Silencing of ZFP36L2 increases sensitivity to temozolomide through G2/M cell cycle arrest and BAX mediated apoptosis in GBM cells

Molecular Biology Reports - Despite the advancements in primary brain tumour diagnoses and treatments, the mortality rate remains high, particularly in glioblastoma (GBM). Chemoresistance,...     

Fecal Microbiota Transplantation Exerts a Protective Role in MPTP-Induced Parkinson’s Disease via the TLR4/PI3K/AKT/NF-κB Pathway Stimulated by α-Synuclein

Neurochemical Research - Gut microbiota is closely related to the Parkinson’s disease (PD) pathogenesis. Additionally, aggregation of α-synuclein (α-syn) is central to PD...     

Synergistic Therapy of Doxorubicin with Cationic Anticancer Peptide L-K6 Reverses Multidrug Resistance in MCF-7/ADR Cancer Cells In Vitro via P-glycoprotein Inhibition

International Journal of Peptide Research and Therapeutics - Multidrug resistance (MDR) is one of the major obstacles to efficient chemotherapy against cancers, resulting from the overexpression of...     

Contribution of P2X4 receptor in pain associated with rheumatoid arthritis: a review

Purinergic Signalling - Pain is the most common symptom reported by patients with rheumatoid arthritis (RA) even after the resolution of chronic joint inflammation. It is believed that...     

Enzymatic deinking of various types of waste paper: Efficiency and characteristics

The aim of the present study was to characterize the enzymatic deinking of various types of waste paper. Studies on the optimization of enzymatic deinking have been performed previously using commercially available enzyme preparations containing cellulase and hemicellulase. The enzymatic deinking of different types of waste paper demonstrated a high efficiency of 86.6% on laser-printed paper, but a low deinking efficiency of 12.9% was obtained with newspaper. All enzymatic treatments significantly improved the drainage rate of the deinked waste paper. Enzymatic deinking increased the tensile index of magazine paper but reduced the tensile index of bubble jet-printed paper, photocopy paper and newspaper. Enzymatic hydrolysis caused a 21.1% reduction in the tear index for bubble jet-printed paper, but a 3.1% increase in the tear index was obtained for laser-printed paper relative to respective blank. In addition, enzymatic hydrolysis increased the burst index by 4.7% relative to blank for laser-printed paper. However, photocopy paper showed the highest reduction (8.3%) in the burst index relative to blank. Taken together, these results suggest that enzymatic hydrolysis is both advantageous and detrimental to the mechanical properties of deinked paper. Thus, the proper regulation of enzymatic hydrolysis is crucial to improve the quality of recycled paper.     

Mechanisms of Siglec-F-Induced Eosinophil Apoptosis: A Role for Caspases but Not for SHP-1, Src Kinases,NADPH Oxidase or Reactive Oxygen

Background

Siglec-F and Siglec-8 are functional paralog proapoptotic cell surface receptors expressed on mouse and human eosinophils, respectively. Whereas Siglec-8 mediated death involves caspases and/or reactive oxygen species (ROS) generation and mitochondrial injury, very little is known about Siglec-F-mediated signaling and apoptosis. Therefore the objective of the current experiments was to better define apoptosis pathways mediated by Siglec-F and Siglec-8. Given that Siglec-F-induced apoptosis is much less robust than Siglec-8-induced apoptosis, we hypothesized that mechanisms involved in cell death via these receptors would differ.

Methods

Consequences of engagement of Siglec-F on mouse eosinophils were studied by measuring ROS production, and by performing apoptosis assays using eosinophils from normal, hypereosinophilic, NADPH oxidase-deficient, src homology domain-containing protein tyrosine phosphatase (SHP)-1-deficient, and Lyn kinase-deficient mice. Inhibitors of caspase and Src family kinase activity were also used.

Results

Engagement of Siglec-F induced mouse eosinophil apoptosis that was modest in magnitude and dependent on caspase activity. There was no detectable ROS generation, or any role for ROS, NADPH oxidase, SHP-1, or Src family kinases in this apoptotic process.

Conclusions

These data suggest that Siglec-F-mediated apoptosis is different in both magnitude and mechanisms when compared to published data on Siglec-8-mediated human eosinophil apoptosis. One likely implication of this work is that models targeting Siglec-F in vivo in mice may not provide identical mechanistic predictions for consequences of Siglec-8 targeting in vivo in humans.