Direct observations of crystallization processes of amorphous GeSn during thermal annealing: A temperature window for suppressing Sn segregation

The solubility limit of tin (Sn) in germanium (Ge) is very small, and, therefore, it is difficult to synthesize high Sn concentration GeSn crystals by conventional methods. An amorphous phase can contain elements beyond the solubility limit of the crystal state, and, therefore, recrystallization of the amorphous alloy is one of the possible ways to realize materials far from the equilibrium state. To suppress Sn precipitation during thermal annealing, knowledge of crystallization processes is required. In the present study, amorphous GeSn thin films with different Sn concentrations were prepared by sputtering, and their crystallization processes were examined by in situ transmission electron microscopy. It was found that the crystallization temperature decreases with increasing Sn concentration, and it became lower than the eutectic temperature when the Sn concentration exceeded ∼25 at. %. Radial distribution function analyses revealed that phase decomposition occurs in the amorphous state of the specimens which crystallize below the eutectic temperature, and Sn crystallites were simultaneously precipitated with crystallization. On the other hand, no remarkable phase decomposition was detected in amorphous GeSn with <25 at. % Sn. Sn precipitation occurred at a higher temperature than the crystallization in these specimens, and the difference between the crystallization and Sn precipitation temperatures became large with decreasing Sn concentration. Because of the existence of this temperature difference, a temperature window for suppressing Sn segregation existed. We demonstrated that large GeSn grains with high Sn concentration could be realized by annealing the specimens within the temperature window

Decreased orbital fat and enophthalmos due to bimatoprost: Quantitative analysis using magnetic resonance imaging.

We quantitatively determined the relation between the decrease in orbital fat and enophthalmos due to bimatoprost using magnetic resonance imaging (MRI). Nine orbits in nine patients were treated unilaterally with bimatoprost for glaucoma or ocular hypertension. The contralateral orbits were used as controls. The volumes of the orbital tissues and the enophthalmos were measured using MRI. The mean volumes on the treated and untreated sides were, respectively, 14.6 ± 2.1 and 17.0 ± 4.3 cm3 for orbital fat (P = 0.04) and 3.4 ± 0.5 and 3.3 ± 0.5 cm3 for total extraocular muscles (P = 0.85). The mean enophthalmos values were 14.7 ± 2.5 and 16.0 ± 2.3 mm on the treated and untreated sides, respectively (P = 0.002). The data acquired by quantitatively measuring the volumes of orbital fat and enophthalmos on MRI showed that each might be reduced by bimatoprost administration. The enophthalmos could be caused by the bimatoprost-induced decrease in orbital fat

Cullin-3 and its adaptor protein ANKFY1 determine the surface level of integrin β1 in endothelial cells

Angiogenesis, the formation of new blood vessels from the pre-existing vasculature, is related to numerous pathophysiological events. We previously reported that a RING ubiquitin ligase complex scaffold protein, cullin-3 (CUL3), and one of its adaptor proteins, BAZF, regulated angiogenesis in the mouse retina by suppressing Notch signaling. However, the degree of inhibition of angiogenesis was made greater by CUL3 depletion than by BAZF depletion, suggesting other roles of CUL3 in angiogenesis besides the regulation of Notch signaling. In the present study, we found that CUL3 was critical for the cell surface level of integrin β1, an essential cell adhesion molecule for angiogenesis in HUVECs. By siRNA screening of 175 BTBPs, a family of adaptor proteins for CUL3, we found that ANKFY1/Rabankyrin-5, an early endosomal BTBP, was also critical for localization of surface integrin β1 and angiogenesis. CUL3 interacted with ANKFY1 and was required for the early endosomal localization of ANKFY1. These data suggest that CUL3/ANKFY1 regulates endosomal membrane traffic of integrin β1. Our results highlight the multiple roles of CUL3 in angiogenesis, which are mediated through distinct CUL3-adaptor proteins

Arthroscopic Reconstruction of the Anterior Talofibular Ligament, Lateral Talocalcaneal Ligament, and Calcaneofibular Ligament Using a Triangle-Shaped Tendon Graft (ALC-Triangle)

The lateral talocalcaneal ligament (LTCL) connects the talus and calcaneus on the lateral side of the hindfoot. Although its function remains has not yet been clearly elucidated, the LTCL is thought to be important for the stabilization of the subtalar joint. Ankle sprains often include not only the talocrural joint but also the subtalar joint; therefore, LTCL injuries occur at a certain rate. Moreover, surgeons often encounter and reluctantly dissect the LTCL during arthroscopic anterior talofibular ligament (ATFL) and calcaneofibular ligament (CFL) reconstruction because the LTCL connects to the ATFL at the talus in 42% of people and connects to the CFL at the calcaneus in 18% of people. As a result, LTCL reconstruction might be necessary for those patients. We describe the arthroscopic reconstruction technique of the ATFL, LTCL, and CFL using a triangle-shaped tendon graft (ALC-triangle). This technique provides a possible advantage of an anatomical and stable talocrural joint and subtalar joint

The Cullin-3-Rbx1-KCTD10 complex controls endothelial barrier function via K63 ubiquitination of RhoB

RhoGTPases control endothelial cell (EC) migration, adhesion, and barrier formation. Whereas the relevance of RhoA for endothelial barrier function is widely accepted, the role of the RhoA homologue RhoB is poorly defined. RhoB and RhoA are 85% identical, but RhoB's subcellular localization and half-life are uniquely different. Here, we studied the role of ubiquitination for the function and stability of RhoB in primary human ECs. We show that the K63 polyubiquitination at lysine 162 and 181 of RhoB targets the protein to lysosomes. Moreover, we identified the RING E3 ligase complex Cullin-3-Rbx1-KCTD10 as key modulator of endothelial barrier integrity via its regulation of the ubiquitination, localization, and activity of RhoB. In conclusion, our data show that ubiquitination controls the subcellular localization and lysosomal degradation of RhoB and thereby regulates the stability of the endothelial barrier through control of RhoBmediated EC contraction

Arthroscopic Reconstruction of the Anterior Tibiotalar Ligament Using a Free Tendon Graft

Deltoid ligament injuries account for 5.1% to 15.8% of ankle sprains and occur with concomitant lateral ankle sprains. The anterior tibiotalar ligament (ATTL), located within the deep layer of the deltoid ligament complex, connects the talus and the tibia on the medial side of the ankle and controls ankle eversion and rotation. If conservative treatment for chronic medial ankle instability after an ankle sprain fails, ATTL repair or reconstruction might be necessary. Arthroscopic reconstruction techniques of the lateral ankle ligaments recently have been reported. Here, we describe arthroscopic reconstruction of the ATTL using a free tendon graft (ARATTL). This technique is less invasive than other treatments and results in a more stable medial ankle joint