Biomedical subjects

Takeshi Shirai

Publications and source records attributed to Takeshi Shirai.

3 recordsLinked to original sources

PubMed2005

[Roles of BPH impact index in the evaluation of impaired urination in patients with BPH].

OBJECTIVE: To assess the significance and current status of the benign prostatic hyperplasia (BPH) impact index (BII) in the evaluation of subjective symptoms of impaired urination in so-called QOL disease, BPH. PATIENTS AND METHODS: Over the past 2 year-period, in 159 patients with the diagnosis of BPH were asked to reply to each of the international prostate symptom score (I-PSS), QOL index and BII questionnaires. The subjective symptom scores (a total of 246 points) were evaluated from the viewpoint of clinical statistics in the search for any these and to find which questions cover the BII, most. RESULTS: 1) Statistically significant but moderate correlations were observed among I-PSS total score, QOL index and BII. The correlations among Qmax, BII and QOL were very weak. 2) Out of the 11 domains in both IPSS and BII, 2 questions of BII ("bothersomeness caused by urinary problems" and "degree of worry about well-being") and 4 questions of IPSS ("residual sense," " pollakisuria," "weak urinary stream" and "nocturia") were shared as QOL indices. Patient satisfaction was affected also by the questions in the BII. 3) Of the 7 BPH symptoms assessed in IPSS, 4 symptoms ("residual sense," "pollakisuria," "weak urinary stream" and "nocturia") affected the QOL index, and 4 symptoms ("urgency on micturition," "residual sense," "nocturia" and "strain at urination") affected BII. 4) Of the 7 symptoms assessed by IPSS, different symptoms affected each of the 4 BII questions. CONCLUSION: It is needed to assess BPH symptoms not only by the IPSS and QOL index but also based on BII to provide the detailed therapeutic instructions and thorough patients consultation.

Aged↗

PubMed2003

Inhibition of excitatory neuronal cell death by cell-permeable calcineurin autoinhibitory peptide.

In glutamate-mediated excitatory neuronal cell death, immunosuppressants (FK506, Cys-A) are powerful agents that protect neurons from apoptosis. Immunosuppressants inhibit two types of enzyme, calcium/calmodulin-dependent protein phosphatase (calcineurin: CaN), and peptidyl-prolyl cis-trans-isomerase (PPIase) activity such as the FKBP family. In this study, we used a protein transduction approach to determine the functional role of CaN and to produce a potential therapeutic agent for glutamate-mediated neuronal cell death. We created a novel cell-permeable CaN autoinhibitory peptide using the 11 arginine protein transduction domain. This peptide was highly efficient at transducing into primary culture neurons, potently inhibited CaN phosphatase activities, and inhibited glutamate-mediated neuronal cell death. These results showed that CaN plays an important role in excitatory neuronal cell death and cell-permeable CaN autoinhibitory peptide could be a new drug to protect neurons from excitatory neuronal death.

Active Transport, Cell Nucleus↗

PubMed2002

Hic-5 interacts with GIT1 with a different binding mode from paxillin.

Hic-5, a member of the paxillin family of adaptor molecules, is localized at focal adhesion and implicated in integrin-mediated signaling. Hic-5 and paxillin exhibit structural homology and share interacting factors, however, diverse functions are suggested for them. In this study, we carried out yeast two-hybrid screening to identify Hic-5 interacting factors using its LD3-4 region, which includes the Hic-5-specific amino acid sequence, as a bait. Through the screening, we identified GIT1, an Arf GTPase-activating protein, as a Hic-5 binding protein. The interaction of these two proteins was mediated by the LD3 motif of Hic-5 and the C-terminal region, which includes a paxillin-binding subdomain, of GIT1. Although GIT1 is known as a paxillin-binding protein, we only observed weak association of paxillin with GIT1 in the overexpression system. In contrast, Hic-5 firmly bound to GIT1 under the same conditions. In addition, the paxillin/GIT1 complex contained PIX, a guanine nucleotide exchange factor, whereas the Hic-5/GIT1 complex contained a smaller amount of PIX. These results suggested that paxillin and Hic-5 associate with GIT1 with different binding modes, and that the Hic-5 complex possesses static features compared with the paxillin complex, which contains both positive and negative regulators of GTPases involved in actin dynamics. Moreover, Hic-5-mediated inhibition of cell spreading was restored by co-expression of the C-terminal fragment of GIT1, which perturbs the interaction of Hic-5 with endogenous GIT1. Thus, it was demonstrated that Hic-5 and GIT1 interact functionally in addition to showing a physical association.

3T3 Cells↗