Influence of Light-Intensity-Dependent Droplet Directionality on Dimensions of Structures Constructed Using an In Situ Light-Guided 3D Printing Method

As an alternative to conventional 3D printing methods that require supports, a new 3D printing strategy that utilizes guided light in situ has been developed for fabricating freestanding overhanging structures without supports. Light intensity has been found to be a crucial factor in modifying the dimensions of structures printed using this method; however, the underlying mechanism has not been clearly identified. Therefore, the light-intensity-dependent changes in the structure dimensions were analyzed in this study to elucidate the associated mechanism. Essentially, the entire process of deposition was monitored by assessing the behavior of photocurable droplets prior to their collision with the structure using imaging analysis tools such as a high-speed camera and MATLAB®. With increasing light intensity, the instability of the ejected falling droplets increased, and the droplet directionality deteriorated. This increased the dispersion of the droplet midpoints, which caused the average midpoints of the deposited single layers to shift further away from the center of the structure. Consequently, the diameter of the structure formed by successive stacking of single layers increased, and the layer thickness per droplet decreased. These led to light-intensity-dependent differences in the diameter and height of structures that were created from the same number of droplets

In-situ 광 가이드를 활용한 3D 프린팅 방법에서 광 강도에 따른 최종 구조물의 치수에 관한 연구

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Catheter based hydrogel microfibers generating device for cerebral aneurysm embolization

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A study on the dimensions of hydrogel 3D structure by light intensity

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Chamber/Capsule-Integrated Self-Healing Coating on Glass for Preventing Crack Propagation

A transparent self‐healing coating incorporating chambers and capsules capable of preventing the propagation of cracks in glass is presented. The main features simultaneously satisfy the requirements of high transmittance (≈90% in the visible region) and the ability to heal random and large‐area cracks in coated‐glass materials (up to 6 cm long, 20 µm wide, and 1 mm deep per chamber). Additionally, the polymerized hydrogel used as the healing agent can stop crack propagation because of its high mechanical strength and good adhesion to glass. Remarkably, the healed glass can withstand a force approximately four times greater than what can be withstood by the unhealed glass after cracking.11sciescopu

Self-Healing Coating for Glass to Stop Crack Propagation

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Feeding and Fasting Signals Converge on the LKB1-SIK3 Pathway to Regulate Lipid Metabolism in <i>Drosophila</i>

<div><p>LKB1 plays important roles in governing energy homeostasis by regulating AMP-activated protein kinase (AMPK) and other AMPK-related kinases, including the salt-inducible kinases (SIKs). However, the roles and regulation of LKB1 in lipid metabolism are poorly understood. Here we show that <i>Drosophila</i> LKB1 mutants display decreased lipid storage and increased gene expression of <i>brummer</i>, the <i>Drosophila</i> homolog of adipose triglyceride lipase (ATGL). These phenotypes are consistent with those of SIK3 mutants and are rescued by expression of constitutively active SIK3 in the fat body, suggesting that SIK3 is a key downstream kinase of LKB1. Using genetic and biochemical analyses, we identify HDAC4, a class IIa histone deacetylase, as a lipolytic target of the LKB1-SIK3 pathway. Interestingly, we found that the LKB1-SIK3-HDAC4 signaling axis is modulated by dietary conditions. In short-term fasting, the adipokinetic hormone (AKH) pathway, related to the mammalian glucagon pathway, inhibits the kinase activity of LKB1 as shown by decreased SIK3 Thr196 phosphorylation, and consequently induces HDAC4 nuclear localization and <i>brummer</i> gene expression. However, under prolonged fasting conditions, AKH-independent signaling decreases the activity of the LKB1-SIK3 pathway to induce lipolytic responses. We also identify that the <i>Drosophila</i> insulin-like peptides (DILPs) pathway, related to mammalian insulin pathway, regulates SIK3 activity in feeding conditions independently of increasing LKB1 kinase activity. Overall, these data suggest that fasting stimuli specifically control the kinase activity of LKB1 and establish the LKB1-SIK3 pathway as a converging point between feeding and fasting signals to control lipid homeostasis in <i>Drosophila</i>.</p></div

Activation of insulin receptor increases phosphorylation of SIK3 by Akt.

<p>(A) Immunoblot analyses showing the effect of 4 hr fasting and constitutively active insulin receptor (InR^CA) on Thr196 phosphorylation of SIK3 protein in larvae (top three panels). Anti-phospho-Thr196 SIK3, -Myc (SIK3 protein), and -β-tubulin (TUB) antibodies were used. Densitometry of phospho-Thr196 SIK3 bands (bottom panel). <i>FB-Gal4</i> was used to drive transgene expression in the fat body. (B) Immunoblot analyses showing the effect of constitutively active insulin receptor (InR^CA) on Akt-dependent phosphorylation of SIK3 protein in larvae (top four panels). The lysates were immunoprecipitated with an anti-Myc (SIK3 protein) antibody, and then immunoblotted with an anti-phospho-Akt substrate antibody. Densitometry of phospho-SIK3 bands (bottom panel). (C) A schematic model for LKB1 and SIK3 function to regulate lipid homeostasis in <i>Drosophila</i> fat body. LKB1 regulates the nucleocytoplasmic localization of HDAC4 via SIK3-dependent phosphorylation. Under feeding condition, DILPs-induced Akt activation leads to SIK3 activation, thereby inhibiting HDAC4 activity by phosphorylation. Under short-term fasting conditions, the AKH pathway inhibits the kinase activity of LKB1 in phosphorylating SIK3 Thr196 residue and controls SIK3 activity via PKA-dependent phosphorylation. Unphosphorylated and nuclear localized HDAC4 deacetylates and activates FOXO to increase <i>bmm</i> expression [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005263#pgen.1005263.ref019" target="_blank">19</a>], thereby reducing lipid storage. AKH-independent signaling modulates the LKB1-SIK3-HDAC4 pathway to induce <i>bmm</i> expression when fasting is prolonged. Data are presented as mean ± SEM (*<i>P</i> < 0.05; **<i>P</i> < 0.01; NS, non-significant).</p

LKB1 and its downstream kinase SIK3 are required for lipid homeostasis.

<p>(A) qPCR analysis of LKB1 and its cofactors required for the catalytic activity, STRAD and MO25, in <i>Drosophila</i> larvae under feeding condition. (B) TAG amounts of wild-type and <i>LKB1</i> mutant larvae (<i>n</i> = 10 per genotype). (C) qPCR analysis for lipogenic genes (<i>SREBP</i>, <i>FAS</i> and <i>ACC</i>) and lipolytic genes (<i>bmm</i> and <i>HSL</i>) in wild-type and <i>LKB1</i> mutant larvae at mid-to-late L2 (60 hr AEL) stage under feeding conditions. (D) qPCR analysis of LKB1, SIKs (SIK2 and SIK3), and AMPK complex (AMPKα, AMPKβ, and AMPKγ) in larvae. (E) TAG amounts in LKB1 mutants following fat body-specific expression of wild-type, kinase-dead (K201I) LKB1, constitutively active (T196E) SIK3 or constitutively active (T184D) AMPK. Genotypes are as follows: FB> (<i>FB-Gal4</i>/+), LKB1^X5,FB> (<i>FB-Gal4/+;LKB1</i>^<i>X5</i><i>/LKB1</i>^<i>X5</i>), LKB1^X5,FB>LKB1^WT (<i>FB-Gal4/UAS-LKB1;LKB1</i>^<i>X5</i><i>/LKB1</i>^<i>X5</i>), LKB1^X5,FB>LKB1^KI (<i>FB-Gal4/UAS-LKB1 K201I;LKB1</i>^<i>X5</i><i>/LKB1</i>^<i>X5</i>), LKB1^X5,FB>SIK3^TE (<i>FB-Gal4/UAS-SIK3 T196E;LKB1</i>^<i>X5</i><i>/LKB1</i>^<i>X5</i>), and LKB1^X5,FB>AMPK^TD (<i>FB-Gal4/UAS-AMPK T184D;LKB1</i>^<i>X5</i><i>/LKB1</i>^<i>X5</i>) (<i>n</i> = 10 per genotype). (F) qPCR analysis of <i>bmm</i> gene expression in <i>LKB1</i> mutants following fat body-specific expression of wild-type LKB1 or constitutively active (T196E) SIK3 at mid-to-late L2 stage under feeding condition. Genotypes are as follows: FB> (<i>FB-Gal4</i>/+), LKB1^X5,FB> (<i>FB-Gal4/+;LKB1</i>^<i>X5</i><i>/LKB1</i>^<i>X5</i>), LKB1^X5,FB>LKB1^WT (<i>FB-Gal4/UAS-LKB1;LKB1</i>^<i>X5</i><i>/LKB1</i>^<i>X5</i>), and LKB1^X5,FB>SIK3^TE (<i>FB-Gal4/UAS-SIK3 T196E;LKB1</i>^<i>X5</i><i>/LKB1</i>^<i>X5</i>). (G) Immunoblot analyses showing the effect of LKB1 on Thr196 phosphorylation of SIK3 protein in larvae. Wild-type and kinase-dead (K70M) SIK3 were highly phosphorylated at Thr196 by LKB1 (second panel). SIK3^T196A was used as a control. <i>FB-Gal4</i> was used to drive transgene expression in the fat body. (H) Immunoblot analyses showing relative amounts of SIK3 Thr196 phosphorylation in wild-type and <i>LKB1</i>^<i>X5</i> mutant larvae. The phosphorylation was absolutely dependent on LKB1 (first panel). <i>FB-Gal4</i> was used to drive transgene expression. (G-H) Anti-LKB1, -phospho-Thr196 SIK3, -Myc (SIK3 protein), and -β-tubulin (TUB) antibodies were used. Data are presented as mean ± SEM (*<i>P</i> < 0.05).</p

Embolization of Vascular Malformations via In Situ Photocrosslinking of Mechanically Reinforced Alginate Microfibers Using an Optical-fiber-integrated Microfluidic Device

Embolization, which is a minimally invasive endovascular treatment, is a safe and effective procedure for treating vascular malformations (e.g., aneurysms). Hydrogel microfibers obtained via spatiotemporally controllable in situ photocrosslinking exhibit great potential for embolizing aneurysms. However, this process is challenging because of the absence of biocompatible and morphologically stable hydrogels and the difficulty in continuously spinning the microfibers via in situ photocrosslinking in extreme endovascular environments such as those involving a tortuous geometry and high absorbance. A double-crosslinked alginate-based hydrogel with tantalum nanopowder (DAT) that exploits the synergistic effect of covalent crosslinking by visible-light irradiation and ionic crosslinking using Ca2+, which is present in the blood, is developed in this study. Furthermore, an effective strategy to design and produce an optical-fiber-integrated microfluidic device (OFI-MD) that can continuously spin hydrogel microfibers via in situ photocrosslinking in extreme endovascular environments is proposed. As an embolic material, DAT exhibits promising characteristics such as radiopacity, nondissociation, nonswelling, and constant mechanical strength in blood, in addition to excellent cyto- and hemo-compatibilities. Using OFI-MD to spin DAT microfibers continuously can help fill aneurysms safely, uniformly, and completely within the endovascular simulator without generating microscopic fragments, which demonstrates its potential as an effective embolization strategy.11Nsciescopu