Travel and changes in routine do not increase the risk of sudden infant death syndrome

We investigated the relationship between travel and changes in routine and the sudden infant death syndrome (SIDS) among 485 SIDS cases compared with 1800 randomly selected control infants. There was no increased risk of SIDS with travel. Special events, such as christenings, were not associated with an increased risk of SIDS. However, visits to and by friends or relatives were associated with a significantly reduced risk of SIDS after controlling for potential confounders (odds ratios = 0.70; 95% confidence interval = 0.52, 0.96). These findings may indicate less social support in SIDS cases.     

Cellular and karyotypic characterization of two doxorubicin resistant cell lines isolated from the same parental human leukemia cell line

Separate mechanisms underlying the multidrug resistant (MDR) phenotype were identified in 2 independent approaches to select tumour cells resistant to low concentrations of doxorubicin (Dox) from the sensitive T cell leukemia cell line CCRF-CEM. The CEM/A7 cell line was selected at an initial concentration of 0.005 microgram/ml of Dox and maintained at 0.07 microgram/ml. In contrast, the CEM/A5 line was selected using an initial concentration of 0.01 microgram/ml and maintained in Dox at a concentration of 0.05 microgram/ml. P-glycoprotein expression was demonstrated in the CEM/A7 line but not the CEM/A5 line. Amplification of the mdrI gene was not observed in the CEM/A7 cell line. Both cell lines showed cross-resistance to a number of structurally unrelated cytotoxic drugs including anthracyclines and etoposide (VP-16), although only the CEM/A7 line was cross resistant to Vinca alkaloids. Immunoblots of total cell lysates of the CEM/A5 line have revealed almost undetectable levels of topoisomerase II alpha and beta in this line. Cytogenetic analyses of both lines revealed numerous karyotypic abnormalities which were present in the parental cell line as well as both resistant cell lines. The CEM/A7 line also demonstrated a duplication of part of the long arm of chromosome 7 which included the region containing the mdrI gene, a finding not seen in the parental or CEM/A5 line. CEM/A5, however, demonstrated an abnormality of chromosome 7, outside the region of the mdrI gene, and it also contained a deletion of the short arm of chromosome 2. Abnormalities in this latter region of genome have been associated with non-P-glycoprotein-mediated MDR.     

von Willebrand factor as a regulator of intrinsic factor X activation

Factor VIII is an important cofactor in the intrinsic activation of factor X. To function effectively as a cofactor, factor VIII must be activated. In plasma, factor VIII circulates in a complex with von Willebrand factor, and although thrombin can activate complexed factor VIII, the activation by activated factor X is inhibited by von Willebrand factor. In this study, the effect of von Willebrand factor on the generation of factor Xa by the factor IXa-VIII complex was investigated. Purified human factors VIII, IXa, and X were incubated on human umbilical vein endothelial cells or phospholipid vesicles in the presence of calcium ions, and the generation of factor Xa was followed. In the presence of von Willebrand factor, a prolonged lag-phase and a dose-dependent inhibition of factor X activation was observed. These effects were not observed when von Willebrand factor was preincubated with a monoclonal antibody directed against von Willebrand factor that blocks factor VIII binding. When factor VIII was activated with thrombin before the incubation, neither the monoclonal antibody nor von Willebrand factor had an effect on the rate of factor X activation. Preincubation of endothelial cells with the monoclonal antibody resulted in a somewhat higher rate of factor X activation. When endothelial cells from a patient with von Willebrand's disease type I were used, preincubation of the monoclonal antibody had no effect on the rate of factor X activation. We conclude that von Willebrand factor on the surface of endothelial cells can modulate the intrinsic factor X activation. This effect is greatly enhanced, however, by the addition of exogenous von Willebrand factor.(ABSTRACT TRUNCATED AT 250 WORDS)     

Salvage surgery for chemorefractory gestational trophoblastic disease

PURPOSE: To investigate and define better the role of salvage surgery for patients with chemorefractory gestational trophoblastic disease (GTD). PATIENTS AND METHODS: A retrospective review of medical records at The University of Texas M.D. Anderson Cancer Center identified 33 patients with chemorefractory GTD who underwent salvage surgery between 1962 and 1991. The end points selected for analysis were serologic response and survival. RESULTS: Initial salvage procedures consisted of 29 hysterectomies, four thoracotomies, and one nephrectomy (in conjunction with a hysterectomy). Fourteen patients (42%) had a serologic complete response (CR) to surgery (normalization of human chorionic gonadotropin [hCG]), 10 (30%) had a partial response (> 50% decrease in hCG level), and nine had no response (< or = 50% decrease in hCG level). Of 19 patients who received further chemotherapy, eight (42%) attained a CR. Four patients underwent a second salvage surgery: two thoracotomies, one craniotomy, and one partial hepatectomy. All achieved a CR. The probability of achieving a CR was influenced by the time from diagnosis to surgery, number of preoperative disease sites, preoperative World Health Organization (WHO) score, and histologic type. Survival was influenced by the type of antecedent pregnancy, number of preoperative regimens, number of preoperative disease sites, time from diagnosis to surgery, and preoperative WHO score. CONCLUSION: Based on the findings of this study, it appears that a select subset of patients with chemorefractory GTD who have a limited number of clinically detectable tumor foci may benefit from salvage surgery.     

Elbow dislocation during overhead skeletal traction therapy: a case report

A dislocation of the elbow occurred in a 7-year-old boy during overhead skeletal traction treatment for a supracondylar fracture of the humerus. Closed reduction of the dislocation was successful. A review of the literature failed to reveal a report of a similar incident.     

beta-endorphin1-31 in the rat pituitary

The behavioral and neural correlates of processing of motor directional information are described for two visuomotor tasks: mental rotation and context-recall. Psychological studies with human subjects suggested that these two tasks involve different time-consuming processes of directional information. Analyses of the activity of single cells and neuronal populations in the motor cortex of behaving monkeys performing in the same tasks provided direct insight into the neural mechanisms involved and confirmed their different nature. In the mental rotation task the patterns of neuronal activity revealed a rotation of the intended direction of movement. In contrast, in the context-recall task the patterns of neural activity identified a switching process of the intended direction of movement.     

Acute respiratory distress syndrome: CT abnormalities at long-term follow-up

Photochemical thrombotic ischemia model was used to study the possible roles of excision repair cross-complementing group 6 (ERCC6), a DNA repair gene, in the neuroprotection of dextromethorphan (DM), a NMDA antagonist, in ischemic brain injury. The results showed that no obvious ERCC6 mRNA expression was found in the perifocal area of irradiated cerebral cortex before 24 h postischemia. Then, the number of ERCC6 mRNA positive cells gradually enhanced, and attained a peak value at 72 h after light irradiation, which followed a declined tendency at 7-day postlesion. These results suggest that DNA repair gene ERCC6 mRNA expression in the perifocal area may be involved in the pathophysiological processes following the photochemical thrombotic cerebral ischemia. By the administration of DM, we observed that it can significantly upregulate the expression of ERCC6 mRNA in the perifocal area at 48 h after ischemic event. The neuroprotective mechanisms of DM may be related to the upregulation of DNA repair gene ERCC6 mRNA.