Stressing State Analysis of Reinforced Concrete Beam Strengthened by CFRP Sheet with Anchoring Device

This paper investigates the working performance of reinforcement concrete (RC) beams strengthened by Carbon-Fiber-Reinforced Plastic (CFRP) with different anchoring under bending moment, based on the structural stressing state theory. The measured strain values of concrete and Carbon-Fiber-Reinforced Plastic (CFRP) sheet are modeled as generalized strain energy density (GSED), to characterize the RC beams’ stressing state. Then the Mann–Kendall (M–K) criterion is applied to distinguish the characteristic loads of structural stressing state from the curve, updating the definition of structural failure load. In addition, for tested specimens with middle anchorage and end anchorage, the torsion applied on the anchoring device and the deformation width of anchoring device are respectively set parameters to analyze their effects on the reinforcement performance of CFRP sheet through comparing the strain distribution pattern of CFRP. Finally, in order to further explore the strain distribution of the cross-section and analyze the stressing-state characteristics of the RC beam, the numerical shape function (NSF) method is proposed to reasonably expand the limited strain data. The research results provide a new angle of view to conduct structural analysis and a reference to the improvement of reinforcement effect of CFRP.

Genetic susceptibility to toxicity of chemotherapy in mice as pharmacokinetics-independent and drug-specific.

e13549 Background: Adverse drug reactions (ADRs) are a significant obstacle in cancer chemotherapy. In spite of the advances in the development of drugs for cancer therapy, ADRs compromise their potential beneficial effects in many patients by imposing reduction of dose or cessation of treatment. Prediction of susceptibility to ADRs in individual patients could significantly improve treatment outcomes by more effectively choosing which drugs to treat with and which dose is appropriate. The pharmacokinetics (PK) of many drugs has been extensively studied and numerous enzymes and transporters that are involved in their activation and processing have been identified. However, when their role in individual susceptibility to ADRs has been tested in numerous studies, the variants of these proteins have not been able to consistently predict specific ADRs. Therefore, additional studies are required for a reliable prediction of toxicity. Methods: We used mouse strains with precisely defined limited genomic differences to evaluate genetic control of ADRs to three drugs commonly used in cancer chemotherapy - irinotecan, gemcitabine, and doxorubicin. We compared strain distribution of susceptibility to ADRs caused by each of these drugs and tested whether there is a correlation with genotypes at the major processing/transport (PK) genes that were reported in humans to affect toxicity of these drugs. Results: The major genetic differences in toxic reactions caused by these drugs do not correlate with the major PK loci and that the strain distribution pattern of susceptibility vs. resistance for each drug is different. Conclusions: This data suggests that a significant part of genetic susceptibility to ADRs is controlled by genes other than the presently known PK-related genes, and that many responsible genes are drug specific, with some possible overlaps. We hypothesize that these genes are likely involved in downstream pharmacodynamic (PD) processes and have remained largely unknown, because most studies in humans have been limited to known PK-related genes. We are proceeding towards identification of these novel genes, as they could help to optimize the selection of therapy for individual patients.

Genetic diversity among Mycobacterium tuberculosis isolates from Mexican patients

Forty-six isolates of the Mycobacterium tuberculosis complex were typified by PCR of the IS6110 region and by Mycobacterium bovis specific primers JB21/JB22. Isolate MVG01 was typified as M. bovis, being the first record of a case of human tuberculosis caused by this species in Mexico. RAPD–PCR was used to describe the genetic diversity of the remaining 45 M. tuberculosis complex isolates. The corrected genotypic diversity value calculated for the analyzed population was 0.96, the estimated mean gene diversity was 0.235, and the corrected Shannon–Weiner index was 2.15. All allele–loci combinations generated showed significant linkage disequilibria. The distribution of genetic variation was analyzed both by the unweighted pair group method with arithmetic averages clustering and by principal coordinates analysis. Unweighted pair group method with arithmetic averages clustering resulted in a tree with four main clusters and one unclustered strain (MVG20), the principal coordinates analysis strain distribution pattern being consistent with this grouping. The obtained results suggest that the studied isolates belong to a clonal population having significant genetic diversity. Our genetic diversity results are comparable with those reported for other populations of M. tuberculosis, although only three RAPD primers were used.

Differential inspiratory timing is genetically linked to mouse chromosome 3

Genetic control of differential inspiratory timing (Ti) at baseline has been previously demonstrated among inbred mouse strains. The inheritance pattern for Ti between C3H/HeJ (C3; 188 ± 3 ms) and C57BL/6J (B6; 111 ± 2 ms) progenitors was consistent with a two-gene model. By using the strain distribution pattern for recombinant inbred strains derived from C3 and B6 progenitors, 100% concordance was established between Ti phenotypes and DNA markers on mouse chromosome 3. This genotype-phenotype hypothesis was tested by typing 52 B6C3F2(F2) progeny by using simple sequence repeat DNA markers ( n = 21) polymorphic between C3 and B6 strains on mouse chromosome 3. Linkage analysis compared marker genotypes to baseline ventilatory phenotypes by computing log-likelihood values. A putative quantitative trait locus located in proximity to D3Mit119 was significantly associated with baseline Ti phenotypes. At the peak (log-likelihood = 3.3), the putative quantitative trait locus determined 25% of the phenotypic variance in Ti among F2 progeny. In conclusion, this genetic model of ventilatory characteristics demonstrated an important linkage between differential baseline Ti and a candidate genomic region on mouse chromosome 3.