Advanced stage IIIB cancer of the cervix treatment by hyperthermia and radiation

Treatment records of patients with primary untreated Stage IIIB carcinoma of the cervix treated at Indiana University Department of Radiation Oncology from November 1964 through January 1979 were reviewed. During this period, 79 patients were treated; 46 received external therapy using cobalt-60, 15 received a 25-MV photon beam, and 18 received a 25-MV photon beam followed by 45 min of 434-MHz microwave hyperthermia producing central tumor core temperatures of 39.5 to 41.5 degrees C. All patients received similar doses of radiation using combination intracavitary radioactive isotopes and external therapy. Patients who received heat therapy in combination with radiation therapy did not have increased acute or chronic complications of normal tissues. Local tumor control was superior when regional heat therapy was given; however, long-term absolute survival rates were not affected as the survival rate at 5 years was not statistically different in any of the three treatment groups.     

Lipoproteins in the progeny of young men with coronary artery disease: children with increased risk

The authors studied 173 progeny from 63 families in which the father had angiographically diagnosed coronary artery disease by 50 years of age. To assess the nature of the coronary risk factors in these families, we measured their height and weight to calculate Quetelet index (wt/ht2), BP, fasting plasma cholesterol, triglyceride, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol were measured in the affected fathers, their wives, and their progeny. These values were compared with age- and sex-specific values from the Lipid Research Clinic data. Sixty-five percent of the affected fathers and 51% of the progeny had elevated triglyceride, elevated low-density lipoprotein cholesterol, diminished high-density lipoprotein cholesterol, or combinations thereof. The distribution of the lipids and lipoproteins in the children bore a close resemblance to those observed in the affected fathers. A significant number of the mothers had diminished high-density lipoprotein cholesterol, which was attributed to their obesity. Screening the progeny of young coronary artery disease patients is therefore highly productive in identifying young people at excessive risk for future coronary artery disease. Early identification of this young high-risk population offers an opportunity for early initiation of preventive measures.     

Respiratory syncytial virus infection in children with bronchopulmonary dysplasia

Little is known about the risk of severe illness from respiratory syncytial virus infection in children with bronchopulmonary dysplasia. A prospective study was done of the natural history of respiratory syncytial virus infection in 30 children less than 2 years of age with bronchopulmonary dysplasia who were in a home oxygen program. Surveillance to identify children with acute respiratory symptoms was done by weekly telephone interview. Symptomatic children were examined, oxygen saturation was determined by oximetry, and nasopharyngeal lavage fluid was collected for virus cultures and rapid respiratory syncytial virus antigen tests. During the 4-month study period (December to April), 27 children had one or more acute respiratory illnesses, and respiratory syncytial virus developed in 16/27 (59%). Passive smoking and greater than or equal to four members in the home increased the risk of symptomatic respiratory syncytial virus (P less than .01 and P less than .03, respectively). Of 16 children, 11 (69%) required hospitalization. Of the 11 hospitalized children with respiratory syncytial virus, nine were either still receiving oxygen at home or required oxygen therapy within the previous 3 months v none of five nonhospitalized children (P less than .005). Five of the hospitalized children were greater than 12 months of age and five had respiratory syncytial virus infection previously that had been confirmed by culture results. Hospitalizations were prolonged and complicated. Seven of 11 children were hospitalized for greater than 1 week; four were admitted to the intensive care unit; four were treated with ribavirin aerosol, and two needed mechanical ventilation. There were no deaths.(ABSTRACT TRUNCATED AT 250 WORDS)     

Increased frequency of dentate granule cells with basal dendrites in the hippocampal formation of schizophrenics

In the hippocampal formation of schizophrenics, the detailed morphology of Golgi-impregnated granule cells was examined. These granule cells of the dentate gyrus are interposed between the rostral entorhinal cortex and the hippocampus proper. In these limbic regions significant cytoarchitectural alterations in schizophrenics are reported, giving rise to the concept of a prenatal limbic maldevelopment in schizophrenia. Compared to controls, the frequency of dentate granule cells with basal dendrites was significantly increased in schizophrenics [43% (+/-3)] vs. [22% (+/-2) in the control group]. In epilepsy, dentate granule cells of epileptic patients also develop basal dendrites, which is explained as an adaptive process of plasticity. Similarly, the hippocampal alterations described in schizophrenics could be the sequela of primary entorhinal cytoarchitectural alterations. Since the increase in basal dendrites seems to reflect a process of continuous plasticity, suggesting an increased rate of postnatal granule cell generation, the synthesis of a prenatal limbic maldevelopment with an ongoing process of plasticity might, therefore, supersede the hypothesis of a neurodegeneration in schizophrenia.     

Targeted inactivation of the mouse locus encoding coagulation factor XIII-A: hemostatic abnormalities in mutant mice and characterization of the coagulation deficit

Blood coagulation factor XIII (FXIII) promotes cross-linking of fibrin during blood coagulation; impaired clot stabilization in human genetic deficiency is associated with marked pathologies of major clinical impact, including bleeding symptoms and deficient wound healing. To investigate the role of FXIII we employed homologous recombination to generate a targeted deletion of the inferred exon 7 of the FXIII-A gene. FXIII transglutaminase activity in plasma was reduced to about 50% in mice heterozygous for the mutant allele, and was abolished in homozygous null mice. Plasma fibrin gamma-dimerization was also indetectable in the homozygous deficient animals, confirming the absence of activatable FXIII. Homozygous mutant mice were fertile, although reproduction was impaired. Bleeding episodes, hematothorax, hematoperitoneum and subcutaneous hemorrhage in mutant mice were associated with reduced survival. Arrest of tail-tip bleeding in FXIII-A deficient mice was markedly and significantly delayed; replacement of mutant mice with human plasma FXIII (Fibrogammin P) restored bleeding time to within the normal range. Thrombelastography (TEG) experiments demonstrated impaired clot stabilization in FXIII-A mutant mice, replacement with human FXIII led to dose-dependent TEG normalization. The mutant mice thus reiterate some key features of the human genetic disorder: they will be valuable in assessing the role of FXIII in other associated pathologies and the development of new therapies.