The Mini-International Neuropsychiatric Interview (MINI) is a short, structured diagnostic interview used as a tool to diagnose 16 axis I (Diagnostic and Statistical Manual) DSM-IV disorders and one personality disorder. Its original version was developed by Sheehan and Lecrubier. We translated the MINI into Japanese, and investigated the reliability and validity of the Japanese version of MINI. Eighty-two subjects participated in the validation of the MINI versus the Structured Clinical Interview for DSM-III-R (SCID-P). One hundred and sixty-nine subjects participated in the validation of the MINI versus an expert's professional opinion. Seventy-seven subjects were interviewed by two investigators and subsequently readministered by a third interviewer blind to the results of initial evaluation 1-2 days later. In general, kappa values indicated good or excellent agreement between MINI and SCID-P diagnoses. Kappa values indicated poor agreement between MINI and expert's diagnoses for most diagnoses. Interrater and test-retest reliabilities were good or excellent. The mean durations of the interview were 18.8 min for MINI and 45.4 min for corresponding sections of SCID-P. Overall, the results suggest that the MINI Japanese version succeeds in reliably and validly eliciting symptom criteria used in making DSM-III-R diagnoses, and can be performed in less than half the time required for the SCID-P.

Natural-food-based compounds show substantial promise for prevention and biotherapy of cancers including leukemia. In general, their mechanism of action remains unclear, hampering rational use of these compounds. Herein we show that the common dietary flavonoid apigenin has anticancer activity, but also may decrease chemotherapy sensitivity, depending on the cell type. We analyzed the molecular consequences of apigenin treatment in two types of leukemia, the myeloid and erythroid subtypes. Apigenin blocked proliferation in both lineages through cell-cycle arrest in G2/M phase for myeloid HL60 and G0/G1 phase for erythroid TF1 cells. In both cell lines the JAK/STAT pathway was one of major targets of apigenin. Apigenin inhibited PI3K/PKB pathway in HL60 and induced caspase-dependent apoptosis. In contrast, no apoptosis was detected in TF1 cells, but initiation of autophagy was observed. The block in cell cycle and induction of autophagy observed in this erythroleukemia cell line resulted in a reduced susceptibility toward the commonly used therapeutic agent vincristine. Thus, this study shows that although apigenin is a potential chemopreventive agent due to the induction of leukemia cell-cycle arrest, caution in dietary intake of apigenin should be taken during disease as it potentially interferes with cancer treatment.

No abstract

Cryoablation in CS within 2 mm of LCx produces Trans-CSM lesions similar to RFA with lower risk of LCx stenosis than RFA.

Pre-osteoblast adhesion attracts increasing interest in both medicine and dentistry. However, how this physiological event alters osteoblast phenotype is poorly understood. We therefore attempted to address this question by investigating key biochemical mechanism that governs pre-osteoblast adhesion on polystyrene surface. Importantly, we found that cofilin activity was strongly modulated by PP2A (Ser/Thr phosphatase), while cell-cycle was arrested. Accordingly, we observed that the profile of cofilin phosphorylation (at Ser03) was similar to phospho-PP2A (at Tyr307). Also, it is plausible to suggest during pre-osteoblast adhesion that PP2A phosphorylation at Y307 was executed by phospho-Src (Y416). In addition, it was observed that MAPKp38, but not MAPK-erk, played a key role on pre-osteoblast adhesion by phosphorylating MAPKAPK-2 and ATF-2 (also called CRE-BP1). Also, the up-modulation of RhoA reported here suggests its involvement at the beginning of osteoblast attachment, while Akt remained active during all periods. Altogether, our results clearly showed that osteoblast adhesion is under an intricate network of signaling molecules, which are responsible to guide their interaction with substrate mainly via cytoskeleton rearrangement.