Study on the Filtration Performance of the Baghouse Filters for Ultra-Low Emission as a Function of Filter Pore Size and Fiber Diameter

The main objective of this study was to determine the effect of filter pore size and fiber diameter on the performance of the baghouse filters for ultra-low emission. In this study, three kinds of conventional polyester filter (depth filtration media) and two kinds of polytetrafluoroethylene membrane-coated polyester filter (surface filtration media), having various filter pore sizes and fiber diameters, were tested to determine the performance of static and dynamic filtration. In order to determine the static filtration performance, the filtration resistance and the filtration efficiency of the clean filter media were measured by the arrestance method. The dynamic filtration performance experiments were conducted to determine the dynamic resistances, dust depositions, and dynamic filtration efficiencies of the dust-containing filter media under the condition of dust airflow filtration through a pulse-cleaning cycle. In the dynamic filtration performance experiments, the size of 50% test dust was less than 2.5 μm, and the mass mean aerodynamic diameter of the dust was 1.5 μm. The filtration velocity was 2 m∙min−1, and the dust concentration was 18.4 g∙m−3. The static filtration performance experiments showed that the filter pore size greatly affected the filtration resistance and the filtration efficiency of the fabric structure of the surface filtration media. In the depth filtration media, the filtration efficiency and the filtration resistance of the fabric structure were improved when the filter pore size and the fiber diameter were smaller in magnitude. For all the five filter media, smaller the pore size of the filter media, greater was the filtration precision (for fine particles, such as PM2.5) of the fabric structure. In the dynamic filtration performance experiments, the filter pore size and the fiber diameter of the depth filtration media affected the dynamic filtration resistance and the dynamic filtration efficiency of the depth filtration media by affecting the deposition rate of dust in the depth filtration media; however, the filter pore size of the surface filtration media affected the blocking rate of dust in the membrane micropores, thus influencing the dynamic filtration resistance and the dynamic filtration efficiency of the surface filtration media

Time-Enabled and Verifiable Secure Search for Blockchain-Empowered Electronic Health Record Sharing in IoT

The collection and sharing of electronic health records (EHRs) via the Internet of Things (IoT) can enhance the accuracy of disease diagnosis. However, it is challenging to guarantee the secure search of EHR during the sharing process. The advent of blockchain is a promising solution to address the issues, owing to its remarkable features such as immutability and anonymity. In this paper, we propose a novel blockchain-based secure sharing system over searchable encryption and hidden data structure via IoT devices. EHR ciphertexts of data owners are stored in the interplanetary file system (IPFS). A user with proper access permissions can search for the desired data with the data owner’s time-bound authorization and verify the authenticity of the search result. After that, the data user can access the relevant EHR ciphertext from IPFS using a symmetric key. The scheme jointly uses searchable encryption and smart contract to realize secure search, time control, verifiable keyword search, fast search, and forward privacy in IoT scenarios. Performance analysis and proof demonstrate that the proposed protocol can satisfy the design goals. In addition, performance evaluation shows the high scalability and feasibility of the proposed scheme

A new model for the treatment of type 2 diabetes mellitus based on rhythm regulations under the framework of psychosomatic medicine: a real-world study

Abstract We aimed to explore a new treatment model for type 2 diabetes mellitus (DM) based on rhythm regulation under the framework of psychosomatic medicine. Using psychotropics as rhythm regulators, 178 patients with DM were evaluated and divided into three groups: the antidiabetic treatment group (AT group), psychotropic treatment group (PT group), and combined antidiabetic + psychotropic treatment group (combined group), for a course of 16 weeks. The West China Psychiatry Association (WCPA) Somatic Symptom Classification Scale (SSCS) was used to evaluate each patient. The levels of hormones in the hypothalamic–pituitary–adrenal (HPA) and hypothalamic-pituitary-thyroid axes and of blood glucose and glycosylated hemoglobin (HbA1c) were evaluated both before and after treatment. After the treatment, the blood glucose and HbA1c levels in all three groups were lower than those at baseline. Furthermore, the incidence of the abnormal HPA axis in the PT group was significantly decreased (P = 0.003), while the incidence of the abnormal HPA axis in the combined group was 0.0%. The five factor scores of the SSCS in the PT and combined groups after treatment were both significantly low (P < 0.01). Both the incidence of abnormal neuroendocrine axes and SSCS scores in the AT group showed no significant difference before and after treatment. “Blood glucose control + rhythm regulation” should be considered as optimised treatment goals for DM. Moreover, some psychotropics could be used as biorhythm regulators, which have good potential value for clinical application. Clinical trial registration number: ChiCTR1800019064. Name of trial registration: Reinterpretation of mechanism and the optimization of treatment for non-infectious chronic diseases under the “stress-dysrhythmia” theory hypothesis. The full trial protocol can be accessed at the Chinese Clinical Trial Registry ( http://www.chictr.org.cn/ )

Toosendanin targeting eEF2 impedes Topoisomerase I & II protein translation to suppress esophageal squamous cell carcinoma growth

Abstract Background Although molecular targets such as HER2, TP53 and PIK3CA have been widely studied in esophageal cancer, few of them were successfully applied for clinical treatment. Therefore, it is urgent to discover novel actionable targets and inhibitors. Eukaryotic translational elongation factor 2 (eEF2) is reported to be highly expressed in various cancers. However, its contribution to the maintenance and progression of cancer has not been fully clarified. Methods In the present study, we utilized tissue array to evaluate eEF2 protein expression and clinical significance in esophageal squamous cell carcinoma (ESCC). Next, we performed knockdown, overexpression, RNA-binding protein immunoprecipitation (RIP) sequence, and nascent protein synthesis assays to explore the molecular function of eEF2. Furthermore, we utilized compound screening, Surface Plasmon Resonance (SPR), Isothermal Titration Calorimetry (ITC) assay, cell proliferation and Patient derived xenograft (PDX) mouse model assays to discover an eEF2 inhibitor and assess its effects on ESCC growth. Results We found that eEF2 were highly expressed in ESCC and negatively associated with the prognosis of ESCC patients. Knocking down of eEF2 suppressed the cell proliferation and colony formation of ESCC. eEF2 bond with the mRNA of Topoisomerase II (TOP1) and Topoisomerase II (TOP2) and enhanced the protein biosynthesis of TOP1 and TOP2. We also identified Toosendanin was a novel inhibitor of eEF2 and Toosendanin inhibited the growth of ESCC in vitro and in vivo. Conclusions Our findings show that Toosendanin treatment suppresses ESCC growth through targeting eEF2 and regulating downstream TOP1 and TOP2 biosynthesis. eEF2 could be supplied as a potential therapeutic target in the further clinical studies

Additional file 1 of Re-interpretation of the mechanism of type 2 diabetes mellitus based on a framework of psychosomatic medicine: a real-world study

Additional file 1: Supplementary table 1. Comparisons of demographic data among the five groups. Supplementary table 2. Comparisons of the scores of five factors of NEO-FFI among the five groups. Supplementary table 3. Comparisons of hormonelevels and abnormal rates among the five groups. Supplementary figure 1. Comparisons of abnormal rates of neuroendocrine axes among the five case groups

Autocrine CTHRC1 activates hepatic stellate cells and promotes liver fibrosis by activating TGF-β signalingResearch in context

Background: Hepatic fibrosis is caused by chronic liver injury and may progress toward liver cirrhosis, and even hepatocellular carcinoma. However, current treatment is not satisfactory. Therefore, there is a mandate to find novel therapeutic targets to improve therapy, and biomarkers to monitor therapeutic response. Methods: Liver fibrosis was induced by carbon tetrachloride (CCl4) or thioacetamide (TAA) in wild type (WT) or CTHRC1−/− mice, followed by immunofluorescence and immunohistochemical analyses. CTHRC1 monoclonal antibody (mAb) was used to abrogate the effect of CTHRC1 in vitro and in vivo. Results: Here, we reported that collagen triple helix repeat containing 1 (CTHRC1), a secreted protein derived from hepatic stellate cells (HSCs), was significantly up-regulated in fibrotic liver tissues. CTHRC1 promoted HSCs transformation from a quiescent to an activated state, and enhanced migratory or contractile capacities of HSCs by activating TGF-β signaling. Meanwhile, CTHRC1 competitively bound to Wnt noncononical receptor and promoted the contractility but not activation of HSCs. CCl4 or TAA-induced liver fibrosis was attenuated in CTHRC−/− mice compared with littermate control, while a monoclonal antibody of CTHRC1 suppressed liver fibrosis in WT mice treated with CCl4 or TAA. Interpretation: We demonstrated that CTHRC1 is a new regulator of liver fibrosis by modulating TGF-β signaling. Targeting CTHRC1 could be a promising therapeutic approach, which can suppress TGF-β signaling and avoid the side effects caused by directly targeting TGF-β. CTHRC1 could also be a potential biomarker for monitoring response to anti-fibrotic therapy. Fund: This study was supported by the National Natural Science Foundation of China (ID 81672358, 81871923, 81872242, 81802890), the Shanghai Municipal Education Commission—Gaofeng Clinical Medicine Grant Support (ID 20181708), the Natural Science Foundation of Shanghai (ID 17ZR1428300, 18ZR1436900), and Shanghai Municipal Health Bureau (ID 2018BR32). The funders did not play a role in manuscript design, data collection, data analysis, interpretation nor writing of the manuscript. Keywords: Liver fibrosis, CTHRC1, HSCs, TGF-β signalin

Cx3cr1 deficiency in mice attenuates hepatic granuloma formation during acute schistosomiasis by enhancing the M2-type polarization of macrophages

Acute schistosomiasis is characterized by pro-inflammatory responses against tissue- or organ-trapped parasite eggs along with granuloma formation. Here, we describe studies in Cx3cr1−/− mice and demonstrate the role of Cx3cr1 in the pathoetiology of granuloma formation during acute schistosomiasis. Mice deficient in Cx3cr1 were protected from granuloma formation and hepatic injury induced by Schistosoma japonicum eggs, as manifested by reduced body weight loss and attenuated hepatomegaly along with preserved liver function. Notably, S. japonicum infection induced high levels of hepatic Cx3cr1 expression, which was predominantly expressed by infiltrating macrophages. Loss of Cx3cr1 rendered macrophages preferentially towards M2 polarization, which then led to a characteristic switch of the host immune defense from a conventional Th1 to a typical Th2 response during acute schistosomiasis. This immune switch caused by Cx3cr1 deficiency was probably associated with enhanced STAT6/PPAR-γ signaling and increased expression of indoleamine 2,3-dioxygenase (IDO), an enzyme that promotes M2 polarization of macrophages. Taken together, our data provide evidence suggesting that CX3CR1 could be a viable therapeutic target for treatment of acute schistosomiasis