Loss of Posterior Occluding Teeth and Its Association with Protein-Micronutrients Intake and Muscle Mass among Thai Elders: A Pilot Study.

Contact between upper and lower posterior teeth is crucial for chewing. However, the influence of posterior occluding teeth loss on protein intake and muscle mass was unclear. This cross-sectional study compared consumption frequency of protein food, amount of protein and relevant micronutrient intakes and muscle mass indices among older adults with different Eichner indices (EI) of posterior occluding teeth loss. Ninety Thai healthy adults were divided into three groups (N=30 each) according EI with statistically comparable characters. Food frequency questionnaire, 4-days diet record, and bioelectrical impedance analysis were used for outcome measurement. Our findings suggested that loss of posterior occluding teeth on both sides was associated with less frequent consumption of meat, nut, egg, fish and dairy products, inadequate intakes of protein (< 0.8 g/kg body weight), iron and vitamin B12, and reduced muscle mass indices in older adults. Future large-scale cohort studies are warranted to confirm these findings.

Effective killing of Gleevec-resistant CML cells with T315I mutation by a natural compound PEITC through redox-mediated mechanism.

Mutation of Bcr-Abl is an important mechanism by which chronic myelogenous leukemia (CML) cells become resistant to Gleevec. The T315I mutation is clinically significant since CML cells harboring this mutation are insensitive to Gleevec and other Bcr-Abl-targeted drugs. Identification of new agents capable of effectively killing CML cells with T315I mutation would have important therapeutic implications in Gleevec-resistant CML. Here, we showed that beta-phenylethyl isothiocyanate (PEITC), a natural compound found in vegetables, is effective in killing CML cells expressing T315I BCR-ABL. Treatment of leukemia cell lines harboring wild-type or mutant Bcr-Abl with 10 microM PEITC resulted in an elevated ROS stress and a redox-mediated degradation of the BCR-ABL protein, leading to massive death of the leukemia cells. Antioxidant NAC attenuated the PEITC-induced oxidative stress in CML cells and prevented the degradation of BCR-ABL, caspase-3 activation and cell death. We further showed that the ROS-induced degradation of BCR-ABL was mediated partially by caspase-3 and the proteasome pathway. The ability of PEITC to effectively kill T315I-positive CML cells was further confirmed using primary leukemia cells isolated from CML patients. Our results suggest that PEITC is a promising compound capable of killing Gleevec-resistant CML cells through a ROS-mediated mechanism and warrants further investigations.