Immunogenicity of tetravalent rhesus rotavirus vaccine administered with buffer and oral polio vaccine.

Between January and November 1989, we studied 174 infants aged 6 to 16 weeks in a randomized clinical trial to (1) determine the immunogenicity of a single dose of tetravalent rhesus rotavirus vaccine (RRV-TV) when administered with three different buffer regimens: no antacid buffer and small-volume (2.5-mL) and large-volume (30-mL) antacid buffer; and (2) examine the potential interference of RRV-TV on the immune response to oral polio vaccine. Immunogenicity of RRV-TV, measured as a fourfold rise in antibody titers to rotavirus, was similar in the groups receiving small- and large-dose buffer (45% and 49%, respectively) and significantly less in the group that received RRV-TV alone (23%). Administration of RRV-TV with oral polio vaccine did not significantly interfere with the neutralization response of oral polio vaccine poliovirus serotypes 1, 2, or 3, and overall, 29%, 87%, and 24% of the infants had a fourfold rise in titer to each serotype, respectively.     

Human leukocyte antigen-DRB1*1104 in the chronic iridocyclitis of pauciarticular juvenile rheumatoid arthritis.

To determine whether genetic markers for chronic iridocyclitis could be identified, we used both serologic and oligonucleotide dot blot techniques to characterize immunogenetically 164 children with early-onset pauciarticular juvenile rheumatoid arthritis. Seventy-eight children (47.6%) had chronic iridocyclitis and 86 (52.4%) had not had evidence of eye disease during a mean follow-up period after the onset of arthritis of 15.8 years (minimum of 5.5 years). Control subjects were 218 healthy, unrelated individuals. The analysis was limited to alleles known to be associated with an increased or decreased risk of early-onset pauciarticular juvenile rheumatoid arthritis or of chronic iridocyclitis in this form of juvenile rheumatoid arthritis. Only one split of human leukocyte antigen (HLA)-DR5, HLA-DRB1* 1104, showed a statistically significant association with a risk of chronic iridocyclitis (chi-square value = 7.52; p = 0.036 adjusted; odds ratio 3.45); HLA-DQA1* 0501 and HLA-DQB1* 0301, both in linkage disequilibrium with HLA-DRB1* 1104, also were significantly associated with eye disease. Patients with both the DRB1* 1104 and DPB1* 0201 genes had a 7.7-fold increased risk for chronic iridocyclitis compared with that for other patients. The presence of HLA-DRB1* 1104 was about four times as specific, but only about one third as sensitive, as antinuclear antibodies in identifying patients at risk for eye disease. Although all children with early-onset pauciarticular juvenile rheumatoid arthritis should undergo periodic slit-lamp examinations, those with the HLA class II gene DRB1* 1104 are at particularly high risk for eye disease, and we recommend that they be monitored carefully for its evolution.     

Studies on the chronic toxicity (inhalation) of four types of refractory ceramic fiber in male Fischer 344 rats

Abstract Refractory ceramic fibers (RCF) are man-made vitreous fibers used primarily in industrial high-temperature applications, especially for insulation of furnaces and kilns. Because of their increasing use and potential for human exposure, a chronic toxicity/carcinogenicity inhalation study was conducted in Fischer 344 (F344) rats. Five groups of 140 weanling male F344 rats were exposed via noseonly inhalation to either HEPA-filtered air (chamber controls) or 30 mg/m(3) (approximately 220 fibers/cm(3)) of three types [kaolin-based, high-purity, and aluminum zirconia silica (AZS)] of "size-selected" RCF fibers (approximately 1μ in diameter and approximately 20 um in length) and an "after-service" heat-treated (2400°F for 24 h) kaolin-based fiber for 6 h/day, 5 days/wk for 24 mo. They were then held unexposed until approximately 20% survival and then sacrificed at 30 mo. A positive control group of 80 F344 rats was exposed to 10 mg/m(3) chrysotile asbestos. Croups of 3-6 animals were sacrificed at 3, 6, 9, 12, 15, 18, and 24 mo to follow the progression of lesions and to determine fiber lung burdens. Additional groups of 3 rats were removed from exposure at 3, 6, 9, 12, and 18 mo and were held until sacrificed at 24 mo (recovery groups) for similar determinations. Lung burdens increased rapidly for all RCFs, appearing to plateau by about 12 mo. By 24 mo, lung burdens ranged from 2.6 to 9.6 × 10(5) fiberslmg of dry lung tissue for the RCFs tested. Treatment-related lesions were restricted to the lungs. To some extent all types of RCF resulted in macrophage infiltration, bronchiolization of proximal alveoli, and microgranuloma formation by 3 mo of exposure. Interstitial fibrosis was observed at 6 mo for all types of RCF, except the "after-service" fiber where fibrosis was not seen until 12 mo. The lesions progressed in severity until 12-15 mo, after which they plateaued. A minimal amount of focal pleural fibrosis was first observed at 9 mo and progressed to a mild severity by the end of the study. Fxposure-related pulmonary neoplasms (bronchoalveolar adenomas and carcinomas combined) were observed with all 4 types of RCF [kaolin, 16 of 123 (13%); AZS, 9 of 121 (7.4%); high-purity, 19 of 121 (15.7%); and "after-service,"4 of 118 (3.4%)], compared to 2 of 120 (1.5%) in the untreated air controls. Pleural mesotheliomas were observed in two kaolin, three AZS, two high-purity, and one "after-service" exposed rats. A comparable but slightly greater amount of fibrosis was observed in the lungs of the positive (chrysotile asbestos) controls. The incidence of bronchoalveolar neoplasms in the chrysotile exposed rats was 13 of 69 (18.8%), and a mesothelioma occurred in 1 (1.4%) animal. The results of this study showed that the four types of RCF studied had carcinogenic activity in rats at the maximum tolerated dose.     

In Vitro Evaluation of an Alternative Neonatal Extracorporeal Life Support Circuit on Hemodynamic Performance and Bubble Trap

The objective of this study was to evaluate an alternative neonatal extracorporeal life support (ECLS) circuit with a RotaFlow centrifugal pump and Better‐Bladder (BB) for hemodynamic performance and gaseous microemboli (GME) capture in a simulated neonatal ECLS system. The circuit consisted of a Maquet RotaFlow centrifugal pump, a Quadrox‐iD Pediatric diffusion membrane oxygenator, 8 Fr arterial cannula, and 10 Fr venous cannula. A “Y” connector was inserted into the venous line to allow for comparison between BB and no BB. The circuit and pseudopatient were primed with lactated Ringer's solution and packed human red blood cells (hematocrit 35%). All hemodynamic trials were conducted at flow rates ranging from 100 to 600 mL/min at 36°C. Real‐time pressure and flow data were recorded using a data acquisition system. For GME testing, 0.5 cc of air was injected via syringe into the venous line. GME were detected and characterized with or without the BB using the Emboli Detection and Classification Quantifier (EDAC) System. Trials were conducted at flow rates ranging from 200 to 500 mL/min. The hemodynamic energy data showed that up to 75.2% of the total hemodynamic energy was lost from the circuit. The greatest pressure drops occurred across the arterial cannula and increased with increasing flow rate from 10.1 mm Hg at 100 mL/min to 114.3 mm Hg at 600 mL/min. The EDAC results showed that the BB trapped a significant amount of the GME in the circuit. When the bladder was removed, GME passed through the pump head and the oxygenator to the arterial line. This study showed that a RotaFlow centrifugal pump combined with a BB can help to significantly decrease the number of GME in a neonatal ECLS circuit. Even with this optimized alternative circuit, a large percentage of the total hemodynamic energy was lost. The arterial cannula was the main source of resistance in the circuit.     

The relationship of axillary venous thrombosis to the thoracic outlet compression syndrome.

In a relatively small personal series (41 patients) of first rib resections for thoracic outlet compression, I have encountered 8 patients in whom venous obstruction at the thoracic outlet was the major component. Four of the 8 had typical "stress" thrombosis of the axillary vein. Angiography demonstrated a tight thoracic outlet to be the underlying cause of the venous thrombosis. In the 4 patients with venous compression but without thrombosis, angiograms suggested that each was a candidate for axillary venous thrombosis unless the underlying thoracic outlet compression syndrome was relieved. Although thoracic outlet compression has been documented as a cause of "stress thrombosis" of the axillary vein, the relationship of the two conditions apparently is often overlooked, even by experienced thoracic surgeons. Representative case histories and angiograms are presented to demonstrate the close relationship of thoracic outlet compression and axillary venous thrombosis.