MicroRNAs in adult high-grade gliomas: Mechanisms of chemotherapeutic resistance and their clinical relevance.

Notorious for its high mortality rate, the current standard treatment for high-grade gliomas remains a challenge. This is largely due to the complex heterogeneity of the tumour coupled with dysregulated molecular mechanisms leading to the development of drug resistance. In recent years, microRNAs (miRNAs) have been considered to provide important information about the pathogenesis and prognostication of gliomas.

New insights into the substrate inhibition of human 17β-hydroxysteroid dehydrogenase type 1.

Human type 1 17β-hydroxysteroid dehydrogenase (17β-HSD1),a member of the short-chain dehydrogenase/reductase family, catalyzes the last step in the bioactivation of the most potent estrogen estradiol with high specificity and is thus involved in estrogen-dependent diseases. As an oxidoreductase, 17β-HSD1 can utilize both triphosphate and diphosphate cofactors in reaction at the molecular level, but more specific with triphosphate cofactor. The NADPH is much higher than NADP+ in living cells leading to preliminary reduction action.

Efficacy of Various Low Temperature and Exposure Time Combinations for Thaumatotibia leucotreta (Meyrick) (Lepidoptera: Tortricidae) Larvae.

A systems approach was developed as an alternative to a standalone quarantine disinfestation treatment for Thaumatotibia leucotreta in citrus fruit exported from South Africa. The systems approach consists of three measures: pre and postharvest controls and measurements, postpacking inspection, and postharvest exposure to low temperatures. Different cold treatment conditions with a range of efficacy levels can be used for this last measure.

CRIF1-CDK2 Interface Inhibitors Enhance Taxol Inhibition of the Lethal Triple-Negative Breast Cancer.

Paclitaxel (taxol), a chemotherapeutic agent, remains the standard of care for the lethal triple-negative breast cancer (TNBC). However, over 50% of TNBC patients become resistant to chemotherapy and, to date, no solution is available. CR6-interacting factor 1 (CRIF1) is reported to act as a negative regulator of the cell cycle by interacting with cyclin-dependent kinase 2 (CDK2).