IMMUNOLOGIC REACTIONS TO HAPTENS ON AUTOLOGOUS CARRIERS : I. PARTICIPATION OF BOTH THYMUS-DERIVED AND BONE MARROW-DERIVED CELLS IN THE SECONDARY IN VITRO RESPONSE

Both thymus-derived (T) and bone marrow-derived (B) lymphocytes participate in the response to a hapten 4-hydroxy-3-iodo-5-nitrophenylacetic acid (NIP), coupled to a nonimmunogenic isologous carrier, mouse gamma globulin (MGG). Spleen cells from mice immunized with NIP-MGG show increased DNA synthesis in vitro when cultured with NIP-MGG. The participation of and requirement for T cells in the response was demonstrated by treating the spleen cells with anti-θ serum. This treatment resulted in a 77% inhibition of the antigen response. Furthermore, adoptively transferred normal thymus cells could be specifically "activated" by NIP-MGG in vivo and they responded secondarily to the antigen in vitro. The active participation of B cells in the secondary response was demonstrated by passing the immune spleen cells through a column coated with polyvalent anti-MGG serum. Column filtration reduced the number of NIP-specific plaque-forming cells and NIP-specific rosette-forming cells (both functions of B cells) and produced a 47% inhibition of the NIP-MGG response. The ability of the cells to respond to phytohemagglutinin (PHA) was not affected by column filtration showing that T cells were not being selectively removed. The participation of B cells in the in vitro NIP-MGG response was also shown by treatment of the spleen cells with antiserum specific for MGG and MGG determinants. B cells were removed by treatment with anti-IgM or polyvalent anti-MGG serum plus complement, resulting in a respective 46 and 49% inhibition of the response to NIP-MGG. (Treatment with anti-IgM serum had no effect on T cells.) The contribution of the hapten NIP to stimulation of T cells was investigated using NIP-MGG-activated thymus cells. These activated T cells responded in vitro very well to the NIP-MGG complex but not to the MGG carrier alone demonstrating the requirement of the hapten for T cell stimulation. The response was also partially inhibited (41%) by incubating the activated cells with NIP coupled to a single amino acid (epsilon-aminocaproic acid) before addition of NIP-MGG. These results demonstrated that T cells recognize the hapten NIP when it is coupled to the isologous carrier MGG

Prevalence and Risk Factors for Upper Airway Obstruction after Pediatric Cardiac Surgery

Objective To determine the prevalence of and risk factors for extrathoracic upper-airway obstruction after pediatric cardiac surgery. Study design A retrospective chart review was performed on 213 patients younger than 18 years of age who recovered from cardiac surgery in our multidisciplinary intensive care unit in 2012. Clinically significant upper-airway obstruction was defined as postextubation stridor with at least one of the following: receiving more than 2 corticosteroid doses, receiving helium-oxygen therapy, or reintubation. Multivariate logistic regression analysis was performed to determine independent risk factors for this complication. Results Thirty-five patients (16%) with extrathoracic upper-airway obstruction were identified. On bivariate analysis, patients with upper-airway obstruction had greater surgical complexity, greater vasoactive medication requirements, and longer postoperative durations of endotracheal intubation. They also were more difficult to calm while on mechanical ventilation, as indicated by greater infusion doses of narcotics and greater likelihood to receive dexmedetomidine or vecuronium. On multivariable analysis, adjunctive use of dexmedetomedine or vecuronium (OR 3.4, 95% CI 1.4-8) remained independently associated with upper-airway obstruction. Conclusion Extrathoracic upper-airway obstruction is relatively common after pediatric cardiac surgery, especially in children who are difficult to calm during endotracheal intubation. Postoperative upper-airway obstruction could be an important outcome measure in future studies of sedation practices in this patient population

Risk Factors for Extubation Failure following Neonatal Cardiac Surgery

Objective: Extubation failure after neonatal cardiac surgery has been associated with considerable postoperative morbidity, although data identifying risk factors for its occurrence are sparse. We aimed to determine risk factors for extubation failure in our neonatal cardiac surgical population. Design: Retrospective chart review. Setting: Urban tertiary care free-standing children’s hospital. Patients: Neonates (0–30 d) who underwent cardiac surgery at our institution between January 2009 and December 2012 was performed. Interventions: Extubation failure was defined as reintubation within 72 hours after extubation from mechanical ventilation. Multivariate logistic regression analysis was performed to determine independent risk factors for extubation failure. Measurements and Main Results: We included 120 neonates, of whom 21 (17.5%) experienced extubation failure. On univariate analysis, patients who failed extubation were more likely to have genetic abnormalities (24% vs 6%; p = 0.023), hypoplastic left heart (43% vs 17%; p = 0.009), delayed sternal closure (38% vs 12%; p = 0.004), postoperative infection prior to extubation (38% vs 11%; p = 0.002), and longer duration of mechanical ventilation (median, 142 vs 58 hr; p = 0.009]. On multivariate analysis, genetic abnormalities, hypoplastic left heart, and postoperative infection remained independently associated with extubation failure. Furthermore, patients with infection who failed extubation tended to receive fewer days of antibiotics prior to their first extubation attempt when compared with patients with infection who did not fail extubation (4.9 ± 2.6 vs 7.3 ± 3; p = 0.073). Conclusions: Neonates with underlying genetic abnormalities, hypoplastic left heart, or postoperative infection were at increased risk for extubation failure. A more conservative approach in these patients, including longer pre-extubation duration of antibiotic therapy for postoperative infections, may be warranted

Passive Peritoneal Drainage versus Pleural Drainage after Pediatric Cardiac Surgery

Background: We aimed to determine whether infants undergoing cardiac surgery would more efficiently attain negative fluid balance postoperatively with passive peritoneal drainage as compared to traditional pleural drainage. Methods: A prospective, randomized study including children undergoing repair of tetralogy of Fallot (TOF) or atrioventricular septal defect (AVSD) was completed between September 2011 and June 2013. Patients were randomized to intraoperative placement of peritoneal catheter or right pleural tube in addition to the requisite mediastinal tube. The primary outcome measure was fluid balance at 48 hours postoperatively. Variables were compared using t tests or Fisher exact tests as appropriate. Results: A total of 24 patients were enrolled (14 TOF and 10 AVSD), with 12 patients in each study group. Mean fluid balance at 48 hours was not significantly different between study groups, −41 ± 53 mL/kg in patients with periteonal drainage and −9 ± 40 mL/kg in patients with pleural drainage (P = .10). At 72 hours however, postoperative fluid balance was significantly more negative with peritoneal drainage, −52.4 ± 71.6 versus +2.0 ± 50.6 (P = .04). On subset analysis, fluid balance at 48 hours in patients with AVSD was more negative with peritoneal drainage as compared to pleural, −82 ± 51 versus −1 ± 38 mL/kg, respectively (P = .02). Fluid balance at 48 hours in patients with TOF was not significantly different between study groups. Conclusion: Passive peritoneal drainage may more effectively facilitate negative fluid balance when compared to pleural drainage after pediatric cardiac surgery, although this benefit is not likely universal but rather dependent on the patient’s underlying physiology

IMMUNITY AND TOLERANCE TO A HAPTEN (NIP) COUPLED TO AN ISOLOGOUS CARRIER (MOUSE GAMMA GLOBULIN)

A hapten, 4-hydroxy-3-iodo-5-nitrophenylacetic acid (NIP) when coupled to isologous mouse gamma globulin (MγG) elicits a hapten-specific immune response in mice if administered in Freund's complete adjuvant. This response is measurable by the capacity of the sera to bind N(125)IP, by detection of NIP-specific plaque-forming cells (B cells), and by in vitro secondary type antigen-driven DNA synthesis (T cells and probably B cells). The in vitro response requires both the hapten and carrier since neither by itself is capable of stimulating the spleen cells. This same antigen gives rise to hapten-specific tolerance when given in the soluble form. Mice pretreated with soluble NIP-MγG and challenged with NIP coupled to a heterologous carrier give a normal antibody response to the carrier but have barely detectable levels of antibody to NIP. Spleen cells from mice made tolerant to NIP-MγG do not respond in vitro with increased DNA synthesis. This implies that thymus-derived cells as well as bone marrow-derived cells are involved in hapten-specific tolerance

Visual estimates of grain size distribution in some Chester sandstones

Bibliography: p. 32-33

Identification and characterization of 3.8 min 134mI

The [gamma]-ray spectra of iodine fractions rapidly separated from the products of slow neutron fission of 235U were studied. A 3.8 +/- 0.2 min species was found and was identified as 134mI from observations of corresponding growth in the intensities of the prominent 847 and 884 keV [gamma]-rays of 53 min 134I. This isomer is analogous to the 2.9 h isomer 134mCs and decays by the sequence 134mI (J[pi] = 8-)(J[pi] = 5+)134I (J[pi] = 4+) by transitions of and 44.4 +/- 0.1 keV(), respectively. For a 316 keV cross-over [gamma]-ray an upper limit of 1 % was obtained, and is near the intensity predicted by M4 systematics. A low-intensity [gamma]-ray of 234.3 +/- 0.5 keV was found This [gamma]-ray is interpreted as evidence for [beta]-decay (2%) of the isomer, possibly to the 0.29 sec 7- isomeric level in 134Xe.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/34159/1/0000445.pd