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Biomedical subjects

C A Davis

Publications and source records attributed to C A Davis.

At least 91 records · Page 5Linked to original sources

Circulating immune complexes in membranoproliferative glomerulonephritis.

Circulating immune complexes (CIC), measured by the solid-phase Clq method, were found to be in abnormal concentration in about half of 39 patients with membranoproliferative glomerulonephritis (MPGN). In contrast, they were present, usually in higher concentration, in nearly all patients with active lupus nephritis. Correlations between clinical course and CIC levels in patients with MPGN showed that complexes were always present when the disease was mild or "silent," but when renal impairment developed or was incipient, complexes were nearly always absent. In patients with disease of intermediate severity, characterized by definite proteinuria but without renal impairment, 50% had complexes. The presence of complexes when glomerular abnormality is relatively slight could be interpreted as indicating that the complexes measured were not nephritogenic, or that they program subsequent events that augment glomerular injury in the absence of complexes. The measurement of CIC in MPGN appears to have minimal value both in diagnosis and in determining prognosis.

Adolescent↗

Refractory hypertension in an otherwise healthy adolescent.

Severe hypertension, for which no cause could be found, developed in an adolescent female. The patient's blood pressure was refractory to intensive pharmacologic intervention. After 11/2 years of medical management, the patient's intra-arterial blood pressures were found to be in the normotensive range. Individuals with labile hypertension may be refractory to pharmacologic control and may require continuous pressure monitoring in order to establish a proper diagnosis.

Adolescent↗

Control of serum C3 levels by beta 1H and C3b inactivator.

In serum specimens from 50 normal adults, a high correlation was found between the sum of the levels of the control proteins of the C3b amplification loop, C3b inactivator and beta 1H, and the sum of the component proteins, C3 and factor B (R = 0.83), when the concentrations are expressed as percent of the normal adult level. The slope for this regression was 0.98 and the y intercept practically zero, indicating that under normal conditions, beta 1H + C3b inactivator = C3 + factor B +/- 35% (95% error of the prediction). Biological significance of the combined values was suggested by the fact that their equality was largely preserved in serum specimens from cord blood, from infants, and from patients with idiopathic nephrotic syndrome, malnutrition, chronic illness, and partial C3b inactivator deficiency even though, individually, control and component protein concentrations deviated from normal in many of these conditions and, as single proteins, did not correlate with each other as in normal subjects. On the other hand, C3 + factor B was disproportionately lower than beta 1H + C3b inactivator in subjects heterozygously deficient in C3 and in those with hypocomplementemic glomerulonephritis and was often disproportionately high in those with an acute-phase reaction. The data indicate that for meaningful interpretation of the serum C3 level, the concurrent levels of factor B, C3b inactivator, and beta 1H must be taken into consideration.

Adolescent↗

Partial properdin deficiency.

The action of properdin in supporting complement consumption has been investigated in the serum from two individuals with partial properdin deficiency. Our studies are in agreement with those in which serum were artificially depleted of properdin in showing that serum deficient in properdin results in less C3 consumption in the presence of activators of both the alternative and classical complement pathways. Properdin deficiency did not lessen C3 consumption by C3NeF or CoF, confirming that properdin is not necessary for the action of these substances. Our findings indicate that partial properdin deficiency is innocuous but that complete absence of properdin may severely limit one's ability amplify complement activation.

Animals↗

Idiopathic rapidly progressive glomerulonephritis with C3 nephritic factor and hypocomplementemia.

A 7-year-old boy with mild renal failure and signs and symptoms of acute poststreptococcal glomerulonephritis including severe hypocomplementemia had, by renal biopsy, numerous crescents but no deposits in the glomerular capillary loops. Instead, deposits identical in location and composition to those described for children with idiopathic rapidly progressive glomerulonephritis were present. The severe hypocomplementemia was found to be due to high levels of C3 nephritic factor; niether nephritic factor nor hypocomplementemia has been reported in rapidly progressive glomerulonephritis of the idiopathic type. Following prompt therapy with methylprednisolone intravenously, serologic abnormalities disappeared and renal function greatly improved, but a later biopsy showed 50% of the glomeruli obliterated by scarring. The case is of importance not only in indicating that severe hypocomplementemia does not rule out idiopathic rapidly progressive glomerulonephritis but also in adding to the list of diseases in which nephritic factor can be found.

Antigen-Antibody Complex↗

Serum complement levels in infancy: age related changes.

Levels of eight complement components and two control proteins, were determined on cord serum from normal full term neonates and serum from healthy infants aged 1 and 6 months. For all proteins, the levels were below the adult normal at birth and rose toward the adult range by age 6 months. In a second group of 271 patients, ages 1-36 months, serum Clq and properdin levels were measured. For both proteins, the mean values in early infancy were more than two SD below the adult range and did not reach the adult range until 18-21 months of age. The Clq concentration was more variable than that for any other component studied. In infants from 11 months-3 yr of age, Clq levels correlated with serum IgG levels, but properdin levels did not.

Adult↗

Observations on the evolution of idiopathic rapidly progressive glomerulonephritis.

Distinctive deposits of C3, C5 and properdin were identified in the minimally proliferative glomerular lesions of a patient with idiopathic rapidly progressive glomerulonephritis. Biopsies of her renal allograft at times of recurrences of her disease and of five other patients with progressive renal failure but less severe crescent formation showed deposits identical composition and position, giving evidence of a common pathogenesis. The deposits were subepithelial and located in that part of the basement membrane in apposition to the mesangium (capillary waist). Breaks in the basement membrane were often exclusively in this area suggesting the deposits were causative. Ancillary observations suggest that the subepithelial deposits become unidentifiable after the scarring of severe extracapillary proliferation develops. Three of the patients had, in addition, intramembranous dense deposits but in other ways their disease was not characteristic of membranoproliferative glomerulonephritis Type II. Instead, the evidence indicated that all six patients were in early or lage stages of idiopathic (non-streptococcal) rapidly progressive glomerulonephritis.

Basement Membrane↗

Vertebral mineral determination by quantitative computed tomography (QCT): accuracy of single and dual energy measurements.

Quantitative CT (QCT) studies of trabecular vertebral bone tissue have been carried out in vitro on a GE CT/T 9800 scanner. Results of both single energy (SE) 80 kVp and dual energy (DE) 80/140 kVp QCT data are compared with chemical mineral analysis to determine accuracy. We examined 62 vertebral specimens, from 28 cadavers (19 male and 9 female with an age range of 19-93 years, mean = 60.4). Averaging the results of all vertebral bodies of the same individual for SEQCT versus ashweight, we found a correlation coefficient (r) of 0.94 (p less than 0.0001), a standard error of the estimate (SEE) of 12.2 mg/cm3 (calibrated to K2HPO4), with a coefficient of variation (CV) of 13.2% and an average underestimation of bone mineral content of 18.7 mg/cm3. The corresponding DEQCT results were r = 0.98 (p less than 0.0001), SEE = 7.4 mg/cm3, CV = 7.0%, and an average underestimation of 4.9 mg/cm3. The SE and DE results are correlated with r = 0.98 (p less than 0.0001), SEE = 8.0 mg/cm3, and CV = 8.7%. From our SEQCT data and the results of the chemical analysis of bone mineral and fat content we calculated a fat sensitivity of 7.7 mg/cm3 K2HPO4 per 100 mg/cm3 fat change for our scanner. Using an average fat variability of 87.5 mg/cm3, this leads to a fat-related uncertainty for the normative SEQCT data of 6.7 mg/cm3, which is far lower than the normal biological variation of 29.4 mg/cm3. Using tabulated normative data on fat content versus age and versus mineral content of 188 vertebral specimens from five collaborating centers, we derived a correction algorithm for QCT measurement that reduces our average underestimation to 0.88 mg/cm3 with an SEE of 12.1 mg/cm3. Hence, this correction procedure can be used to estimate the fat corrected absolute mineral density for research purposes or for scanners with high fat sensitivity. For the GE CT/T 9800 scanner, with a relatively low fat to mineral sensitivity at 80 kVp, the correction procedure is generally not recommended for clinical studies since it minimizes the average fat induced error but does not reduce the residual, partially fat related uncertainty. Finally, since the fat related uncertainty is small compared to biological variation, the correlation is high between SEQCT and DEQCT, and the radiation dose is lower and the precision higher for SEQCT, we suggest that most clinical diagnostic studies using the GE CT/T 9800 scanner for bone mineral determination employ SEQCT at 80 kVp.

Adult↗

Postoperative catecholamine response to onychectomy in isoflurane-anesthetized cats. Effects of analgesics.

Twenty-four healthy adult cats were anesthetized with isoflurane in oxygen. Six cats (group 1) served as controls; onychectomy of the forefeet was performed in the other three groups. Saline was administered intravenously to group 1, and morphine, xylazine, and salicylate were administered to groups 2, 3, and 4, respectively. Mixed venous blood samples were drawn for catecholamine analysis before induction of anesthesia, after recovery from anesthesia, and 30 minutes and 60 minutes after administration of the analgesic agent. Plasma catecholamine concentrations were determined by high performance liquid chromatography. Isoflurane anesthesia alone induced a transient increase in epinephrine concentration. Norepinephrine and epinephrine concentrations increased significantly after onychectomy. Morphine and xylazine significantly decreased postoperative norepinephrine and epinephrine concentrations; salicylate did not.

Analgesics↗

Wrist pain syndrome in the gymnast. Pathogenetic, diagnostic, and therapeutic considerations.

Gymnast wrist pain syndrome presents a difficult diagnostic and therapeutic challenge. It is common and debilitating among gymnasts, resulting in a reduction in training and performance, and may be the result of a response to repetitive trauma during the period of growth and development. This study was undertaken to define and characterize factors contributing to the causes and development of gymnast wrist pain and to establish an effective means of systematic and comprehensive evaluation and treatment. Thirty-eight collegiate gymnasts (20 UCLA: 9 female, 11 male; 18 NCAA: all male) were evaluated by radiograph and questionnaire. Seventy-five percent (22) of the males and 33% (3) of the females had had wrist pain for at least 4 months. The UCLA males averaged 2.82 +/- 1.94 mm positive ulnar variance; this was significantly greater than that of the NCAA males, who averaged 1.28 +/- 1.02 mm (P less than 0.02). The UCLA females averaged 1.44 +/- 1.88 mm positive ulnar variance. All of the gymnasts had significantly greater variance than had the controls, who averaged -0.52 mm (P less than 0.0001). The pommel horse routine was consistently responsible for wrist pain among the males. Anatomical and histological correlation of cryosections with magnetic resonance imaging (MRI) was performed to establish the usefulness of MRI in the diagnosis of wrist pain. MRI was able to differentiate the complex transitions between cortical and trabecular bone, articular surfaces, the ligaments, and the triangular fibrocartilage (TFC) complex of the wrist joint. A therapeutic algorithm was established to facilitate the evaluation and management of gymnast wrist pain. Arthroscopic surgery was successful, and arthroscopic findings correlated well with those of MRI and arthrography. Prospective studies are now underway in the pediatric and adolescent population to define further the causes and development of wrist pain problems in gymnasts.

Adolescent↗

Effects of gamma-aminobutyric acid on the compound action potential of the rat superior cervical ganglion.

The effects on the ganglionic transmission of gamma-aminobutyric acid (GABA) and related drugs were studied in the rat isolated superior cervical ganglion. The extracellularly recorded postganglionic compound action potential was used as an index for ganglionic transmission. GABA reversibly inhibited the ganglionic transmission by blocking the action potential. The effect of GABA is markedly antagonized by bicuculline (20 microM) or picrotoxin (200 microM). Furosemide (1 mM) was also effective in antagonizing the ganglionic effect of GABA. The antagonism by bicuculline was not affected in the presence of pentobarbital (50 microM). Baclofen inhibited the ganglionic transmission through an activation of GABAB receptors since it was markedly antagonized by phaclofen. Muscimol and isoguvacine were less effective than GABA in blocking the ganglionic transmission. The GABA uptake inhibitor isonipecotic acid blocked the ganglionic transmission, probably by activating GABAA receptors, because the effect was antagonized by bicuculline, but the GABA uptake inhibitor guvacine had no significant effect on the ganglionic transmission. These results suggest that GABA causes a ganglionic blockade by activation of both GABAA and GABAB receptor subtypes.

Action Potentials↗