Hybrid Control of Seismic Structures with Optimal Placement of Control Devices

A theoretical study is carried out for optimal controller placement and effectiveness of a hybrid seismic response control system comprising a viscous fluid damper and a servovalve-controlled hydraulic actuator. A stochastic seismic response of controlled structures is first investigated with nonorthogonal damping and stiffness; then a statistical method for optimal placement of control devices on seismic-resistant structures is developed. With such placement, a hybrid system can achieve greater performance in that much less control force is required to reduce structural seismic response to a given level. This study also shows the hybrid system is superior to both active and passive control systems in control capacity. Numerical simulation for the seismic response of a building structure is presented to demonstrate the effectiveness of the proposed control strategy

Optimum Control of a Hybrid System for Seismic Excitations with State Observer Technique

This paper presents a theoretical study of a hybrid seismic response control system comprising a passive fluid viscous damper and an active control system with a hydraulic actuator and acceleration sensors. The analytical model of this system is derived in the discrete time domain with actuator and clamper dynamics considered. Based on digital control theory, a state observer is established for optimal control strategies of the hybrid system. This study shows that the hybrid system gains the advantages of both active and passive control techniques currently in vogue; and that, with the state observer technique, a seismic response control system is more effective and less complicated because full-state feedback seismic control algorithms can be implemented by means of acceleration sensors, and a smaller number of sensors is required. A numerical simulation for seismic response of a building structure with a hybrid control system is presented to demonstrate the effectiveness of this control strategy for the hybrid system

COMPARISON OF CHLOROPHYLL A AND THE ALGAL GROWTH POTENTIAL IN THE WEST LAKE

The present work studied environmental factors, such as temperature, nitrogen, phosphorus, chlorophyll a and transparency of the West Lake. Algal growth potential test (AGP) was performed to determine the influence of the environment elements on the potential of algal growth, and to explain what conditions were necessary for algal reproduction.Article信州大学理学部附属諏訪臨湖実験所報告 11: 35-39(1999)departmental bulletin pape

An Enhanced Plane Wave Expansion Method to Solve Piezoelectric Phononic Crystal with Resonant Shunting Circuits

An enhanced plane wave expansion (PWE) method is proposed to solve piezoelectric phononic crystal (PPC) connected with resonant shunting circuits (PPC-C), which is named as PWE-PPC-C. The resonant shunting circuits can not only bring about the locally resonant (LR) band gap for the PPC-C but also conveniently tune frequency and bandwidth of band gaps through adjusting circuit parameters. However, thus far, more than one-dimensional PPC-C has been studied just by Finite Element method. Compared with other methods, the PWE has great advantages in solving more than one-dimensional PC as well as various lattice types. Nevertheless, the conventional PWE cannot accurately solve coupling between the structure and resonant shunting circuits of the PPC-C since only taking one-way coupling from displacements to electrical parameters into consideration. A two-dimensional PPC-C model of orthorhombic lattice is established to demonstrate the whole solving process of PWE-PPC-C. The PWE-PPC-C method is validated by Transfer Matrix method as well as Finite Element method. The dependence of band gaps on circuit parameters has been investigated in detail by PWE-PPC-C. Its advantage in solving various lattice types is further illustrated by calculating the PPC-C of triangular and hexagonal lattices, respectively

Repression of Esophageal Neoplasia and Inflammatory Signaling by Anti-miR-31 Delivery In Vivo.

BACKGROUND: Overexpression of microRNA-31 (miR-31) is implicated in the pathogenesis of esophageal squamous cell carcinoma (ESCC), a deadly disease associated with dietary zinc deficiency. Using a rat model that recapitulates features of human ESCC, the mechanism whereby Zn regulates miR-31 expression to promote ESCC is examined. METHODS: To inhibit in vivo esophageal miR-31 overexpression in Zn-deficient rats (n = 12-20 per group), locked nucleic acid-modified anti-miR-31 oligonucleotides were administered over five weeks. miR-31 expression was determined by northern blotting, quantitative polymerase chain reaction, and in situ hybridization. Physiological miR-31 targets were identified by microarray analysis and verified by luciferase reporter assay. Cellular proliferation, apoptosis, and expression of inflammation genes were determined by immunoblotting, caspase assays, and immunohistochemistry. The miR-31 promoter in Zn-deficient esophagus was identified by ChIP-seq using an antibody for histone mark H3K4me3. Data were analyzed with t test and analysis of variance. All statistical tests were two-sided. RESULTS: In vivo, anti-miR-31 reduced miR-31 overexpression (P = .002) and suppressed the esophageal preneoplasia in Zn-deficient rats. At the same time, the miR-31 target Stk40 was derepressed, thereby inhibiting the STK40-NF-κΒ-controlled inflammatory pathway, with resultant decreased cellular proliferation and activated apoptosis (caspase 3/7 activities, fold change = 10.7, P = .005). This same connection between miR-31 overexpression and STK40/NF-κΒ expression was also documented in human ESCC cell lines. In Zn-deficient esophagus, the miR-31 promoter region and NF-κΒ binding site were activated. Zn replenishment restored the regulation of this genomic region and a normal esophageal phenotype. CONCLUSIONS: The data define the in vivo signaling pathway underlying interaction of Zn deficiency and miR-31 overexpression in esophageal neoplasia and provide a mechanistic rationale for miR-31 as a therapeutic target for ESCC

Clinicopathological Analysis of 11 Cases of SMARCA4 (BRG1)-deficient Carcinoma

ObjectiveTo investigate the clinicopathological features, immunophenotype, diagnosis and treatment of SMARCA4 (BRG1)-deficient carcinoma. MethodsClinical data of 11 patients with SMARCA4 (BRG1)-deficient cancer were collected. The morphologic and immunohistochemical features of this tumour were summarized, and the relevant literature was reviewed. ResultsAmong the 11 cases of SMARCA4 (BRG1)-deficient carcinoma, eight were male and three were female, with median age of 60. Seven patients underwent radical resection, and four underwent traditional joint targeted chemotherapy and immunotherapy. Microscopically, the tumor cells were epithelioid, rhabdoid or spindle-shaped, with prominent eosinophilic nucleoli and frequent mitoses (>5/10 HPF). Multiple foci of necrosis were found in the tumor tissue, a large number of tumor emboli in the blood vessels and myxoid stromal degeneration. Among these cases, 11 cases showed loss of SMARCA4 (BRG1) expression, whereas the CK and Vim markers were expressed, SMARCB1 (INI1) expression was retained, and p53 mutation was detected. The tumor cells showed high proliferation activity (Ki-67>60%), and synaptophsin was moderately positive. Three cases were mismatch repair deficient and respectively showed the loss of MLH1/PMS2, PMS2 and MSH6 expression. ConclusionThe incidence of SMARCA4 (BRG1) -dificient carcinoma is low. It can be easily confused with other tumors and is difficult to be diagnosed before operation, which requires confirmation by immunohistochemistry

A triton X-100 assisted PMAxx-qPCR assay for rapid assessment of infectious African swine fever virus

IntroductionAfrican Swine Fever (ASF) is a highly infectious disease of pigs, caused by African swine fever virus (ASFV). The lack of vaccines and drugs makes strict disinfection practices to be one of the main measurements to curb the transmission of ASF. Therefore, it is important to assess if all viruses are inactivated after disinfection or after long time exposure in their natural conditions. Currently, the infectivity of ASFV is determined by virus isolation and culture in a biosafety level 3 (BSL-3) laboratory. However, BSL-3 laboratories are not readily available, need skilled expertise and may be time consuming.MethodsIn this study, a Triton X-100 assisted PMAxx-qPCR method was developed for rapid assessment of infectious ASFV in samples. PMAxx, an improved version of propidium monoazide (PMA), can covalently cross-link with naked ASFV-DNA or DNA inside inactivated ASFV virions under assistance of 0.1% (v/v) TritonX-100, but not with ASFV-DNA inside live virions. Formation of PMAxx-DNA conjugates prevents PCR amplification, leaving only infectious virions to be detected. Under optimum conditions, the limit of detection of the PMAxx-qPCR assay was 2.32log10HAD50/mL of infectious ASFV. Testing different samples showed that the PMAxx-qPCR assay was effective to evaluate intact ASFV virions after treatment by heat or chemical disinfectants and in simulated samples such as swine tissue homogenate, swine saliva swabs, and environmental swabs. However, whole-blood and saliva need to be diluted before testing because they may inhibit the PCR reaction or the cross-linking of PMAxx with DNA.ConclusionThe Triton X-100 assisted PMAxx-qPCR assay took less than 3 h from sample to result, offering an easier and faster way for assessing infectious ASFV in samples from places like pig farms and pork markets

Zinc deficiency activates S100A8 inflammation in the absence of COX-2 and promotes murine oral-esophageal tumor progression

Zinc (Zn)-deficiency (ZD) is implicated in the pathogenesis of human oral-esophageal cancers. Previously, we showed that in ZD mice genetic deletion of cyclooxygenase-2 (Cox-2) enhances N-nitrosomethylbenzylamine-induced forestomach carcinogenesis. By contrast, Cox-2 deletion offers protection in Zn-sufficient (ZS) mice. We hypothesize that ZD activates pathways insensitive to COX-2 inhibition, thereby promoting carcinogenesis. This hypothesis is tested in a Cox-2−/− mouse tongue cancer model that mimics pharmacologic blockade of COX-2 by firstly examining transcriptome profiles of forestomach mucosa from Cox-2−/− and wild-type mice on a ZD vs. ZS diet, and secondly investigating the roles of identified markers in mouse forestomach/tongue preneoplasia and carcinomas. In Cox-2−/− mice exposed to the tongue carcinogen 4-nitroquinoline 1-oxide, dietary ZD elicited tongue/esophagus/forestomach carcinomas that were prevented by ZS. The precancerous ZD:Cox-2−/−vs. ZS:Cox-2−/− forestomach had an inflammatory signature with upregulation of the proinflammation genes S100a8 and S100a9. Bioinformatics analysis revealed overrepresentation of inflammation processes comprising S100a8/a9 and an nuclear factor (NF)-κB network with connectivity to S100A8. Immunohistochemistry revealed co-overexpression of S100A8, its heterodimeric partner S100A9, the receptor for advanced glycation end-products (RAGE), NF-κB p65, and cyclin D1, in ZD:Cox-2−/− forestomach/tongue preneoplasia and carcinomas, evidence for the activation of a RAGE-S100A8/A9 inflammatory pathway. Accumulation of p53 in these carcinomas indicated activation of additional inflammatory pathways. Zn-replenishment in ZD:Cox-2−/−mice reversed the inflammation and inhibited carcinogenesis. Thus, ZD activates alternative inflammation-associated cancer pathways that fuel tumor progression and bypass the antitumor effect of Cox-2 ablation. These findings have important clinical implications, as combination cancer therapy that includes Zn may improve efficacy