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The chicken industry, in which broiler chickens are bred, is the largest poultry industry in Taiwan. In a traditional poultry house, breeders must usually observe the health of the broilers in person on the basis of their breeding experience at regular times every day. When a breeder finds unhealthy broilers, they are removed manually from the poultry house to prevent viruses from spreading in the poultry house. Therefore, in this study, we designed and constructed a novel small removal system for dead chickens for Taiwanese poultry houses. In the mechanical design, this system mainly contains walking, removal, and storage parts. It comprises robotic arms with a fixed end and sweep-in devices for sweeping dead chickens, a conveyor belt for transporting chickens, a storage cache for storing chickens, and a tracked vehicle. The designed system has dimensions of approximately 1.038 × 0.36 × 0.5 m3, and two dead chickens can be removed in a single operation. The walking speed of the chicken removal system is 3.3 cm/s. In order to enhance the automation and artificial intelligence in the poultry industry, the identification system was used in a novel small removal system. The conditions of the chickens in a poultry house can be monitored remotely by using a camera, and dead chickens can be identified through deep learning based on the YOLO v4 algorithm. The precision of the designed system reached 95.24% in this study, and dead chickens were successfully moved to the storage cache. Finally, the designed system can reduce the contact between humans and poultry to effectively improve the overall biological safety.

Spark plasma sintering (SPS) is a fairly novel powder metallurgy (PM)-based process. Compared with more traditional PM processes, SPS technology provides greater sintering efficiency for the Ti-48Al alloy, due to its fast heating and cooling rates, combined with an applied pressure and electric field during the process. In this study, three fundamental processing parameters (i.e. sintering temperature, time and particle size) are investigated, and their effects on densification, hardness and phase transformations are studied. Three grain morphologies were found in the microstructures, present in different ratios in the samples, depending on the sintering parameters. A model is proposed to explain the (α 2 ) grain-phase growth and the transformation of two types (fine and coarse) of lamellar structural development. The pore configurations (i.e. size and quantity) are examined, and their interactions with the phases, which suggest the phase-formation sequence and sintering state, are also discussed.

Pulmonary artery intimal sarcoma is a rare disorder arising from the intima of the pulmonary artery. Histopathology reveals that it is a tumour cell of mesenchymal origin. The signs and symptoms include chronic shortness of breath and other features of right ventricular failure, which mimic chronic pulmonary thromboembolism. The definitive diagnosis can rarely be made based on the symptoms and signs alone, and other investigations including echocardiography, computed tomography, magnetic resonance imaging (MRI), and positron emission tomography (PET) are often required. The gold standard for diagnosis is tissue biopsy. The mainstay for treatment is surgery, and complete surgical resection with endarterectomy provides survival benefit. According to recent evidences, however, multimodal treatment provides better survival outcomes than monotherapy such as surgery alone. Despite the newer upcoming treatment strategies, patients with pulmonary intimal sarcoma continue to have a poor prognosis. We present a case of pulmonary artery intimal sarcoma and review the literature associated with the disease. Pulmonary artery intimal sarcoma is a rare disorder arising from the intimal wall of the pulmonary artery. As the tumour decreases the lumen of the pulmonary artery, patients usually present with symptoms and signs of right ventricular failure, and it has often been misdiagnosed as pulmonary thromboembolism. In this report, we present the case of a patient in whom the diagnosis of pulmonary artery sarcoma was made promptly and surgery was performed soon after.

Asparaginyl endopeptidase （AEP） is an endo/lysosomal cysteine endopeptidase with a preference for an asparagine residue at the P1 site and plays an important role in the maturation of toll-like receptors 3/7/9. AEP is known to undergo autoproteolytic maturation at acidic pH for catalytic activation. Here, we describe crystal structures of the AEP proenzyme and the mature forms of AEP. Structural comparisons between AEP and caspases revealed similarities in the composition of key residues and in the catalytic mechanism. Mutagenesis studies identified N44, R46, H150, E189, C191, S217/S218 and D233 as residues that are essential for the cleavage of the peptide substrate. During maturation, autoproteolytic cleavage of AEP＇s cap domain opens up access to the active site on the core domain. Unexpectedly, an intermediate autoproteolytic maturation stage was discovered at approximately pH 4.5 in which the partially activated AEP could be reversed back to its proenzyme form. This unique feature was confirmed by the crystal structure of AEPpH4.s （AEP was matured at pH 4.5 and crystallized at pH 8.5）, in which the broken peptide bonds were religated and the structure was transformed back to its proenzyme form. Additionally, the AEP inhibitor cystatin C could be digested by the fully activated AEP, but could not be digested by activated cathepsins. Thus, we demonstrate for the first time that cystatins may regulate the activity of AEP through substrate competition for the active site.

Restenosis is resulted from the proliferation and migration of vascular smooth muscle cells (VSMCs) from the arterial media into the intima within the vessel lumen following percutaneous transluminal coronary angioplasty (PTCA). OSU-03012, a synthetic compound (2-amino- N -{4-[5-(2-phenanthrenyl)-3-(trifluoromethyl)-1 H -pyrazol-1-yl]-phenyl} acetamide) acting as a PDK-1 inhibitor, is used as an apoptosis-promoting anticancer drug. However, whether OSU-03012 can inhibit VSMC proliferation and migration following PTCA remains unclear. In this study, we used A10 smooth muscle cells cultured in 10% FBS for stimulating proliferation and evaluated the inhibitory effects of OSU-03012 on cell proliferation and migration. The data demonstrated that OSU-03012 dose-dependently inhibited A10 cell proliferation examined by Trypan blue, MTT and morphological alteration assays, and inhibited the levels of proliferation-related proteins, proliferating cell nuclear antigen (PCNA), phosphorylated ERK examined by western blotting. Additionally, 10 μM OSU-03012 also enhanced apoptosis examined using DAPI assay by regulating apoptosis-related proteins. Furthermore, compared with the control group, A10 cells treated with 10 μM OSU-03012 showed a lower number of migrating cells examined by Boyden Chamber assay, and a dose-dependently reduced NF k B-dependent and interferon-stimulated response element (ISRE) promoter luciferase activities, implying the anti-migration and anti-inflammation effects of OSU03012. Taken together, this study provides insights into the pharmacological mechanisms of OSU-03012 in preventing smooth muscle cell proliferation, migration, and inflammation supporting the novel discovery of OSU-03012 as an adjuvant therapy for balloon injury-induced restenosis.

Sighting and binding of double-stranded DNA （ds- DNA） by a sensor in the cytoplasm trigger the activation of the immune-surveillance pathways [1]. The crystal structure of absent in melanoma 2 （AIM2） bound with DNA conclusively defines the role of AIM2 as a sensor in the innate immune system [2]. AIM2 belongs to the PYHIN family of proteins and contains a pyrin domain （PYD） followed by a hematopoietic interferon-inducible nuclear protein （HIN） domain （Figure 1A）. AIM2 binds DNA via the HIN domain and recruits the adaptor pro- tein apoptosis-associated speck-like protein containing a caspase recruitment domain （ASC） via the PYD. ASC in turn recruits caspase-1 via CARD-CARD interaction, resulting in the formation of inflammasomes comprised of AIM2, ASC and caspase-1. The molecular crowding of the AIM2 inflammasome ensures the proteolysis and transactivation of caspase-1. Activated caspase-1 cleaves pro-IL-1 ]3 and pro-IL-18 into their mature proinflamma- tory forms [3, 4]. The termination of inflammatory responses originated from inflammasomes can be accomplished by employing naturally occurring dominant-negative antagonists [4]. Dominant-negative proteins are similar to their canoni- cal counterparts except for a missing effector domain, so that they cannot relay the signals any further. They out- compete their canonical counterparts for ligands or bind- ing sites and thus block the downstream signal transduc- tion. Such regulation is essential for maintaining cellular homeostasis. To regulate inflammasome activation, mice have evolved a strategy that has so far not been discov- ered in humans. Mice use the H1N-only protein, p202, to sequester cytoplasmic dsDNA and render it unavailable for its canonical sensor, AIM2 [4]. p202 contains two HIN domains （HINa and H1Nb）, but lacks the PYD （Fig- ure 1A）. Therefore, p202 is unable to recruit the adaptor ASC, and its binding to DNA results in the termination of inflammasome signaling. The significance of p202 in the regulation of the innate immune responses is exem- plified by the fact that dysregulation of p202 function hasbeen linked to increased susceptibility to systemic lupus erythematosus [5]. To more clearly understand the mechanism of inhibi- tion of AIM2-mediated signaling by p202, it is essential to solve the structure of p202 in complex with DNA and compare it with that of AIM2 complexed with DNA. p202 has so far only been detected in mice. To compare the structure of AIM2 and p202 from the same species, we first solved the structure of the H1N domain of mu- rine AIM2 （mAIM2） in complex with dsDNA to 2.23 A resolution （Supplementary information, Table S1）. Although a 12-base pair （bp） long dsDNA was used for the crystallization, the HIN domain of mAIM2 seems to have lined up the DNA oligonucleotides end to end, gen- erating an appearance of a long and contiguous stretch of B-form DNA with putative major and minor grooves. As expected, the overall structure of the H1N domain of mAIM2 （Figure 1B） closely mirrors the structure of its human counterpart [2] （Supplementary information, Fig- ure S 1）. Minor deviations are observed at the N-terminus and in the loop regions. The surface electrostatic poten- tial distribution is similar, implying that the mechanism of tethering dsDNA is similar between human and mouse AIM2. The HIN domain of AIM2 consists of two oligonucle- otide/oligosaccharide （OB） folds [6] linked via a flexible linker （Figure 1B）. The proximal and distal OB folds are referred to as OB1 and OB2, respectively. Similar to the human ortholog, mAIM2 uses the helix-loop-helix motif located in the linker to engage DNA （Figure 1C）. Specifically, a short helix containing two turns is inserted horizontally to the vertical axis of the DNA spiral （Figure 1C）. Amino acids from the loop connecting helices ul and a2, and from helix ct2 interact with the major groove （Figure 1C）. A couple of interactions between OB2 and the DNA backbone are also observed. Residues N244, N245, K248, R249, R251, R255, K258, 0262 K273,

Organic electronic materials and processing techniques have attracted considerable attention for developing organic thin-film transistors (OTFTs), since they may be patterned on flexible substrates which may be bent into a variety of shapes for applications such as displays, smart cards, solar devices and sensors Various fabrication methods for building pentacene-based OTFTs have been demonstrated. Traditional vacuum deposition and vapor deposition methods have been studied for deposition on plastic and paper, but these are unlikely to scale well to large area printing. Researchers have developed methods for processing OTFTs from solution because of the potential for low-cost and large area device manufacturing, such as through inkjet or offset printing. Most methods require the use of precursors which are used to make pentacene soluble, and these methods have typically produced much lower carrier mobility than the best vacuum deposited devices. We have investigated devices built from solution-processed pentacene that is locally crystallized at room temperature on the polymer substrates. Pentacene crystals grown in this manner are highly localized at pre-determined sites, have good crystallinity and show good carrier mobility, making this an attractive method for large area manufacturing of semiconductor devices.

Uch37 is a de-ubiquitinating enzyme that is activated by Rpn13 and involved in the proteasomal degradation of proteins. The full-length Uch37 was shown to exhibit low iso-peptidase activity and is thought to be auto-inhibited. Structural comparisons revealed that within a homo- dimer of Uch37, each of the catalytic domains was blocking the other＇s ubiquitin （Ub）-binding site. This blockage likely prevented Ub from entering the active site of Uch37 and might form the basis of auto-inhibition. To understand the mode of auto-inhibition clearly and shed light on the activation mechanism of Uch37 by Rpn13, we investigated the Uch37-Rpn13 complex using a combi- nation of mutagenesis, biochemical, NMR, and small- angle X-ray scattering （SAXS） techniques. Our results also proved that Uch37 oligomerized in solution and had very low activity against the fluorogenic substrate ubi- quitin-7-amino-4-methylcoumarin （Ub-AMC） of de-ubiq- uitinating enzymes. Uch37AHb＇Hc＇KEKE, a truncation removal of the C-terminal extension region （residues 256- 329） converted oligomeric Uch37 into a monomeric form that exhibited iso-peptidase activity comparable to that of a truncation-containing the Uch37 catalytic domain only. We also demonstrated that Rpn13C （Rpn13 residues 270- 407） could disrupt the oligomerization of Uch37 by sequestering Uch37 and forming a Uch37-Rpn13 com- plex. Uch37 was activated in such a complex, exhibiting 12-fold-higher activity than Uch37 alone. Time-resolved SAXS （TR-SAXS） and FRET experiments supported the proposed mode of auto-inhibition and the activation mechanism of Uch37 by Rpn13. Rpn13 activated Uch37 by forming a 1：1 stoichiometric complex in which the active site of Uch37 was accessible to Ub.

Separating molecules or ions with sub-Angstrom scale precision is important but technically challenging. Achieving such a precise separation using membranes requires Angstrom scale pores with a high level of pore size uniformity. Herein, we demonstrate that precise solute-solute separation can be achieved using polyamide membranes formed via surfactant-assembly regulated interfacial polymerization (SARIP). The dynamic, self-assembled network of surfactants facilitates faster and more homogeneous diffusion of amine monomers across the water/hexane interface during interfacial polymerization, thereby forming a polyamide active layer with more uniform sub-nanometre pores compared to those formed via conventional interfacial polymerization. The polyamide membrane formed by SARIP exhibits highly size-dependent sieving of solutes, yielding a step-wise transition from low rejection to near-perfect rejection over a solute size range smaller than half Angstrom. SARIP represents an approach for the scalable fabrication of ultra-selective membranes with uniform nanopores for precise separation of ions and small solutes. Separating molecules or ions with sub-Angstrom scale precision is important but technically challenging. Here, the authors demonstrate that precise solute-solute separation can be achieved using polyamide membranes formed via surfactant-assembly regulated interfacial polymerization.

FOLFOX (5-fluorouracil, leucovorin, and oxaliplatin), a 5-fluorouracil (5-FU)-based chemotherapy regimen, is one of most common therapeutic regimens for colorectal cancer. However, intestinal mucositis is a common adverse effect for which no effective preventive strategies exist. Moreover, the efficacy and the safety of fecal microbiota transplants (FMT) in cancer patients treated with anti-neoplastic agents are still scant. We investigated the effect of FMT on FOLFOX-induced mucosal injury. BALB/c mice implanted with syngeneic CT26 colorectal adenocarcinoma cells were orally administered FMT daily during and two days after five-day injection of FOLFOX regimen for seven days. Administration of FOLFOX significantly induced marked levels of diarrhea and intestinal injury. FMT reduced the severity of diarrhea and intestinal mucositis. Additionally, the number of goblet cells and zonula occludens-1 decreased, while apoptotic and NF-κB-positive cells increased following FOLFOX treatment. The expression of toll-like receptors (TLRs), MyD88, and serum IL-6 were upregulated following FOLFOX treatment. These responses were attenuated following FMT. The disrupted fecal gut microbiota composition was also restored by FMT after FOLFOX treatment. Importantly, FMT did not cause bacteremia and safely alleviated FOLFOX-induced intestinal mucositis in colorectal cancer-bearing mice. The putative mechanism may involve the gut microbiota TLR-MyD88-NF-κB signaling pathway in mice with implanted colorectal carcinoma cells.