Brain plasticity following psychophysiological treatment in learning disabled/ADHD pre-adolescents.

This research investigated the effects of a psychophysiological treatment methodology on brain plasticity as reflected in event-related brain potential topographic mapping and morphology along with School-marks and Mangina-Test performance in three different groups of pre-adolescents at baseline and 8 months later: (a) Learning Disabled/ADHD pre-adolescents who were treated; (b) Non-treated Learning Disabled/ADHD pre-adolescents; (c) Normal controls. Results indicate that: (1) the Event-Related Brain Potentials topographic mapping was significantly modified in post-treatment condition for the treated Learning/Disabled/ADHD group as opposed to pre-treatment baseline (P < 0.001). This was mainly due to the enhanced pre-frontal and frontal N450 amplitudes along with higher P450 components over posterior regions in post-treatment condition (P < 0.001); (2) for group comparisons at baseline, no significant topographic mapping differences were found between the treated Learning Disabled/ADHD group and the non-treated Learning Disabled/ADHD control group (P > 0.05) and significant differences were present between the treated Leaning Disabled/ADHD and the normal control group (P < 0.001); (3) 8 months later, in post-treatment condition, group comparisons revealed significant topographic mapping differences between the treated Learning Disabled/ADHD group and the non-treated Learning Disabled/ADHD control group (P < 0.001) and none between the treated Learning Disabled/ADHD group and the normal control group (P > 0.05); (4) the topographic mapping of both components was similar at baseline and 8 months later in both control groups (P > 0.05); (5) at baseline, school-marks and Mangina-Test performance of treated Learning Disabled/ADHD were not significantly different than those of the non-treated Learning Disabled/ADHD (P > 0.05) and significantly lower than those of the normal control group (P < 0.001); (6) the treated Learning Disabled/ADHD group in post-treatment condition had significantly higher school-marks and Mangina-Test performance than those of non-treated Learning Disabled/ADHD controls (P < 0.001) and were similar to those of normal controls 8 months later (P > 0.05); (7) school-marks and Mangina-Test performance at baseline for non-treated Learning Disabled/ADHD controls were not modified 8 months later (P > 0.05) and normal controls maintained their high performance within the same time interval (P > 0.05). These findings provide evidence of the impact of the psychophysiological treatment methodology on brain plasticity and regulation as reflected in significantly improved neurophysiology of pre-frontal, frontal and posterior brain regions concomitantly with higher school-marks and neuropsychometric performance in the Mangina-Test.     

European system for cardiac operative risk evaluation predicts long-term survival in patients with coronary artery bypass grafting.

OBJECTIVE: To evaluate the accuracy of predicting long-term mortality in patients with coronary artery bypass grafting (CABG) by using the European system for cardiac operative risk evaluation (EuroSCORE). METHODS: Medical records of patients with CABG (n=3760) between January 1992 and March 2002 were retrospectively reviewed and their predicted surgical risk was calculated according to the standard (study A) and logistic (study B) EuroSCORE. In study A the patients were divided into six groups: 0-2 (n=610), 3-5 (n=1479), 6-8 (n=1099), 9-11 (n=452), 12-14 (n=103) and >14 (n=17). In study B the patients were divided into seven groups: 0.00-2.00 (n=447), 2.01-5.00 (n=1190), 5.01-10.00 (n=890), 10.01-20.00 (n=686), 20.01-30.00 (n=234), 30.01-60.00 (n=254) and >60.00 (n=59). Long-term survival was obtained by the National Death Index and Kaplan-Meier curves were constructed and compared employing the log-rank test. Multivariate Cox regression analysis was performed in order to control for pre, intra and postoperative factors and adjusted hazard ratios were calculated for standard and logistic EuroSCORE groups. The receiver operating characteristic (ROC) curves were plotted to assess the discrimination ability of the EuroSCORE. RESULTS: In study A there were differences among the six groups in 30-day mortality (0.7%, 1.0%, 3.1%, 4.6%, 13.6% and 23.5%; P<0.001), in major complications (8.5%, 10.4%, 16.2%, 20.4%, 31.1% and 35.3%; P<0.001) as well as in actuarial long-term survival (86.2%, 79.6%, 53.6%, 37.9%, 24.9% and 0% from EuroSCORE 0-2 to >14; P<0.001). In study B there were differences among the seven groups in 30-day mortality (0.9%, 1.1%, 1.2%, 3.6%, 3.4%, 8.7% and 15.3%; P<0.001), major complications (8.5%, 10.1%, 12.1%, 18.4%, 16.2%, 26.0% and 30.5%; P<0.001) as well as in actuarial long-term survival (89.5%, 79.9%, 66.9%, 51.0%, 40.3%, 38.4% and 13.7% from EuroSCORE 0.00-2.00 to >60.00; P<0.001). Multivariate Cox regression analysis confirmed that EuroSCORE (standard or logistic) was a statistically significant predictor for long-term mortality, while the area under the ROC curve was 0.72 for either standard or logistic EuroSCORE. CONCLUSION: The predicted surgical risk in CABG patients as calculated by standard or logistic EuroSCORE is a strong predictor for long-term survival in addition to predicting operative survival for which it was originally designed.     

Outcomes of 829 neonates with complete transposition of the great arteries 12-17 years after repair.

OBJECTIVE: Between 1985 and 1989, the surgical management of neonates with complete transposition (TGA) underwent a transition from atrial to arterial repair. We sought to examine the intermediate outcomes and their associated risk factors in neonates repaired during the era of transition. PATIENTS AND METHODS: Twenty-four institutions entered 829 neonates age less than 15 days in a prospective study. Diagnosis was simple TGA (n=631), TGA with ventricular septal defect (VSD) (n=167), TGA with VSD and pulmonary stenosis (TGA/VSD/PS) (n=30), or TGA with PS (n=1). Repair was by arterial switch (n=516), atrial repair (Senning=175, Mustard=110) or Rastelli (n=28). Time-related events were analysed by parametric hazard function modeling and incremental risk factors for mortality, re-intervention, and late functional assessment were sought. RESULTS: Survival estimates at 6 months, 5, 10, and 15 years are 85, 83, 83, and 81%, respectively. The hazard function for death after repair has two phases: an early rapidly declining phase and an ongoing constant one. Constant phase mortality is less likely after the arterial switch operation and in children with simple TGA. During follow up, at least one re-intervention was required in 167 children (pacemaker, n=35; percutaneous intervention, n=32; baffle re-intervention, n=27; re-operation, n=125). Freedom from re-intervention at 6 months, 5, 10 and 15 years is 93, 82, 77, and 76%, respectively. Of survivors, 87% have been followed up to the last 3 years, including an assessment of functional ability of 562 children (83%). Functional class 15 years after repair is class I in 76%, II in 22%, III in 2%. The proportion in functional class I decreased over time. Psychosocial deficits, especially learning disorders are prevalent. CONCLUSIONS: Survival 15 years after TGA repair is good with most children functioning well, and results are best after an arterial switch operation. There is an ongoing risk of death that is less after the arterial switch operation. With the exception of Rastelli patients, the likelihood of survivors needing re-intervention after 5 years is low. There is need for improved neurodevelopmental outcomes.     

Smooth muscle of rabbit isolated aorta contains the NK-2 tachykinin receptor

Summary Neurokinin A, neurokinin B and substance P caused concentration-related contractions of rabbit isolated aorta with pD₂ values of 8.1, 6.9 and 6.0, respectively. [D-Pro², D-Trp^7,9]-substance P, a competitive tachykinin antagonist, had pA₂ values of 5.3 against neurokinin A, 5.1 against neurokinin B and 5.2 against substance P indicating that tachykinin receptors mediated responses to the agonists. [pGIu⁵,MePhe⁸,-McGly⁹]-substance P 5–11 (DiMe-C7), senktide and septide did not contract the aorta. It is concluded that of the known tachykinin receptors smooth muscle of the rabbit isolated aorta contains only the NK-2 type. Send offprint requests to J. W. Constantine at the above address     

Translocation t(12;22)(q13;q12.2–12.3) in a clear cell sarcoma of tendons and aponeuroses

Cytogenetic analysis of a short-term culture from a clear cell sarcoma revealed a complex karyotype with the mainline of 49,XY,t(7;18)(p11.2;q21.3), + der(7)t(7;18)(p11.2;q21.3), + 8, + der(8;17)(q10;q10),t(12;22)(q13;q12.2–12.3),add(13)(p13). An apparently identical translocation t(12;22) has been described recently in four clear cell sarcomas, indicating that this constitutes a primary cytogenetic change specific for this type of tumor. In our case, the breakpoint on chromosome 22 could be assigned to band 22q12.2 or 22q12.3. Together with the present case, trisomy or tetrasomy 8 has been found in six of nine clear cell sarcomas, suggesting that, as in Ewing's sarcoma and myxoid liposarcoma, trisomy/tetrasomy 8 represents a nonrandom secondary aberration. We conclude that the finding of the specific translocation t(12;22) may prove to be an important marker in the differential diagnosis of clear cell sarcoma from some other soft tissue sarcomas and malignant melanoma. © 1993 Wiley-Liss, Inc.     

Passive intranasal monoclonal antibody prophylaxis against murine Pneumocystis carinii pneumonia

Passive antibody immunoprophylaxis is one method used to protect patients against infection if they are unable to mount an adequate active immune response. Topical application of antibody may be effective against infections at mucosal sites. Using a SCID mouse model of Pneumocystis carinii pneumonia, we were able to demonstrate protection against an airborne challenge with P. carinii by intranasal administration of antibody. Immunoglobulin M (IgM) monoclonal antibodies to an epitope shared by mouse and human P. carinii organisms reduced organism numbers by more than 99% under the conditions described. An IgG1 switch variant of one of the IgM monoclonal antibodies was also protective. These experiments provide a model for exploring the utility of this approach in protecting at-risk patients from infection with P. carinii.     

Epitope mapping of a protective monoclonal antibody against Pneumocystis carinii with shared reactivity to Streptococcus pneumoniae surface antigen PspA

Pneumocystis carinii is an opportunistic fungal pathogen that causes pneumonia in the immunocompromised host. A protective monoclonal antibody (MAb) termed 4F11 generated against mouse-derived P. carinii was shown by indirect immunofluorescence assay (IFA) to bind surface antigens of P. carinii derived from multiple host species, including humans. We have identified multiple epitopes recognized by MAb 4F11 in two recombinant mouse P. carinii antigens. The epitopes mapped have similar proline content and positive charge distribution. The consensus 8-mer epitope recognized by MAb 4F11 is K/RPA/RPK/QPA/TP. Immune sera raised against intact mouse P. carinii recognized native antigens affinity purified with MAb 4F11 and a recombinant antigen reactive with MAb 4F11. Database searches for short, nearly exact matches to the mapped MAb 4F11 epitopes identified a bacterial surface antigen, Streptococcus pneumoniae PspA, with a similar proline-rich region. In an IFA, MAb 4F11 detected antigens on the S. pneumoniae surface, and Western blotting identified a protein in S. pneumoniae lysates consistent with the M(r) of PspA. A fragment of the S. pneumoniae PspA gene was cloned and sequenced, and the deduced amino acid sequence contained a region with strong similarity to the MAb 4F11 epitopes identified in P. carinii. The PspA recombinant polypeptide was recognized by MAb 4F11 in a Western blot. The ability of MAb 4F11 to recognize similar proline-rich epitopes may explain its ability to recognize P. carinii derived from multiple hosts and will permit testing of the epitopes recognized by this antibody in immunization against P. carinii.