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Introduction: Bubble continuous positive airway pressure (b CPAP) is associated with a decreased risk for chronic lung disease (CLD) in preterm neonates. This report examined the effectiveness of adopting b CPAP to reduce respiratory complications and medication usage in a community hospital NICU., Methods: The efficacy of b CPAP was assessed by retrospective examination and comparison of 45 neonates who received b CPAP and 87 neonates who received conventional ventilation only. Data on medication usage were also collected and analyzed., Results: After introduction of the b CPAP protocol, the median number of days on oxygen decreased in the b CPAP group compared with the conventional ventilation only group (median = 33 days, IQR = 7.5-66 vs median = 0, IQR = 0-0; P < 0.001). The exposure to conventional ventilation decreased in the b CPAP group compared with the conventional ventilation only group (median = 18 days, IQR = 5-42.5 vs median = 0, IQR = 0-7; P < 0.001). Postimplementation of b CPAP revealed decreases in CLD from 26 (30%) in the conventional ventilation only group to 2 (4%) in the b CPAP group ( P = 0.002); there was also a significant decrease in the use of sedative medications in the b CPAP group compared with the conventional ventilation only group (mean = 5.20 doses, SD = 31.97 vs mean = 1.43, SD = 9.98; P < 0 .001)., Conclusion: The use of b CPAP results in significant decreases in the use of conventional ventilation, the risk for CLD, and the need for sedative medication., (Copyright © 2020 the Author(s). Published by Wolters Kluwer Health, Inc.)

The immunological events mediated by, and antigen specificity of, allograft-bound lymphocytes (ABLs) are poorly understood. To further define the role of antibody-mediated rejection, a rejected allograft from a patient with primary anti-TBM disease was sterilely minced and pressed through a microscreen. The ABLs were isolated by density gradient centrifugation. Using this technique, 8.5 X 10(6) ABLs were isolated. Then 1 X 10(6) washed ABLs/ml were suspended in RPMI 1640 with 20% fetal calf serum and cultured in microtiter plates with media only, or with pokeweed mitogen (PWM) (100 micrograms/culture). The cells were incubated for 7 days and supernatants were collected and assayed for total IgG and IgM by a solid-phase enzyme immunoassay (EIA) and reactivity with normal human kidney targets by indirect immunofluorescence (IF) and immunoperoxidase (IP) techniques. Total IgG production was 500 ng/ml for both spontaneous and PWM stimulated cells. No IgM production was detected. IF and IP studies demonstrated IgG-anti-TBM antibodies in the spontaneous supernatants only. IgG antibodies reactive with peritubular capillaries (anti-PTC) were also noted. IgG-anti-TBM anti-bodies and antibodies reactive with arterioles were subsequently demonstrated by direct immunofluorescence techniques in the rejected allograft. Analysis of serum samples obtained at the time of allograft rejection showed no IF or IP reactivity with the kidney targets. Subsequent analysis of anti-TBM production by the patient's peripheral blood mononuclear cells (PBMs) showed IgM-anti-TBM only. These studies suggest that the IgG-anti-TBM and IgG-anti-PTC antibodies reactive with the allograft resulted from in situ antibody production by ABLs; the role of anti-TBM antibodies in mediating the AR is unclear, but their presence suggests recurrence of the original disease in the allograft. Anti-PTC antibodies could be important in mediation of the vascular AR.

Blood transfusions (BT) administered prior to renal allograft transplantation are known to enhance allograft survival. One proposed mechanism for this effect is through the induction of antiidiotypic antibodies that modify the immune response to subsequently presented graft antigens. In an attempt to determine if antiidiotypic antibodies are generated post-BT, we studied sera from post-BT patients for the presence of antiidiotypic antibodies to anti-HLA class I IgG (i.e., anti-anti-HLA). Anti-HLA antiidiotypes were demonstrated by idiotype-specific inhibition of an enzyme immunoassay (EIA) for anti-HLA antibodies. Using this inhibition technique, test sera from 8 of 16 post-BT patients showed significant inhibition of the anti-HLA target sera (P less than 0.05). Sera from normal individuals showed no inhibition of the target sera, and test sera did not inhibit other antigen-antibody systems. Protein A absorption of test sera eliminated the inhibitory effect, suggesting that the antiidiotypic activity was limited to the IgG fraction of the sera. The EIA binding activity of F(ab')2 fragments of anti-HLA IgG was suppressed by sera from patients post-BT but not by sera from normal volunteers. Studies of serially obtained sera from a post-BT patient showed that anti-HLA antiidiotype levels fluctuate with time and transfusion status. These studies demonstrate that anti-HLA antiidiotypic antibodies are generated post-BT. Their importance in mediating the known allograft-enhancing effect of pretransplant BT remains to be clarified.