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K B Miller

Publications and source records attributed to K B Miller.

108 records · Page 6Linked to original sources
PubMed1982

Immune regulatory abnormalities produced by procainamide.

The pathogenesis of procainamide-induced autoantibody production is unknown. To test the effect of procainamide on the immune system, we studied in vitro suppressor cell function and immunoglobulin G (IgG) secretion in 11 patients who developed autoantibodies while taking procainamide. The procainamide group was compared with patients with spontaneous systemic lupus erythematosus (n = 15) and a normal control population (n = 40). Impaired in vitro suppressor cell function was found in 11 of 14 patients with spontaneous systemic lupus erythematosus but in none of the patients taking procainamide. However, total in vitro IgG secretion was significantly increased in the procainamide group with regard to the control and systemic lupus erythematosus groups. There was a direct correlation between the circulating anti-SS DNA antibody titer and in vitro IgG secretion. Furthermore, T cells isolated from the procainamide-treated patients stimulated IgG secretion by normal allogeneic peripheral blood lymphocytes. The added T cells did not affect in vitro suppressor cell function. We postulate that autoantibody production in patients taking procainamide is due to enhanced helper T cell function and not to impaired suppression. However, the development of clinical disease requires the participation of additional genetic or immunologic factors.

Adolescent↗
PubMed1981

Unusual roentgenologic manifestations of Meckel's diverticulum.

Five cases illustrating rare roentgenographic manifestations of Meckel's diverticulum are presented. Small bowel studies in 2 patients demonstrated a mucosal pattern identifiable as heterotopic gastric rugae, and in 2 other cases peptic ulcers were seen within the diverticulum. In 1 patient the diverticulum located in the right upper quadrant contained calcified enteroliths, and in another patient the diverticulum had fistulous communication with the appendix.

Adult↗
PubMed1981

Normal immunoregulation of in vitro antibody secretion in autoimmune thyroid disease.

Defective suppressor cell function may be a causative factor in autoimmune disease in animals and man. In autoimmune thyroid disease, decreased suppressor cell activity could, under appropriate conditions, account for excess production of thyroid autoantibodies. We evaluated suppressor cell function in patients with Graves' disease and Hashimoto's thyroiditis and in normal controls. The method used is based on the principle that immunoglobulin synthesis by pokeweed mitogen (PWM)-stimulated lymphocytes is inhibited by Concanavalin A (Con A) stimulation of suppressor T cells. We studied suppressor cell control of polyclonal immunoglobulin G (IgG) and the thyroid-specific autoantibody, antimicrosomal antibody. PWM-stimulated IgG secretion (mean +/- SD) by lymphocytes from patients with Graves' disease (2797 +/- 718 ng/ml) and Hashimoto's thyroiditis (2201 +/- 423 ng/ml) did not differ from normal subjects (2431 +/- 485 ng/ml). The addition of Con A to PWM-stimulated lymphocytes suppressed IgG production in all three groups: Graves', 475 +/- 137 ng/ml; Hashimoto's, 507 +/- 74 ng/ml; and normal subjects, 460 +/- 156 ng/ml. The degree of suppression by the disease groups did not differ from the normal controls. Antimicrosomal antibody was detected in the concentrated, PWM-stimulated culture media of two of four Hashimoto's lymphocytes, three of five Graves' lymphocytes, and none of nine normal controls. Con A induced marked suppression of this organ-specific antibody in all cases. We conclude that Con A-stimulated lymphocytes from patients with Hashimoto's thyroiditis and Graves' disease can suppress antimicrosomal antibody and polyclonal IgG synthesis. These findings do not support the postulate of a generalized defect of suppressor cell function in these thyroid disorders.

Adult↗
PubMed1980

The role of delayed hypersensitivity in the enhancement of host resistance to infection.

Swiss-Webster mice were vaccinated by the intraperitoneal route (i.p.) with Mycobacterium tuberculosis BCG and challenged i.p. 4-10 weeks later with 10(4) virulent Salmonella typhimurium in the presence or absence of purified derivative (PPD) of tuberculin. Normal control mice were similarly challenged. Such an infection was fatal to the normal mice within 12 days. BCG vaccination prolonged the survival time and protected about 36% of the salmonella-infected mice from death. In contrast, tuberculin sensitivity, elicited in the BCG-vaccinated mice, significantly increased the survival time and protected about 70% of the mice against an otherwise fatal challenge. When these experiments were repeated using an infective dose of 10(6) organisms, the protective effect of the tuberculin reaction became substantially reduced, but there remained a statistically significant improvement in the survival distribution of the challenged mice as compared with that among the BCG-vaccinated mice. The examination of peritoneal washings obtained from BCG-vaccinated mice stimulated with PPD showed that the enhanced resistance to salmonella infection was directly associated with a quantitatively increased influx of phagocytic leukocytes accumulating at the site of infection as a result of the elicitation of tuberculin sensitivity.

Animals↗
PubMed1979

Familial abnormalities of suppressor-cell function in systemic lupus erythematosus.

We tested the hypothesis that abnormalities of central immune function are genetically controlled in patients with systemic lupus erythematosus. We used an in vitro suppressor-cell assay to evaluate central immunoregulation in 15 patients, 50 of their clinically healthy family members and 41 normal persons. Impaired suppressor-cell function was found in 11 patients; there was no correlation between disease activity and test results. Abnormal suppressor-cell activity was also found in 13 first-degree relatives, 12 of whom were women. We found no correlation between results of the suppressor-cell assay and the presence or absence of lymphocytotoxic antibodies in the relatives. Impaired suppressor-cell function cannot by itself explain the pathogenesis of systemic lupus erythematosus. Our results support the hypothesis that certain abnormalities of suppressor cells are genetic markers. We propose that the development of systemic lupus erythematosus requires the participation of at least two functionally distinct classes of genes.

Adolescent↗
PubMed1978

Evidence for structural homology between human red cell phosphoglycerate mutase and 2,3-bisphosphoglycerate synthase.

Previous reports have suggested the possibility of extensive structural homology between human erythrocyte bisphosphoglycerate synthase (glycerate-1,3-P2 leads to glycerate-2,3-P2) and phosphoglycerate mutase (glycerate-3-P in equilibrium glycerate-2-P). This study lends credence to that conjecture through comparative physicochemical investigations involving peptide mapping, circular dichroism, and immunological techniques. The data indicate that despite differences in function, both enzymes apparently manifest a high degree of similarity in primary, secondary, and tertiary structure. Mapping data also indicate that each protein is comprised of two apparently identical subunits.

Bisphosphoglycerate Mutase↗
PubMedDate not supplied

Nosocomial klebsiella infection in a neonatal unit: identification of risk factors for gastrointestinal colonization.

Sequential outbreaks of infection due to gentamicin-resistant Klebsiella pneumoniae (GRKP) types 30 and 19 occurred in the neonatal intensive care unit (NICU) at the Medical College of Virginia in 1977 and 1978. The extensive epidemiologic investigation carried out included a case-control study, careful review of aseptic technique, and cultures from nursery staff and environment. The gastrointestinal (GI) tracts of the patients were the reservoirs for GRKP, and the epidemic strain was transmitted by hands of personnel. The case-control study showed a significant relationship between acquisition of GRKP by patients and oropharyngeal and GI instrumentation, including use of bag resuscitation, oropharyngeal suctioning, and use of nasogastric feeding tubes. The findings of the case-control study were supported by observation of the patient care techniques practiced by NICU staff. Institution of control measures based on results of the epidemiologic investigation of the first outbreak rapidly brought the second outbreak under control, even though cohorting or use of routine isolation was not possible. Whereas GI colonization and hand transmission have been described previously in outbreaks of K. pneumoniae infections in NICUs, this study is the first to document the mode of inoculation of patients' GI tracts by contaminated hands of personnel.

Cross Infection↗