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Pancreatic cancer remains one of the most challenging malignancies to date and is associated with poor survival. Cancer-associated fibroblasts (CAFs) are key stromal cells in the tumor microenvironment (TME) that play a crucial role in tumor progression in pancreatic cancer. Thus, uncovering the key genes involved in CAF progression and determining their prognostic value is critically important. Herein, we report our discoveries in this research area. Analysis of The Cancer Genome Atlas (TCGA) dataset and investigation of our clinical tissue samples indicated that COL12A1 expression was aberrantly highly expressed in pancreatic cancer. Survival and COX regression analyses revealed the significant clinical prognostic value of COL12A1 expression in pancreatic cancer. COL12A1 was mainly expressed in CAFs but not in tumor cells. This was verified with our PCR analysis in cancer cells and CAFs. The knocking down of COL12A1 decreased the proliferation and migration of CAFs and down-regulated the expression of CAF activation markers actin alpha 2 (ACTA2), fibroblast activation protein (FAP), and fibroblast-specific protein 1 (FSP1). Meanwhile, the interleukin 6 (IL6), CXC chemokine Ligand-5 (CXCL5), and CXC chemokine Ligand-10 (CXCL10) expressions were inhibited, and the cancer-promoting effect was reversed by COL12A1 knockdown. Therefore, we demonstrated the potential prognostic and target therapy value of COL12A1 expression in pancreatic cancer and elucidated the molecular mechanism underlying its role in CAFs. The findings of this study might provide new opportunities for TME-targeted therapies in pancreatic cancer.

We know that society is the sum of human relations. Similarly, in the insurance industry, we should also consider the impact of various factors on the decision-making of the insurance company. The main purpose of this paper is to obtain the optimal investment-reinsurance strategy of the insurer when it is closer to the real economic environment and considering the relationship between insurance market and financial market. In addition, this paper assumes that the risk model considered by the insurance company is uncertain. So based on the risk model of ambiguity aversion, the optimal problem is found and the corresponding HJB equation is derived by using the relevant knowledge and theories of mathematics, actuarial science, economics and probability theory. Finally, this paper will give some suggestions on how to make the company more satisfied with reinsurance and investment strategy.

Pancreatic cancer (PC) is one of the most lethal malignant tumors and has the lowest survival rate due to early metastasis and drug resistance. Exosomes derived from bone marrow mesenchymal stem cells (BM-MSCs) have emerged as crucial regulators of the progression of various tumors. These vesicles contain abundant circRNAs that have important biological functions. This study aimed to elucidate the role of exosomal circRNAs in PC progression. In this study, we successfully isolated BM-MSCs from human bone marrow based on their surface marker expression and osteogenic and adipogenic differentiation potential. We found that BM-MSC-derived exosomes significantly reduced the invasion, migration, and proliferation of PC cells, as well as tumor stemness. According to whole-transcriptome resequencing and clustering heat map analysis, we identified the key molecule circ_0030167 and miR-338-5p, its downstream target. We revealed that circ_0030167 mainly regulates miR-338-5p, enhances Wif1 expression, and inhibits the Wnt8/β-catenin pathway, thereby inhibiting the stemness of PC cells and tumor progression. Overall, BM-MSC exosomal circ_0030167 contributes to the progression and stemness of PC cells via the miR-338-5p/wif1/Wnt 8/β-catenin axis. Our study provides a new perspective for the treatment of PC.

To explore whether miR-573 can suppress pancreatic cancer cell proliferation, migration, and invasion by targeting TSPAN1. The expression of miR-573 and TSPAN1 in pancreatic cancer tissues and cells lines was analyzed using RT-qPCR. The human pancreatic cancer cell line PANC‑1 was transfected with miR-573 mimic, pcDNA3.1-TSPAN1, or genOFFTM st-h-TSPAN1. The effects of miR-573 and TSPAN1 on cell proliferation, colony formation, migration, and invasion were analyzed by CCK‑8, colony formation, transwell migration, and invasion assay, respectively. Target genes of miR-573 were screened using bioinformatics tools and confirmed by dual-luciferase reporter assay and real-time PCR. The effects of miR-573 in vivo were observed using tumor xenografts. We found that miR-573 is downregulated and TSPAN1 is upregulated in pancreatic cancer tissues and cells lines. Function assays demonstrated that overexpression of miR-573 inhibited cell proliferation, colony formation, migration, and invasion of pancreatic cancer cells, as well as suppressing tumor growth in vivo. Target genes of miR-573 were predicted using bioinformatics tools and confirmed by dual-luciferase reporter assay and RT-qPCR or western blotting. Downregulation of TSPAN1 also inhibited cell proliferation, colony formation, migration, and invasion of pancreatic cancer cells. Furthermore, overexpression of TSPAN1 attenuated miR-573-induced inhibition of pancreatic cancer cell proliferation and migration. Our findings indicated that miR-573 suppresses pancreatic cancer cell proliferation, migration, and invasion through targeting TSPAN1. TSPAN1 targeted by miR-573 might be a potential therapeutic target for clinical treatment of pancreatic cancer.

Islet transplantation is considered as one of the promising treatment options for curing diabetes. However, the extracellular matrix (ECM) is destroyed during the process of islet isolation and extraction, which leads to decreased islet activity

The biomimetic pancreatic microenvironment improves the differentiation efficiency and function of human embryonic stem cell-derived β-cells (SC-β cells). Thus, a laminin subunit alpha 2-gelatin methacrylate (LAMA2-GelMA) hybrid hydrogel as a bionics carrier for the formation and maturation of endocrine lineage was developed in our research, based on pancreas proteomics analysis of postnatal mice. Pancreatic endocrine cells cultured on the hybrid hydrogel in vitro, which was composed of 0.5 μg/mL LAMA2 protein and 4% GelMA, the expression of transcription factors (TFs), including NKX6.1, NKX6.2, and NEUROD1 were upregulated. Single-cell transcriptomics was performed after LAMA2 knockdown during the early differentiation of pancreatic progenitor (PP) cells, a marked decrease in the forkhead box protein A2 (FOXA2

Islet transplantation has poor long-term efficacy because of the lack of extracellular matrix support and neovascularization; this limits its wide application in diabetes research. In this study, we develop a 3D-printed islet organoid by combining a pancreatic extracellular matrix (pECM) and hyaluronic acid methacrylate (HAMA) as specific bioinks. The HAMA/pECM hydrogel was validated in vitro to maintain islet cell adhesion and morphology through the Rac1/ROCK/MLCK signaling pathway, which helps improve islet function and activity. Further, in vivo experiments confirmed that the 3D-printed islet-encapsulated HAMA/pECM hydrogel increases insulin levels in diabetic mice, maintains blood glucose levels within a normal range for 90 days, and rapidly secretes insulin in response to blood glucose stimulation. In addition, the HAMA/pECM hydrogel can facilitate the attachment and growth of new blood vessels and increase the density of new vessels. Meanwhile, the designed 3D-printed structure was conducive to the formation of vascular networks and it promoted the construction of 3D-printed islet organoids. In conclusion, our experiments optimized the HAMA/pECM bioink composition and 3D-printed structure of islet organoids with promising therapeutic effects compared with the HAMA hydrogel group that can be potentially used in clinical applications to improve the effectiveness and safety of islet transplantation in vivo. STATEMENT OF SIGNIFICANCE: The extraction process of pancreatic islets can easily cause damage to the extracellular matrix and vascular system, resulting in poor islet transplantation efficiency. We developed a new tissue-specific bioink by combining pancreatic extracellular matrix (pECM) and hyaluronic acid methacrylate (HAMA). The islet organoids constructed by 3D printing can mimic the microenvironment of the pancreas and maintain islet cell adhesion and morphology through the Rac1/ROCK/MLCK signaling pathway, thereby improving islet function and activity. In addition, the 3D-printed structures we designed are favorable for the formation of new blood vessel networks, bringing hope for the long-term efficacy of islet transplantation.

Bentonite was modified with cetyltrimethylammonium bromide (CTAB). The organically modified bentonite (OMB) was used to remove phenol from aqueous solution, the microstructural changes were characterized by X-ray diffraction (XRD) and scanning electronic microscopy (SEM), and phenol adsorption kinetic was obtained using batch adsorption test results. The results indicated that the rate of adsorption of phenol onto the OMB was positively correlated with the initial concentration, and the maximum adsorption capacity was found to be 10.1 mg/g at the initial concentration of 150 mg/L at 25 °C and pH 10. The investigations of adsorption kinetics models showed that the adsorption kinetic was better reflected by the pseudo-second-order kinetic model. Furthermore, the properties of the OMB samples with different adsorption times were obtained by SEM and XRD. The statistic analysis revealed that the pore diameter of the OMB samples decreased with the increasing adsorption time and gradually reached equilibrium.

Qingsong Guo,1,2,* Yuhua Lu,1,* Yan Huang,1,2 Yibing Guo,2 Shajun Zhu,1,2 Qiuqiang Zhang,1 Donghui Zhu,3 Zhiwei Wang,1 Jia Luo4 1Department of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Nantong University, Nantong, 226001, People’s Republic of China; 2Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong, 226001, People’s Republic of China; 3Nantong University Medical School, Nantong, 226001, People’s Republic of China; 4Department of Pharmacy, Affiliated Hospital of Nantong University, Nantong, 226001, People’s Republic of China*These authors contributed equally to this workCorrespondence: Jia LuoDepartment of Pharmacy, Affiliated Hospital of Nantong University, Xi Si Road, Nantong, 226001, People’s Republic of ChinaEmail tdfylj@163.comZhiwei WangDepartment of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Nantong University, Xi Si Road, Nantong, 226001, People’s Republic of ChinaEmail wzw3639@163.comObjective: Exosomes have emerged as potential tools for the differentiation of induced pluripotent stem cells (iPSCs) into insulin-producing cells (IPCs). Exosomal microRNAs are receiving increasing attention in this process. Here, we aimed at investigating the role of exosomes derived from a murine pancreatic β-cell line and identifying signature exosomal miRNAs on iPSCs differentiation.Methods: Exosomes were isolated from MIN6 cells and identified with TEM, NTA and Western blot. PKH67 tracer and transwell assay were used to confirm exosome delivery into iPSCs. qRT-PCR was applied to detect key pancreatic transcription gene expression and exosome-derived miRNA expression. Insulin secretion was determined using FCM and immunofluorescence. The specific exosomal miRNAs were determined via RNA-interference of Ago2. The therapeutic effect of 21 day-exosome-induced IPCs was validated in T1D mice induced by STZ.Results: iPSCs cultured in medium containing exosomes showed sustained higher expression of MAFA, Insulin1, Insulin2, Isl1, Neuroud1, Nkx6.1 and NGN3 compared to control iPSCs. In FCM analysis, approximately 52.7% of the differentiated cells displayed insulin expression at the middle stage. Consistent with the gene expression data, immunofluorescence assays showed that Nkx6.1 and insulin expression in iPSCs were significantly upregulated. Intriguingly, the expression of pancreatic markers and insulin was significantly decreased in iPSCs cultured with siAgo2 exosomes. Transplantation of 21 day-induced IPCs intoT1D mice efficiently enhanced glucose tolerance and partially controlled hyperglycemia. The therapeutic effect was significantly attenuated in T1D mice that received iPSCs cultured with siAgo2 exosomes. Of the seven exosomal microRNAs selected for validation, miR-706, miR-709, miR-466c-5p, and miR-423-5p showed dynamic expression during 21 days in culture.Conclusion: These data indicate that differentiation of exosome-induced iPSCs into functional cells is crucially dependent on the specific miRNAs encased within exosomes, whose functional analysis is likely to provide insight into novel regulatory mechanisms governing iPSCs differentiation into IPCs.Keywords: diabetes, exosomes, iPSCs, differentiation, miRNA, insulin

Type 1 diabetes mellitus (T1DM), as an autoimmune deficiency disease, is associated with an absolute deficiency of insulin subject to islet β-cell destruction. Insulin-producing cells (IPCs) differentiated from induced pluripotent stem cells are an ideal replacement origin of β-cells, which can be applied for cell transplantation therapies in T1DM. At present, more strategies focus on inducing and differentiating to obtain IPCs; however, the unsatisfactory differentiation efficiency and the lack of ideal carriers for in vivo transplantation limited their application. It is necessary to consider the cell microenvironment by constructing a biomimetic niche to improve the differentiation and transplantation efficiency. The main components of the extracellular matrix derived from pancreatic (the niche of β-cells) decellularization were retained, which could provide the ideal extracellular microenvironment for IPCs. In this research, a hydrogel prepared with alginate (Alg) and the pancreatic extracellular matrix (pECM) was assessed for the beneficial outcomes on encapsulated IPCs. The results showed that pECM/Alg improved the differentiation efficiency and promoted insulin secretion and the expression of insulin-related genes as well. Besides, pECM/Alg-encapsulated IPCs exhibited obvious biocompatibility in vivo, which can prolong the transplantation effect and hypoglycemic function by reducing the inflammatory reaction. RNA-seq indicated that the PI3K/Akt pathway may be related to the improvement of the differentiation efficiency and function of IPCs. In general, the pECM/Alg hydrogel provides an ideal biomimetic microenvironment for IPCs and is suitable for in vivo transplantation.

BackgroundHepatocellular carcinoma (HCC) is one of the world’s most lethal malignant tumors with a poor prognosis. Growing evidence has been demonstrating that immune-related long non-coding RNAs (lncRNAs) are relevant to the tumor microenvironment (TME) and can help assess the effects of immunotherapy and evaluate one’s prognosis. This study aims to identify an immune-related lncRNA signature for the prospective assessment of the immunotherapy and prognosis in HCC.MethodWe downloaded HCC RNA-seq data and clinical information from The Cancer Genome Atlas (TCGA) project database. We first used ESTIMATE to evaluate the TME. Then, we conducted a cox regression analysis to construct a prognostic signature and the riskScore. We then applied the univariate Cox regression, multivariate Cox regression, principal components analysis (PCA), receiver operating characteristic (ROC) curve, and stratification analyses to confirm our previous assessments. Afterward, we employed a gene set enrichment analysis (GSEA) to explore the biological processes and pathways. Besides, we used CIBERSORT to estimate the abundance of tumor-infiltrating immune cells (TIICs). Furthermore, we investigated the relationship between the immune-related lncRNA signature and immune checkpoint genes. Finally, we used the quantitative real-time polymerase chain reaction (qRT-PCR) assays to demonstrate the expression of the six lncRNAs.ResultsWe identified six immune-related lncRNAs — MSC-AS1, AC145207.5, SNHG3, AL365203.2, AL031985.3, NRAV — which show the ability to stratify patients into high-risk and low-risk groups with significantly different survival rates. The univariate Cox regression, multivariate Cox regression, ROC, and stratification analyses confirmed that the immune-related six-lncRNA signature was a novel independent prognostic factor in HCC patients. The high-risk group and low-risk group illustrated contrasting distributions in PCA. The GSEA suggested that the immune-related six-lncRNA signature was involved in the immune-related biological processes and pathways. Besides, the immune-related six-lncRNA signature was associated with the infiltration of immune cells. Furthermore, it was linked with the expression of critical immune genes and could predict immunotherapy’s clinical response. Finally, the qRT-PCR demonstrated that the six lncRNAs were significantly differentially expressed in HCC cell lines and normal hepatic cell lines.ConclusionIn summary, we identified an immune-related six-lncRNA signature that can predict the outcomes, immune cell infiltration, and immunotherapy response in patients with hepatocellular carcinoma.

The energy efficiency and stability of wireless sensor networks (WSNs) have always been a hot issue in the research. Clustering is a typical architecture for WSNs, and cluster heads (CHs) play a vital role. Unreasonable CH selection causes a lot of energy consumption. In this paper, we propose a competition-based unequal clustering multihop approach (CUCMA). CHs are selected by competition. First, the cluster radius (CR) of a node is calculated according to the distance to base station (BS). Then, CR is resized based on the number of around nodes. Only the nodes with high residual energy and appropriate distances to the selected CHs maybe become CHs, which are usually closer to the surrounding nodes. CUCMA and four related approaches are simulated in different scenarios. The results are analyzed, and it is proved that CUCMA balances the energy consumption of the CHs and reduces the energy consumption of the whole networks, thus leading to prolong the lifetime of WSNs.

Background. An increasing number of systematic reviews/meta-analyses (SRs/MAs) of clinical trials have begun to investigate the effects of traditional Chinese medicine (TCM) nursing in patients with stroke. To systematically appraise and synthesize these results, we conducted an overview of SRs/MAs. Methods. Eight databases from their inception to April 2020 were searched to include all SRs/MAs on TCM nursing for stroke. Methodological quality assessment was performed using Assessing the Methodological Quality of Systematic Reviews 2 (AMSTAR-2) and evidence quality assessment was performed using the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE). Results. Eleven SRs/MAs regarding TCM nursing for stroke were included. The assessments with AMSTAR-2 indicated that the methodological quality of all included SRs/MAs was critically low. According to the evaluation results of GRADE, 10 (40%) outcomes were rated as critically low-quality evidence, 7 (28%) low-quality evidence, and 8 (32%) moderate-quality evidence. Descriptive analysis results showed that TCM nursing was effective for stroke. Conclusions. All included SRs/MAs suggested positive findings of TCM nursing for stroke, but the credibility of the results is limited. Studies with methodologically rigorous and adequately powered are still needed in this field.

Cancer cells have developed chemoresistance and have improved their survival through the upregulation of autophagic mechanisms that protect mitochondrial function. Here, we report that the traditional Chinese anticancer agent tubeimoside I (Tub), which is a potent inhibitor of autophagy, can promote mitochondria-associated apoptosis in lung cancer cells. We found that Tub disrupted both mitochondrial and lysosomal pathways. One of its mechanisms was the induction of DRP1-mediated mitochondrial fragmentation. Another mechanism was the blocking of late-stage autophagic flux via impairment of lysosomal acidification through V-ATPase inhibition; this blocks the removal of dysfunctional mitochondria and results in reactive oxygen species (ROS) accumulation. Excessive ROS accumulation causes damage to lysosomal membranes and increases lysosomal membrane permeability, which leads to the leakage of cathepsin B. Finally, cathepsin B upregulates Bax-mediated mitochondrial outer membrane permeability and, subsequently, cytosolic cytochrome C-mediated caspase-dependent apoptosis. Thus, the cancer cell killing effect of Tub is enhanced through the formation of a positive feedback loop. The killing effect of Tub on lung cancer cells was verified in xenografted mice. In summary, Tub exerts a dual anticancer effect that involves the disruption of mitochondrial and lysosomal pathways and their interaction and, thereby, has a specific and enhanced killing effect on lung cancer cells.

Type 1 diabetes mellitus is a serious disease comprising approximately 10% of all diabetes cases, and the global incidence of type 1 diabetes mellitus is steadily rising without any promise of a cure in the near future. Although islet transplantation has proven to be an effective means of treating type 1 diabetes mellitus and promoting insulin independence in patients, its widespread implementation has been severely constrained by instances of post-transplantation islet cell death, rejection, and severe adverse immune responses. Islet encapsulation is an active area of research aimed at shielding implanted islets from immunological rejection and inflammation while still allowing for effective insulin and nutrient exchange with donor cells. Given their promising physical and chemical properties, hydrogels have been a major subject of focus in the field of islet transplantation and encapsulation technology, offering promising advances towards immunologically privileged islet implants. The present review therefore summarizes the current state of research regarding the use of hydrogels in the context of islet transplantation, including both natural molecular hydrogels and artificial polymer hydrogels, with the goal of understanding the current strengths and weaknesses of this treatment strategy.

Pancreas transplantation is considered as a promising therapeutic option with the potential to cure diabetes. However, efficacy of current clinical transplantation is limited by the donor organ. With regard to creating a functional pancreas-tissue equivalent for transplantation, vascularization remains a large obstacle. To enhance the angiogenic properties of pancreatic decellularized scaffold, surface modification of the vasculature was used to promote endothelialization efficiency. In this study, an endothelialized pancreatic decellularized scaffold was obtained through heparin modification under mild conditions. The immobilization of heparin was performed through 1-ethyl-3–(3-dimethylaminopropyl)-carbodiimide and N-Hydroxysuccinimide. The morphology, ultra-structure and porosity of the heparinized scaffold were characterized by toluidine blue staining, scanning electron microscope and infrared spectrum. The adhesion, proliferation and angiogenesis of human umbilical vein endothelial cells on heparin-pancreatic decellularized scaffold were also researched in vitro. In vivo transplantation was also performed to observe the location of human umbilical vein endothelial cells and the formation of new blood vessel, which exhibited significant differences with pancreatic decellularized scaffold group (p

This paper analyzes the shortcomings of two setting methods which is commonly used in security chip communication rate, and proposes an improved setting method. The basic communication rate instruction parameters are set in a security chip for setting the communication rate in different communication modes. The interface device sends the communication rate instructions to the security chip. The security chip executes the communication rate instructions so as to complete the setting of the communication rate. This method can switch the communication mode freely, so it can be applied to diversified application scenarios.

This study investigated the emission and diffusion of hydrogen sulfide (H2S), as one of the odorous gases generated from landfills, in a municipal solid waste landfill of a south Chinese city. To this end, the flux of the H2S emissions in the working area of the landfill and its diffusion in the surrounding area were measured. The diffusion of the H2S was simulated at different wind speeds, wind directions, bare working areas of the landfill, heights of the landfill, and angles between the wind direction and the long side of the working area. The results indicated that the concentration of the H2S around the monitoring point ranged from 0 to 60 µg/m3, and the simulated data were consistent with the measured results. At a uniform wind direction, the pollution range of the H2S was narrow. Furthermore, with an increase in the height of the waste dump, the concentration of the H2S decreased in the working area but rose in the surrounding area. Notably, when the angle between the long side of the working area and the wind direction was 0°, the H2S largely spread along the extension cord of the long side of the working area. When the angle increased to 90°, the influence range of the H2S extended significantly. The working area in the landfill site should be regulated based on the monitored data to reduce the effect of this harmful gas on the living environment, and the health of the landfill staff and nearby residents.

PAQR3 is a tumor suppressor in breast cancer and its expression regulation mechanism has not been well elucidated. In this study, we found that PAQR3 expression was downregulated in breast cancer tissues, and the downregulation of PAQR3 expression was found to be significantly associated with aberrant methylation of the gene promoter. Methylation‑specific PCR showed that hypermethylation of the PAQR3 gene was observed in 71.8% of the breast cancers, whereas it was found in only 28.2% of the corresponding non‑tumor tissues. Moreover, we found that the PAQR3 promoter methylation status was related to lymph node metastasis (P=0.01). In addition, overexpression of PAQR3 inhibited breast cancer cell invasion and growth. Furthermore, PAQR3 expression was restored in MCF‑7 cells after treatment with the demethylating agent, 5-aza-2'-deoxycytidine, and the effect of demethylation induced invasion and proliferation suppression of MCF‑7 cells. Collectively, our results suggested that the aberrant methylation of PAQR3 underlies its downregulation in breast cancer and our data indicated that epigenetic silencing of PAQR3 gene expression by promoter hypermethylation may play an important role in breast cancer.

Anaplasma phagocytophilum is an obligate intracellular bacterium that causes febrile illness in humans and livestock. A 49-year-old woman was suffering from feverish symptoms, fatigue, arthralgia, general body pain, and anorexia for 2 weeks. Later, she visited the Bayannur Centers for Disease Control and Prevention Hospital in Inner Mongolia, China. Molecular-based diagnostic analysis of the patient's blood revealed that A. phagocytophilum p44 DNA was positive, but Brucella omp31, spotted fever group Rickettsia gltA, Orientia tsutsugamushi 16S rDNA, and Ehrlichia p28 were negative. The amino acid sequences of 9 A. phagocytophilum p44 clones obtained from the patient shared 44-100% similarity among them and were closely related to those of previously identified p44 clones from Canis familiaris (accession no. KJV64194) and from Ixodes persulcatus tick (no. BAN28309). Serological tests using the patient's serum showed that immunoglobulin M (IgM) and IgG titers to A. phagocytophilum antigens were 160 and 20, respectively, determined using indirect immunofluorescence assay, and the reaction to recombinant P44 proteins (rP44-1, rP44-18ES, and/or rP44-47) was confirmed using Western blot analysis. Thus, the results obtained in this study strongly suggest that the patient was infected with A. phagocytophilum. To our knowledge, this is the first case of human anaplasmosis infection in the Inner Mongolia Autonomous Region.

In order to provide direction guidance for the heat loss of steam pipeline and ensure the safe and energy-saving operation of steam pipe network, it is very important to realize rapidly and accurate diagnosis of high-temperature area of the pipeline. This paper is aimed at the problem of the complicated working environment of the steam pipe, which causes the infrared image obtained have strong background interference. A neural immune ensemble learning algorithm, based on the ensemble learning theory and the coordination between nervous system and immune system, is proposed to diagnose abnormal high temperature region in infrared steam pipeline image. Experimental results show that the proposed algorithm can effectively diagnose the high temperature region of steam pipeline. Compared with other image classification algorithms, the results show that the neural immune ensemble learning algorithm has higher diagnostic accuracy and can meet the needs of actual engineering applications.

Figure S2. Quantitative RT-PCR for the expression levels of 13 candidate miRNAs. U6 was used as the internal control for mRNA. Error bars show the SD (nâ =â 3). (PDF 565 kb)

Figure S1. Identification of iPSCs. a The GFP-iPSCs were purple which showed positive alkaline phosphatase staining. Scale bar: 20 μm. b Five weeks following injection, a 1.5 × 1.5 × 1 cm3 size tumor formed. c H&E staining image showed that tumor tissue was noted to be derived from all three embryonic layers obviously, containing glandular epithelium (endoderm), cartilage (mesoderm), and cornified epithelium (ectoderm). Scale bar: 20 μm. (PDF 731 kb)

Bone marrow-derived mesenchymal stem cells (BMSCs) have the ability to differentiate into insulin-producing cells (IPCs). Bio-scaffolds derived from decellularized organs can act as a carrier for seed cells and may have broad applications in regenerative medicine. This study investigated the effect of native pancreatic stroma obtained from decellularized pancreas on the proliferation, migration and differentiation of BMSCs into IPCs, and explored the potential underlying molecular mechanism. The decellularized pancreas bio-scaffold was obtained by perfusion with Triton X-100/ammonium hydroxide, followed by digestion with a mixture of pepsin and hydrochloric acid to prepare the stroma solution. Islet-like cells were differentiated from BMSCs by a three-step induction method. The differences on the cytological behavior with or without stroma were evaluated by morphological observation, insulin release assay, qRT-PCR assay and western blot analysis. Our results showed that, stroma derived from decellularized pancreas could promote the proliferation and migration of BMSCs. Furthermore, the formation of IPCs could also be promoted, which possessed similar morphology to endogenous islets. During the induced differentiation process, the presence of stroma significantly increased the expression of insulin 1, insulin 2 and Pdx-1, as well as insulin release. This was accompanied by an increase in the phosphorylation of Akt and ERK in third stage cell clusters, which was prevented by the addition of the inhibitors PD98059 and LY294002, respectively. In summary, decellularized pancreatic stroma could promote the proliferation, migration and differentiation of BMSCs into IPCs, and this involved the activation of Akt and ERK signal pathways.

Anaplasma phagocytophilum is an obligate intracellular bacterium that causes febrile illness in humans and livestock. A 49-year-old woman was suffering from feverish symptoms, fatigue, arthralgia, general body pain, and anorexia for 2 weeks. Later, she visited the Bayannur Centers for Disease Control and Prevention Hospital in Inner Mongolia, China. Molecular-based diagnostic analysis of the patient's blood revealed that A. phagocytophilum p44 DNA was positive, but Brucella omp31, spotted fever group Rickettsia gltA, Orientia tsutsugamushi 16S rDNA, and Ehrlichia p28 were negative. The amino acid sequences of 9 A. phagocytophilum p44 clones obtained from the patient shared 44-100% similarity among them and were closely related to those of previously identified p44 clones from Canis familiaris (accession no. KJV64194) and from Ixodes persulcatus tick (no. BAN28309). Serological tests using the patient's serum showed that immunoglobulin M (IgM) and IgG titers to A. phagocytophilum antigens were 160 and 20, respectively, determined using indirect immunofluorescence assay, and the reaction to recombinant P44 proteins (rP44-1, rP44-18ES, and/or rP44-47) was confirmed using Western blot analysis. Thus, the results obtained in this study strongly suggest that the patient was infected with A. phagocytophilum. To our knowledge, this is the first case of human anaplasmosis infection in the Inner Mongolia Autonomous Region.

Whole-organ decellularization has been identified as a promising choice for tissue engineering. The aim of the present study was to engineer intact whole rat liver scaffolds and repopulate them with hepatocytes and endothelial progenitor cells (EPCs) in a bioreactor. Decellularized liver scaffolds were obtained by perfusing Triton X-100 with ammonium hydroxide. The architecture and composition of the original extracellular matrix were preserved, as confirmed by morphologic, histological, and immunolabeling methods. To determine biocompatibility, the scaffold was embedded in the subcutaneous adipose layer of the back of a heterologous animal to observe the infiltration of inflammatory cells. Hepatocytes were reseeded using a parenchymal injection method and cultured by continuous perfusion. EPCs were reseeded using a portal vein infusion method. Morphologic and functional examination showed that the hepatocytes and EPCs grew well in the scaffold. The present study describes an effective method of decellularization and recellularization of rat livers, providing the foundation for liver engineering and the development of bioartificial livers.