Search

The present study was conducted to investigate the regulatory mechanism of liver injury in largemouth bass Micropterus salmoides (LMB) fed low protein high starch diets. Two isolipidic and isoenergetic diets were formulated with different protein and starch ratios, being named as diets P49S9 (48.8 % protein and 9.06 % starch) and P42S18 (42.4 % protein and 18.2 % starch). Each diet was fed to triplicate replicates of LMB (initial body weight, 4.65 ± 0.01 g) juveniles. Fish were fed to visual satiation for 8 weeks. The results indicated that though the P42S18 fish up-regulated the feeding ratio to meet their protein requirements, feeding efficiency ratio and growth performance were impaired in treatment P42S18 as compared to treatment P49S9. Periodic acid-Schiff (PAS) staining showed glycogen accumulated in the liver of LMB fed low protein high starch diets, and the reason should be attributed to down-regulated expression of the glycogenolytic glycogen debranching enzyme. Lower liver lipid level was associated with feeding low protein high starch diets in LMB, which should be resulted from the changes in hepatic glycerolipid metabolism regulated by lipoprotein lipase (representative of triglyceride synthesis, up-regulated) and diacylglycerol acyltransferase (representative of triglyceride breakdown, down-regulated). Though fasting plasma glucose level was comparable, treatment P42S18 performed inferior glucose tolerance to treatment P49S9. Hematoxylin-eosin (HE) and TdT-mediated dUTP Nick-End Labeling (TUNEL) staining suggested that feeding low protein high starch diets induced disruption of structural integrity, inflammation and apoptosis in the hepatocytes of LMB. As expected, KEGG pathways analysis indicated that many of the up-regulated differentially expressed genes were enriched in AGE (advanced glycation end product)/RAGE (receptor for AGE), Toll-like receptor and apoptosis signaling pathways. Our transcriptome data revealed that feeding low protein high starch diets might promote the accumulation of AGEs in LMB, which bound to RAGE and subsequently induced PI3K/Akt signal pathway. The activation of Akt induced NF-κB translocation into the nucleus thus releasing proinflammatory factors including tumor necrosis factor-α (TNF-α) and interleukin-8. The release of these inflammatory factors concomitantly induced T cell stimulation and natural killer cells chemotactic effects through Toll-like receptor signaling pathway. Besides mediating inflammation and immune response, TNF-α signal transduction participated in mediating apoptosis through the receptor of TNF (TNF-R1) pathway by up-regulating the expression of caspase 8 and cytochrome c. In conclusion, our results demonstrated that feeding low protein and high starch diets induced hepatocytes inflammation and apoptosis in LMB through the PI3K/Akt/NF-κB signaling pathway.

Isoflurane (ISO) elicits protective effects on ischemia-induced brain injury. We investigated whether sub-anesthetic (0.7%) ISO post-conditioning attenuates the inflammation and apoptosis in oxygen-glucose deprivation (OGD)-insulted co-cultures (microglia and neurons) in vitro and the brain injury of the middle cerebral arterial occlusion (MCAO) rat. We demonstrated that ISO augmented the viability of OGD-treated microglia and neurons. ISO reduced the expression and activation of COX2 and iNOS in OGD-challenged microglia. ISO repressed the production of tumor necrosis factor-α, interleukin (IL)-1β, IL-6, IL-8, and monocyte chemoattractant protein-1 in OGD-exposed microglia. ISO also decreased nucleosomal fragmentation and caspase-3 activity but increased mitochondrial membrane potential in OGD-stimulated microglia and neurons. Mechanistically, ISO suppressed OGD-induced microglial inflammation by blocking ROS-regulated p38 MAPK/NF-κB signaling pathway and hampered OGD-triggered microglial apoptosis in a ROS- or NO-dependent fashion. In vivo results with MCAO rats were partly consistent with the in vitro observation. These findings indicate that sub-anesthetic ISO post-conditioning abates the inflammation and apoptosis in OGD-stimulated rat microglia and the apoptosis of OGD-exposed neurons and the brain injuries of MCAO rats, suggesting it as a potentially effective therapeutic approach for ischemic brain damages.

Summary Osteosarcopenic obesity (OSO) is a complex disease commonly seen in the elderly. We found that resistance training may improve bone mineral density, skeletal muscle mass, and body fat percentage in patients with OSO. Therefore, resistance training is beneficial for elderly OSO patients and is worth being promoted. Purpose Investigate effects of resistance training on body composition and physical function in elderly osteosarcopenic obesity (OSO) patients. Methods PubMed, Web of Science, Embase, Cochrane Library, Medline, SinoMed, CNKI, and Wanfang Database were searched from inception until October 13, 2021.Two independent researchers extracted the key information from each eligible study. The methodological quality of included studies was assessed using the Physiotherapy Evidence Database (PEDro) scale. The Cochrane Risk of Bias Tool was used to assess the risk of bias. Grading of Recommendations Assessment Development and Evaluation (GRADE) was used to evaluate the quality of the outcomes. Sensitivity analysis indicated the stability of the results. Statistical analysis was performed using Review Manager 5.3. Results Four randomized controlled studies meeting the inclusion criteria were included, with 182 participants. Twelve weeks of resistance training improved bone mineral density (BMD, mean difference (MD) = 0.01 g/cm2, 95% confidence interval (CI): 0.001, 0.02, P = 0.03, I2 = 0%), skeletal muscle mass (SMM, MD = 1.19 kg, 95% CI: 0.50, 1.89, P = 0.0007, I2 = 0%), Z score, timed chair rise test (TCR), and body fat percentage (BFP, MD = − 1.61%, 95% CI: − 2.94, − 0.28, P = 0.02, I2 = 50%) but did not significantly affect skeletal muscle mass index (SMI, MD = 0.20 kg/m2, 95% CI: − 0.25, 0.64, P = 0.38, I2 = 0%) or gait speed (GS). Conclusions Resistance training is a safe and effective intervention that can improve many parameters, including BFP, SMM, and Z score, among OSO patients and is a good option for elderly individuals to improve their physical fitness.

We recently published that type 2 diabetes promotes cell centrosome amplification via upregulation of Rho-associated protein kinase 1 (ROCK1) and 14-3-3 protein-σ (14-3-3σ). This study further investigates the molecular mechanisms underlying diabetes-associated centrosome amplification. We found that treatment of cells with high glucose, insulin, and palmitic acid levels increased the intracellular and extracellular protein levels of Wingless-type MMTV integration site family member 6 (Wnt6) as well as the cellular level of β-catenin. The treatment also activated β-catenin and promoted its nuclear translocation. Treatment of cells with siRNA species for Wnt6, Frizzled-4 (FZD4), or β-catenin as well as introduction of antibodies against Wnt6 or FZD4 to the cell culture medium could all attenuate the treatment-triggered centrosome amplification. Moreover, we showed that secreted Wnt6-FZD4-β-catenin was the signaling pathway that was upstream of ROCK1 and 14-3-3σ. We found that advanced glycation end products (AGEs) were also able to increase the cellular and extracellular levels of Wnt6, the cellular protein level of β-catenin, and centrosome amplification. Treatment of the cells with siRNA species for Wnt6 or FZD4 as well as introduction of antibodies against Wnt6 or FZD4 to the cell culture could all inhibit the AGEs-elicited centrosome amplification. In colon tissues from a diabetic mouse model, the protein levels of Wnt6 and 14-3-3σ were increased. In conclusion, our results showed that the pathophysiological factors in type 2 diabetes, including AGEs, were able to induce centrosome amplification. It is suggested that secreted Wnt6 binds to FZD4 to activate the canonical Wnt6 signaling pathway, which is upstream of ROCK1 and 14-3-3σ, and that this is the cell signaling pathway underlying diabetes-associated centrosome amplification.

The patients with sarcopenic obesity (SO) have the characteristics of both sarcopenia and obesity, that is, less muscle mass and increased fat mass, and their morbidity, disability and mortality are higher than patients with sarcopenia or obesity alone.To investigate the effects of whole-body electromyostimulation (WB-EMS) training and protein supplementation intervention on body composition, physical function, metabolism and inflammatory biomarkers in middle-aged and elderly patients with SO.We searched for randomized controlled trials in seven databases, including PubMed, Web of Science, Embase, Cochrane Library, Scopus, SinoMed, and CNKI as of July 3, 2021. The methodological quality of each included study was assessed using the Physiotherapy Evidence Database (PEDro) scale. The Cochrane Risk of Bias Tool was used to assess the risk of bias. Statistical analysis was performed using Review Manager 5.3.Eleven randomized controlled studies with a total of 779 participants were included in this meta-analysis. WB-EMS training improved sarcopenia Z-score (MD = -1.52, 95 % CI: -2.27, -0.77, P 0.0001) and waist circumference (WC) (MD = -1.41, 95 % CI: -2.62, -0.20, P = 0.02), and increased skeletal muscle mass index (SMI) (MD = 1.27, 95 % CI: 0.66,1.88, P 0.0001) and appendicular skeletal muscle mass (ASMM) (MD = 0.68, 95 % CI: 0.08, 1.27, P = 0.03). Protein supplementation intervention reduced body fat rate (BF%) (MD = -1.28, 95 % CI: -1.88, -0.68, P 0.0001, IAs things stand, protein supplementation intervention can effectively reduce body fat percentage, fat mass, and increase grip strength in SO patients. Both WB-EMS and protein supplementation intervention had no significant effects on metabolic and inflammatory biomarkers. WB-EMS combined with protein supplementation intervention was beneficial for SO patients in many ways. Due to the small number of studies, further studies are needed to confirm the efficacy of WB-EMS alone or in combination with protein supplementation intervention in SO patients.INPLASY202190096 DOI:10.37766/inplasy2021.9.0096.

In this study, we investigated the role of ubiquitin-specific protease 22 (USP22) in the growth and progression of gastric cancer (GC). USP22 mRNA and protein levels were significantly higher in GC tissue samples and GC cell lines than in adjacent noncancerous tissue samples and a normal gastric mucosal epithelial cell line (GES1), respectively. USP22 knockdown significantly decreased in vitro survival, proliferation, migration, and invasiveness of GC cells compared with the controls. Western blot analysis of control and USP22-silenced GC cells showed that USP22 modulates the c-Myc/NAMPT/SIRT1-dependent FOXO1 and YAP signaling pathways. Subcutanenous injection of USP22-silenced GC cells into SCID mice generated significantly smaller xenograft tumors than did control cells. Moreover, USP22-silenced GC cells showed less lung metastasis than the controls following tail vein injection in SCID mice. In addition, high USP22 expression correlated positively with tumor size, advanced stage and metastasis, and correlated negatively with tumor differentiation and prognosis in GC patients. These results show that USP22 regulates growth and progression of GC via the c-Myc/NAMPT/SIRT1-dependent FOXO1 and YAP signaling pathways.

Background Laparoscopic pancreaticoduodenectomy (LPD) is widely used in several centers. This study analyzed the postoperative complications rate curve, possible cause, and solution of LPD and open pancreaticoduodenectomy (OPD). Methods Between January 2015 and December 2019, the study included 213 and 204 patients undergoing OPD and LPD, respectively. Postoperative outcomes, complications, and complication risk, along with operation time were analyzed, and the learning curve was determined. Results The OPD group (378.7±8.98 min) had shorter operation time than the LPD group (402.5±7.12 min) (P=0.037). Blood loss was significantly lower in the LPD group (389.9±19.05 mL) than in the OPD group (530.1±33.55 mL) (P

Feeding restriction (FR) is a scientific strategy to attenuate nutrient excess-mediated liver metabolic syndromes in human beings. However, it is still unclear whether liver health could benefit from FR in cultured animals including fish. In this regard, the regulatory role of FR in liver health of juvenile largemouth bass Micropterus salmoides were investigated in this study using single-molecule real-time sequencing and next-generation sequencing. Groups of fish (20 fish per group) with an initial body weight of 6.9 g were randomly allocated into 12 rectangular tanks (250 L each) operating as a recirculating aquaculture system. The satiation (ST) fish was fed to satiation, while ration levels of the moderately restricted (MR) and highly restricted (HR) fish were maintained at 85% and 70% of the ST fish, respectively. All fish were fed a commercial extruded diet containing 49.9% crude protein and 13.2% crude lipid. After a 9-week feeding trial, growth performance of the MR fish was not affected through improving the feed utilization as compared with the ST fish. Even though feed utilization was further improved, growth of the HR fish was still impaired. The MR fish obtained superior antioxidant status in the plasma and liver (based on glutathione or malondialdehyde concentration, and total antioxidant capacity and superoxide dismutase activities) together with better liver integrity (based on HE and TUNEL staining) than the other treatments. A total of 38,909 full-length transcripts were generated from the sequencing. GO enrichment analysis of the differentially expressed genes (DEGs) showed that many terms related to immunization and wound repair were enriched in the feed restricted fish (especially the MR fish). A total of 701 DEGs were identified in the liver of the MR fish as compared with the ST fish, and the apoptosis was enriched as the prominent pathway by KEGG pathway analysis. Our results suggested that the intrinsic apoptosis pathway played an important role in the hepatocyte apoptosis inhibition in the MR fish. Specifically, the activation of Akt might mediate an anti-apoptosis role through inhibiting the release of direct IAP binding protein with low pI (DIABLO) from mitochondria and promoting the transcription of pro-survival genes such as X-linked inhibitor-of-apoptosis protein (xiap), which coordinately activated the inhibitor of apoptosis protein (IAP). Besides the intrinsic apoptosis pathway, our results indicated that the lysosome pathway and endoplasmic reticulum stress pathway might also participate in regulating hepatocyte apoptosis inhibition of the MR fish.

The study reported here is the first to systematically investigate the postprandial change in glucose metabolism in the adipose tissue (AT) of an omnivorous fish. Sub-adult Genetically Improved Farmed Tilapia (GIFT) Oreochromis niloticus were sampled at 0, 1, 3, 8 and 24 h after feeding (HAF), and the time course of changes in glucose transport and glycolipid metabolism at the transcript level were analyzed in the AT. The plasma glucose level increased between 1 and 8 HAF, and the expression of glucose transporter 1a (glut1a) and glut4 in the AT were stimulated at the same time. Concomitantly, the mRNA levels of glycolytic genes, such as hexokinase 1a (hk1a), hk1b, glucokinase and liver type of phosphofructokinase, were upregulated. The expression of glycogen synthase 1 and glycogen level in the AT increased between 3 and 8 HAF, suggesting that AT has the capacity to store excess glucose in tilapia. The decreased glycogen level together with upregulated transcription of glucose-6-phosphatase catalytic subunit a2 (g6pca2) at 24 HAF suggests that glycogen breakdown and glucose release from AT might contribute to circular glucose in tilapia. The opposite expression patterns between g6pca2 and phosphoenolpyruvate carboxykinase (pck) paralogs suggest that pck might participate in glyceroneogenesis rather than gluconeogenesis in the AT of tilapia. The mRNA levels of both cytosolic pck1 and mitochondrial pck2 increased during the period 1–8 HAF, and the expressions of lipogenic genes, such as acetyl-CoA carboxylase α and fatty acid synthase, were upregulated between 3 and 8 HAF, suggesting that glyceroneogenesis was probably stimulated as a source of glyceride–glycerol for triglyceride synthesis in the AT of tilapia. Taken together, our preliminary data suggest that AT plays an important role in the regulation of postprandial glucose homeostasis in the omnivorous tilapia, at least at the molecular level.

// Ling Qin 1,* , Zhi-qiang Yao 2,* , Qi Chang 3,* , Ya-li Zhao 2,* , Ning-ning Liu 2,* , Xiao-shan Zhu 2 , Qin-qin Liu 2 , Li-feng Wang 4 , An-gang Yang 5 , Chun-fang Gao 2 and Jun-tang Li 2,3,4,5 1 Department of Hematology, First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, Henan, China 2 Centre of Inflammation and Cancer Research, 150th Central Hospital of PLA, Luoyang, Henan, China 3 Centre of Biomaterial and Biophysics Research, Institute of Training Medicine, 150th Central Hospital of PLA, Luoyang, Henan, China 4 State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, Fourth Military Medical University, Xi’an, Shaanxi, China 5 State Key Laboratory of Cancer Biology, Department of Immunology, Fourth Military Medical University, Xi’an, Shaanxi, China * These authors have contributed equally to this work Correspondence to: Jun-tang Li, email: // Chun-fang Gao, email: // Ling Qin, email: // Keywords : chronic colitis, swimming, inflammation, oxidative stress, apoptosis, Immunology and Microbiology Section, Immune response, Immunity Received : March 28, 2016 Accepted : December 15, 2016 Published : December 21, 2016 Abstract Increasing evidence suggests that regular physical exercise suppresses chronic inflammation. However, the potential inhibitory effects of swimming on dextran sulfate sodium (DSS)-induced chronic colitis, and its underlying mechanisms, remain unclear. In this study, rats were orally administered DSS to induce chronic colitis, and subsequently treated with or without swimming exercise. A 7-week swimming program (1 or 1.5 hours per day, 5 days per week) ameliorated DSS-caused colon shortening, colon barrier disruption, spleen enlargement, serum LDH release, and reduction of body weight gain. Swimming for 1.5 hours per day afforded greater protection than 1 hour per day. Swimming ameliorated DSS-induced decrease in crypt depth, and increases in myeloperoxidase activity, infiltration of Ly6G + neutrophils and TNF-α- and IFN-γ-expressing CD3 + T cells, as well as fecal calprotectin and lactoferrin. Swimming inhibited pro-inflammatory cytokine and chemokine production and decreased the protein expression of phosphorylated nuclear factor-κB p65 and cyclooxygenase 2, whereas it elevated interleukin-10 levels. Swimming impeded the generation of reactive oxygen species, malondialdehyde, and nitric oxide; however, it boosted glutathione levels, total antioxidant capacity, and superoxide dismutase and glutathione peroxidase activities. Additionally, swimming decreased caspase-3 activity and expression of apoptosis-inducing factor, cytochrome c, Bax, and cleaved-caspase-3, but increased Bcl-2 levels. Overall, these results suggest that swimming exerts beneficial effects on DSS-induced chronic colitis by modulating inflammation, oxidative stress, and apoptosis.

Ubiquitin-specific protease 22 (USP22) aberrance has been implicated in several malignancies; however, whether USP22 plays a role in anaplastic thyroid carcinoma (ATC) remains unclear. Here, we report that USP22 expression is highly elevated in ATC tissues, which positively correlated with tumor size, extracapsular invasion, clinical stages, and poor prognosis of ATC patients. In vitro assays showed that USP22 depletion suppressed ATC cell survival and proliferation by decreasing Rb phosphorylation and cyclin D2, inactivating Akt, and simultaneously upregulating Rb; USP22 silencing restrained cell migration and invasion by inhibiting epithelial-mesenchymal transition; USP22 knockdown promoted mitochondrion- mediated and caspase-dependent apoptosis by upregulating Bax and Bid and promoting caspase-3 activation. Consistent with in vitro findings, downregulation of USP22 in ATC cells impeded tumor growth and lung metastasis in vivo. These results raise the applicability for USP22 as a useful predictor of ATC prognosis and a potential therapeutic target for ATC.

// Jun-Tang Li 1,2,3,* , Wei-Qi Wang 4,5,6,* , Ling Wang 7,* , Ning-Ning Liu 1,* , Ya-Li Zhao 1,* , Xiao-Shan Zhu 1 , Qin-Qin Liu 1 , Chun-Fang Gao 1 , An-Gang Yang 2 and Lin-Tao Jia 3 1 Centre of Inflammation and Cancer Research, 150th Central Hospital of PLA, Luoyang, Henan, China 2 State Key Laboratory of Cancer Biology, Department of Immunology, Fourth Military Medical University, Xi’an, Shaanxi, China 3 State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, Fourth Military Medical University, Xi’an, Shaanxi, China 4 State Key Laboratory of Military Stomatology, Department of Oral and Maxillofacial Surgery, School of Stomatology, Fourth Military Medical University, Xi’an, China 5 National Clinical Research Center for Oral Diseases, Department of Oral and Maxillofacial Surgery, School of Stomatology, Fourth Military Medical University, Xi’an, China 6 Shaanxi Clinical Research Center for Oral Diseases, Department of Oral and Maxillofacial Surgery, School of Stomatology, Fourth Military Medical University, Xi’an, China 7 Department of Anesthesiology, 150th Central Hospital of PLA, Luoyang, Henan, China * These authors have contributed equally to this work Correspondence to: Jun-Tang Li, email: // An-Gang Yang, email: // Lin-Tao Jia, email: // Keywords : isoflurane, zymosan, neutrophil, NMDA receptor, TLR2, Immunology and Microbiology Section, Immune response, Immunity Received : September 07, 2015 Accepted : April 18, 2016 Published : April 28, 2016 Abstract Neutrophil release of NO/ONOO – induces endothelial cell barrier dysfunction in inflammatory acute lung injury (ALI). Previous studies using zymosan-triggered inflammation and ALI model revealed that zymosan promotes inducible NO synthase (iNOS) expression in neutrophils, and that isoflurane inhibits zymosan-induced oxidative stress and iNOS biosynthesis. However, the underlying mechanisms remain largely unknown. We found here that in zymosan-primed neutrophils, iNOS is transcriptionally activated by NF-κB, whose nuclear translocation is triggered by excessive reactive oxygen species (ROS) and consequently activated p38 MAPK. ROS production is attributed to zymosan-initiated Toll-like receptor 2 (TLR2) signaling, in which the adaptor MyD88 recruits and activates c-Src, and c-Src activates NADPH oxidase to generate ROS. Subanesthetic isoflurane counteracts the aforementioned zymosan-induced signaling by targeting N-methyl-D-aspartic acid (NMDA) glutamate receptor and thereby suppressing calcium influx and c-Src activation. Whereas iNOS accelerates NO/ONOO – production in neutrophils which eventually promote protein leak from pulmonary microvascular endothelial cells (PMVEC), isoflurane reduced NO/ONOO – release from zymosan-treated neutrophils, and thus relieves trans-PMVEC protein leak. This study provides novel insights into the roles of neutrophils and the underlying mechanisms in zymosan-induced ALI, and has implications for the therapeutic potential of subanesthetic isoflurane in attenuating inflammatory responses causing lung endothelial cell damage.

We have recently published that type 2 diabetes can induce cell centrosome amplification due to the action of high glucose, palmitic acid, and insulin, and ROCK1 and 14-3-3σ are signal mediators. In this study, we further investigated the molecular mechanisms of the centrosome amplification in colon cancer HCT116 cells. Treatment of the cells with high glucose, palmitic acid, and insulin increased the expression of peroxisome proliferator-activated receptor γ (PPARγ) as well as the spindle and kinetochore associated protein 1 (SKA1), knockdown of each of which resulted in the inhibition of the treatment-triggered centrosome amplification. Knockdown of PPARγ inhibited the treatment-evoked increase in the SKA1 level, whereas knockdown of SKA1 did not modify the treatment-increased PPARγ level. We found a predicted binding site for PPARγ in the promoter region of the SKA1 gene from the JASPAR database. Experimental results showed that the treatment increased the messenger RNA level of SKA1, which could be inhibited by PPARγ chemical inhibitor or small interfering RNA. Moreover, we were able to show that PPARγ could bind to the binding site in the SKA1 gene promoter, which was increased by the experimental treatment. In conclusion, it is suggested that the pathophysiological factors in type 2 diabetes, high glucose, palmitic acid, and insulin, induce the cell centrosome amplification through the PPARγ-SKA1 pathway, in which PPARγ increases the expression of SKA1 via directly enhancing the SKA1 gene transcription.

Whereas miR-101 is involved in the development and progression of breast cancer, the underlying molecular mechanisms remain to be elucidated. Here, we report that miR-101 expression is inversely correlated with the clinical stage, lymph node metastasis and prognosis in breast cancers. Introduction of miR-101 inhibited breast cancer cell proliferation and invasion in vitro and suppressed tumor growth and lung metastasis of in vivo. CX chemokine receptor 7 (CXCR7) is a direct target of miR-101, positively correlating with the histological grade and the incidence of lymph node metastasis in breast cancer patients. The effects of miR-101 were mimicked and counteracted by CXCR7 depletion and overexpression, respectively. STAT3 signaling downstream of CXCR7 is involved in miR-101 regulation of breast cancer cell behaviors. These findings have implications for the potential application of miR-101 in breast cancer treatment.

Based on the calculation method and the analysis method of the ventilation requirement, the paper discussed the necessary ventilation referring to the standard of the allowed indoor CO2concentration, the necessary ventilation with oxygen as the standard and the calculation method and correction method of the full amount of required ventilation to remove the waste heat or wet. According to the pros and cons of the methods described above, the paper proposed the corresponding countermeasures to meet the indoor air quality and the fresh air needed by indoor personnel.

Granite is a kind of acid stone which has the advantages of high strength, high wear resistance, etc. However, the poor adhesion between the granite and asphalt often fail to meet the corresponding design requirements, and the application of granite asphalt mixture is often affected. Based on the analysis of the comparative tests of common treatment methods in projects, the paper tried to explore the best countermeasures to improve the water stability of granite asphalt mixture, and provide guidance for engineering practice.

Firstly, based on contrast to the the merits of conventional asphalt, natural colored asphalt, bitumen thermoset and thermoplastic light colored asphalt, the paper proposed the base asphalt selection method. Then on the basis of comparison of the performance of organic pigments and inorganic pigments of paint, the pigmentselection method was identified. Thirdly, the paper compared the color characteristics of different types of stone and provided some recommendations on aggregate selection. Finally, the paper briefly introduced the design method and technical requirement of colored hot-mix asphalt material.

Due to the perturbation between multiple PV Grid-connected power system can’t be synchronized easily, the islanding detection often lose efficacy when multiple PV Grid-connected inverters are running simultaneously. The paper show the in-depth analysis of the principle and the advantages and disadvantages of the detection method of AFDPF and SMS, a composition controller is designed aim at the non-detection zone in multiple PV Grid-connected system in the practical application. Through the software simulation, it shows that the method mentioned in the paper practically improves the effect of the islanding detection.

An enormous research effort is presently being directed towards the improvement of efficient visible light driven photocatalysts for renewable energy applications including water splitting and CO2 reduction. Hybrids of semiconductors and layered double hydroxides (LDHs) are promising nanomaterials due to their flexible properties and the large number of compositions/preparation variables obtainable for fine-tuning. Recent advancements have been confirmed that semiconductor/LDHs nanocomposites can be envisioned as the most privileged and promising novel catalysts in the photocatalytic and photoelectrochemical applications. Moreover, this study gives an advanced review important developments in the production of the LDHs/semiconductor photocatalysts for energy generation and ecological clean up, such as degradation of dyes, O2 evolution, hydrogen production and CO2 reduction. We desire that this review article will promote the researchers to expand the applications of LDHs/semiconductor composite in the field of photocatalysis in a green approaches.

This paper studied the impact of silicon oxide layer on photovoltaic characteristic of iron-doped amorphous carbon film/silicon heterojunction (a-C:Fe/Si). The results show that a native SiO2 layer on the silicon surface can provide a significant improvement of the a-C:Fe/Si devices’ photovoltaic performances, especially for the short circuit current and fill factor. This improvement partly may be attributed to the electron recombination process is suppressed and the interface is modified by the SiO2 film based on the open circuit voltage decay measurement.

The title compound Fe2Mo3O12 is prepared using a wet chemical method from aqueous solutions of ferrous nitrate and ammonium molybdate. The various process parameters were optimized to get a suitable precursor, which upon calcination at 700°C for 2 h gave a well crystalline product. The product was characterized by powder XRD to have a monoclinic unit cell of Fe2Mo3O12. Its thermal expansion property was investigated by thermomechanical analyzer and high-temperature XRD. The typical monoclinic to orthorhombic phase transition happened at about 500°C, and Fe2Mo3O12 shows great NTE (macro -13.43×10-6°C-1 and micro -21.77×10-6°C-1) property during the temperature range from 500°C to 800°C.

To reveal the mechanical property on the interface between the surrounding rock and the supporting structure, inducting the definition of the interface, based on ABAQUS software, two finite element models were established to compare and analysis the interaction through the aspects of stress, deformation and plastic region of surrounding rocks and the resistance of supporting structure. At last, compare the simulative and the metrical results. The result shows that the ideal full-constraint between the surrounding rock and the supporting structure isn’t possibility. It becomes more reasonable to define an interface during the numerical analysis and design calculations, the selection of the constitutive relation of the interface is directly related to the accuracy of the numerical calculation results.

Negative thermal expansion (NTE) material ZrWMoO8 was prepared by hydrothermal method. The phase structure and morphology of the obtained precursor and final product were examined by XRD and SEM, respectively. To study its negative thermal expansion property, two methods were utilized. One is based on the in-situ XRD results and the thermal expansion coefficient (CTE) was calculated by the cell parameters obtained at different temperatures. Another is based on the thermo-mechanical analysis (TMA) and the CTE was calculated by the length of ZrWMoO8 bar at different temperatures. The differences between these two methods were also discussed.

In order to solve the transmission error from the backlash in precision gear transmission, this paper proposes a mechanism which uses slider and pendulum to eliminate backlash. Based on the force analysis of the new-typed auto-eliminate backlash mechanism, genetic algorithm is selected to optimize the design. The simulation experiment by Matlab shows that spring force of the mechanism is minimum and its performance is ideal, meanwhile the configuration parameters of the mechanism are ensured.

It is inclined to lose the tracking of a GPS receiver's carrier loop in noisy jamming or high dynamic environment, therefore, INS's velocity information is often used to expand the equivalent bandwidth of GPS receiver's tracking loop, reduce loop's bandwidth, improve high dynamic adaptability and Signal-noise ratio. However, because of the discretization of INS's velocity, the rapidly changing control quantity for NCO under high dynamic environment makes the loop tracking unstable. For this reason, tracking loop with INS's acceleration information aiding based on LM algorithm of BP neural network is proposed. Firstly, the effect of INS's update frequency on a typical second-order tracking loop is analyzed, then the model of BP neural network based on LM algorithm is built, and the INS instantaneous velocity and acceleration as input variables to obtain the estimate of the loop NCO through training the network and compensation the loop NCO, after training is completed, we can create the appropriate database, which the data can be called directly. The results show that this method enhances loop's tracking speed and stability, improves loop's adaptability to dynamic stress.

To explore the tumor growth inhibition of gamma secretase inhibitor MRK003 on human multiple myeloma xenograft mice by inhibition of AKT and Notch1 expression.NOD/SCID mice were injected with human multiple myeloma cell lines RPMI8226 to establish a xenograft mouse model. Mice were randomized into two groups：the experimental group were injected with MRK003 at a dose of 5 mg× kg⁻¹×d⁻¹ for 14 days; the inhibitor was replaced by an equal saline in the control group. Mice were sacrificed by cervical dislocation on the next day after the last injection and tumor tissue was removed to detect the expression of Notch1 and AKT by immunohistochemistry.After subcutaneous injection with RPMI8226, mice had tumor formation in 5-7 days and the largest tumor block in 10-12 days. Before RPMI8226 injection, the mean sizes of tumor block in the experimental and the control groups were 509.2 mm³, 511.2 mm³(P0.05). 9 days after injection, the mean sizes of tumor tissue in the experimental and the control groups were 636.6 mm³, 691.2 mm³(P0.01). On the next day after the last injection, the tumor sizes of the experimental and the control groups were 683.5 mm³ and 1798.7 mm³(P0.01). The size of tumor block in the experimental group was significantly smaller than that of the control group(P0.01). Immunohistochemistry staining showed that the positive expression rates of Notch1(11.1%, P0.01) and AKT(13.3%, P0.01) in experimental group were significantly decreased compared with the control group(Notch1: 95.6%; AKT: 93.3%). Western blot results showed that Notch1 and AKT protein in experimental group were significantly lower than those in the control group.MRK003 could inhibit the tumor growth of human multiple myeloma xenograft mice by downregulated expression of Notch1 signaling pathway.

The current case report presents a patient with acute monocytic leukemia (AML-M5) occurring 14 years following the successful treatment of severe aplastic anemia (SAA) with immunosuppressants and androgens. The patient was treated with induction chemotherapy, but did not achieve remission. The patient succumbed to central nervous system bleeding 2 weeks following the first cycle of chemotherapy. Chromosomal examination revealed 47,XX,+21[10]/46,XX[1]. To the best of our knowledge the present case is the first to be reported of SAA 14 years preceding AML-M5 with acquired trisomy 21.