Vision-Based Estimation of Force Balance of Near-Suspended Melt Pool for Drooping and Collapsing Prediction.

Wire-arc additive manufacturing (WAAM) is favored by the industry for its high material utilization rate and low cost. However, wire-arc additive manufacturing of lattice structures faces problems with forming accuracy such as broken rod and surface morphology defects, which cannot meet the industrial demand. This article innovatively combines the melt pool stress theory with visual perception algorithms to visually study the force balance of the near-suspended melt pool to predict the state of the melt pool. First, the method for melt pool segmentation was studied. The results show that the optimized U-net achieved high accuracy in melt pool segmentation tasks, with accuracies of 98.18%, MIOU 96.64%, and Recall 98.34%. In addition, a method for estimating melt pool force balance and predicting normal, sagging, and collapsing states of the melt pool is proposed. By combining experimental testing with computer vision technology, an analysis of the force balance of the melt pool during the inclined rod forming process was conducted, showing a prediction rate as high as 90% for the testing set. By using this method, monitoring and predicting the state of the melt pool is achieved, preemptively avoiding issues of broken rods during the printing process. This approach can effectively assist in adjusting process parameters and improving welding quality. The application of this method will further promote the development of intelligent unmanned WAAM and provide some references for the development of artificial intelligence monitoring systems in the manufacturing field.

IL-17A signaling in colonic epithelial cells inhibits pro-inflammatory cytokine production by enhancing the activity of ERK and PI3K.

Our previous data suggested that IL-17A contributes to the inhibition of Th1 cell function in the gut. However, the underlying mechanisms remain unclear. Here we demonstrate that IL-17A signaling in colonic epithelial cells (CECs) increases TNF-α-induced PI3K-AKT and ERK phosphorylation and inhibits TNF-α induced expression of IL-12P35 and of a Th1 cell chemokine, CXCL11 at mRNA level. In a co-culture system using HT-29 cells and PBMCs, IL-17A inhibited TNF-α-induced IL-12P35 expression by HT-29 cells and led to decreased expression of IFN-γ and T-bet by PBMCs. Finally, adoptive transfer of CECs from mice with Crohn's Disease (CD) led to an enhanced Th1 cell response and exacerbated colitis in CD mouse recipients. The pathogenic effect of CECs derived from CD mice was reversed by co-administration of recombinant IL-17A. Our data demonstrate a new IL-17A-mediated regulatory mechanism in CD. A better understanding of this pathway might shed new light on the pathogenesis of CD.

Identify the key amino acid of BAFF binding with TACI.

B-cell activating factor (BAFF) has been used as a therapeutic target. To develop BAFF-specific small molecular inhibitors, it is necessary to know the key amino acid in the BAFF binding with its receptor. The key binding amino acid of BAFF interacting with its receptor TACI (trans-membrane activator and calcium modulator and cyclophilin ligand interactor) was analyzed based on the computer-guided molecular modeling method. According to theoretical prediction, a series of key amino acid mutants of BAFF, including M204 (Lys(204) to Ala), M208 (Met(208) to Ala), M209 (Gly(209) to Ala), M210 (His(210) to Ala), M234 (Gln(234) to Ala), M236 (Met(236) to Ala), and M237 (Pro(237) to Ala) were designed and evaluated with biological experiments. The results show that M208, M209, M236, and M237 of BAFF were the key amino acids and in accord with the theoretical results. The results highlight clues for the further development of BAFF-specific small molecular inhibitors.

Acitretin exhibits inhibitory effects towards UDP-glucuronosyltransferase (UGT)1A9-mediated 4-methylumbelliferone (4-MU) and propofol glucuronidation reaction.

The present study aimed to evaluate the potential risk of drug-drug interactions associated with acitretin which is a drug for therapy of psoriasis approved by the Food and Drug Administration (FDA). The initial screening of acitretin's inhibition towards 4-methylumbelliferone (4-MU) glucuronidation catalyzed by important UDP-glucuronosyltransferase (UGT) isoforms in the liver showed that UGT1A9 activity was strongly inhibited by acitretin with other UGT isoforms negligibly influenced. The inhibition type is best fit to competitive inhibition, and the inhibition kinetic parameter (K(i)) was determined to be 3.5 microM. The inhibition behaviour of acitretin towards UGT1A9 activity did not exhibit probe substrate-dependent behaviour when selecting human liver microsomes (HLMs)-catalyzed propofol-O-glucuronidation as probe reaction of UGT1A9. The same inhibition type and similar inhibition parameters (K(i) = 3.2 microM) were obtained. Using the maximum plasma exposure dose of acitretin (C(max)), the C(max)/K(i) values were calculated to be 0.23 and 0.25 when selecting 4-MU and propofol as probe substrates, respectively. All these results indicate a potential clinical drug-drug interaction between acitretin and 4-MU or propofol.

Responses, actions and health-promoting behavior among rural Taiwanese women with abnormal Papanicolaou test.

OBJECTIVES: The incidence and mortality rate of cervical cancer in Taiwan are higher than in other developed countries. This study aimed to explore women's responses and actions after receiving their test reports and their practice of health-promoting behaviors. DESIGN: This study employed a cross-sectional descriptive design. SAMPLE: A convenient sample of 101 women living in a rural area. MEASUREMENTS: Demographic characteristics, semistructured questions and Chinese Adult Health Promotion scale were used in this study. RESULTS: The mode of the duration of their marriages was 20 years. Nearly 14% were diagnosed as precancerous and underwent further treatment. 24 percent of the women took no action during the 3 months after receiving the results. As many as 96% of the participants were not aware of the 90% 5-year survival rate for localized cervical cancer. From semistructured interviews, 4 behavioral responses and 5 actions were identified. Notably, many women in this study practiced health-promoting behaviors for health responsibility, regular exercise and stress management with low frequency. CONCLUSIONS: These analytical results may prove useful in developing intervention strategies to assist women with positive Papanicolaou test results to choose treatment modalities and adopt healthy behaviors.

Distinct components of Janus kinase/signal transducer and activator of transcription signaling pathway mediate the regulation of systemic and tissue localized renin-angiotensin system.

In an attempt to demonstrate the linkage between the Janus kinase (Jak)/signal transducer and activator of transcription (STAT) signaling and the activity of the systemic or local renin-angiotensin system in vivo, we produced transgenic mice harboring angiotensinogen (ANG) promoter containing the wild-type or mutant STAT target site (St-domain) fused to the luciferase reporter. The ANG-promoter-driven luciferase expression was dependent upon phosphorylation of Jak2, as administration of tyrphostin AG490, a potent inhibitor of Jak2, down-regulated the ANG promoter activity and abolished the stimulated endogenous ANG mRNA level in the liver. Administration of angiotensin II peptide to the mice resulted in prominent expression of luciferase in the liver and heart of animals containing wild type St-domain, but not in transgenes with mutant St-domain. Angiotensin II-induced signaling caused activation of STAT proteins in the liver (systemic), the pattern of which was distinct from that in the heart (local). The inducible expression of ANG promoter appears to be mediated by physical association of p300 with STAT 5B in liver and STAT 3 and STAT 5A in heart. Taken together, these results point to the differences in signaling mechanisms in the circulating and localized renin-angiotensin system and identify at least two molecular steps, the tyrosyl phosphorylation of Jak2 and the STAT/St-domain interaction, as pivotal in the regulation of ANG gene transcription.