Experimental Bearing Capacity Determination of Bonded Rock Bolts

Import 26/02/2015Diplomová práce se zabývá únosností tmelených horninových svorníků a jejím experimentální stanovením. Tato práce analyzuje a poukazuje na možné způsoby porušení, které vznikají zatížením v těsné blízkosti svorníkové tyče a to především v prstenci tmele na kontaktech svorník – tmel a tmel – hornina. V teoretické části byl navržen způsob měření a stanovení pevnostních a deformačních charakteristik tahem zatížených tmelených svorníků napodobujících zatížení v kořenové délce svorníkové výztuže. V praktické části byly pak navržené postupy uskutečněny sérií laboratorních zkoušek. Výstupem z provedených zkoušek je pracovně-deformační charakteristika tmelené svorníkové výztuže zvoleného testovaného materiálu.The thesis focuses on the bearing capacity of bonded rock bolts and experimental determination of this capacity. Possible ways of failure, which is caused by the load near the rock bolt, especially in the circular ring of the grout and between the rock bolt - the grout and between the grout - the rock, are analysed. The theoretical part includes design of measuring and assessment of strength and deformation characteristics on drawn rock bolts as it simulates the load in the root length of bolt reinforcement. This theory was applied in the laboratory tests and presents the practical part of the thesis. In conclusion, the load - deformation characteristics of bonded rock bolt reinforcement made from chosen material are stated.224 - Katedra geotechniky a podzemního stavitelstvívýborn

Decreased prothrombin conversion and reduced thrombin inactivation explain rebalanced thrombin generation in liver cirrhosis

<div><p>Impaired coagulation factor synthesis in cirrhosis causes a reduction of most pro- and anticoagulant factors. Cirrhosis patients show no clear bleeding or thrombotic phenotype, although they are at risk for both types of hemostatic event. Thrombin generation (TG) is a global coagulation test and its outcome depends on underlying pro- and anticoagulant processes (prothrombin conversion and thrombin inactivation). We quantified the prothrombin conversion and thrombin inactivation during TG in 30 healthy subjects and 52 Child-Pugh (CP-) A, 15 CP-B and 6 CP-C cirrhosis patients to test the hypothesis that coagulation is rebalanced in liver cirrhosis patients. Both prothrombin conversion and thrombin inactivation are reduced in cirrhosis patients. The effect on pro- and anticoagulant processes partially cancel each other out and as a result TG is comparable at 5 pM tissue factor between healthy subjects and patients. This supports the hypothesis of rebalanced hemostasis, as TG in cirrhosis patients remains within the normal range, despite large changes in prothrombin conversion and thrombin inactivation. Nevertheless, <i>in silico</i> analysis shows that normalization of either prothrombin conversion or thrombin inactivation to physiological levels, by for example the administration of prothrombin complex concentrates would cause an elevation of TG, whereas the normalization of both simultaneously maintains a balanced TG. Therefore, cirrhosis patients might require adapted hemostatic treatment.</p></div

The contribution of changes in prothrombin conversion, antithrombin levels and a₂-macroglobulin levels to the altered thrombin generation profile in cirrhosis patients.

<p>Prothrombin conversion (A-B), antithrombin levels (C-D) and α₂-macroglobulin levels (E-F) were normalized <i>in silico</i> to the average level found in the healthy subjects group. Thrombin generation was simulated (black) in healthy subjects (○), Child-Pugh A patients (●), Child-Pugh B patients (Δ), Child-Pugh C patients (▲) and compared to the experimental values found in the same group of subjects (grey). The simulated and experimental TG curves in the healthy subject group are almost completely superimposed. The ratio of simulated and experimental ETP values were compared between patients and healthy subjects. *p<0.05, **p<0.01, ***p<0.001 compared to healthy subject values.</p

APC sensitivity in cirrhosis patients and healthy subjects.

<p>(A-B) Thrombin generation and prothrombin conversion curves measured at 1 pM TF in the absence (gray) or presence of 0.56 nM thrombomodulin (black) in healthy subjects (○), Child-Pugh A patients (●), Child-Pugh B patients (Δ), Child-Pugh C patients (▲). (C) (C-F) The percentage of the ETP, peak height, total prothrombin conversion and the maximum prothrombin conversion rate in plasma with thrombomodulin compared to plasma without thrombomodulin. *p<0.05, **p<0.01, ***p<0.001 compared to healthy subject values.</p

Coagulation factor levels.

<p>Coagulation factor levels.</p

The <i>in silico</i> effect prothrombin complex concentrates with or without co-supplementation of antithrombin in cirrhosis.

<p><i>In silico</i> experimentation was performed to predict the effect of prothrombin complex concentrate administration on thrombin generation in cirrhosis patients in the absence (A) or presence (B) of antithrombin supplementation. Prothrombin conversion curves were increased <i>in silico</i> to 110% (- -), 120% (- -), ad 130% (- ∙ -) with or without co-administration of 100%, 120%, or 130% AT. The effects of PCC with or without antithrombin were quantified by the ETP (C-D) and the peak height (E-F). Healthy subjects are shown in black, CP-A patients in red, CP-B patients in blue and CP-C patients in green. *p<0.05, **p<0.01, ***p<0.001 compared to healthy subject values.</p

Thrombin inactivation capacity in cirrhosis patients and healthy subjects.

<p>The thrombin decay capacity was calculated based on the antithrombin, α₂-macroglobulin and fibrinogen level of the sample.*p<0.05, **p<0.01, ***p<0.001 compared to healthy subject values.</p

Patient characteristics.

<p>Patient characteristics.</p