Cells from the T-lymphoblastoid cell line, CCRF-CEM, have been exposed in vitro to a quasirectangular, asymmetric electromagnetic field pulsed at 72 Hz at 37 degrees for periods of 30 min to 24 h. RNA synthesis, assessed by incorporation of 3H-uridine, increased (relative to control cells) 2-fold after 30 min in exposed cells and achieved its greatest increase of 3.2-fold relative to controls after 2 h exposure. Increased precursor incorporation was observed at all subsequent exposure times up to 24 h. Synthesis of mRNA was similar, but not identical to that observed with total cellular RNA. Additionally, protein synthesis, determined by incorporation of radioactive precursor into acid-precipitable material, was increased 2.8-fold, compared to controls, after 2 h exposure. Longer exposure times resulted in an exponential decrease in precursor incorporation to 1.1-times control levels after 24 h. Using a dye reduction assay, mitochondrial activity was also found to be increased over a 24 h exposure period. No effect of electromagnetic field exposure was found on cellular synthesis of DNA. These data are generally consistent with other reports documenting effects of electromagnetic field exposure on macromolecular synthesis in vitro.

DNA, Neoplasm↗

PubMed1987

Drug-induced esophageal strictures.

A retrospective study of 55 patients with a benign esophageal stricture showed that in 11 patients (20%) the cause was a drug-induced lesion due to potassium chloride (3), tetracyclines (3), aspirin (2), vitamin C (1), phenytoin (1), and quinidine (1). Five of the 11 patients would have been diagnosed as having a reflux etiology of their stricture if 24-hour esophageal pH monitoring was not performed. Six patients responded to dilatation and five patients required resection or bypass. A prospective study of 18 asymptomatic volunteers showed a high incidence of esophageal lodgment of a radiolabeled medicinal capsule, with subsequent dissolution and release of the isotope. This occurred most frequently in elderly subjects and was reduced by increasing the volume of water chaser. The sites of lodgment correspond to the location of the observed strictures in the patient population. An in vitro study showed that, when the causative drugs were mixed with saliva, dissolution occurred within 60 minutes and was associated with significant changes in pH. These investigations show that drug-induced esophageal strictures are more common than previously appreciated, and can be confused with a reflux etiology. Diagnosis is suggested by a history of drug ingestion, location of the stricture, and a normal esophageal acid exposure on 24-hour pH monitoring. The severity of the esophageal injury is variable and requires dilatation to resection for therapy.

Adolescent↗

PubMed1987

Factors influencing the transit of a gelatin capsule in the esophagus.

The tendency of a gelatin capsule to lodge in the esophagus, dissolve, and release its contents, as a potential etiology of drug-induced esophageal injury, was studied in 18 asymptomatic volunteers. Their ages ranged from 21 to 81 years, with nine subjects over 70 years old. Esophageal transit time of liquids was measured in all subjects after which the esophageal transit time of a #00 gelatin capsule containing technetium (99mTc) sulfur colloid was measured with a 120 ml and a 15 ml water bolus. The capsule lodged in three subjects (17 percent) with the 120 ml bolus and in 11 subjects (61 percent) with the 15 ml bolus. Esophageal manometry demonstrated a lower mean amplitude of esophageal contractions in subjects in whom the capsule lodged with the 120 ml bolus and in the elderly subjects. We conclude that the esophageal transit time of a gelatin capsule is related to the volume of fluid chaser. Our findings that a lower amplitude of esophageal contractions was associated with elderly patients and those in whom the capsule lodged with the large fluid bolus are worthy of further investigation.

Adult↗

PubMed1985

Regulation of T cell proliferation by cloned interferon-alpha mediated by Leu-11b-positive cells.

The autologous T lymphocyte proliferative response (AMLR) induced by a B lymphocyte-enriched non-T, nonadherent cell population (NT, NAC) and by a macrophage-enriched population were both suppressed by the addition of a cloned interferon-alpha (IFN-alpha Con1) directly to the cultures. Preincubation of the stimulating NT, NAC with IFN-alpha Con1 resulted in comparable suppression. In contrast, preincubation of the macrophages with IFN-alpha Con1 resulted in significant augmentation of T cell proliferation. Depletion of Leu-11b-positive cells from the NT, NAC exposed to IFN-alpha Con1 restored the autologous T cell response. Addition of IFN-alpha Con1 activated Leu-11b-positive cells, isolated from the NT, NAC population, was suppressive of the AMLR. Although NK cytotoxicity was irradiation sensitive, suppression of the AMLR by IFN-alpha Con1-activated NT, NAC was resistant, suggesting that different subsets of cells or mechanisms by the same cells may have been responsible. These observations may offer insights into the potential role of cells with the NK phenotype, Leu-11b, and IFN in contributing to immuno-regulatory changes observed in clinical states associated with elevated concentrations of IFN.

Antibodies, Monoclonal↗

PubMed1984

Characterization of the defective autologous mixed lymphocyte response in rheumatoid arthritis.

In order to characterize the autologous mixed lymphocyte response (AMLR) in patients with rheumatoid arthritis (RA) and to define the relationship with disease activity, peripheral blood T lymphocytes were stimulated with either a B lymphocyte-enriched (B cells) or a macrophage-enriched (macrophages) population. A significant reduction (P less than 0.01 to P less than 0.001) of T cell proliferation stimulated both by B cells and macrophages was observed in patients with active disease. The B lymphocytes were significantly less stimulatory (P less than 0.02 to P less than 0.001) than macrophages in the patients compared with the controls. In the normal controls, macrophages in higher concentrations were capable of suppressing the B lymphocyte-stimulated AMLR, but macrophages from patients with RA were not excessively suppressive. A significant association (P less than 0.02) was observed between disease activity and the AMLR. Using the B-enriched population, the AMLR proliferative response was significantly associated (P less than 0.001) with the production of interleukin-2. Defects in proliferation could only be partially restored by the addition of interleukin-2. These data indicate that the defective AMLR observed in patients with RA is related to disease activity and is associated with altered cellular interactions among T lymphocytes, macrophages, and the B lymphocyte-enriched population.

Arthritis, Rheumatoid↗

PubMedDate not supplied

Leflunomide, a potential immunosuppressant for pancreatic islet transplantation.

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Animals↗