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Background: Early diagnosis of mesenteric ischemia can be life saving. The aim of this study is to investigate the time-dependent diagnostic value of plasma D-dimer and other ancillary laboratory evaluations such as creatine phosphokinase, lactic dehydrogenase, aspartate aminotransferase, alanine aminotransferase, amylase, and leukocyte count in an experimental superior mesenteric arterial occlusion (SMA-O) model in rats. Methods: Forty male Wistar-Albino rats were separated into 4 groups: 2-, 4-, 6-, and 12-hour SMA-O groups. After laparotomy, the SMA was identified and ligated for 2, 4, 6 and 12 h in the 4 respective study groups. Blood samples were taken for laboratory tests 2 h after laparotomy in the control group and at the end of the ischemic period in the study groups. Results: The longer the duration of mesenteric ischemia, the higher were the serum D-dimer levels in the study groups, and statistical significance was obtained at 2 h (p = 0.021). Sensitivity, positive predictive value, negative predictive value, and accuracy of the relation were 88.8, 88.8, 100 and 90%, respectively. Leukocyte count was significantly higher than controls after 12 h. No other laboratory parameter correlated positively with the duration of mesenteric ischemia. Conclusion: Serum D-dimer measurements may be a valuable diagnostic parameter in the early diagnosis of mesenteric ischemia.

Boron is an essential micronutrient for plants and it is either necessary or beneficial for animals. Studies identified only few genes related to boron metabolism thus far and details of how boron is imported into cells and used in cell metabolism are largely unknown. In order to identify genes that play roles in boron metabolism, we screened the entire set of yeast haploid deletion mutants and identified 6 mutants that were resistant to toxic levels of boron, and 21 mutants that were highly sensitive to boron treatment. Furthermore, we performed a proteomic approach to identify additional proteins that are significantly up-regulated by boron treatment. Our results revealed many genes and pathways related to boron stress response and suggest a possible link between boron toxicity and translational control.

Background: Hemodynamic and hemostatic abnormalities are reportedly frequent in chronic obstructive pulmonary disease (COPD). Objectives: We investigated the changes in systolic pulmonary artery pressure (PAPs) and hemostatic status and the effects of systemic steroid treatment (SST) during COPD exacerbation. Methods: Consecutive 26 male and 4 female patients as well as 10 controls were enrolled. The nonsteroid treatment (NST) group received standard treatment without steroids, and the other group received additional SST. Initial values of blood gases, spirometry and PAPs, P-selectin, D-dimer and fibrinogen levels, activities of thrombocyte aggregation, antithrombin III (AT III), protein C (PC), protein S, activated PC resistance (APCR), prothrombin time and partial thromboplastin time were obtained and compared with values at day 10. Results: Improvement in spirometry and blood gases was more prominent with SST. At presentation, patients had higher PAPs, P-selectin, D-dimer and fibrinogen but lower AT III levels than controls. PAPs and fibrinogen levels significantly decreased in the SST group while P-selectin levels further increased in the NST group. The D-dimer level significantly decreased in both groups. Means of AT III, PC and protein S increased in the SST and decreased in the NST group, but only the decrease in PC in the NST group was meaningful. Compared with the controls, AT III levels in the NST group and activated PC resistance in the SST group were significantly decreased. Thrombocyte aggregation tests suggested an incline after 10 days in both groups. Conclusions: We suggest that in patients with COPD exacerbation, addition of systemic corticosteroids to treatment results in better outcome in normalization of PAPs, hemostasis, pulmonary functions and blood gases.

Pentoxifylline, IFN-alpha and their combination have no beneficial effect on experimental fibrosis induced by biliary obstruction.