Topochemical polymerization of dumbbell-shaped diacetylene monomers: relationship between chemical structure, molecular packing structure, and gelation property.

Herein, we have synthesized novel photopolymerizable dumbbell-shaped diacetylene liquid crystal (LC) monomers by locating a diacetylene dicarboxylic acid group at the center and chemically connecting swallow-tails, such as hydrophobic alkyl chains (abbreviated as AT3DI) and amphiphilic biphenyl mesogens (abbreviated as BP3DI), with bisamide groups. Major phase transitions of dumbbell-shaped diacetylene monomers were identified using differential scanning calorimetry (DSC), polarized optical microscopy (POM), and Fourier transform infrared spectroscopy (FT IR). Molecular packing structures were studied based on structure-sensitive wide-angle X-ray diffraction (WAXD) and small-angle X-ray scattering (SAXS) analyses. Mainly, due to nanophase separations and strong intermolecular hydrogen bonding, AT3DI formed a low-ordered lamellar LC phase at room temperature. BP3DI self-assembled into highly-ordered crystal phases (K1 and K2) at lower temperatures below a low-ordered lamellar LC phase, in which BP3DI were intercalated with each other to compensate the mutual volume differences. From the photopolymerization of AT3DI and BP3DI, it was realized that the topochemical reactions of dumbbell-shaped diacetylene monomers were closely related to their chemical structures as well as molecular packing structures.

Donor-Site Morbidity Analysis of Thenar and Hypothenar Flap.

Background For the small glabrous skin defect, Thenar and Hypothenar skin are useful donors and they have been used as a free flap. Because of similar skin characteristics, both flaps have same indications. We will conduct comparative study for the donor morbidity of the Free thenar flap and Hypothenar free flap. Methods From January 2011 to December 2021, demographic data, characteristics of each flap, and complications using retrospective chart review were obtained. Donor outcomes of the patient, who had been followed up for more than 6 months, were measured using photographic analysis and physical examination. General pain was assessed by Numeric Rating Scale (NRS) score, neuropathic pain was assessed by Douleur Neuropathique 4 Questions (DN4) score, scar appearance was assessed by modified Vancouver Scar Scale (mVSS), and patient satisfaction was assessed on a 3-point scale. Statistical analysis was performed on the outcomes. Results Out of the 39 survey respondents, 17 patients received Free thenar flaps, and 22 patients received Hypothenar free flaps. Thenar group had higher NRS, DN4, and mVSS ( p < 0.05). The average scores for the Thenar and Hypothenar groups were 1.35 and 0.27 for NRS, 2.41 and 0.55 for DN4, and 3.12 and 1.59 for mVSS, respectively. Despite the Hypothenar group showing greater satisfaction on the 3-point scale (1.82) compared with the Thenar group (1.47), the difference was not significant ( p = 0.085). Linear regression analysis indicated that flap width did not have a notable impact on the outcome measures, and multiple linear regression analysis revealed no significant interaction between flap width and each of the outcome measures. Conclusion Despite the limited number of participants, higher donor morbidity in general pain, neuropathic pain, and scar formation was noted in the Thenar free flap compared with the Hypothenar free flap. However, no difference in overall patient satisfaction was found between the two groups.

The integrin-coupled signaling adaptor p130Cas suppresses Smad3 function in transforming growth factor-beta signaling.

Reciprocal cooperative signaling by integrins and growth factor receptors at G1 phase during cell cycle progression is well documented. By contrast, little is known about the cross-talk between integrin and transforming growth factor (TGF)-beta signaling. Here, we show that integrin signaling counteracts the inhibitory effects of TGF-beta on cell growth and that this effect is mediated by p130Cas (Crk-associated substrate, 130 kDa). Adhesion to fibronectin or laminin reduces TGF-beta-induced Smad3 phosphorylation and thus inhibits TGF-beta-mediated growth arrest; loss of p130Cas abrogates these effects. Loss and gain of function studies demonstrated that, once tyrosine-phosphorylated via integrin signaling, p130Cas binds to Smad3 and reduces phosphorylation of Smad3. That in turn leads to inhibition of p15 and p21 expression and facilitation of cell cycle progression. Thus, p130Cas-mediated control of TGF-beta/Smad signaling may provide an additional clue to the mechanism underlying resistance to TGF-beta-induced growth inhibition.