3D printers for Rapid Prototyping and Additive Manufacturing have been widely accepted by large and small-scale industries or by many hobbyists. Due to its nature of layer by layer addition of material, identifying de...
3D printers for Rapid Prototyping and Additive Manufacturing have been widely accepted by large and small-scale industries or by many hobbyists. Due to its nature of layer by layer addition of material, identifying defects between the layers can be a crucial strategy to determine the quality of a 3D printed product by carefully monitoring the layerwise process during part building. This kind of approach gives an advantage in the applications where 3D printing of products requires high customization without compromise on part quality. In this work, a low-cost camera is installed in an open 3D printer, and computer vision algorithms are used to implement an in-situ monitoring system. The defects can be evaluated by comparing the printed layer to the deposition path of the open ISO G-code. The G-code printing file is modified to introduce the image capture step after each layer. The value of the area of missing or exceeding material is returned to the user with the corresponding images. A decision can be made to abort the job in case of important defects to avoid unnecessary waste in material, time, and costs.
Background: Inactivating mutations of SMAD4 are frequent in metastatic colorectal carcinomas. In previous analyses, we were able to show that restoration of Smad4 expression in Smad4-deficient SW480 human colon carcin...
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Background: Inactivating mutations of SMAD4 are frequent in metastatic colorectal carcinomas. In previous analyses, we were able to show that restoration of Smad4 expression in Smad4-deficient SW480 human colon carcinoma cells was adequate to suppress tumorigenicity and invasive potential, whereas in vitro cell growth was not affected. Using this cellular model system, we searched for new Smad4 targets comparing nuclear subproteomes derived from Smad4 re-expressing and Smad4 negative SW480 cells. Methods: High resolution two-dimensional (2D) gel electrophoresis was applied to identify novel Smad4 targets in the nuclear subproteome of Smad4 re-expressing SW480 cells. The identified candidate protein Keratin 23 was further characterized by tandem affinity purification. Immunoprecipitation, subfractionation and immunolocalization studies in combination with RNAi were used to validate the Keratin 23-14-3-3 epsilon interaction. Results: We identified keratins 8 and 18, heat shock proteins 60 and 70, plectin 1, as well as 14-3-3 epsilon and gamma as novel proteins present in the KRT23-interacting complex. Co-immunoprecipitation and subfractionation analyses as well as immunolocalization studies in our Smad4-SW480 model cells provided further evidence that KRT23 associates with 14-3-3 epsilon and that Smad4 dependent KRT23 up-regulation induces a shift of the 14-3-3 epsilon protein from a nuclear to a cytoplasmic localization. Conclusion: Based on our findings we propose a new regulatory circuitry involving Smad4 dependent up-regulation of KRT23 (directly or indirectly) which in turn modulates the interaction between KRT23 and 14-3-3 epsilon leading to a cytoplasmic sequestration of 14-3-3 epsilon. This cytoplasmic KRT23-14-3-3 interaction may alter the functional status of the well described 14-3-3 scaffold protein, known to regulate key cellular processes, such as signal transduction, cell cycle control, and apoptosis and may thus be a previously unappreciated facet of t
Background - Sleep apnoea disorders affect a large proportion of patients with renal failure. However, it is unknown whether body composition and visceral adiposity predispose haemodialysis patients to sleep apnoea di...
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Background - Sleep apnoea disorders affect a large proportion of patients with renal failure. However, it is unknown whether body composition and visceral adiposity predispose haemodialysis patients to sleep apnoea disorders. Methods - Forty-one dialysis patients were divided in two groups according to the BMI score as;the Lean group (N=21, 1F/20M, BMI = 21.3 +/- 2.1) and the Overweight group (N=20, 9F/11M, BMI = 28.3 +/- 2.8). Sleep disturbances assessed by a full polysomnography (PSG), visceral adipose tissue (VAT), calculated by computed tomography, the quality of life, assessed by the SF-36, and the body composition, measured by DEXA. Results - None of the PSG parameters were different between the two groups. Only visceral adiposity was correlated significantly with sleep apnoea disorders. Conclusions - BMI and percent of total body fat do not seem to predispose for sleep apnoea disorders. Rather it is the increased fat deposition in abdominal area that plays the pivotal role.
J chains prepared from human serum IgA and human secretory IgA both contained 7.6% total carbohydrate. The monosaccharide compositions were similar and on the basis of a molecular weight of 26 000 each J chain contain...
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