General corrosion during metal-assisted etching of n-type silicon using different metal catalysts of silver, gold, and platinum.

Metal-assisted etching is a promising technique for microfabrication of semiconductors. In this method, porous silicon (Si) can be produced with a very simple procedure, and various nanostructures can be designed by changing the catalyst patterns. The kind of metal catalysts is one of the key factors to control the porous structure. In this work, we performed the etching of n-type Si (100) in a hydrofluoric acid solution containing hydrogen peroxide in the dark using silver, gold, and platinum particles electrolessly deposited at a constant coverage, and demonstrated the difference in the porous structures obtained for the different kind of metal catalysts. By comparing the mass loss of substrates with the depth of pores formed under the metal particles, we found that general corrosion occurred on the top-surface of the Si substrate around the metal particles even under the dark condition. The general corrosion depended on the metal species and it was explained by the formation and dissolution of a mesoporous layer. The kind of metal catalysts influences the dissolution of the Si surface not only under the metal catalysts but also between them.

In vivo kinematics of a low contact stress rotating platform total knee arthroplasty system under weight bearing and non-weight bearing condition.

BACKGROUND: The patterns and magnitudes of axial femorotibial rotation are variable due to the prosthesis design, ligamentous balancing, and surgical procedures. We aimed to investigate the effects of the weight bearing (WB) condition on the kinematics of mobile-bearing total knee arthroplasty (TKA). METHODS: We examined 12 patients (19 knees) implanted with a low contact stress (LCS) mobile-bearing TKA system using a two-dimensional to three-dimensional registration technique. The in vivo kinematics of dynamic deep knee flexion under WB and non-WB (NWB) conditions were compared. We evaluated the knee range of motion, femoral axial rotation relative to the tibial component, anteroposterior translation, and kinematic pathway of the femorotibial contact point for both the medial and lateral sides. RESULTS: Under the WB condition, the mean range of motion was 117.8° ± 16.7°. Under the NWB condition, the mean range of motion was 111.0° ± 4.4°. The mean range of axial rotation from full extension to maximum flexion was 3.0° ± 1.5° under the WB condition and 2.2° ± 1.0° under the NWB condition. With regard to the anteroposterior translation, the LCS mobile-bearing TKA system showed the same kinematic patterns under both conditions, except for axial rotation at 0°, 10°, and 110°. From hyperextension to maximum flexion, the kinematic pattern reflected a central pivot under both conditions. CONCLUSIONS: In conclusion, this study demonstrated that, in an LCS mobile-bearing TKA system, knee kinematics showed the same patterns under NWB and WB conditions, except for axial rotation at the early phase. Further understanding of knee kinematics could provide us with useful information for future design concepts of TKA implants.

Thrombin-stimulated proliferation is mediated by endothelin-1 in cultured rat gingival fibroblasts.

Abstract Endothelin-1 (ET-1) appears to be involved in drug-induced proliferation of gingival fibroblasts. Thrombin induces proliferation of human gingival fibroblasts via protease-activated receptor 1 (PAR1). In this study, using cultured rat gingival fibroblasts, we investigated whether thrombin-induced proliferation of gingival fibroblasts is mediated by ET-1. Thrombin-induced proliferation (0.05-2.5 U/mL). Proliferation was also induced by a PAR1-specific agonist (TFLLR-NH(2,) 0.1-30 microm), but not by a PAR2-specific agonist (SLIGRL-NH(2)). Thrombin (2.5 U/mL) induced an increase in immunoreactive ET-1 expression, which was inhibited by cycloheximide (10 microg/mL), and an increase in preproET-1 mRNA expression, as assessed by reverse transcription polymerase chain reaction. TFLLR-NH(2) increased ET-1 release into the culture medium in both a concentration (0.01-10 microm)- and time (6-24 h)-dependent manner, as assessed by solid phase sandwich enzyme-linked immunosorbent assay. The thrombin (2.5 U/mL)-induced proliferation was inhibited by a PAR1-selective inhibitor, SCH79797 (0.1 microm) and an ET(A) antagonist, BQ-123 (1 microm), but not by an ET(B) antagonist, BQ-788 (1 microm). These findings suggest that thrombin, acting via PAR1, induced proliferation of cultured rat gingival fibroblasts that was mediated by ET-1 acting via ET(A).

Inhibition of angiotensin II- and endothelin-1-stimulated proliferation by selective MEK inhibitor in cultured rabbit gingival fibroblastsdagger.

We investigated the implication of extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) in the proliferation stimulated by angiotensin II (Ang II) and endothelin-1 (ET-1) in cultured rabbit gingival fibroblasts (CRGF). Ang II stimulated activation of ERK1/2 and the activation was inhibited by CV-11974, an AT1 antagonist, and saralasin, an AT1/AT2 antagonist, but not by PD123,319, an AT2 antagonist in the CRGF. Ang II-stimulated proliferation was inhibited by PD98059 or U0126, selective MEK inhibitors. Furthermore, ET-1 stimulated proliferation via G-protein-coupled ETA receptors, which were identified by Western blot analysis of membrane protein from the CRGF. ET-1 also stimulated activation of ERK1/2 and the activation was inhibited by BQ-123, an ETA inhibitor, and TAK044, an ETA/ETB inhibitor, but not by BQ-788, an ETB inhibitor. ET-1-stimulated proliferation was inhibited by PD98059 or U0126. These findings suggest that ERK1/2 play a role in the signaling process leading to proliferation stimulated by Ang II and ET-1 via G-protein-coupled receptors, AT1 and ETA in CRGF.

Pharmacological properties of angiotensin II receptors in cultured rabbit gingival fibroblasts.

We demonstrated that angiotensin II (Ang II, 10-1000 nM) induced proliferation of cultured rabbit gingival fibroblasts in a concentration-dependent manner. The Ang II-induced proliferation was inhibited by CV-11974 (AT1 antagonist; 1 microM) and saralasin (AT1/AT2 antagonist; 1 microM), but not by PD123,319 (AT2 antagonist; 1 microM), suggesting that Ang II-induced proliferation was mediated via AT1 receptors present in and/or on gingival fibroblasts. The results of Western blot analysis indicated the presence of AT1 and AT2 receptors in/on the fibroblasts. In a subsequent radioligand binding assay, the binding of [3H]Ang II to the fibroblasts was specific and saturable with both high- and low-affinity sites. Competition binding experiments indicated that Ang II completely displaced [3H]Ang II binding, and CV-11974 and PD123,319 maximally displaced up to approximately 63% and 37% of the total binding, respectively. Ang II and CV-11974 completely displaced the [3H]DuP753 binding but PD123,319 did not, indicating a single population of binding site. These findings demonstrate that gingival fibroblasts contain both AT1 and AT2 receptor subtypes for Ang II, and support that Ang II stimulation of AT1 receptors results in proliferation of the fibroblasts.

Proliferative effects of angiotensin II and endothelin-1 on guinea pig gingival fibroblast cells in culture.

We investigated whether phenytoin (PHT) and nifedipine (NIF) induce angiotensin II (Ang II) and endothelin-1 (ET-1) generation by cultured gingival fibroblasts derived from guinea pigs and whether Ang II and ET-1 induce proliferation of these cells. Immunohistochemical experiments showed that PHT (250 nM) and NIF (250 nM) increased the immunostaining intensities of immunoreactive Ang II and ET-1 (IRET-1) in these cells. Captopril (3 microM), an angiotensin-converting enzyme inhibitor, reduced these enhanced intensities to control levels. Ang II (100 nM) enhanced the immunostaining intensity of IRET-1. PHT (250 nM) and NIF (250 nM)-induced cell proliferation. Both PHT- and NIF-induced proliferation was inhibited by captopril (3 microM). Ang II (100 nM) and ET-1 (100 nM) also induced cell proliferation. Ang II-induced proliferation was inhibited by CV11974 (1 microM), an AT(1) receptor antagonist and saralasin (1 microM), an AT(1)/AT(2) receptor antagonist, but not by PD123,319 (1 microM), an AT(2) receptor antagonist. ET-1-induced proliferation was inhibited by BQ123 (10 microM), an ET(A) receptor antagonist, but not by BQ788 (1 microM), an ET(B) receptor antagonist. These findings suggest that PHT- and NIF-induced gingival fibroblast proliferation is mediated indirectly through the induction of Ang II and ET-1 and probably mediated through AT(1) and ET(A) receptors present in or on gingival fibroblasts.