Software model checking without source code

We present a framework, called air, for verifying safety properties of assembly language programs via software model checking. air extends the applicability of predicate abstraction and counterexample guided abstraction refinement to the automated verification of low-level software. By working at the assembly level, air allows verification of programs for which source code is unavailable—such as legacy and COTS software—and programs that use features—such as pointers, structures, and object-orientation—that are problematic for source-level software verification tools. In addition, air makes no assumptions about the underlying compiler technology. We have implemented a prototype of air and present encouraging results on several non-trivial examples.     

Initial high beta operation of the HBT-EP Tokamak

HBT-EP is a new research tokamak designed and built to investigate passive and active feedback techniques to control MHD instabilities. In particular, HBT-EP will be able to test techniques to control fast MHD instabilities occurring at high Troyon-normalized beta, _N Ba/I_p [Tm/MA], since it is equipped with a thick, close-fitting, and adjustable conducting shell. The major goals of the initial operation of HBT-EP have been the achievement of high beta operation (_N 3) using only ohmic heating and the observation of MHD instabilities. By using a unique fast startup technique, we have successfully achieved these goals. A variety of MHD phenomena were observed during the high beta operation of HBT-EP. At modest beta (_N 2), discharges have been maintained for more than 10 msec, and these discharges exhibit saturated resistive instabilities. When _N approaches 3, major disruptions occur preceded by oscillating, growing precursors. During start-up, one or more minor disruptions are usually observed. A 1-D transport code has been used to simulate the evolution of the current profile, and these early minor instabilities are predicted to be double tearing modes. The simulation also reproduces the observed high beta operation when saturated neo-Alcator energy confinement scaling is assumed.     

Validation chez les adolescents d'une version francophone d'un instrument de mesure de la peur du jugement négatif d'autrui.

The popularity of the Fear of Negative Evaluation scale (FNE; Watson & Friend, 1969) stems from the centrality of this construct in personality, social and clinical psychology. In order to meet the needs of the Francophone researchers community, Kéroack, Boisvert, and Prévost (1987) traduced the short version of this instrument. Since social anxiety is most salient in adolescence, there is a need for normative and psychometric data for this population. This research aims at documenting the psychometric properties and norms for Francophone adolescents. Five hundred and seventy-eight participants aged from 14 to 19 years completed the French versions of the short FNE and the Social Avoidance and Distress scale. The factorial structure, the internal consistency and the convergent validity analyses confirm the traduction's quality and the questionnaire's validity. Norms are presented separately for females and males. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Maintenance of recombinant type A gamma-aminobutyric acid receptor function: role of protein tyrosine phosphorylation and calcineurin

In the present study, rundown of gamma-aminobutyric acid (GABA)-activated Cl- channels was studied in recombinant GABAA receptors stably expressed in human embryonic kidney cells (HEK 293), with conventional whole-cell and amphotericin B-perforated patch recording. When [ATP]i was lowered to 1 mM and resting [Ca++]i was buffered to a relatively high level, the response of alpha 3 beta 2 gamma 2 GABAA receptors to relatively low [GABA] (up to 50 microM) did not show rundown in the whole-cell configuration. However, high [GABA] (greater than 200 microM) induced significant rundown, which was observed by decreases in both the maximum GABA-induced current and GABA EC50. Rundown was prevented completely with a solution containing 4 mM Mg(++)-ATP and low resting [Ca++]i, or during perforated patch recording. The magnitude of rundown was comparable in alpha 1 beta 2 gamma 2 and beta 2 gamma 2 receptors. Neither stimulation nor inhibition of protein kinase A or protein kinase C had a significant effect on rundown. However, sodium metavanadate, an inhibitor of protein tyrosine phosphatase, significantly reduced rundown. In addition, inhibition of protein tyrosine kinase activity by either genistein or lavendustin A induced rundown of the GABA response. Inhibition of the Ca++/calmodulin-dependent phosphatase calcineurin with fenvalerate also prevented rundown of the response to GABA. Our results demonstrate that rundown of GABAA receptor function is concentration-dependent, due to depletion of ATP and/or unbuffered [Ca++]i, and does not depend on the presence or subtype of the alpha subunit. We propose that protein phosphorylation at a tyrosine kinase-dependent site, and a distinct unidentified site, which is dephosphorylated by calcineurin, maintains the function of GABAA receptors.     

Car insurance and the risk of car crash injury

Despite speculation about the role of vehicle insurance in road traffic accidents, there is little research estimating the direction or extent of the risk relationship. Data from the Auckland Car Crash Injury Study (1998–1999) were used to examine the association between driving an uninsured motor vehicle and car crash injury. Cases were all cars involved in crashes in which at least one occupant was hospitalized or killed anywhere in the Auckland region. Controls were 588 drivers of randomly selected cars on Auckland roads. Participants completed a structured interview. Uninsured drivers had significantly greater odds of car crash injury compared to insured drivers after adjustment for age, sex, level of education, and driving exposure (odds ratio 4.77, 95% confidence interval 2.94–7.75). The causal mechanism for insurance and car crash injury is not easily determined. Although we examined the effects of multiple potential confounders in our analysis including socioeconomic status and risk-taking behaviours, both of which have been previously observed to be associated with both insurance status and car crash injury, residual confounding may partly explain this association. The estimated proportion of drivers who are uninsured is between 5 and 15% in developed countries, representing a significant public health problem worthy of further investigation.     

Creativity of undergraduates with and without family history of alcohol and other drug problems

BACKGROUND: Colonoscopic surveillance is a standard procedure in many patients with long standing, extensive ulcerative colitis (UC), in order to avoid death from colorectal cancer. No conclusive proof of its benefits has been presented however. AIMS: To evaluate the association between colonoscopic surveillance and colorectal cancer mortality in patients with UC. PATIENTS: A population based, nested case control study comprising 142 patients with a definite UC diagnosis, derived from a study population of 4664 patients with UC, was conducted. METHODS: Colonoscopic surveillance in all patients with UC who had died from colorectal cancer after 1975 was compared with that in controls matched for age, sex, extent, and duration of the disease. Information on colonoscopic surveillance was obtained from the medical records. RESULTS: Two of 40 patients with UC and 18 of 102 controls had undergone at least one surveillance colonoscopy (relative risk (RR) 0.29, 95% confidence interval 0.06 to 1.31). Twelve controls but only one patient with UC had undergone two or more surveillance colonoscopies (RR 0.22, 95% confidence interval 0.03 to 1.74), indicating a protective dose response relation. CONCLUSION: Colonoscopic surveillance may be associated with a decreased risk of death from colorectal cancer in patients with long standing UC.     

Regulation of BRCA1 and BRCA2 expression in human breast cancer cells by DNA-damaging agents

Germline mutations in the breast cancer susceptibility genes BRCA1 and BRCA2 have been linked to the development of breast cancer, ovarian cancer, and other malignancies. Recent studies suggest that the BRCA1 and BRCA2 gene products may function in the sensing and/or repair of DNA damage. To investigate this possibility, we determined the effects of various DNA-damaging agents and other cytotoxic agents on the mRNA levels of BRCA1 and BRCA2 in the MCF-7 and other human breast cancer cell lines. We found that several agents, including adriamycin (a DNA intercalator and inhibitor of topoisomerase II), camptothecin (a topoisomerase I inhibitor), and ultraviolet radiation induced significant decreases in BRCA1 and BRCA2 mRNA levels. Decreased levels of BRCA1 and BRCA2 mRNAs were observed within 6-12 h after treatment with adriamycin and persisted for at least 72 h. Adriamycin also induced decreases in BRCA1 protein levels; but these decreases required several days. U.V. radiation induced dose-dependent down-regulation of BRCA1 and BRCA2 mRNAs, with significant decreases in both mRNAs at doses as low as 2.5 J/m2, a dose that yielded very little cytotoxicity. Adriamycin-induced down-regulation of BRCA1 and BRCA2 mRNAs was first observed at doses that yielded relatively little cytotoxicity and little or no apoptotic DNA fragmentation. Adriamycin and U.V. radiation induced distinct dose- and time-dependent alterations in the cell cycle distribution; but these alterations did not correlate well with corresponding changes in BRCA1 and BRCA2 mRNA levels. However, the adriamycin-induced reduction in BRCA1 and BRCA2 mRNA levels was correlated with p53 functional status. MCF-7 cells transfected with a dominant negative mutant p53 (143 val-->ala) required at least tenfold higher doses of adriamycin to down-regulate BRCA1 and BRCA2 mRNAs than did parental MCF-7 cells or control-transfected MCF-7 clones. These results suggest that BRCA1 and BRCA2 may play roles in the cellular response to DNA-damaging agents and that there may be a p53-sensitive component to the regulation of BRCA1 and BRCA2 mRNA expression.     

Neuronal stress and injury in C57/BL mice after systemic kainic acid administration

Kainate-induced seizures are widely studied as a model of human temporal lobe epilepsy due to behavioral and pathological similarities. While kainate-induced neuronal injury is well characterized in rats, relatively little data is available on the use of kainate and its consequences in mice. The growing availability of genetically altered mice has focused attention on the need for well characterized mouse seizure models in which the effects of specific genetic manipulations can be examined. We therefore examined the kainate dose-response relationship and the time-course of specific histopathological changes in C57/BL mice, a commonly used founder strain for transgenic technology. Seizures were induced in male C57/BL mice (kainate 10-40 mg/kg i.p.) and animals were sacrificed at various time-points after injection. Seizures were graded using a behavioral scale developed in our laboratory. Neuronal injury was assayed by examining DNA fragmentation using in situ nick translation histochemistry. In parallel experiments, we examined the expression an inducible member of the heat shock protein family, HSP-72, another putative marker of neuronal injury, using a monoclonal antibody. Seizure severity paralleled kainate dosage. At higher doses DNA fragmentation is seen mainly in hippocampus in area CA3, and variably in CA1, thalamus and amygdala within 24 h, is maximal within 72 h, and is largely gone by 7 days after administration of kainate. HSP-72 expression is also highly selective, occurring in limbic structures, and it evolves over a characteristic time-course. HSP-72 is expressed mainly in structures that also manifest DNA fragmentation. Using double-labeling techniques, however, we find essentially no overlap between neurons expressing HSP-72 and DNA fragmentation. These findings indicate that DNA fragmentation and HSP-72 expression are complementary markers of seizure-induced stress and injury, and support the notion that HSP-72 expression is neuroprotective following kainate-induced seizures.