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Histone deacetylase (HDAC) inhibitors can protect the brain from ischemic injury. This study aimed to identify the regulation of HDAC3 in cerebral ischemic injury. Middle cerebral artery occlusion (MCAO) was performed to establish a mouse model with cerebral ischemic injury, in which expression of HDAC3 and miR-19a was evaluated using RT-qPCR. In MCAO mice with silencing of HDAC3, infarct volume was determined using 2,3,5-triphenyl tetrazolium chloride (TTC) staining, and serum levels of TNF-α, IL-6, and IL-8 were measured using ELISA. An in vitro model was constructed in human umbilical vein endothelial cells (HUVECs) with oxygen-glucose deprivation/reoxygenation (OGD/R), followed by gain- and loss-of-function experiments. Relationships among miR-19a, HDAC3, and syndecan-1 (SDC1) were explored using RIP, ChIP, and dual-luciferase reporter assays. The expression of HDAC3, SDC1, JAK1, and STAT3 along with the extent of JAK1 and STAT3 phosphorylation was measured by Western blot analysis. HUVEC viability, apoptosis, and angiogenesis were assessed by CCK-8, flow cytometry, and angiogenesis assays in vitro separately. We found elevated HDAC3 and downregulated miR-19a expression in the MCAO mice. Decreased TNF-α, IL-6, and IL-8 serum levels were observed in response to silencing of HDAC3. HDAC3 inhibited the expression of miR-19a, which in turn targeted SDC1, leading to JAK1/STAT3 signaling pathway activation. HDAC3 overexpression or miR-19a inhibition repressed HUVEC viability and angiogenesis but enhanced HUVEC apoptosis. Our data unraveled the mechanism whereby HDAC3 inhibition ameliorated cerebral ischemic injury by activating the JAK1/STAT3 signaling pathway through miR-19a-mediated SDC1 inhibition.

Dexmedetomidine (Dex) possesses analgesic and anaesthetic values and reported being used in cerebral ischaemic injury therapeutics. Accumulating studies have determined the effect of microRNAs (miRNAs) on the cerebral ischaemic injury. Thus, the present study aimed to unravel the molecular mechanism of miR‐381 and Dex in cerebral ischaemic injury. For this purpose, the cerebral ischaemic injury rat model was established by induction of middle cerebral artery occlusion (MCAO) and expression of miR‐381 and IRF4 was determined. Thereafter, MCAO rats were treated with Dex, miR‐381 mimic, miR‐381 inhibitor and oe‐IRF4 respectively, followed by evaluation of neurological function. Furthermore, neuron cells were isolated from the hippocampus of rats and subjected to oxygen‐glucose deprivation (OGD). Then, OGD‐treated neuron cells and primary neuron cells were examined by gain‐ and loss‐of‐function assay. Neuron cell apoptosis was detected using TUNEL staining and flow cytometry. The correlation between interferon regulatory factor 4 (IRF4) and interleukin (IL)‐9 was detected. Our results showed down‐regulated miR‐38 and up‐regulated IRF4 in MCAO rats. Besides, IRF4 was targeted by miR‐381 in neuron cells. Dex and overexpressed miR‐381, or silenced IRF4 improved the neurological function and inhibited neuron cell apoptosis in MCAO rats. Additionally, in MCAO rats, Dex was found to increase the miR‐381 expression and reduced IRF4 expression to decrease the IL‐9 expression, which suppressed the inflammatory response and cell apoptosis both in vivo and in vitro. Importantly, our study demonstrated that Dex elevated the expression of miR‐381, which ultimately results in the inhibition of inflammation response in rats with cerebral ischaemic injury.

Cell death after spinal cord ischemia/reperfusion (I/R) can occur through necrosis, apoptosis, and autophagy, resulting in changes to the immune environment. However, the molecular mechanism of this immune regulation is not clear. Accumulating evidence indicates that microRNAs (miRs) play a crucial role in the pathogenesis of spinal cord I/R injury. Here, we hypothesized miR-22-3p may be involved in spinal cord I/R injury by interacting with interferon regulatory factor (IRF) 5. Rat models of spinal cord I/R injury were established by 12-min occlusion of the aortic arch followed by 48-hr reperfusion, with L4-6 segments of spinal cord tissues collected. MiR-22-3p agomir, a lentivirus-delivered siRNA specific for IRF5, or a lentivirus expressing wild-type IRF5 was injected intrathecally to rats with I/R injury to evaluate the effects of miR-22-3p and IRF5 on hindlimb motor function. Macrophages isolated from rats were treated with miR-22-3p mimic or siRNA specific for IRF5 to evaluate their effects on macrophage polarization. The levels of IL-1β and TNF-α in spinal cord tissues were detected by ELISA. miR-22-3p was down-regulated, whereas IRF5 was up-regulated in rat spinal cord tissues following I/R. IRF5 was a target gene of miR-22-3p and could be negatively regulated by miR-22-3p. Silencing IRF5 or over-expressing miR-22-3p relieved inflammation, elevated Tarlov score, and reduced the degree of severity of spinal cord I/R injury. Increased miR-22-3p facilitated M2 polarization of macrophages and inhibited inflammation in tissues by inhibiting IRF5, thereby attenuating spinal cord I/R injury. Taken together, these results demonstrate that increased miR-22-3p can inhibit the progression of spinal cord I/R injury by repressing IRF5 in macrophages, highlighting the discovery of a promising new target for spinal cord I/R injury treatment.

In this paper, melamine was used as porogen to prepare porous polyimide film by in-situ polymerization. The mechanical properties, thermal properties, dielectric properties, oil content and friction and wear properties of polyimide films with different porosity were investigated. The tensile strength of porous films decreases obviously with increase of melamine content. It shows the lower thermal decomposition temperature and the faster decomposition speed compared with the non-porous film, indicating higher heat exchange rate due to holes in porous films. As the porogen content increases, the dielectric constant decreases significantly, and the film with melamine content of 20 wt.% has the lowest dielectric constant of 2.43. The holes lead to good oil storage performance and the wear rate and the friction coefficient decrease with the increase of porosity. Keywords: polyimide; porous; melamine; dielectric; friction

NF-κB is a core transcription factor, the activation of which can lead to hypoxic-ischemic brain damage (HIBD), while RCAN1 plays a protective role in HIBD. However, the relationship between NF-κB and RCAN1 in HIBD remains unclear. This study aimed to explore the mechanism of NF-κB signaling pathway in hippocampal neuron apoptosis and cognitive impairment of neonatal rats with HIBD in relation to RCAN1. Initially, microarray analysis was used to determine the differentially expressed genes related to HIBD. After the establishment of HIBD rat models, gain- or loss-of-function assay was performed to explore the functional role of NF-κB signaling pathway in HIBD. Then, the learning and memory ability of rats was evaluated. Expression of RCAN1, NF-κB signaling pathway-related genes and glial fibrillary acidic protein (GFAP), S-100β and acetylcholine (Ach) level, and acetylcholinesterase (AchE) activity were determined with neuron apoptosis detected to further explore the function of NF-κB signaling pathway. RCAN1 could influence the development of HIBD. In the HIBD model, the expression of RCAN1 and NF-κB-related genes increased, and NF-κB p65 showed a significant nuclear shift. By activation of NF-κB or overexpression of RCAN1, the number of neuronal apoptosis, S-100β protein level, and AchE level increased significantly, Ach activity decreased significantly, and GFAP positive cells increased. In addition, after the activation of NF-κB or overexpression of RCAN1, the learning and memory ability of HIBD rats was inhibited. All the results show that activation of NF-κB signaling pathway promotes RCAN1 expression, thus increasing neuronal apoptosis and aggravating cognitive impairment in HIBD rats.

Long noncoding RNAs play critical roles in cellular homeostasis, and long noncoding RNA H19 (H19) is implicated in several pathologic conditions. The putative role of H19 in the pathogenesis and progression of hypoxic-ischemic brain damage (HIBD) is not yet understood. Therefore, a series of in vivo and in vitro experiments were designed to investigate the potential roles of H19 in neuronal apoptosis and cognitive dysfunction in HIBD. H19 expression was decreased in HIBD rat models established by partial occlusion of carotid artery. H19 bound to and decreased the expression of miR-107, which also increased VEGF expression. H19 overexpression reduced neuronal apoptosis and alleviated cognitive dysfunction in HIBD rats. The up-regulation of miR-107 reversed the protective effects conferred by H19. In addition, the cell model of HIBD was established by oxygen-glucose deprivation in neuronal cells used. H19 overexpression in oxygen-glucose deprivation neurons increased B-cell lymphoma-2 and decreased B-cell lymphoma-2–associated X, total and cleaved caspase-3 expressions. Taken together, the results showed that H19 expresses at a low level in HIBD. H19 overexpression decreased miR-107 and increased VEGF expression, which resulted in repressed neuronal apoptosis and alleviated cognitive dysfunction. Thus, H19 may serve as a molecular target for translational research for HIBD therapy.

Background We conducted a randomized clinical trial to determine whether adjunctive lidocaine diminishes the incidence of adverse effects in pediatric patients sedated with ketamine. Methods This case‐control study involved 586 consecutive pediatric patients necessitating anesthesia. Then systolic blood pressure, heart rate, respiratory rate, and blood oxygen saturation were observed. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea nitrogen (BUN), and creatinine (Cr) levels were tested. General dose of ketamine, the time of onset and duration of anesthesia and postoperative recovery, anesthesia effect, and adverse reaction were subsequently compared. High‐performance liquid chromatography was employed to detect ketamine concentration at different time points after administration, and the postoperative cognition function was further evaluated. Results Intra‐ and post‐operation, the rising degree of ALT, AST, BUN, and Cr in patients treated with ketamine was higher than those in patients treated with the ketamine‐lidocaine complex. General dose of ketamine, the time of onset and duration of anesthesia, postoperative recovery time, and the incidence rate of adverse reaction in patients treated with ketamine‐lidocaine complex were lower, but the concentration of ketamine was higher compared to the patients treated with ketamine. In patients treated with the ketamine‐lidocaine complex, elimination half‐life of ketamine was prolonged, the area under curve was increased, and the plasma clearance rate was decreased relative to those with ketamine alone. Conclusions Ketamine combined with lidocaine may be beneficial in shortening the onset of anesthesia, promoting postoperative awake, prolonging elimination half‐life, increasing area under curve, and decreasing plasma clearance rate and incidence of adverse reactions.

Long noncoding RNAs have been documented to be protective against ischemia/reperfusion (I/R) injury. However, few research works have focused on the protective effects of PRR34-AS1 on I/R injury after total knee arthroplasty (TKA). The objective of the present study was to investigate the possible effect of PRR34-AS1 on I/R injury after TKA. A mouse model with I/R injury after TKA was established. The interaction between PRR34-AS1 and Janus kinase 1 (JAK1) was examined and thoroughly investigated. Next, the effects of PRR34-AS1 on the expression of apoptosis-related proteins, JAS-signal transducer and activator of transcription (STAT) signaling pathways, and inflammation-related genes, chondrocyte proliferation, and apoptosis were analyzed after gain- and loss-of-function experiments. Attenuated symptoms were observed in mice pretreated with propofol, which was evidenced by decreased positive expression rate of JAK1 protein and superoxide dismutase content along with increased malondialdehyde content and IL-10 levels. PRR34-AS1 was poorly expressed in mice with I/R injury after TKA. JAK1 was a target of PRR34-AS1. Upregulated PRR34-AS1 diminished expression of JAK1, STAT1, JAK2, and STAT3 as well as cell apoptosis, while enhancing cell proliferation in vitro. Furthermore, JAK1 silencing could reverse the suppressed cell proliferation and enhanced cell apoptosis of chondrocytes imposed by silencing PRR34-AS1. Upregulation of PRR34-AS1 can potentially relieve I/R injury after TKA in mice pretreated with propofol through inhibition of the JAS-STAT signaling pathway by targeting JAK1.

Hypoxic-ischemic brain damage (HIBD) is a common neurological disorder. Emerging reports reveal that long non-coding RNAs and microRNAs (miRs) are implicated in the progress of HIBD. In this study we tried to ascertain whether lncRNA MALAT1, with the involvement of miR-429 and WNT1, affects HIBD. Initially, a HIBD mouse model was established. Then, we treated HIBD mice with dexmedetomidine (DEX) and then up- or down-regulated the expression of MALAT1, miR-429 and WNT1 in HIBD mice and neurons. Meanwhile, brain injury and hippocampal neuronal apoptosis were evaluated. Moreover, the interaction among MALAT1, miR-429 and WNT1 in HIBD was investigated. MALAT1 and WNT1 were high-expressed in brain tissues of HIBD mice while miR-429 was low-expressed in brain tissues from HIBD mice. Interestingly, MALAT1 silencing was observed to enhance the cerebral protection of DEX against HIBD. In addition, it was confirmed that MALAT1 sponged miR-429 downregulating expression of miR-429, thereby promoting apoptosis of hippocampal neurons. This effect was achieved through up-regulating the level of WNT1. Taken together, this study demonstrates that silencing of MALAT1 enhances the cerebral protection of DEX against HIBD by suppressing WNT1 expression through miR-429.

Emerging evidence showed that functional polymorphisms in the IL-10 gene may have effects on individuals' susceptibility to nasopharyngeal, oral and esophageal cancers, yet individually published findings are inconsistent. We therefore designed the meta-analysis to investigate the correlations of IL-10 genetic polymorphisms with susceptibility to nasopharyngeal, oral and esophageal cancers. The EMBASE, MEDLINE, CINAHL, Web of Science and the Chinese Biomedical Database (CBM) databases were searched with no language restrictions. We use Comprehensive Meta-analysis 2.0 software to carry out statistical analysis. Ten case-control studies with a number of 1,883 patients and 2,857 healthy subjects were enrolled. Our results revealed that IL-10 rs1800872 T>G and rs1800896 A>G polymorphisms has a significantly association with the increased risk of esophageal cancer under the allele and dominant models; rs1800871 T>G, rs1800872 T>G and rs1800896 A>G under allele and dominant models could increase the risk of nasopharyngeal cancer; rs1800871T>G, rs1800872T>G and rs1800896 A>G SNPs under allele model were closely related to the susceptibility to oral cancer. Our findings support the point that IL-10 genetic polymorphisms may play essential role in identifying esophageal cancer, nasopharyngeal cancer and oral cancer at early stage.

Genetic analysis of 111 patients with phenylketonuria or hyperphenylalaninemia has uncovered a novel 8 bp deletion variant in the phenylalanine hydroxylase gene. The novel deletion mutation c.1034_1041del generated a protein-coding frameshift and resulted in a premature stop codon rendering severe disruption of enzymatic activity. Molecular and clinical evidence also implies that the missense mutation c.301G>A is likely to be mildly pathogenic, although it was previously reported as a benign variant.

Through gene mutation analysis of patients with non-syndromic hearing loss (NSHL) correct genetic counseling for patients with NSHL and their family members were provided. A total of 116 patients suffering from NSHL were selected, and Sanger sequencing was applied to analyze 31 mutation sites in four deafness genes [gap junction β-2 (GJB2), solute carrier family 26, member 4 (SLC26A4), GJB3 and mitochondria 12S ribosomal ribonucleic acid (12SrRNA)]. Based on detection results, for the families with reproductive needs, amniotic fluid was extracted from pregnant women during proper gestational weeks to identify fetal genotypes and predict hearing state. Among 116 patients with NSHL, 51 patients carrying definite pathogenic mutation were found, including 35 patients with GJB2 mutations, 14 patients with SLC26A4 gene mutations and 2 patients with mitochondrial deoxyribonucleic acid 12SrRNA (mtDNA 12SrRNA) mutations. No GJB3 gene mutation site was detected. In addition, prenatal diagnosis to 17 pregnant women who had given birth to babies with deafness was performed, and results suggested that genotypes of 6 fetuses were consistent with those of probands, genotypes of 8 fetuses were consistent with those of their parents, and no mutation was found in the other 3 fetuses. Gene mutation analysis of patients with NSHL can identify the etiology and provide appropriate genetic counseling and birth guiding for patients with NSHL and their family members. In addition, prenatal diagnosis to the families who plan to give birth again can avoid the natality of fetuses with hearing loss.

Two new species of the genus Oxyporus Fabricius, 1775 are described based on specimens collected in Yunnan Province, China, namely Oxyporus (Oxyporus) fentianae sp. nov. from Mojiang County and Oxyporus (Oxyporus) ningerius sp. nov. from Ninger County. The number of Oxyporus species worldwide is thus increased to 130. Color images of the habitus and aedeagi of the two new species are included. A key to the Oxyporus species of Yunnan Province is provided.

Objective Hypoxic-ischemic brain damage (HIBD) is a major cause of acute mortality and chronic neurological morbidity in infants and children. Dexmedetomidine (DEX) is an effective choice in HIBD treatment. Recent findings have revealed that microRNA-128 (miR-128) is implicated in cerebral ischemia reperfusion. Hence, this study aimed to investigate the role of miR-128 in HIBD. Methods HIBD models of neonatal mice were established. HIBD mice were treated with DEX, and injected with agomir (ago)-miR-128 or antagomir (anti)-miR-128 into the lateral ventricles to explore the influence of miR-128 on the neuroprotective effects of DEX on HIBD. Subsequently, the mice body weight, left/right (L/R) brain weight ratio, left-brain water content as well as learning and memory abilities were measured. Furthermore, the pathological changes of brain tissues and apoptosis rate of nerve cells were determined. The potential relationship between miR-128 and WNT1 was analyzed. Results Over-expression of miR-128 caused an increase in mouse body weight, L/R brain weight ratio, and learning and memory abilities, while led to a decline in left-brain water content, brain tissue injury and apoptosis rate of nerve cells in DEX-treated HIBD mice. WNT1 was targeted and negatively regulated by miR-128. Silencing of WNT1 exerted the same effect as miR-128 on enhancing the neuroprotective effect of DEX on HIBD mice. Conclusion Collectively, miR-128 enhanced neuroprotective effect of DEX on HIBD neonatal mice by inhibiting WNT1.

To meet the need of multi-channel DC power supply to activate multiple macro fiber composite (MFC) material simultaneously, a novel multi-channel adjustable DC supply using single-input single-output transformer based on spectral separation is proposed. A hybrid signal containing multiple frequency bands is boosted to obtain a high-voltage signal without bands change. Several frequency selection circuits are then used to separate individual signals in different frequency band from the high-voltage signal. Finally, these signals are rectified and filtered respectively to obtain multiple channel DC voltages. The feasibility of the proposed scheme is analyzed theoretically and verified by simulation. Experimental results prove that each part of the scheme runs reliable and the output is stable and adjustable.

A visual tracking system based on ultrasonic motors is designed in view of shortcoming of traditional video surveillance system, which has a large volume, complicated structure. The pan-tilt can rotate in horizontal and vertical directions by using two ultrasonic motors served as the driving units. The image from video camera is processed and the target is identified and real-time tracked by rotating the pan-tilt which is controlled by ultrasonic motor. Compared with electromagnetic motor, the ultrasonic motor has advantages of high torque at low speed, quick response, high precision and self-locked, which makes the structure simpler and control more convenient. Experimental results show that the system can be stably tracking the selected target with fast response speed and relatively high tracking accuracy.

A lumped parameter model is developed to study thermal management system performance of underwater vehicle equipping large power proton exchange membrane fuel cell propulsion unit. Fuel cell voltage current characteristic and heat release characteristic are represented by models which take effect of cooling water temperature into considered. Fuel cell stack performance models are validated against experimental data. Cooperated with experimental based models of water pump and heat exchanger, thermal management system performance is analyzed while fuel cell stack fresh cooling water outlet temperature is set to be at a certain value. The results show that inlet seawater temperature variation has little effect on opening of regulating valve, but engine power output variation results in notably regulating valve opening fluctuation. Modeling results would be employed in design of a underwater vehicle 300kW fuel cell engine system..

The present study aims to explore the role of stromal cell-derived factor-1α (SDF-1α)/stromal cell-derived factor receptor-4 (CXCR4) signaling pathway to the clinicopathological features and prognosis of patients with nasopharyngeal carcinoma (NPC). From January 2009 to December 2010, 102 patients with NPC and 80 patients with chronic nasopharyngitis were enrolled for the study. Immunohistochemical staining, quantitative real-time polymerase chain reaction (qRT-PCR), and Western blotting were employed to determine the expressions of SDF-1α and CXCR4 proteins in NPC tissues and chronic nasopharyngitis tissues. Chi-square test was conducted to analyze the associations of the expressions of SDF-1α and CXCR4 proteins with the clinicopathological features of NPC patients. Spearman rank correlation analysis was used to analyze the correlation between the SDF-1α protein expression and CXCR4 protein expression. The mRNA and protein expressions of SDF-1α and CXCR4 in NPC tissues were significantly higher than those in chronic nasopharyngitis tissues. The expressions of SDF-1α and CXCR4 proteins showed associations with T staging, N staging, tumor node metastasis (TNM) staging, skull base invasion, and cervical lymph node metastasis of NPC patients. Compared with NPC patients showing negative expressions of SDF-1α and CXCR4 proteins, those with positive expressions of SDF-1α and CXCR4 proteins had a significantly shorter survival time. SDF-1α protein, CXCR4 protein, EBV-IgG status, T staging, N staging, TNM staging, skull base invasion, and cervical lymph node metastasis were independent risk factors for the prognosis of NPC. The findings indicated that SDF-1α/CXCR4 signaling pathway might be associated with the clinicopathological features and prognosis of patients with NPC.

Neurotrophic factor (NF) and Trk signaling mechanisms underlying the promotion of motor recovery following acute spinal cord injury (SCI) in rats were investigated. Thirty-six adult Sprague-Dawley rats of both genders were randomly divided into three groups: Sham-operated, model, and NF/Trk. Each group consisted of 12 rats, with four subgroups in each group: 1, 3, 5 and 7 days. Sham-operated rats received a laminectomy without SCI, while in model group rats, SCI was induced using an improved version of the Allen's method. After analepsia, sham-operated and model group rats were given normal saline via gavage, while the NF/Trk group received NFs and Trk. Lower limb function was measured using the Basso, Beattie and Bresnahan scale 1, 3, 5 and 7 days before and after surgery. Results were analyzed statistically. Six rats from each group were randomly selected for sacrifice at 1, 3, 5 and 7 days after the operation. Morphological changes in motor neurons in the anterior gray column were observed by hematoxylin and eosin, and Nissl staining. Brain-derived expression of NF (BNDF) and neurotrophin-3 (NT-3) was detected by immunofluorescence, and the number of positive cells was counted. Expression of Trk B and Trk protein C receptor was measured by western blotting. In the NF/Trk group, the expression of NF/Trk pathway components remarkably increased. In addition, the morphology of motor neurons in the anterior gray column was improved. Expression of BNDF and NT-3 was significantly increased in motor neurons of the anterior gray column in NF/Trk rats compared with those of sham-operated and model rats (P

The progression of glioblastoma (GBM) is driven by dynamic alterations in the activity and connectivity of gene pathways. Revealing these dynamic events is necessary in order to understand the pathological mechanisms of, and develop effective treatments for, GBM. The present study aimed to investigate dynamic alterations in pathway activity and connectivity across radiotherapy and chemoradiation conditions in GBM, and to give system‑level insights into molecular mechanisms for GBM therapy. A total of two differential co‑expression networks (DCNs) were constructed using Pearson correlation coefficient analysis and one sided t‑tests, based on gene expression profiles and protein‑protein interaction networks, one for each condition. Subsequently, shared differential modules across DCNs were detected via significance analysis for candidate modules, which were obtained according to seed selection, module search by seed expansion and refinement of searched modules. As condition‑specific differential modules mediate differential biological processes, the module connectivity dynamic score (MCDS) was implemented to explore dynamic alterations among them. Based on DCNs with 287 nodes and 1,052 edges, a total of 28 seed genes and seven candidate modules were identified. Following significance analysis, five shared differential modules were identified in total. Dynamic alterations among these differential modules were identified using the MCDS, and one module with significant dynamic alterations was identified, termed the dynamic module. The present study revealed the dynamic alterations of shared differential modules, identified one dynamic module between the radiotherapy and chemoradiation conditions, and demonstrated that pathway dynamics may applied to the study of the pathogenesis and therapy of GBM.

Multislice CT angiography represents one of the most exciting technological revolutions in cardiac imaging and it has been increasingly used in the diagnosis of coronary artery disease. Rapid improvements in multislice CT scanners over the last decade have allowed this technique to become a potentially effective alternative to invasive coronary angiography in patients with suspected coronary artery disease. High diagnostic value has been achieved with multislice CT angiography with use of 64- and more slice CT scanners. In addition, multislice CT angiography shows accurate detection and analysis of coronary calcium, characterization of coronary plaques, as well as prediction of the disease progression and major cardiac events. Thus, patients can benefit from multislice CT angiography that provides a rapid and accurate diagnosis while avoiding unnecessary invasive coronary angiography procedures. The aim of this article is present an overview of the clinical applications of multislice CT angiography in coronary artery disease with a focus on the diagnostic accuracy of coronary artery disease; prognostic value of coronary artery disease with regard to the prediction of major cardiac events; detection and quantification of coronary calcium and characterization of coronary plaques. Limitations of multislice CT angiography in coronary artery disease are also briefly discussed, and future directions are highlighted.

Purpose Family with sequence similarity 83 member H (FAM83H) plays key roles in tumorigenesis. However, the specific roles of FAM83H in cervical cancer (CC) have not been well studied. Materials and methods The RNA-seq data of 306 CC tissues and three normal samples downloaded from The Cancer Genome Atlas were used to analyze the expression of FAM83H. The Kaplan-Meier method was used to draw survival curves. Associations between FAM83H expression and clinicopathological factors were analyzed by chi-square test. Cox proportional hazards model was used to analyze prognostic factors. Loss-of-function assays were conducted to discover the biological functions of FAM83H in cell proliferation, colony formation, invasion, and migration. Real-time Quantitative Reverse Transcription PCR (qRT-PCR) and Western blotting were used to measure the expression levels of FAM83H in CC cell lines. Results Our results demonstrated that FAM83H is overexpressed in CC tissues and that high FAM83H expression is associated with worse overall survival (OS). High FAM83H expression in CC was associated with clinical stage, pathologic tumor, and pathologic node. Univariate analysis suggested that FAM83H expression was significantly related to the OS of CC patients. Although multivariate analysis showed that FAM83H expression was not an independent prognostic factor for the OS of CC patients, the effects of FAM83H on CC cell growth and motility was significant. Loss-of-function experiments demonstrated that knockdown of FAM83H inhibited proliferation, colony formation, migration, and invasion of CC cells by inactivating PI3K/AKT pathway. Conclusion FAM83H might play a crucial role in CC progression and could act as a novel therapeutic target in CC.

An organic compound containing N, B and O was synthesised by reacting 3-hydroxymethyl-quinazolin-4-ones and formalin in 1, 4-dioxane solution, the resulting product then being reacted with butanol and boric acid in dimethylbenzene solution. The tribological performance of the novel compound when added to liquid paraffin was evaluated using a four-ball tester and a ring-on-block machine. The relationship between performance and concentration was analysed, and the results showed that the compound possesses good anti-wear, friction-reducing and load-carrying properties. The mechanism of action of the additive was investigated using X-ray photoelectron spectroscopy. Surface analysis indicated the formation of a protective film containing borate, Fe(3)O(4), and an organonitrogen compound. This protective film formed during sliding processes contributes to the increase in wear resistance. Copyright (C) 2010 John Wiley & Sons, Ltd.

The smoothed particle hydrodynamics (SPH), as a fully Lagrangian particle method, has been suc- cessfully applied to astrophysical problems and extended to elastic dynamics and computational fluid dynamics. High order derivatives have to be approximated when elastic dynamics problems are modeled. However, the approximation errors in SPH could lead to computational failure in the case that the order of derivative is high. A novel method was proposed in order to improve the accuracy of SPH method, which shows the relationship between the selected functions and their SPH approximations. The entire involved system was represented by a finite number of particles that carry individual mass and occupy individual space, and the integral interpo- lation was approximated by a summation interpolation. In addition, error comparison was made between SPH method with and without the present improvement.

The double-bond isomerization of 1-pentene over zeolites has been investigated by using density functional theory at the B3LYP/6-31G(d,p) level. The calculated results indicate that the double-bond isomerization may proceed via either a stepwise or a concerted reaction pathway. The stepwise reaction consists of two elementary steps: firstly, the formation of an alkoxy intermediate by addition of a proton from zeolites, and then the decomposition of this alkoxy intermediate to yield an adsorbed 2-pentene. The calculated activation barriers are 17.9 and 31.5 kcal/mol for the first and second step, respectively. The concerted reaction occurs via one-shift proton transfer, which avoids the formation of highly stable alkoxide species. The resulting activation energy, 20.5 kcal/mol, is close to that of the first step of the stepwise reaction. From an energetic point of view, it is expected that at low temperatures, the concerted reaction mechanism dominates the overall isomerization reaction due to the lower activation energy, while at higher temperatures, the two reaction pathways compete against each other because the alkoxy formation will occur relatively easily. The results can well explain the experimental phenomena observed.

The smoothed particle hydrodynamics (SPH) is a mesh-free particle method, which has been successfully applied to a wide range of astrophysical problems. So far, the SPH method has been extended to ...

The double-bond isomerization of 1-pentene to cis -2-pentene on the surface of the molecular sieves has been investigated by using density functional theory with a cluster model simulating the zeolite materials. The microcosmic interaction of the pentene molecule with the Bronsted acid site of the zeolite leads to the formation of a π-complex, where the C C double bond is weakly coordinated to the proton of the Bronsted acid site. The transition state has an eight-member cyclic structure, in which two hydrogen atoms are situated between one oxygen atom of the zeolite and one carbon atom of the migrating double bond, respectively. The calculations of the intrinsic reaction coordinate indicate that the double-bond isomerization of 1-pentene proceeds via a concerted proton transfer between the Bronsted acid sites of the zeolite and the pentene molecules. The calculated activation energy of 11.74 kcal/mol is close to the experimental data.

Oxyporus (Oxyporus) kunmingius sp. nov. is described from Yunnan, China. Color images of the habitus and aedeagus of the new species are included. A key to the genus Oxyporus of Yunnan species is provided.