Relationship between chlorofluorocarbon chemical structure and their Salmonella mutagenicity

This paper is a quantitative analysis of the relationship between the chemical structure and the Salmonella mutagenicity of a number of chlorofluorocarbons (CFC). The molecules were characterized by both molecular orbital and physical chemical parameters. The results of the analysis indicated that the CFC mutagenicity is correlated with two parameters: the free energy of binding to biological receptors, and the energy of the highest occupied molecular orbital (HOMO). Since these are the same factors that would favor the cytochrome P-450-catalyzed metabolism, it would appear that the CFC mutagenicity is determined more by the rate of initial activation than by the rate of DNA attack.     

Pre-surgical treatment of uterine myomas with LH-RH agonists.

Twenty-five non-menopausal women with uterine myomas were treated with LHRH-analogues for 3-6 months. An average reduction of 40% in uterine volume was observed. One patient refused to complete her therapy, three had no more menses after the interruption of treatment, nine underwent myomectomy within four weeks of their final administration, while in 12 cases hysterectomy was performed. In all cases the decrease in uterine volume induced by the analogue allowed a more limited intervention and prevented excessive blood loss.     

Chronic painful physical conditions, disturbed sleep and psychiatric morbidity: results from an elderly survey.

BACKGROUND: The main purpose of this study is to investigate the association of disturbed sleep, chronic physical pain and psychiatric morbidity in people aged 60 years and over. METHODS: A population-based random sample of 7040 household residents aged 60 years and over, was examined in a face-to-face interview. Painful medical conditions were assessed through questions evaluating medical treatment, hospitalizations, and consultations for medical problems. Disturbed sleep was assessed through questions concerning the presence of sleeping problems in the past 4 weeks. RESULTS: The overall prevalence of disturbed sleep is 33.7% (95% CI: 32.5-34.8) and the 6-month prevalence of any chronic pain was 76.2% (95% CI: 74.2-78.2%). A substantial burden of disturbed sleep is associated with the presence of physical pain morbidity, 42.5% for back pain to 49.7% for headaches. The prevalence of pain among persons with disturbed sleep ranges from 25.8% for gastrointestinal pain to 54.6% for joint pain. The presence of comorbid pain and disturbed sleep has an important disability impact as assessed by socioecomomic/professional data, health care utilization, self-rated health and physical activity. In logistic regression models, headaches, psychiatric morbidity, rural origin, Caucasians, self-rated health and number of chronic pain conditions were significantly associated with disturbed sleep after controlling for demographic variables and comorbidities. Age has a negative effect on sleep complaints. CONCLUSIONS: Disturbed sleep is highly comorbid with other pain conditions particularly headaches and psychiatric morbidity in later life. The combination of pain and disturbed sleep leads to important role disability and increased utilization of medical services.     

Relationships between total plasma load of torquetenovirus (TTV) and TTV genogroups carried

In 239 torquetenovirus-positive people, multiple-genogroup infections were common and associated with higher viral loads than would be expected from simple additive effects. The latter observation was restricted to the infections which included both genogroups 1 and 3, pointing to the possible existence of some kind of infection facilitation between these genogroups.     

Predominance of null mutations in ataxia-telangiectasia

Ataxia-telangiectasia (A-T) is an autosomal recessive disorder involving cerebellar degeneration, immunodeficiency, chromosomal instability, radiosensitivity and cancer predisposition. The responsible gene, ATM, was recently identified by positional cloning and found to encode a putative 350 kDa protein with a Pl 3-kinase-like domain, presumably involved in mediating cell cycle arrest in response to radiation-induced DNA damage. The nature and location of A-T mutations should provide insight into the function of the ATM protein and the molecular basis of this pleiotropic disease. Of 44 A-T mutations identified by us to date, 39 (89%) are expected to inactivate the ATM protein by truncating it, by abolishing correct initiation or termination of translation, or by deleting large segments. Additional mutations are four smaller in-frame deletions and insertions, and one substitution of a highly conserved amino acid at the Pl 3-kinase domain. The emerging profile of mutations causing A-T is thus dominated by those expected to completely inactivate the ATM protein. ATM mutations with milder effects may result in phenotypes related, but not identical, to A-T.