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Plasma FN (pFN) is known to regulate cell growth, differentiation or survival of osteoblasts in vitro. It is also speculated to be important for the early phase of osseointegration, however its actual in vivo behavior is unknown. The objective of this study is to clarify the role of pFN during osseointegration. We developed a titanium ion-plated acrylic implant (Ti-acryl) for thin sectioning without removal of the implant.Either Ti-acryl or pFN-coated Ti-acryl (FN-Ti-acryl) was implanted in the mouse femur.Samples were taken on day 1 to day 7 and on day 14 after the operation, and were decalcified and paraffin embedded. The bone healing process and immunofluorescence localization of pFN and cellular fibronectin (cFN), a marker for fibroblastic cells were examined. Simultaneously, the effect of pFN on chemotaxis, proliferation and differentiation of bone marrow stromal cells (BMSCs) was analyzed in vitro. The in vivo results showed that faster direct bone formation was seen for the FN-Ti-acryl group compared to the Ti-acryl group. The in vitro results showed that, pFN significantly promoted BMSCs chemotaxis, however had no effect on proliferation or differentiation.The results indicate that pFN regulated chemotaxis of osteogenic cells and coating the implant with pFN enhanced earlier osseointegration.

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Progressive neuronal loss in Alzheimer's disease (AD) is considered to be a consequence of the neurotoxic properties of amyloid-␤ peptides (A␤). T-817MA (1-{3-[2-(1-benzothiophen-5-yl) ethoxy] propyl}-3-azetidinol maleate) was screened as a candidate therapeutic agent for the treatment of AD based on its neuroprotective potency against A␤-induced neurotoxicity and its effect of enhancing axonal regeneration in the sciatic nerve axotomy model. The neuroprotective effect of T-817MA against A␤(1-42) or oxidative stress-induced neurotoxicity was assessed using a coculture of rat cortical neurons with glia.

Concurrent treatment with tadalafil and an α -blocker seems to be safe and well tolerated in Japanese patients with lower urinary tract symptoms suggestive of benign prostatic hyperplasia. Adding tadalafil to baseline α -blocker therapy does not translate in adverse effects on the blood pressure. Patients tend to prefer combination therapy over monotherapy, and there seems to be a clinical benefit when using combination therapy.

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ABSTRACT-a,-Adrenoceptors in the rat prostate were characterized by a binding assay using the newlypropyl]-2 methoxybenzenesulfonamide HCI) and an in vitro assay. Specific [3H]-YM617 binding in the rat prostate was saturable and of high affinity (KD = 61.5 ± 5.9 pM) with 23.2 ± 6.9 fmol/mg of protein as the maximal number of binding sites (Bmax). a-Adrenoceptor agonists and antagonists inhibited the binding of the radioligand with the following order of effectiveness: YM617 > prazosin = bunazosin > WB4 101 >5-methyl urapidil = phenoxybenzamine > phentolamine > S(+ )-isomer of YM617 > yohimbine > norepinephrine > phenylephrine>methoxamine.a,-Adrenoceptors in the rat prostate preferred the R(-)-isomer of YM617 to the S(+)-isomer. Preincubation with chlorethylclonidine (CEC; 10-5 M, 10 min) just slightly changed the Bmax value for [3H]-YM617 without changing the KD value in the prostate; however, CEC reduced the Bmax in the aorta. In the isolated tissue, pretreatment with CEC (10-5 M, 10 and 30 min) time-dependently shifted to the right the dose-response curve for phenylephrine and decreased the maximal contraction of aortas induced by phenylephrine, but did not shift or decrease those of prostates. The present results indi cate that the a,-adrenoceptors in the rat prostate are mainly CEC-insensitive (a,A), whereas those in the aorta are CEC-sensitive (a,B).