0-7.5 and a temperature range of 25-37 degrees C. The K(m) and V(max) values for O-nitrophenol-beta-D-galactopyranoside Selleckchem PLX3397 (ONPG) were 1.20 mM and 1,000 mu mol/min.mg protein, respectively. The response surface methodology was found to be useful in optimizing and determining the interactions among process variables in beta-galactosidase enzyme production. Hence, this study fulfills the lack of using mathematical

and statistical techniques in optimizing beta-galactosidase enzyme production in stirred tank bioreactor.”
“Portulacerebroside A (PCA) is a novel cerebroside compound isolated from Portulaca oleracea L. The present results showed that PCA significantly inhibited cell viability time-and dose-dependently, elicited chromatin aggregation and fragmented nuclei, and enhanced the percentage of apoptotic cells. Furthermore PCA remarkably increased the protein phosphorylation of p38 MAPK and JNK, disrupted mitochondrial membrane penetrability, and triggered the release AZD6094 of mitochondrial cytochrome c and AIF to cytosol. Treatment with PCA also evidently activated caspase-9 and caspase-3 but not caspase-8. These results suggest that PCA-induced apoptosis is associated with activation of the p38 MAPK-and JNK-triggered mitochondrial death pathway. PCA possibly has the high potential for clinical applications in treating liver cancer and improving cancer chemotherapy.

(C) 2013 Phytochemical Society of Europe. Published by Elsevier B.V. All rights reserved.”
“Introduction: The response of Crohn’s disease (CD) to infliximab is initially good, although a loss of efficacy is observed over time. Dose escalation has been recommended in such cases.

Aims: To study the response to an intensified infliximab regimen in patients with CD; and to evaluate the adverse effects associated with intensification of therapy and identify predictors of loss of response.

Methods: We performed EVP4593 research buy a retrospective multicenter survey of all patients with CD who had been treated with at least the 3 induction doses of standard infliximab therapy, and for whom treatment had to be intensified due to loss of response. We analyzed the efficacy of the intensified regimen.

Results:

Thirty-three patients were included. After the first intensification dose, 79% of patients had a clinical response (33.5% complete response, 45.5% partial response). In the long term, 83%, 69%, 47%, and 29% of patients who had an initial response to the intensification maintained the response at 6, 12, 18, and 36 months, respectively. The loss of efficacy after escalation was 43% per patient-year of follow-up. One patient had an infusion reaction after 36 doses. One patient developed a herpes zoster infection.

Conclusions: A high proportion of patients whose dose of infliximab is increased due to loss of efficacy respond initially. However, nearly half lose the response after one year. The safety profile of an intensified infliximab regimen is good. (C) 2011 Published by Elsevier B.V.