Degradation and inactivation of chromosomal and plasmid encoded resistance genes/ARBs and the impact of different matrices on UV and UV/HO based advanced oxidation process.

This study reports a structured investigation on the degradation kinetics of different types (gyrA,tetA, qnrS) and conformational forms (chromosomal, plasmids) of ARGs and mobile genetic elements (intl-1, plasmids) as a function of water matrix (DI water, phosphate buffer, wastewater) with UV and UV/HO treatments. Extracellular, intracellular and the free-ARGs fate were tracked to infer the impact of various parameters on the degradation efficacy of the treatment process. The degradation profile of e-ARGs (118-454 bp) showed 1-4 log reductions but did not correlate strongly to amplicon size indicating the importance of active sites distribution and/or types of ARGs for UV induced gene damage.

Inhibition of metastasis of syngeneic murine melanoma in vivo and vasculogenesis in vitro by monoclonal antibody C11C1 targeted to domain 5 of high molecular weight kininogen.

Metastasis of malignant tumors is a major cause of morbidity and mortality. Inhibition of tumor growth in distant organs is of clinical importance. We have demonstrated that C11C1, a murine monoclonal antibody to the light chain region of high molecular weight kininogen (HK), reduces growth of murine multiple myeloma in normal mice and human colon cancer in nude mice.

Towards a targeted multi-drug delivery approach to improve therapeutic efficacy in breast cancer.

Importance Of The Field: Significant improvements in breast cancer treatments have resulted in a significant decrease in mortality. However, current breast cancer therapies, for example, chemotherapy, often result in high toxicity and nonspecific side effects. Other treatments, such as hormonal and antiangiogenic therapies, often have low treatment efficacy if used alone.

Myofibril-inducing RNA (MIR) is essential for tropomyosin expression and myofibrillogenesis in axolotl hearts.

The Mexican axolotl, Ambystoma mexicanum, carries the naturally-occurring recessive mutant gene 'c' that results in a failure of homozygous (c/c) embryos to form hearts that beat because of an absence of organized myofibrils. Our previous studies have shown that a noncoding RNA, Myofibril-Inducing RNA (MIR), is capable of promoting myofibrillogenesis and heart beating in the mutant (c/c) axolotls. The present study demonstrates that the MIR gene is essential for tropomyosin (TM) expression in axolotl hearts during development.