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Background Dysimmunity plays a key role in diabetes, especially type 1 diabetes mellitus. Islet-specific autoantibodies (ISAs) have been used as diagnostic markers for different phenotypic classifications of diabetes. This study was aimed to explore the relationships between ISA titers and the clinical characteristics of diabetic patients. Methods A total of 509 diabetic patients admitted to Department of Endocrinology and Metabolism at the Affiliated Hospital of Nantong University were recruited. Anthropometric parameters, serum biochemical index, glycosylated hemoglobin, urinary microalbumin/creatinine ratio, ISAs, fat mass, and islet β-cell function were measured. Multiple linear regression analysis was performed to identify relationships between ISA titers and clinical characteristics. Results Compared with autoantibody negative group, blood pressure, weight, total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), visceral fat mass, fasting C-peptide (FCP), 120 minutes C-peptide (120minCP) and area under C-peptide curve (AUCCP) of patients in either autoantibody positive or glutamate decarboxylase antibody (GADA) positive group were lower. Body mass index (BMI), waist circumference, triglycerides (TGs), body fat mass of patients in either autoantibody positive group were lower than autoantibody negative group. GADA titer negatively correlated with TC, LDL-C, FCP, 120minCP, and AUCCP. The islet cell antibody and insulin autoantibody titers both negatively correlated with body weight, BMI, TC, TG, and LDL-C. After adjusting confounders, multiple linear regression analysis showed that LDL-C and FCP negatively correlated with GADA titer. Conclusion Diabetic patients with a high ISA titer, especially GADA titer, have worse islet β-cell function, but less abdominal obesity and fewer features of the metabolic syndrome.

This paper presents a machine learning method, Gaussian Mixture Hidden Markov Model (GMM-HMM), for device-free activity recognition using WiFi channel state information (CSI). The basic concept of CSI is introduced and signal changes caused by human activity are described, which demonstrates that human activity can be identified using a unique mapping between action and signal variations. The phase difference expanded matrix is built by the mean and standard deviation of phase difference as feature matrix after linear correction and Savitzky-Golay filter is performed on the CSI raw phase information. The GMM-HMM is used for classification as the human activity can be modeled as the Markov process and the complex activity patterns can be fitted by multiple Gaussian density functions, respectively. The proposed system is verified on the self-collected datasets and several factors affecting the recognition accuracy are analyzed. Furthermore, the system has compared with the previous work. High accuracy and robustness in universal scenarios are realized. Experimental results show that the average recognition accuracy of the proposed system is over 97%.

This study aims to determine the efficacy of Zinc finger protein ZBTB20 in treatment of post‐infarction cardiac remodelling. For this purpose, left anterior descending (LAD) ligation was operated on mice to induce myocardial infarction (MI) with sham control group as contrast and adeno‐associated virus (AAV9) system was used to deliver ZBTB20 to mouse heart by myocardial injection with vehicle‐injected control group as contrast two weeks before MI surgery. Then four weeks after MI, vehicle‐treated mice with left ventricular (LV) remodelling underwent deterioration of cardiac function, with symptoms of hypertrophy, interstitial fibrosis, inflammation and apoptosis. The vehicle‐injected mice also showed increase of infarct size and decrease of survival rate. Meanwhile, the ZBTB20‐overexpressed mice displayed improvement after MI. Moreover, the anti‐apoptosis effect of ZBTB20 was further confirmed in H9c2 cells subjected to hypoxia in vitro. Further study suggested that ZBTB20 exerts cardioprotection by inhibiting tumour necrosis factor α/apoptosis signal‐regulating kinase 1 (ASK1)/c‐Jun N‐terminal kinase 1/2 (JNK1/2) signalling, which was confirmed by shRNA‐JNK adenoviruses transfection or a JNK activator in vitro as well as ASK1 overexpression in vivo. In summary, our data suggest that ZBTB20 could alleviate cardiac remodelling post‐MI. Thus, administration of ZBTB20 can be considered as a promising treatment strategy for heart failure post‐MI. Significance Statement: ZBTB20 could alleviate cardiac remodelling post‐MI via inhibition of ASK1/JNK1/2 signalling.

Background The aim of this study was to investigate the correlation between serum uric acid level and central body fat distribution in patients with type 2 diabetes (T2DM). Methods A total of 867 patients with T2DM were enrolled. Measurements of central fat distribution were obtained by dual energy X-ray absorptiometry. Patients were stratified into three groups according to their levels of serum uric acid (SUA). Multiple linear regression analysis was used to determine the association between SUA and central body fat distribution. Logistic regression analysis was used to estimate the risk factors for hyperuricemia (HUA). Mediation analysis was applied to assess the overall, direct, and indirect mediators of SUA levels. Results Multiple linear regression analysis showed that SUA levels were significantly positively correlated with waist circumference (WC), body mass index (BMI), visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), Android fat mass, Gynoid fat mass, fasting c-peptide (F-CP), and area under the curve of C-peptide (P < 0.05 for all). VAT [odds ratio (OR), 2.367; 95% confidence interval (CI), 1.078-5.197; P < 0.001)], WC (OR, 1.041; 95% CI, 1.011-1.072; P < 0.001), high-density lipoprotein (OR, 0.274; 95% CI, 0.104-0.727; P < 0.001), and estimated glomerular filtration rate (OR, 0.966; 95% CI, 0.959-0.973; P < 0.001) were found to be independent risk factors for T2DM patients with HUA. After mediation analysis, BMI and central obesity were found to have different partial effects on the association between SUA and F-CP (P < 0.001). Conclusion In patients with T2DM, HUA was positively correlated with F-CP and central body fat distribution, especially VAT. These results suggest that central obesity may play a role in the positive correlation between HUA and insulin resistance (IR).

It is still a challenging task to segment ultrasound medical images automatically and accurately because of the poor quality of images. To address these problems, a two-stage automatic segmentation scheme based on local entropy and a proposed active contour model for ultrasound images are put forward in this paper. First, a new region-based active contour model in the level set formulation, driven by global and local intensity information, is established for the segmentation. Furthermore, for automatically segmenting the ultrasound images, a coarse segmentation is performed utilizing local entropy information of the ultrasound images, then the coarse segmentation result is used as the initial value of the explicit segmentation based on the proposed model. Several experiments on real ultrasound images demonstrate that the proposed method outperforms other methods on both visual perception and objective evaluation metrics.

Medical image fusion is one of the hot research in the field of medical imaging and radiation medicine, and is widely recognized by medical and engineering fields. In this paper, a new fusion scheme for medical images based on sparse representation of classified image patches is proposed. In this method, first, the registered source images are divided into classified patches according to the patch geometrical direction, from which the corresponding sub-dictionary is trained via the online dictionary learning (ODL) algorithm, and the least angle regression (LARS) algorithm is used to sparsely code each patch; second, the sparse coefficients are combined with the “choose-max” fusion rule; Finally, the fused image is reconstructed from the combined sparse coefficients and the corresponding sub-dictionary. The experimental results showed that the proposed method outperforms other methods in terms of both visual perception and objective evaluation metrics.

NLRP3, a member of the nucleotide-binding oligomerization domain (NOD)-like receptor family, is involved in cardiac inflammation. However, the functional role of NLRP3 in cardiac remodeling is not clear. To investigate the roles of NLRP3 in pressure overload-induced cardiac remodeling, NLRP3 knockout and wild-type mice were subjected to aortic banding to induce cardiac remodeling. The data showed that NLRP3 expression was downregulated in the remodeling process. NLRP3 deficiency accelerated cardiac hypertrophy, fibrosis, and inflammation responses with deteriorating cardiac dysfunction in the pressure overload-induced cardiac remodeling mouse model. Neonatal rat cardiomyocytes were isolated and stimulated with phenylephrine (PE). We identified NLRP3 as a negative regulator of cardiomyocyte remodeling in PE-stimulated cardiomyocyte remodeling using adenovirus-NLRP3 and NLRP3 siRNA. Mechanistically, we found that the expression of Toll-like receptor (TLR) 4 was upregulated in NLRP3-deficient mouse hearts and PE-stimulated cardiomyocytes. NLRP3 knockout mice subjected to a TLR4 inhibitor revealed a relieved cardiac remodeling response with improved cardiac dysfunction. Our data suggested that NLRP3 could be a therapeutic target for cardiac remodeling and heart failure. KEY MESSAGES: NLRP3 expression was downregulated in the remodeling process. NLRP3 deficiency accelerated pressure overload-induced cardiac remodeling. NLRP3 acted as a negative regulator of cardiomyocyte remodeling via downregulating TLR4.

Orientin is a flavonoid extracted from Chinese traditional herb, Polygonum orientale L. Previous study has reported that orientin protected myocardial from ischemia reperfusion injury. However, whether orientin could protect against cardiac remodeling after myocardial injury remains unclear. The aim of our study is to investigate the effects of orientin in the progression of cardiac remodeling after myocardial infarction (MI). Mice cardiac remodeling model was established by left coronary artery ligation surgery. Experimental groups were as follows: vehicle-sham, orientin-sham, vehicle-MI, and orientin-MI. Animals were treated with vehicle or orientin (40 mg/kg) for 25 days starting 3 days after surgery. After 4 weeks of MI, mice with orientin treatment had decreased mortality and improved cardiac function. Significantly, at 4 weeks post-MI, orientin treatment decreased fibrosis, inflammatory response, and cardiomyocyte apoptosis. Furthermore, orientin treatment attenuated the hypoxia-induced neonatal rat cardiomyocyte apoptosis and increased cell viability. Additionally, orientin supplementation mitigated oxidative stress in remodeling heart tissue and cardiomyocytes exposed to hypoxia as measured by 2′,7′-dichlorodihydrofluorescein diacetate fluorescent probe. Mechanistically, orientin promotes cardioprotection by activating the eNOS/NO signaling cascades, which was confirmed by eNOS inhibitor (L-NAME) in vitro and in vivo. Inhibition of oxidative stress by orientin via eNOS/NO signaling cascades in the heart may represent a potential therapy for cardiac remodeling.

Background/Aims: Nuclear localization leucine-rich-repeat protein 1 (NLRP1) is a cytoplasmic protein, involved in autoimmune diseases, mammalian reproduction, neuronal cell death, and stroke. However, the role of NLRP1 in cardiac hypertrophy remains unclear. We used in vivo and in vitro models to investigate the effects of NLRP1 on cardiac hypertrophy. Methods: We used NLRP1-deficient mice and cultured neonatal rat cardiomyocytes with gain and loss of NLRP1 function. Cardiac hypertrophy was estimated by echocardiographic and hemodynamic measurements, and by pathological and molecular analysis. Results: Eight weeks after aortic banding (AB), NLRP1 deficiency significantly inhibited aortic banding–induced cardiac hypertrophy, inflammation, and fibrosis. Activation of MAPK, NF-κB, and TGF-β/Smad pathways was reduced in NLRP1-knockout (KO) mice compared with that in wild-type (WT) mice. Consistent with these results, in vitro studies, performed using cultured neonatal mouse cardiomyocytes, confirmed that NLRP1 deficiency protects against cardiomyocyte hypertrophy induced by isoproterenol (PE); this protective activity was associated with the arrest of MAPK and NF-κB signaling. Conclusions: Our data illustrates that NLRP1 plays a crucial role in the development of cardiac hypertrophy via positive regulation of the MAPK, NF-κB, and TGF-β/Smad signaling pathways.

The Approach and Landing (A&L) trajectory optimization is important for reusable launch vehicle (RLV) to deliver it to its landing site safely and reliably. And the trajectory should satisfy multi-constraints and path features. In this paper, the 3D dynamics of RLV in the A&L phase is introduced. and the the adaptive Gauss pseudo-spectral method (AGPM) is used to solve the A&L trajectory optimization problem. The adaptive method in GPM can improve the accuracy of the trajectory and accelerate convergence velocity of algorithm effectively. The simulation results of the typical RLV (X-33) demonstrate the feasibility of the trajectory optimization scheme which can let the RLV land securely.

Fixed-wing unmanned aerial vehicle (UAV) should be under control in the presence of model uncertainty and external disturbance, which is considered as torque perturbation in this paper. Such a challenge imposes tight requirements to the enhanced robustness and accuracy of the vehicle autopilot. The key of this paper is to introduce the model of attitude dynamics and propose a novel finite-time observer-based super twisting sliding mode control scheme for fixed-wing UAV. The observer designed in this paper can not only estimate the attitude rate but also the torque perturbation exactly in finite time. Then combined with the observer, a continuous homogeneous second-order sliding mode controller based on the terminal sliding mode and super twisting algorithm is designed to achieve a finite-time and exact attitude tracking with chattering attenuation. Finally, some simulations are provided to verify the effectiveness and robustness of the integrated control scheme in attitude tracking.

Icariin, the major active component isolated from plants of the Epimedium family, has been reported to have potential protective effects on the cardiovascular system. However, it is not known whether icariin has a direct effect on angiotensin II (Ang II)-induced cardiomyocyte enlargement and apoptosis. In the present study, embryonic rat heart-derived H9c2 cells were stimulated by Ang II, with or without icariin administration. Icariin treatment was found to attenuate the Ang II-induced increase in mRNA expression levels of hypertrophic markers, including atrial natriuretic peptide and B-type natriuretic peptide, in a concentration-dependent manner. The cell surface area of Ang II-treated H9c2 cells also decreased with icariin administration. Furthermore, icariin repressed Ang II-induced cell apoptosis and protein expression levels of Bax and cleaved-caspase 3, while the expression of Bcl-2 was increased by icariin. In addition, 2',7'-dichlorofluorescein diacetate incubation revealed that icariin inhibited the production of intracellular reactive oxygen species (ROS), which were stimulated by Ang II. Phosphorylation of c-Jun N-terminal kinase (JNK) and p38 in Ang II-treated H9c2 cells was blocked by icariin. Therefore, the results of the present study indicated that icariin protected H9c2 cardiomyocytes from Ang II-induced hypertrophy and apoptosis by inhibiting the ROS-dependent JNK and p38 pathways.

The cytoplasmic signaling protein tumor necrosis factor (TNF) receptor-associated factor 5 (TRAF5), which was identified as a signal transducer for members of the TNF receptor super-family, has been implicated in several biological functions in T/B lymphocytes and the innate immune response against viral infection. However, the role of TRAF5 in cardiac hypertrophy has not been reported. In the present study, we investigated the effect of TRAF5 on the development of pathological cardiac hypertrophy induced by transthoracic aorta constriction (TAC) and further explored the underlying molecular mechanisms. Cardiac hypertrophy and function were evaluated with echocardiography, hemodynamic measurements, pathological and molecular analyses. For the first time, we found that TRAF5 deficiency substantially aggravated cardiac hypertrophy, cardiac dysfunction and fibrosis in response to pressure overload after 4 weeks of TAC compared to wild-type (WT) mice. Moreover, the mitogen-activated protein/extracellular signal-regulated kinase kinase (MEK)-extracellular signal-regulated kinases 1/2 (ERK1/2) signaling pathway was more activated in TRAF5-deficient mice than WT mice. In conclusion, our results suggest that as an intrinsic cardioprotective factor, TRAF5 plays a crucial role in the development of cardiac hypertrophy through the negative regulation of the MEK-ERK1/2 pathway. J. Cell. Biochem. 115: 349-358, 2014. © 2013 Wiley Periodicals, Inc.

Nucleotide-binding oligomerization domain-2 (NOD2, also designated CARD15), a member of the NOD-leucine-rich repeat (LRR) protein family (also called the CATERPILLAR family), is upregulated in atheroma lesions and has an important role in regulating the intracellular recognition of bacterial components by immune cells. However, the effect of NOD2 on cardiac hypertrophy induced by a pathological stimulus has not been determined. Here, we investigated the effects of NOD2 deficiency on cardiac hypertrophy induced by aortic banding (AB) in mice. Cardiac hypertrophy was evaluated by echocardiographic, hemodynamic, pathological, and molecular analyses. NOD2 expression was upregulated in cardiomyocytes after aortic banding surgery in wild-type (WT) mice. NOD2 deficiency promoted cardiac hypertrophy and fibrosis 4 weeks after AB. Further, the enhanced activation of TLR4 and the MAPKs, NF-κB and TGF-β/Smad pathways were found in NOD2-knockout (KO) mice compared with WT mice. Our results suggest that NOD2 attenuates cardiac hypertrophy and fibrosis via regulation of multiple pathways.

Cardiac hypertrophy is an adaptive process of the heart in response to various stimuli, but sustained cardiac hypertrophy will finally lead to heart failure. Sulforaphane—extracted from cruciferous vegetables of the genus Brassica such as broccoli, brussels sprouts, and cabbage—has been evaluated for its anticarcinogenic and antioxidant effects. To investigate the effect of sulforaphane on angiotensin II (Ang II)-induced cardiac hypertrophy in vitro. Embryonic rat heart-derived H9c2 cells were co-incubated with sulforaphane and Ang II. The cell surface area and mRNA levels of hypertrophic markers were measured to clarify the effect of sulforaphane on cardiac hypertrophy. The underlying mechanism was further investigated by detecting the activation of Akt and NF-κB signaling pathways. We found that H9c2 cells pretreated with sulforaphane were protected from Ang II-induced hypertrophy. The increasing mRNA levels of ANP, BNP, and β-MHC in Ang II-stimulated cells were also down-regulated after sulforaphane treatment. Moreover, sulforaphane repressed the Ang II-induced phosphorylation of Akt, GSK3β, mTOR, eIF4e, as well as of IκBα and NF-κB. Based on our results, sulforaphane attenuates Ang II-induced hypertrophy of H9c2 cardiomyocytes mediated by the inhibition of intracellular signaling pathways including Akt and NF-κB.

Cardiac remodeling is a key determinant in the clinical course and outcome of heart failure and characterized by cardiac hypertrophy, fibrosis, cardiomyocyte apoptosis and inflammation. The anti-inflammatory, anti-apoptotic and anti-fibrotic effects of paeoniflorin have been identified in various types of tissue and cells. However, the role of paeoniflorin in cardiac remodeling remains unclear. We performed aortic banding (AB) in mice to induce a cardiac remodeling model in response to pressure overload. Paeoniflorin (20 mg/kg) was administered by daily intraperitoneal (i.p.) injection. Paeoniflorin treatment promoted the survival rate and improved cardiac function of mice at 8 weeks post surgery. AB-induced cardiac hypertrophy, as assessed by heart weight, gross heart, HE and WGA staining, cross-sectional area of cardiomyocyte and mRNA expresssion of hypertrophic makers, was attenuated by paeoniflorin. Paeoniflorin also inhibited collagen deposition, expression of TGFβ, CTGF, collagen Iα and collagen IIIα, and phosphorylation of Smad2 and Smad3 in the heart exposed to pressure overload. Cardiomyocyte apoptosis and induction of Bax and cleaved caspase3 in response to AB were suppressed by paeoniflorin. Furthermore, paeoniflorin decreased the quantity of CD68+ cells, protein levels of TNF-α and IL-1β, and phosphorylation of IκBα and NFκB-p65 in the heart after AB. In conclusion, paeoniflorin attenuated cardiac hypertrophy, fibrosis, apoptosis and inflammation, and improved left ventricular function in pressure overloaded mice. The cardioprotective effect of paeoniflorin is associated with the inhibition of TGFβ/Smads and NF-κB pathways.

Phenolic glucoside gastrodin (Gas), which is a main component extracted from the Chinese herbs Gastrodia elata Bl, is a well-known natural calcium antagonist with antioxidant and anti-inflammatory functions. It has long been used clinically for treatment of cardiovascular and cerebrovascular diseases. Previous studies have shown that gastrodin possesses comprehensive pharmacological functions. However, very little is known about whether gastrodin has protective role on cardiac hypertrophy. The aim of this study was to determine whether gastrodin attenuates pressure overload-induced cardiac hypertrophy in mice and to clarify the underlying molecular mechanisms. Our data demonstrated that gastrodin prevented cardiac hypertrophy induced by aortic banding (AB), as assessed by heart weight/body weight and lung weight/body weight ratios, echocardiographic parameters, and gene expression of hypertrophic markers. The inhibitory effect of gastrodin on cardiac hypertrophy is mediated by ERK1/2 signaling and GATA-4 activation. Further studies showed that gastrodin attenuated fibrosis and collagen synthesis through abrogating ERK1/2 signaling pathway. Therefore, these findings indicated that gastrodin, which is a potentially safe and inexpensive therapy for clinical use, has protective potential in targeting cardiac hypertrophy and fibrosis through suppression of ERK1/2 signaling.

The GIS 3D modelling and its topology relationship are introduced and which is used into describe space topology of tunnel in mine ventilation sytem. Based on mathematical modeling and data structure, 3D visualized modeling and airflow simulation of mine ventilation system are realized with OpenGL. Further more some algorithms and key technologies used in prototype systems are profiled. This study has a great significance in increasing performance of mine ventilation management and enjoys a bright prospect for future applications.

Rosai-Dorfman disease (RDD) is a rare histioproliferative disorder that only occasionally involves the central nervous system. We present the diagnosis and treatment of five patients with intracranial RDD. The patients were preoperatively misdiagnosed as meningioma or eosinophilic granuloma. All five patients were treated by total or subtotal surgical resection and none of them experienced recurrence. Histopathological examination showed a characteristic emperipolesis, the lymphocytes were engulfed in the S-100 protein and CD68 positive histiocytes, with negative expression of CD1a. Preoperative diagnosis of intracranial RDD is still challenging because the lesion is usually a dural-based lesion that mimics a meningioma. Surgical resection is an effective treatment and radiotherapy, steroid and chemotherapy has not demonstrated reliable therapeutic efficiency.

Obstructive Sleep Apnea Syndrome (OSAS) is the most common sleep-disordered breathing medical condition and a potentialy life-threatening affliction. Upper airway defense is based on the secreted mucus. The primary factors involved in the airway surface liquid (ASL) are not completely understood. In this study, identification of ASL proteins was demonstrated by using proteomic approach. 30 OSAS patients and 15 normal subjects between the ag e s of 30 and 50 (males=23; females=22) underwent collection of ASL sample. Proteomic approach involving two-dimensional polyacrylamide gel electrophoresis (2D PAGE) and mass spectrometry (MS). Querying the SWISSPROT database with the MS data yielded the identity of 10 proteins in the spots. Three of these proteins showing significant difference in abundance were identified to be Carbonic Anhydrase VI, immunoglobulin (Ig) heavy chain, and Calgranulin A. Overal, differential expression of proteins in the A S L proteome of OSAS patients suggests that the hypoxia associated with OSAS may lead to changes in catabolism of these proteins and their excretion in ASL.

Objective To study the modeling method of animal model of upper stenosis-airway of rats and air flow characteristic. Methods Totally 30 3-month old rats were randomly divided into a control group and a model group. Sodium Hyaluronte 0.1ml was injected into mucosa of the soft palate and the uvula of each rat from the model group in the anesthetic state. After 3-month feeding under the same conditions, the two rat groups were carried out CT Scanning and respiratory experimental examinations, respectively. The Computational Fluid Dynamic Method was then employed to simulate the airflow in upper airway. The flow characteristics are compared between a control rat and a model rat. The minimum cross sectional area of pharyngeal of the model group rats was reduced remarkably than that of the control group, which implies that the airway of the model rats is significantly narrower than that of the control rats with a P-value P

An alternative technique to improve the electric performance of shrunk MOSFET devices is strained engineering. Considering SiGe channel layer as a global strain capping a Si layer to prevent Ge diffusion from the SiGe channel layer and soften the stress between SiON gate dielectric and SiGe channel is a possible way. To favor NMOSFET, depositing silicon nitride on gate as contact etching stop layer (CESL) process providing the tensile effect is more appreciated. In this study, besides the electrical characteristics with different strain processes, the conduction path and channel location of electron carrier through body bias adjustment is an attractive exploration. Because the charge profile in channel shown as a quantum mechanical effect is not a uniform distribution, the chief inversion layer thickness of electron carrier will be shifted when the substrate bias is applied. This evidence will be exhibited in gamma factor. Observing the gamma shift, the main conductive path of electron carrier can be diagnosed and analyzed about the quality of SiGe layer in growth.

Channels of FinFET are 3 dimensional fin-like structures which are thin enough to be fully depleted as the gate is appropriately biased leaving no leaky neutrally-charged leaky body. Different widths (fin thickness), different gate materials, and the Vt-adjustment using different implant energies are taken into account in this paper. It is then found that different fin thicknesses do affect the electrical performance. But cobalt silicide replacing the gate poly-silicon does not show apparent benefits on n-channel FinFET.

FinFET devices have the structure of 3-D fins as channels, which are capable of being fully depleted as the gate is biased and potentially suppress the leakage currents. In this paper, one compares poly-silicon gates with fully cobalt silicide gate to see how much they are affected by the fin widths. Two channel lengths (0.1 micron and 0.12 micron) at two different fin widths (namely, 110nm, and 120nm) are taken into account.

Fin-FET is so expected because it protects Ioff current from outrageously leaky as the channel length gets shorten continuously. It thus keeps the threshold voltage and the swing from rolling-up. Those good characteristics are manifested by the fully depleted region and the lack of leaky body as the gate is biased. In this study, the fin-thickness effect is to be noticeably discussed. The correlated swings are to be determined and compared between the two kinds. The P-well Vt adjustment at two different energies, 10KeV and 6KeV, are also put into split.

We aimed to investigate metabolic parameters in children with adenoid hypertrophy (AH) only or adenotonsillar hypertrophy (ATH) and compare them with healthy controls.Forty-four prepubertal children aged 6-12 years who were obstructive symptoms and 16 healthy children were recruited in this study. All children underwent a complete otolaryngologic examination and sleep screening. The patients were divided into three groups according to obstruction type: normal, AH (adenoid grade III or IV, tonsil grade 1 or 2), and ATH (adenoid grade III or IV, tonsil grade 3 or 4). All participants underwent hematologic and biochemical tests including fasting blood glucose, insulin, and plasma lipids.(1) The children with AH and ATH had lower high-density lipoprotein cholesterol (HDL-C), when compared to normal children. (2) The level of HDL-C was negatively correlated with the sum of adenoid and tonsillar size scores and the apnea-hypopnea index (AHI) (r=-0.477, p0.001 vs. r=-0.548, p0.001, respectively). There was a modest association between HDL-C and minimal SpO₂ (r=0.332, p=0.009). (3) Stepwise multiple regression analysis identified the AHI, triglycerides, and fasting insulin as independent predictors for HDL-C.Patients with adenoid and tonsil hypertrophy had low HDL-C. HDL-C levels are inversely related to the sum of adenoid and tonsillar size scores and AHI in SDB children. HDL-C may be a sensitive indicator of serum lipids changes in SDB children.

Stem cell antigen (Sca) 1, a glycosyl phosphatidylinositol-anchored protein localized to lipid rafts, is upregulated in the heart during myocardial infarction and renovascular hypertension-induced cardiac hypertrophy. It has been suggested that Sca-1 plays an important role in myocardial infarction. To investigate the role of Sca-1 in cardiac hypertrophy, we performed aortic banding in Sca-1 cardiac-specific transgenic mice, Sca-1 knockout mice, and their wild-type littermates. Cardiac hypertrophy was evaluated by echocardiographic, hemodynamic, pathological, and molecular analyses. Sca-1 expression was upregulated and detected in cardiomyocytes after aortic banding surgery in wild-type mice. Sca-1 transgenic mice exhibited significantly attenuated cardiac hypertrophy and fibrosis and preserved cardiac function compared with wild-type mice after 4 weeks of aortic banding. Conversely, Sca-1 knockout dramatically worsened cardiac hypertrophy, fibrosis, and dysfunction after pressure overload. Furthermore, aortic banding–induced activation of Src, mitogen-activated protein kinases, and Akt was blunted by Sca-1 overexpression and enhanced by Sca-1 deficiency. Our results suggest that Sca-1 protects against cardiac hypertrophy and fibrosis via regulation of multiple pathways in cardiomyocytes.

Electronic resources purchased by library mostly only allow access of authorized users who own on-campus IP address. Some off-campus users who get on the Internet by dialing, etc and have no fixed IP address cannot access library resources. In this paper, building one secure and reliable virtual private network is presented by utilizing VPN technology on the basis of campus network to be specially used by library management system.

The design of information center library management system (LMS) database and the realization process of system functions are introduced. The system is network library management system operated on the company backbone network and it consists of eight subsystems of book cataloging, book acquisitioning, book circulation, periodical management, standard management, data management, system maintenance and Web query. The technology mode combined the Client/Server with the Browser/Server is adopted, through which functions of computer network management and Web query of books and reference materials are realized.

Baicalein, a flavonoid present in the root of Scutellaria baicalensis, is well known for its antibacterial, antiviral, anti-inflammatory, antithrombotic, and antioxidant effects. Here we show that baicalein also attenuates cardiac hypertrophy. Aortic banding (AB) was performed to induce cardiac hypertrophy secondary to pressure overload in mice. Mouse chow containing 0.05% baicalein (dose: 100 mg/kg/day baicalein) was begun 1 week prior to surgery and continued for 8 weeks after surgery. Our data demonstrated that baicalein prevented cardiac hypertrophy and fibrosis induced by AB, as assessed by echocardiographic and hemodynamic parameters and by pathological and molecular analysis. The inhibitory action of baicalein on cardiac hypertrophy was mediated by effects on mitogen-activated protein kinase kinase (MEK)-extracellular signal-regulated kinases (ERK1/2) signaling and GATA-4 activation. In vitro studies performed in rat cardiac H9c2 cells confirmed that baicalein attenuated cardiomyocyte hypertrophy induced by angiotensin II, which was associated with inhibiting MEK-ERK1/2 signaling. In conclusion, our results suggest that baicalein has protective potential for targeting cardiac hypertrophy and fibrosis through suppression of MEK-ERK1/2 signaling. Baicalein warrants further research as a potential antihypertrophic agent that might be clinically useful to treat cardiac hypertrophy and heart failure.

Background Puerarin is the most abundant isoflavonoid in kudzu root. It has been used to treat angina pectoris and myocardial infarction clinically. However, little is known about the effect of puerarin on cardiac hypertrophy. Methods Aortic banding (AB) was performed to induce cardiac hypertrophy in mice. Puerarin premixed in diets was administered to mice after one week of AB. Echocardiography and catheter-based measurements of hemodynamic parameters were performed at 7 weeks after starting puerarin treatment (8 weeks post-surgery). The extent of cardiac hypertrophy was also evaluated by pathological and molecular analyses of heart samples. Cardiomyocyte apoptosis was assessed by measuring Bax and Bcl-2 protein expression and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. In addition, the inhibitory effect of puerarin (1 μM, 5 μM, 10 μM, 20 μM, 40 μM) on mRNA expression of atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) in Ang II (1 μM)-stimulated H9c2 cells was investigated using quantitative real-time reverse transcription-polymerase chain reaction. Results Echocardiography and catheter-based measurements of hemodynamic parameters at 7 weeks revealed the amelioration of systolic and diastolic abnormalities. Puerarin also decreased cardiac fibrosis in AB mice. Moreover, the beneficial effect of puerarin was associated with the normalization in gene expression of hypertrophic and fibrotic markers. Further studies showed that pressure overload significantly induced the activation of phosphoinositide 3-kinase (PI3K)/Akt signaling and c-Jun N-terminal kinase (JNK) signaling, which was blocked by puerarin treatment. Cardiomyocyte apoptosis and induction of Bax in response to AB were suppressed by puerarin. Furthermore, the increased mRNA expression of ANP and BNP induced by Ang II (1 μM) was restrained to a different extent by different concentrations of puerarin. Conclusion Puerarin may have an ability to retard the progression of cardiac hypertrophy and apoptosis which is probably mediated by the blockade of PI3K/Akt and JNK signaling pathways.