ABSTRACT
Objective To observe the effect of massage at Tiantu (CV22) in promoting expectoration in craniocerebral trauma patients, and to lessen complications. Method Fifty craniocerebral trauma patients after extubation were randomized into a control group and a treatment group, 25 cases each. The control group was intervened by nebulization plus tapping back to promote cough and expectoration, while the treatment group was additionally given massage at Tiantu. For successive 3 days, the oxygen saturation, atelectasis and arrhythmias were observed and recorded before and after treatment in the morning, at midday and night, as well as the re-intubation rate, cough and expectoration induced by the treatment in the morning, at midday and night during the 3 days. Result The total effective rate in causing cough and expectoration and the increase of oxygen saturation in the treatment group were significantly higher than those in the control group, while the occurrence of complications including atelectasis and arrhythmias and re-intubation rate in the treatment group were significantly lower than those in the control group (P<0.05). Conclusion Massage at Tiantu is helpful to enhance the oxygen saturation and promote cough and expectoration in craniocerebral trauma patients, and it can lessen the occurrence of complications, thus worth applying in clinic.
ABSTRACT
PURPOSE: The normal function of tumor suppressor genes is thought to be related to their ability to regulate cell proliferation and the loss of such function presumably leads to malignant transformation by releasing the transformed cells from growth regulation. One approach to identify these tumor suppressor genes is by loss of heterozygosity (LOH) studies. The rationale of these studies is that the mutation of one allelic copy of a tumor suppressor gene followed by the loss of the remaining wild type allele will result in the total loss of the function of the tumor suppressor gene. Chromosomal loci with frequent LOH in malignant tumors is likely to contain tumor suppressor genes. We want to identify deletions of putative tumor suppressor gene loci in pediatric brain tumors by polymerase chain reaction (PCR)-based LOH studies using microsatellite polymorphic markers of chromosome 9, 22 and 17p as most frequent cytogenetic abnormalities involve chromosome 17p, 22 and 9 in pediatric brain tumors. MATERIAL AND METHOD: Blood and tumor samples were obtained from 12 pediatric brain tumor patients who were operated at Texas Children's Cancer Center from April 1996 to January 1997. The 12 tumors consist of 5 cases of medulloblastomas, 4 cases of juvenile pilocytic astrocytomas, and 1 case each of ependymoma, atypical teratoid rhabdoid tumor and desmoplastic infantile ganglioglioma. Genomic DNA extracted from blood and tumor tissues were amplified by PCR using [gamma-32P]ATP endlabeled primer pairs for the microsatellite polymorphic markers on chromosome 9, 22 and 17p which were D9S171, D9S169, D9S168, D9S165, D9S156, D9S110, D9S146, D9S971, D9S757,D9S176, D9S2105, D9S177, D9S2127, D9S1849, D9S1817, D22S303, D22S33, D22S315, D22S275, D22S299, D22S301, TOP1P2, PDGFB, D22S274, D22S304, D17S1866, D17S1810, D17S796, D17S1566 and D17S1574. The PCR products were separated by electrophoresis in a denaturing 6% polyacrylamide gel and exposed on X-ray films to analyze LOH. RESULTS: 1) There was no evidence of LOH on chromosome 9 in all 12 pediatric brain tumors. 2) Among 12 pediatric brain tumors, only one allelic loss on chromosome 22 (D22S274 : 22q13.31-22q13.33) was observed in an atypical teratoid rhabdoid tumor. 3) LOH for loci on chromosome 17p were detected in 6 cases (50%) of 12 various pediatric brain tumors including 4 cases of medulloblastomas and 1 case each of ependymoma and atypical teratoid rhabdoid tumor. Among 5 cases of medulloblastomas, 4 cases(80%) showed LOH on at least one of 5 markers of chromosome 17p. 4) There was no allelic loss on chromosome 9, 22 and 17p in juvenile pilocytic astrocytomas. CONCLUSION: Our data indicate that there may be a putative tumor suppressor gene located on chromosome 22q13.3 associated with tumorigenesis of atypical teratoid rhabdoid tumor, and other putative tumor suppressor genes located on chromosome 17p13.1-17p13.3 associated with tumorigenesis of medulloblastoma, ependymoma and atypical teratoid rhabdoid tumor. But we need to collect more pediatric brain tumor samples to be studied and allelotype the suggested LOH region in detail.