PATIENTS AND METHODS: We measured the EPO concentration in plasma and urine of 26 patients with NS by an immunologic assay using a rabbit antiserum against recombinant human EPO. The results were compared with those obtained in a group of 12 normal control subjects. RESULTS: Despite a significant reduction in the hemoglobin concentration in the NS group compared with the control group (125 +/- 25 g/L versus 148 +/- 11 g/L, p less than 0.05), the plasma EPO concentration in the NS group was not significantly different from that seen in the control group (6.2 +/- 4.5 mU/mL versus 6.7 +/- 2.4 mU/mL, p = NS). No significant correlations were found between plasma EPO and hemoglobin concentration, serum creatinine, serum albumin, or urinary albumin excretion rate. Moreover, comparison of the NS patients with serum creatinine concentrations less than or equal to 1.5 mg/dL (133 mumol/L) with those exhibiting creatinine concentrations exceeding 1.5 mg/dL did not reveal a significant difference in mean plasma EPO concentration. Significant amounts of EPO were found in the urine of the patients with NS, while none was detected in the urine of the control subjects. CONCLUSION: We conclude that plasma EPO is inappropriately low in patients with NS. This is due, at least in part, to the urinary/renal losses of this protein and can potentially contribute to anemia in NS patients or compound the problem in those with concurrent renal insufficiency and diminished EPO production.

Adolescent↗
PubMed1992

Mapping Creb-1 to chromosome 1 in the mouse.

The gene CREB1 encoding the cyclic AMP response element DNA binding protein was previously assigned to human 2q32.3-q34. In this study, a panel of 207 backcross mice made between C57BL/10ScSn (=B10) females and (B10 x B10.L-Lsh)F1 males were used to map Creb-1 with respect to Cryg and Lsh/Vil on mouse chromosome 1. A reverse-transcribed, polymerase chain reaction-amplified cDNA probe covering bp 39 to 554 of the human sequence identified restriction fragment length polymorphisms with 7/18 restriction endonucleases used to digest whole genomic mouse DNA from the parental strains. BglII and DraI RFLPs for Creb-1 were scored on a subpanel of 16/207 known recombinants between Cryg and Lsh/Vil, yielding 2/16 recombinants between Cryg and Creb-1 and 14/16 recombinants between Creb-1 and Lsh/Vil. The 16/207 recombinants observed between Lsh/Vil and Cryg provide an estimated recombination frequency of 0.077 +/- 0.019, equivalent to a map distance of 7.7 +/- 1.9 cM. This is in good agreement with previously published map distances. The number of recombinants observed between Creb-1 and the other markers place Creb-1 approximately 1 cM distal to Cryg and 7 cM proximal to Lsh/Vil.

Animals↗
PubMed1991

Genetic regulation of macrophage priming/activation: the Lsh gene story.

This paper describes functional and genetic studies on the macrophage resistance gene Lsh/Ity/Bcg first described almost two decades ago. Working in vitro with resident peritoneal, liver (Kupffer cells) and bone marrow derived macrophages from congenic B10 (LshS) and B10.L-LshR mice it has been possible to demonstrate that the final effector mechanism for the gene in regulating antileishmanial activity involves production of reactive nitrogen rather than reactive oxygen intermediates. This in turn is dependent upon priming/activation of macrophages for enhanced TNF-alpha release which acts back on the macrophage in an autocrine manner to increase nitric oxide production. The precise point at which Lsh acts to control macrophage priming/activation has not been identified, but studies of early response gene expression show differences in KC mRNA levels at 2 h after LPS stimulation, and in c-fos mRNA as early as 20 min after stimulation with PMA plus ionophore, in peritoneal macrophages from congenic LshS and LshR mice. Data available suggest that both negative and positive signals may be involved in macrophage priming/activation, with LshS macrophages down-regulating their capacity for continued response to the autocrine loop. Work in progress will examine the role of TPA and cAMP response element-binding proteins in regulating gene expression in Lsh congenic mice. A major new initiative has also commenced to clone the Lsh gene by reverse genetics using yeast artificial chromosomes to walk towards Lsh from the closet proximal and distal markers on mouse chromosome 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Factor XIII and its substrates, fibronectin, fibrinogen, and alpha 2-antiplasmin, in plasma and urine of patients with nephrosis.

Plasma and urine concentrations of factor XIII and its circulating substrates (fibronectin, fibrinogen, and alpha 2-antiplasmin) were measured in a group of 36 patients with nephrotic syndrome. The results were compared with those obtained in a group of 32 normal volunteers (control group) and 12 patients with end-stage renal disease (ESRD). A mild but significant reduction in plasma level and an abnormal urinary excretion of alpha 2-antiplasmin was found in the nephrotic group. Plasma concentrations of factor XIII, fibronectin, and fibrinogen were significantly elevated in patients with nephrosis. In contrast, patients with ESRD showed no significant difference in the plasma concentrations of either factor XIII, fibronectin, or alpha 2-antiplasmin and only a modest elevation of fibrinogen when compared with normal controls. No significant correlation was found between serum creatinine concentration and plasma levels of factor XIII and its circulating substrates in the nephrotic group. No measurable quantities of factor XIII and only small quantities of fibronectin were found in the urine of patients with nephrosis. Elevation of plasma factor XIII, fibronectin, and fibrinogen concentrations in the nephrotic group is considered to be the result of a combination of increased synthesis and possibly contracted intravascular distribution of these macromolecular proteins in the face of their negligible urinary losses. The presence of the observed abnormalities in the nephrotic group and their absence in the non-nephrotic ESRD group tends to exclude renal failure as a cause of these abnormalities. Although the clinical significance of these abnormalities is uncertain, they can potentially contribute to the thrombophilic diathesis and platelet hyperaggregability in nephrotic syndrome.

Adolescent↗
PubMed1990

Characterization of the human N-CAM promoter.

In contrast with the complex series of splicing choices that generate the various membrane-associated isoforms of the neural cell-adhesion molecule alternative splicing of 5' exons does not contribute to additional molecular diversity. A single regulatory unit in genomic DNA, mapping to a 5 kb restriction-endonuclease-HindIII fragment, controls the expression of all major RNA size classes. DNA sequence analysis of a 2 kb fragment spanning the two major identified transcriptional initiation sites (194 and 188 bp from the ATG codon) and translation start codon indicates that the regulatory unit does not possess classical TATA or CCAAT motifs. The region of the putative promoter exhibits a GC-rich content and a high frequency of the dinucleotide CpG, both characteristics of a HTF(HpaII tiny fragments)-island. Introduction of deletion-mutant chimaeric-gene constructs into human and rodent N-CAM-expressing cell lines defines an active promoter region of 467 bp (-144 to -611 bp from the ATG codon). This region of genomic DNA contains consensus sites for the interaction of known transcriptional factors.

Animals↗
PubMed1979

Cimetidine in the management of metabolic alkalosis induced by nasogastric drainage.

Metabolic alkalosis resulting from nasogastric drainage is a well recognized and potentially serious clinical problem. In the postoperative patient with acute renal failure, the management of the metabolic alkalosis is particularly difficult, and established modalities of therapy are sometimes ineffective and can be hazardous to the patient. In this article, we report on the successful use of cimetidine (an H2-receptor antagonist) as an adjunct in the treatment of severe metabolic alkalosis in a postsurgical renal failure patient. To our knowledge, this is the first reported successful use of cimetidine in the treatment of metabolic alkalosis due to gastric acid loss.

Acute Kidney Injury↗
PubMed1979

Renal tubular dysfunction in transplanted kidneys.

We studied 15 renal transplant recipients for evidence of tubular dysfunction. Eight patients were hypophosphatemic, and two had systemic acidosis with a urinary acidification defect. Mild aminoaciduria and bicarbonaturia were present in four and 14 patients, respectively. Elevated parathyroid hormone level was found in only one patient. Tubular reabsorption of phosphorus was depressed in all eight hypophosphatemic patients, while no such abnormalities were observed in 14 control subjects. Defective tubular reabsorption of phosphorus was the most striking abnormality. None of the parameters studied, including immunosuppressant therapy, parathyroid hormone levels, creatinine clearance, or acid-base balance, clearly account for the pathogenesis of this abnormality.

Acidosis↗
PubMed1979

Thyroid function studies in the nephrotic syndrome.

Total serum and urinary thyroxine (T4), triiodothyronine (T3), and thyroxine-binding globulin (TBG) as well as serum free T4, thyroid-stimulating hormone (TSH), and T3 resin uptake (T3RU) were measured in seven patients with the nephrotic syndrome. The nephrotic syndrome was defined by proteinuria exceeding 3 g/24 h. All patients were clinically euthyroid. Most values for total serum T4, free T4, T3, T3RU, TBG, and TSH were within normal limits. However, the mean serum T3 and TBG values were significantly lower in patients compared with the control group. The values (mean +/- 2 SD) for urinary T4 were 24.3 +/- 20.3 in the patient group and 1.5 +/- 0.7 microgram/24 h in the control group. Urinary T3 values for patients and the control group were 2100 +/- 856 and 848 +/- 253 ng/24 h respectively. Urinary TBG was 2.1 +/- 1.8 mg/24 h in the patients and undetectable in the control group. There was no correlation between daily urinary T3 and T4 and urinary TBG. There was a weak correlation between daily urinary protein excretion and urinary T4 (r = 0.5).

Adult↗
PubMed1979

Peritoneal dialysis clearance of cimetidine.

Peritoneal dialysis clearance of cimetidine was determined in two patients undergoing peritoneal dialysis treatment. The peritoneal dialysis clearance of cimetidine was approximately 10 ml./min. under optimal dialyzing conditions. The average cimetidine to creatinine extraction ratio was 0.45, which represents significant peritoneal dialyzability. The amount of cimetidine removed, however, constituted only a small fraction of the total administered dose. Therefore, only minor dose adjustments may be necessary during peritoneal dialysis treatment.

Adult↗
PubMed1978

Dialysability of theophylline.

We have shown that theophylline is highly dialysable with an average dialysis clearance of 76 ml/min approaching 63% of urea clearance with hemodialysis. Implications include dose adjustment during dialysis and efficacy of dialytic technique in the treatment of theophylline intoxication.

Blood Glucose↗
PubMed1978

Hemodialysis clearance of cimetidine.

Hemodialysis clearance of cimetidine was determined in three patients and was found to range between 41.34 to 75.91 ml/min. Notwithstanding its substantial dialyzability, the amount of cimetidine removed by four hours of hemodialysis constituted only 8% to 14% of the administered dose. Accordingly, major dose adjustment on the days of dialysis treatment, as suggested in the available literature, may not be necessary.

Adult↗
PubMedDate not supplied

Central retinal vein occlusion associated with hemodialysis.

Central retinal vein occlusion (CRVO) occurred in 3 of 15 maintenance hemodialysis patients over a two-week period. There have been no previous reports of this ophthalmologic catastrophe observed in the dialysis setting. Lupus nephritis, Henoch-Schönlein purpura and nephrosclerosis constituted the patients' major underlying diseases. Moderate hypertension was also present. Impaired vision of the left eye noted 24 to 36 hours following dialysis was the presenting symptom in all cases. Findings included decreased visual acuity, retinal vein engorgement, hemorrhage, and disc edema. All three patients subsequently lost the vision in their left eye (two received anticoagulation therapy). With the exception of hypertension, there were no known underlying predisposing conditions present. Although we are unable to offer a definite explanation for these unusual cases of CRVO, we feel a hypercoagulable state may have been responsible. Because our three cases occurred during a two-week period, some transient unidentified procoagulant factor associated with hemodialysis could have been present.

Adolescent↗