Research on trust mechanism of supply chain finance under Industrial Internet embedded with blockchain.

In traditional supply chain finance, the financing of enterprise mainly relies on the credit segmentation of the core enterprise, resulting in a short trust transmission radius and poor financing ability. The development of Internet technology, while expanding financing channels, has also seen an increasing severity in issues such as information fraud and data breaches, which has further aggravated the trust crisis in supply chain finance. This paper integrates blockchain technology into the industrial internet platform and analyzes the applicability of both in empowering supply chain financial trust. Then a supply chain financial trust framework, which emphasizes information sharing, data security, and trust circulation, is proposed. Furthermore, combined with the theories of Funk-SVD and entropy value, this paper designs a global trust evaluation mechanism that facilitates the trust circulation in supply chain finance and proposes a recommendation algorithm for global trust. With the testing conducted using the Epinions dataset, it is found that the algorithm proposed in this paper has a strong data dimensionality reduction and concentration ability, especially for large sample data, it can obtain more accurate evaluation values with less space occupation, thus enhancing the trust circulation ability of supply chain finance. Finally, the paper puts forward specific policy recommendations for the implementation of the supply chain finance information mechanism, aiming to better improve the financing accessibility of enterprises in supply chain, particularly small and medium-sized enterprises.

Extralobar pulmonary sequestration with a cyst: a case report.

Extralobar pulmonary sequestration (EPS) is a congenital malformation. In contrast with intralobar sequestration, EPS located outside the normal lung tissue and with a distinct pleural covering. In the current case report, we present a rare case of EPS. To our knowledge, this is the first report of a cyst occurring within the EPS. A 17-year-old male patient presented with chest pain for 1 month. Computed tomography (CT) scan demonstrated a sharply circumscribed mass at the left side of the lower thoracic vertebrae. No aberrant vessel was observed on contrast-enhanced CT. The preoperative diagnosis was a posterior mediastinal tumor or EPS and surgical resection was recommended to the patient. During the operation, an extrapulmonary sequestration lobe was found in the left chest cavity. There was an aberrant artery connecting the sequestration lobe and the descending aorta. A cyst was located in the apex of the sequestration lobe. Surgical resection was performed via thoracoscopy. The postoperative histopathology confirmed an extrapulmonary sequestration combined with a cyst. The patient recovered successfully and was discharged on the sixth day postoperatively. He did not present with recurrent chest pain at the 6-month follow up. EPS should be considered when a posterior mediastinal conical mass is shown on chest CT.

LncRNA NKILA upregulation mediates oxygen glucose deprivation/re-oxygenation-induced neuronal cell death by inhibiting NF-κB signaling.

Oxygen glucose deprivation (OGD)/re-oxygenation (OGDR) induces severe injury to neuronal cells. The expression and potential function of NKILA (NF-κB Interacting LncRNA) in OGDR-treated neuronal cells were tested in this study. We show that OGDR induced NKILA upregulation to in-activate NF-κB signaling in SH-SY5Y cells and primary murine hippocampal neurons. Conversely, shRNA-mediated NKILA silencing almost reversed OGDR-induced NF-κB inhibition. OGDR-induced neuronal cell viability reduction, apoptosis and necrosis were largely attenuated by NKILA shRNA as well. Conversely, ectopic overexpression of NKILA by a lentiviral vector enhanced OGDR-induced SH-SY5Y cell death. For the mechanism study, we show that OGDR downregulated miR-103 and miR-107 to induce NKILA upregulation in neuronal cells. Transfection of miR-103 mimic or miR-107 mimic almost reversed OGDR-induced NKILA upregulation, NF-κB in-activation and SH-SY5Y cell death. Taken together, OGDR induces NKILA upregulation to in-activate NF-κB signaling, which mediates subsequent neuronal cell death. NKILA could be a novel therapeutic target of ischemic neuronal injury.

Potential Vaccine Targets against Rabbit Coccidiosis by Immunoproteomic Analysis.

The aim of this study was to identify antigens for a vaccine or drug target to control rabbit coccidiosis. A combination of 2-dimensional electrophoresis, immunoblotting, and mass spectrometric analysis were used to identify novel antigens from the sporozoites of Eimeria stiedae. Protein spots were recognized by the sera of New Zealand rabbits infected artificially with E. stiedae. The proteins were characterized by matrix-assisted laser desorption ionization time of flight mass spectrometry (MALDI-TOF/TOF-MS) analysis in combination with bioinformatics. Approximately 868 protein spots were detected by silver-staining, and a total of 41 immunoreactive protein spots were recognized by anti-E. stiedae sera. Finally, 23 protein spots were successfully identified. The proteins such as heat shock protein 70 and aspartyl protease may have potential as immunodiagnostic or vaccine antigens. The immunoreactive proteins were found to possess a wide range of biological functions. This study is the first to report the proteins recognized by sera of infected rabbits with E. stiedae, which might be helpful in identifying potential targets for vaccine development to control rabbit coccidiosis.

Pathological and ultrastructural observations and liver function analysis of Eimeria stiedai-infected rabbits.

To study the pathogenicity of Eimeria stiedai, sporulated oocysts were given orally to coccidian-free two-month-old New Zealand rabbits(1000±20g). After 30days, blood samples from the rabbit hearts were collected for routine blood tests, liver functions and four characteristics of blood coagulation. Additionally, specimens of the liver, bile duct and duodenum were collected to observe the changes in pathology and ultrastructure. E. stiedai severely restricted the growth and development of rabbits. Blood tests showed that glutamine transferase (GGT) and serum cholinesterase (ChE) were significantly different from the non-infected controls. Other extremely significant differences were observed in the biochemical indices of routine blood tests, liver function and four blood coagulation characteristics, indicating that the liver functions were significantly affected. Staining showed that, compared with the negative control group, the liver, bile duct and duodenum contained significant numbers of lesions, and organs and cell structures suffered severe damage in ultrastructure, which greatly affecting bodily functions. E. stiedai-infected rabbits model was successfully established, which might provide a theoretical basis for research on the pathogenesis of rabbit coccidia, and the diagnosis and prevention of coccidiosis in rabbits.

[Fine mapping of mutant gene related corneal opacity mouse with SNPs].

To further investigate the genetic mechanism of the mutant mice(B6-Co) with hereditary corneal opacity phenotype obtained by ENU-induced mutagenesis from B6 in previous study, SNP markers were used to map the mutant gene of B6-Co mice. F2 generation mice were bred by backcrossing (B6-CoPxD2 )F1 with D2 and the DNA samples of F2 mutant mice were extracted from the tails. Five SNP sites that showed differences between B6 and D2 strains nearby the located region on chromosome 13 were screened from MGI database. Five SNPs, PCR-RFLP and linkage analyses were carried out to map the mutant gene. The result showed that the mutant gene was located between 112 546 283~113 397 654 bp on chromosome 13. There are five identified genes including Map3k1 that is associated with eye morphogenesis and eyelid closure of mouse in this region. This suggests that Map3k1 is the most probable candidate mutant gene of B6-Co mice.