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Objective: To investigate whether miR-483-5p regulates osteoclast generation by targeting Timp2. miR-483-5p can promote osteoclast differentiation and bone destruction. Methods: Target genes of miR-483-5p were predicted by miRNAs target gene prediction software TargetScan8.0, and wild type and mutant 3' UTR plasmids were constructed. Dual luciferase reporter genes were used to verify whether target genes had a targeted regulatory relationship with miR-483-5p. Western blotting was used to detect the corresponding changes in the expression level of target protein after adjusting the level of miR-483-5p in cells. Cells were transfected or infected with target gene siRNA or target protein lentivirus, and TRAP staining and q-PCR assays were performed. In addition, for osteoclast induction experiment, RAW264.7 cells were co-transfected with ago-miR-483-5p and target protein-overexpressed lentiviruses q-PCR and TRAP staining were performed respectively. Results: Bioinformatics software was used to predict the target gene of miR-483-5p, and the Timp2 gene was found to regulate osteoclasts, and the dual luciferase reporter detection system found that miR-483- 5p could be associated with the 3-UTR of the predicted target gene Timp2 gene. There are complementary loci and targeted regulatory relationship between them. Subsequently, we upregulated miR-483-5p in RAW264.7 cells to reduce the expression of Timp2. Compared with the normal group, the number of osteoclasts and the expression of osteoclast-specific genes increased significantly after the induction of Timp2 in knockdown cells. After co-transfection of target gene and miR-483-5p into cells, the number of osteoclasts and the expression of specific genes decreased significantly compared with the normal group. Conclusion: Timp2 is a downstream target gene of miR-483-5p and is involved in and inhibits osteoclast generation. [ABSTRACT FROM AUTHOR]

Objective: To study the effect of borneol combined with astragaloside IV and Panax notoginseng saponins (BAP) on promoting neurogenesis by regulating microglia polarization after cerebral ischaemia–reperfusion(CI/R) in rats. Methods: A focal CI/R injury model was established. Evaluated the effects of BAP on ischaemic brain injury, on promoting neurogenesis, on inhibiting Inflammatory microenvironment and TLR4/MyD88/NFκB signalling pathway. A microglia oxygen-glucose deprivation reoxygenation (OGD/R) model was established that evaluated the effects of BAP on regulating the polarization of microglia and inflammatory microenvironment. Results: BAP can inhibit the expression of TLR4, MyD88 and NFκB proteins, reduce IL-1β and increase IL-10, reduce M1 type microglia and increase M2 microglia. The proliferation of neural stem cells increased, synaptic gap decreased, synaptic interface curvature increased, expression of SYN and PSD95 proteins increased, which improved the neurological dysfunction and reduced the volume of cerebellar infarction and nerve cell injury. Conclusion: BAP can reduce CI/R injury and promote neurogenesis, the effect is related to inhibition of the activation of TLR4/MyD88/NFκB, regulating the polarization of microglia from M1 type to M2 type and inhibition of inflammatory response. [ABSTRACT FROM AUTHOR]

Aims: Low caspofungin exposure is frequently encountered in patients with invasive candidiasis caused by Candida albicans. This study aimed to investigate the effects of caspofungin on C. albicans at sub‐inhibitory concentrations. Methods and Results: First, a comparative transcriptomics analysis was performed on C. albicans receiving caspofungin at sub‐minimum inhibitory concentrations (sub‐MICs). The results showed that caspofungin significantly changed the mRNA expression profile in DAY185, with DE‐mRNAs enriched in the functions of cell wall biosynthesis, metabolism, etc. Subsequently, cellular fitness, cell aggregation, energy metabolism activity and the proportion of persister cells of C. albicans were quantitatively and/or qualitatively assessed after sub‐MIC caspofungin exposure. No significant changes in cell fitness and aggregation formation were observed during treatment of C. albicans with sub‐MIC caspofungin. In C. albicans aggregation treated with sub‐MIC caspofungin, we observed a decrease in respiratory metabolism and an increase in persister cells; this effect was more pronounced in als1ΔΔ than in DAY185. Conclusions: Pre‐exposure to sub‐MIC caspofungin suppresses C. albicans respiratory metabolism and promotes persister cell development. Significance and Impact of the Study: Caspofungin should be used with caution in patients with C. albicans infections, as anti‐infection therapy may fail due to persister cells. [ABSTRACT FROM AUTHOR]

BACKGROUND: The widespread use of chemical insecticides has resulted in the development of resistance in German cockroaches worldwide, and biopesticides based on entomopathogenic fungi as active ingredients have become a promising alternative strategy. Resistance can change many of the physiological and biochemical characteristics of insect pests, such as cuticle thickness, detoxification enzyme activity, and even intestinal flora composition. Thus, potential interactions between pathogenic fungi and insecticide resistance may lead to unpredictable changes in pest susceptibility to fungi. RESULTS: Beta‐cypermethrin‐resistant German cockroaches were more susceptible to infection with the fungus Metarhizium anisopliae regardless of age and sex. Histopathological results showed that the infection of resistant strains (R) by M. anisopliae was visibly faster than that of susceptible strains (S). The gut microbiota of the S strain indicated a stronger ability to inhibit fungi in vitro. The abundance of Parabacteroides, Lachnoclostridium, and Tyzzerella_3 decreased significantly in the R strain, and most demonstrated the ability to regulate glucose and lipid metabolism, and antifungal infections. The expression levels of Akirin, BgTPS, and BgPo genes in the R strain were significantly lower than those in the S strain, while BgChi and CYP4G19 gene expression were significantly higher. The mortality of cockroaches infected with M. anisopliae decreased to varying degrees after RNA interference, reflecting the role of these genes in antifungal infection. CONCLUSIONS: Results confirmed that insecticide resistance may enhance cockroach susceptibility to fungi by altering intestinal flora and gene expression. Fungal biopesticides have high utilization value in pest control and insecticide resistance management strategies. © 2021 Society of Chemical Industry. [ABSTRACT FROM AUTHOR]

Airway epithelial cells, the first barrier of the respiratory tract, play an indispensable role in innate immunity. Integrin β4 (ITGB4) is a structural adhesion molecule that is involved in the pathological progression of acute inflammatory diseases and is downregulated in asthmatic patients. Research has shown that endothelial ITGB4 has proinflammatory properties in acute lung injury (ALI). However, the role of epithelial ITGB4 in a murine ALI model is still unknown. This study investigated the role of ITGB4 in lipopolysaccharide (LPS)‐induced ALI. We found that ITGB4 in the airway epithelium had remarkably increased after the introduction of LPS in vivo and in vitro. Then, we constructed airway epithelial cell‐specific ITGB4 knockout (ITGB4−/−) mice to study its role in ALI. At a time point of 12 h after the tracheal injection of LPS, ITGB4−/− mice showed increased macrophages (mainly M1‐type macrophages) and neutrophil infiltration into the lungs; inflammation‐related proteins including interleukin (IL)‐6, tumor necrosis factor, and IL‐17A were significantly elevated compared to their levels in ITGB4+/+ mice. Furthermore, we investigated the role of ITGB4 in the anti‐inflammatory response. Intriguingly, in the ITGB4−/− + LPS group, we found significantly reduced expression of anti‐inflammatory factors, including IL‐10 messenger RNA (mRNA) and ARG‐1 mRNA. We also observed that monocyte chemotactic protein (MCP‐1) increased significantly both in vivo and in vitro. Airway epithelium activates macrophages, most likely driven by MCP‐1, which we confirmed in the coculture of epithelia and macrophages. These phenomena indicate that ITGB4 in airway epithelial cells plays an important role in the process of inflammation and activation of macrophages in ALI. Overall, these data demonstrated a novel link between airway epithelial ITGB4 and the inflammatory response in LPS‐induced ALI. [ABSTRACT FROM AUTHOR]

To explore the main active components and effects of cell cycle regulation mechanism of Astragali radix (AR) and Angelicae sinensis radix (ASR) on oxidative damage in vascular endothelial cells, a model of oxidative damage in human umbilical vein endothelial cells (HUVECs) induced by oxidized low-density lipoprotein (ox-LDL) treatment was developed. Based on the "knock-out/knock-in" model of the target component, cell viability, intracellular reactive oxygen species (ROS), and lactate dehydrogenase (LDH) leakage were assessed by Cell Counting Kit-8 assay, fluorescent probe 2,7-dichlorodihydrofluorescein diacetate (DCFH-DA), and colorimetric assay, respectively, to evaluate the protective effect of the active components of AR and ASR (astragaloside IV (AS IV), astragaloside I (AS I), formononetin (FRM), calycosin (CAL), calycosin-7-O-β-D glucoside (CLG), and ferulic acid (FRA)) against oxidative damage. The cell cycle and expression of genes encoding cyclins and cyclin-dependent kinases (CDKs) were observed using flow cytometry and quantitative real-time polymerase chain reaction. The results showed that the combination of active components (ACC) significantly inhibited the decrease in cell viability as well as the increase in ROS and LDH release in HUVECs induced by ox-LDL treatment. AS IV and FRM promoted the proliferation of HUVECs but the proliferation index was decreased in the AS I and FRA groups; this inhibitory effect was counteracted by the ACC. The ACC reduced and increased the proportion of positive cells in G1 and S phases, respectively, followed by the upregulation of cyclin A (CCNA), cyclin E (CCNE), and CDK2 mRNA expression and downregulation of cyclin B (CCNB), cyclin D1 (CCND1), CDK1, CDK4, and CDK6 mRNA expression, which significantly mitigated inhibition of HUVECs proliferation induced by ox-LDL treatment. Taken together, AS IV, AS I, FRM, CAL, CLG, and FRA were the primary pharmacodynamic substances of AR and ASR that alleviated oxidative injury in HUVECs. ACC mitigated the upregulation of intracellular ROS levels and LDH release induced by ox-LDL treatment, which promoted the cell cycle procession of HUVECs by regulating the expression of genes encoding cyclins and CDKs and thus preventing oxidative damage in HUVECs. [ABSTRACT FROM AUTHOR]

In inter-satellite laser communication, four-quadrant detector is often used in precise tracking unit for spot location. The positioning error directly affects the angular measurement accuracy of fine tracking unit. In order to achieve the tracking precision of micro-radian magnitude, this paper studies various noise factors that affect the positioning accuracy of the detector, simplifying the analysis according to the practice of inter-satellite laser communication, and putting forward the specific calculation method of positioning error. Finally, we evaluate the influence degree of each factor through a specific example. The results show that the signal-to-noise ratio of the received signal increases with the increasing of emitting power in a certain range with reduced positioning error. However, positioning error does not decrease linearly with the increase of transmitting power. When the transmitting power increases to a certain extent, the reduction of tracking error is limited. At this time, it will be very expensive to improve the tracking precision simply by increasing the transmitting power. [ABSTRACT FROM AUTHOR]

Multiple congenital anomalies-hypotonia-seizures syndrome 1 (MCAHS1) caused by phosphatidylinositol-glycan biosynthesis class N (PIGN) mutations is an autosomal recessive disease involving many systems of the body, such as the urogenital, cardiovascular, gastrointestinal, and central nervous systems. Here, compound heterozygous variants NM_012327.6:c.2427-2A > G and c.963G > A in PIGN were identified in a Chinese proband with MCAHS1. The features of the MCAHS1 family proband were evaluated to understand the mechanism of the PIGN mutation leading to the occurrence of MCAHS1. Ultrasound was conducted to examine the fetus, and his clinical manifestations were evaluated. Genetic testing was performed by whole-exome sequencing and the results were verified by Sanger sequencing of the proband and his parents. Reverse transcription-polymerase chain reaction was performed, and the products were subjected to Sanger sequencing. Quantitative PCR (Q-PCR) was conducted to compare gene expression between the patient and wild-type subjects. The compound heterozygous mutation NM_012327.6:c.2427-2A > G and c.963G > A was identified by whole-exome sequencing and was confirmed by Sanger sequencing. The NM_012327.6:c.2427-2A > G mutation led to skipping of exon 26, which resulted in a low expression level of the gene, as measured by Q-PCR. These findings provided a basis for genetic counseling and reproduction guidance in this family. Phenotype-genotype correlations may be defined by an expanded array of mutations. [ABSTRACT FROM AUTHOR]

Autosomal dominant non-syndromic hearing loss (ADNSHL) has a broad phenotypic spectrum which includes bilateral, symmetrical, and high-frequency sensorineural hearing loss, that eventually progresses into hearing loss at all frequencies. Several genetic variations have been identified as causal factors underlying deafness, autosomal dominant 5 (DFNA5) gene-related hearing loss. Here, we report a novel mutation (c.991-1G > C) in DFNA5 , which co-segregated with late-onset ADNSHL in a Chinese family and was identified via exome sequencing and Sanger sequencing of DNA from peripheral blood of the family members. Further sequencing of cDNA derived from peripheral blood mRNA revealed that the c.991-1G >C mutation led to the skipping of exon 8, which is a known pathogenic mechanism for DFNA5-related hearing loss. [ABSTRACT FROM AUTHOR]

Objective: To analyze the correlation between the Kellgren–Lawrence (K‐L) score of knee osteoarthritis (KOA) patients with different degrees and their urine concentration of C‐terminal telopeptide of collagen type II (CTX‐II) and interleukin‐1β (IL‐1β), and to further evaluate the diagnostic value of CTX‐II and IL‐1β during the pathological process by producing an experimental osteoarthritis (OA) model in rabbits. Methods: From 1 January 2017 to 31 December 2018, a total of 34 subjects (7 mild, 9 moderate, 9 severe arthritis patients, and 9 healthy individuals) comprising 16 men and 18 women were included in this study. Patients were diagnosed according to the American College of Rheumatology (ACR) criteria. The urine of all subjects was collected to detect the concentration of CTX‐II and IL‐1β. The rabbits in the KOA group were subjected to protease (control group with saline) injection into the articular cavity of their right knees and immobilization with gypsum. We used radiological and histological examination to identify the KOA model. ELISA was applied to investigate the concentrations of CTX‐II and IL‐1β in urine and serum, and Spearman's rank correlation analysis was used to analyze the correlation. Results: There was no significant difference in the mean ages and body mass index (BMI) between groups. The mean ages of mild, moderate, and severe arthritis patients and healthy individuals were 54.29 ± 5.76, 58.44 ± 6.44, 59.89 ± 6.75, and 56.67 ± 4.18 years, respectively. The mean BMI of mild, moderate, and severe arthritis patients and healthy individuals were 23.59 ± 1.56, 23.57 ± 2.06, 24.46 ± 1.64, and 23.42 ± 1.35 kg/m2, respectively. The Kellgren–Lawrence (K‐L) score was higher with the aggravation of KOA. The K‐L scores of mild, moderate, and severe KOA patients were 1.14 ± 0.38, 2.56 ± 0.53, and 3.63 ± 0.52, respectively. The KOA symptoms of patients became more severe, with not only increased K‐L scores but also elevated concentrations of CTX‐II and IL‐1β. Moreover, there was a positive correlation between CTX‐II and IL‐1β of all subjects (r = 0.974, P < 0.001), between K‐L score and urine concentration of CTX‐II (r = 0.900, P < 0.001), and between K‐L score and IL‐1β (r = 0.813, P < 0.001) of all subjects. Both were significantly increased in KOA group rabbits at all time points after surgery. The serum concentration of CTX‐II and IL‐1β was elevated as early as in the 2nd week (3.69 and 4.25 times) and reached a peak (5.41 and 7.23 times) in the 4th week after surgery. Then, until 12 weeks after surgery, the CTX‐II and IL‐1β concentrations in the KOA group were slightly reduced and remained around 4.5 and 6.3 times that in the control group. Moreover, there was a positive correlation between the serum concentration of IL‐1β and CTX‐II (r = 0.967, P < 0.001). Conclusion: CTX‐II and IL‐1β, which were significantly increased during the process of KOA, can be used as biomolecular markers to provide guidelines for early diagnosis and treatment of KOA. [ABSTRACT FROM AUTHOR]

Silver–Russell syndrome (SRS) is a rare, well-recognized disorder characterized by growth restriction, including intrauterine and postnatal growth. Most SRS cases are caused by hypomethylation of the paternal imprinting center 1 (IC1) in chromosome 11p15.5 and maternal uniparental disomy in chromosome 7 (UPD7). Here, we report on a Chinese family with a 4 year old male proband presenting with low birth weight, growth retardation, short stature, a narrow chin, delayed bone age, and speech delays, as a result of a rare molecular etiology. Whole-exome sequencing was conducted, and a novel de novo IGF2 splicing variant, NM_000612.4: c.157+5G > A, was identified on the paternal allele. In vitro functional analysis by RT-PCR and Sanger sequencing revealed that the variant leads to an aberrant RNA transcript lacking exon 2. Our results further confirm the IGF2 variant mediates SRS and expand the pathogenic variant and phenotypic spectrum of IGF2 -mediated SRS. The results indicate that, beyond DNA methylation and UPD7 and CDKN1C variant tests, IGF2 gene screening should also be considered for SRS molecular diagnoses. [ABSTRACT FROM AUTHOR]

Oxidative stress induced by hypoxia/ischemia resulted in the excessive reactive oxygen species (ROS) and the relative inadequate antioxidants. As the initial barrier to environmental pollutants and allergic stimuli, airway epithelial cell is vulnerable to oxidative stress. In recent years, the antioxidant effect of hydrogen sulfide (H2S) has attracted much attention. Therefore, in this study, we explored the impact of H2S on CoCl2-induced cell injury in 16HBE14o- cells. The effect of CoCl2 on the cell viability was detected by Cell Counting Kit (CCK-8) and the level of ROS in 16HBE14o- cells in response to varying doses (100–1000 μmol/L) of CoCl2 (a common chemical mimic of hypoxia) was measured by using fluorescent probe DCFH-DA. It was shown that, in 16HBE14o- cells, CoCl2 acutely increased the ROS content in a dose-dependent manner, and the increased ROS was inhibited by the NaHS (as a donor of H2S). Moreover, the calcium ion fluorescence probe Fura-2/AM and fluorescence dye Rh123 were used to investigate the intracellular calcium concentration ([Ca2+]i) and mitochondria membrane potential (MMP) in 16HBE14o- cells, respectively. In addition, we examined apoptosis of 16HBE14o- cells with Hoechst 33342. The results showed that the CoCl2 effectively elevated the Ca2+ influx, declined the MMP, and aggravated apoptosis, which were abrogated by NaHS. These results demonstrate that H2S could attenuate CoCl2-induced hypoxia injury via reducing ROS to perform an agonistic role for the Ca2+ influx and MMP dissipation. [ABSTRACT FROM AUTHOR]

Background: To analyze existing cohort studies and provide evidence for the use of prenatal selective serotonin reuptake inhibitor (SSRI) monotherapy and the associated risk of gestational hypertension and preeclampsia. Methods: A comprehensive search of English language articles published before 30th April 2017 was conducted on PubMed, EMBASE, and the Web of Science databases. Using data acquired, we summarized the relative risks (RRs) and 95% confidence intervals (CIs) of gestational hypertension and preeclampsia using the random-effects model. Heterogeneity between studies was also assessed with the I2 statistic. Results: Seven cohort studies with 1,108,261 individuals were included for analysis. Compared with nonusers, those undertaking prenatal SSRI monotherapy were more likely to develop gestational hypertension or preeclampsia (summarized RR = 1.21, 95% CI: 1.05–1.40, I2 = 71.3%), gestational hypertension (summarized RR = 1.14, 95% CI: 1.00–1.30, I2 = 5.7%), and preeclampsia (summarized RR = 1.32, 95% CI: 0.99–1.78, I2 = 83.3%). In addition, although subgroup analyses, which were stratified by study design, number of cases, geographic location, duration of SSRI monotherapy, registry databases, and adjustment for potential confounders and risk factors, were consistent with the main findings, not all of these showed statistical significance. No evidence of publication bias was detected. Conclusions: Women who receive SSRI monotherapy during pregnancy are at increased risk of gestational hypertension and preeclampsia. [ABSTRACT FROM AUTHOR]

Aim To perform a meta-analysis of available cohort studies on the association between sertraline use by pregnant women in the first trimester and the findings of congenital anomalies in infants. Methods A comprehensive search of articles published from the index date up to 31st December 2015 investigating the aforementioned associations was conducted on PubMed and Web of Science. Mesh headings used included the terms 'serotonin reuptake inhibitor,' 'sertraline,' 'congenital anomalies' and 'obstetrical outcome.' Results Twelve cohort studies that involved 6 468 241 pregnant women were identified. We summarized odds ratios (ORs) and 95% confidence intervals (CIs) of congenital anomalies using the random-effects model. Pregnant women who used sertraline in the first trimester had a statistically significant increased risk of infant cardiovascular-related malformations (OR = 1.36; 95% CI = 1.06-1.74; I2 = 64.4%; n = 12) as well as atrial and/or ventricular septal defects (OR = 1.36, 95% CI = 1.06-1.76; I2 = 62.2%; n = 8). Additionally, positive but nonsignificant associations between sertraline use and congenital anomalies of the nervous system (OR = 1.39; 95% CI = 0.83-2.32; I2 = 0%; n = 5), digestive system (OR = 1.23; 95% CI = 0.76-1.98; I2 = 0%; n = 5), eye, ear, face and neck (OR = 1.08; 95% CI = 0.33-3.55; I2 = 32.1%; n = 3), urogenital system (OR = 1.03; 95% CI = 0.73-1.46; I2 = 0%; n = 5), and musculoskeletal system (OR = 0.97; 95% CI = 0.69-1.36; I2 = 0%; n = 5) were observed. Conclusion This meta-analysis suggested that the use of sertraline use by pregnant women in the first trimester had an increased risk of cardiovascular-related malformations as well as atrial and/or ventricular septal defects in infants. Meanwhile, nonsignificant associations between sertraline use and other congenital anomalies were found. More cohort studies are warranted to provide detailed results of other congenital anomalies. [ABSTRACT FROM AUTHOR]

Selecting plant species that can overcome unfavorable conditions and increase the recovery of degraded mined lands remains a challenge. A pot experiment was conducted to evaluate the feasibility of using transplanted tree seedlings for the phytoremediation of lead/zinc and copper mine tailings. One-year-old bare-root of woody species (Rhus chinensisMill,Quercus acutissimaCarruth,Liquidambar formosanaHance,Vitex trifoliaLinn. var.simplicifoliaCham,Lespedeza cuneataandAmorpha fruticosaLinn) were transplanted into pots with mine tailings and tested as potential metal-tolerant plants. Seedling survival, plant growth, root trait, nutrient uptake, and metal accumulation and translocation were assessed. The six species grew in both tailings and showed different tolerance level.A. fruticosawas highly tolerant of Zn, Pb and Cu, and grew normally in both tailings. Metal concentrations were higher in the roots than in the shoots of the six species. All of the species had low bioconcentration and translocation factor values. However,R. chinensisandL. formosanahad significantly higher translocation factor values for Pb (0.88) and Zn (1.78) than the other species. The nitrogen-fixing species,A. fruticosa,had the highest tolerance and biomass production, implying that it has great potential in the phytoremediation of tailing areas in southern China. [ABSTRACT FROM AUTHOR]

Previous studies investigating the relationship between passive maternal smoking and preterm birth reveal inconsistent results. We conducted the current meta-analysis of observational studies to evaluate the relationship between passive maternal smoking and preterm birth. We identified relevant studies by searching PubMed, EMBASE, and ISI Web of Science databases. We used random-effects models to estimate summary odds ratios (SORs) and 95% confidence intervals (CIs) for aforementioned association. For the analysis, we included 24 studies that involved a total of 5607 women who experienced preterm birth. Overall, the SORs of preterm birth for women who were ever exposed to passive smoking versus women who had never been exposed to passive smoking at any place and at home were 1.20 (95%CI = 1.07–1.34,I2 = 36.1%) and 1.16 (95%CI = 1.04–1.30,I2 = 4.4%), respectively. When we conducted a stratified analysis according to study design, the risk estimate was slightly weaker in cohort studies (SOR = 1.10, 95%CI = 1.00–1.21,n = 16) than in cross-sectional studies (SOR = 1.47, 95%CI = 1.23–1.74,n = 5). Additionally, the associations between passive maternal smoking and preterm birth were statistically significant for studies conducted in Asia (SOR = 1.26, 95%CI = 1.05–1.52), for studies including more than 100 cases of preterm birth (SOR = 1.22, 95%CI = 1.05–1.41), and for studies adjusted for maternal age (SOR = 1.27,95%CI = 1.09–1.47), socioeconomic status and/or education (SOR = 1.28, 95%CI = 1.10–1.49), body mass index (SOR = 1.33, 95%CI = 1.04–1.71), and parity (SOR = 1.27, 95%CI = 1.13–1.43). Our findings demonstrate that passive maternal smoking is associated with an increased risk of preterm birth. Future prospective cohort studies are warranted to provide more detailed results stratified by passive maternal smoking during different trimesters of pregnancy and by different types and causes of preterm birth. [ABSTRACT FROM AUTHOR]

Detecting the state mechanism of protocol can effectively improve the test comprehensiveness when testing the stability of network. This paper proposed a detection method of the state mechanism of protocol based on finite state machine. First, this method established an FSM model of certain message sending entity of testing protocol and determined the input set. Second, during the test, it monitored state transitions of sending entity and generated a state transition diagram. Finally, it determined the state mechanism of protocol message and defined trigger conditions of stateful message according to the state transition diagram. It determined the state mechanism of protocol after summarizing and classifying the tested messages. This paper built a lab environment to test and verify the effectiveness of this method. [ABSTRACT FROM AUTHOR]

For the purpose of a quantitative understand for IMS network's attack effect, this paper introduced an evaluation method for IMS's attack effect based on fuzzy comprehensive evaluation. It constructed the attack index tree on the basis of analyzing the possible attack flow, and introduced analytic hierarchy process to compute the indexes' power, and made comprehensive evaluation for IMS attack effects using the fuzzy comprehensive evaluation. To reduce the warp brought by the single fuzzy operator's properties, it selected several operators with different properties to evaluate and took the mean as the finally result. Finally, the examples validate the evaluation method is able to distinguish the attack effects resulted by different attack methods effectively, and can provide a reference to the security of IMS. [ABSTRACT FROM AUTHOR]

Background: Association between parity and colorectal cancer (CRC) risk has been investigated by several epidemiological studies but results are controversial, yet a comprehensive and quantitative assessment of this association has not been reported so far. Methods: Relevant published studies of parity and CRC were identified using MEDLINE, EMBASE and Web of Science databases through end of April 2013. Two authors independently assessed eligibility and extracted data. Eleven prospective studies reported relative risk (RR) estimates and 95% confidence intervals (CIs) of CRC risk associated with parity. We pooled the RR from individual studies using fixed- or random-effects models and carried out heterogeneity and publication bias analyses. Results: The summary RR for the ever parity vs. nulliparous was 0.95 (95% CI: 0.88–1.02), with no heterogeneity (Q = 9.04, P = 0.443, I2 = 0.5%). Likewise, no significant association was yielded for the highest vs. lowest parity number (RR = 1.02, 95% CI: 0.89–1.17), with moderate heterogeneity (Q = 17.48, P = 0.094, I2 = 37.1%). Dose-response analysis still indicated no effect of parity on CRC risk and the summary RR of per one livebirth was 0.99 (95% CI: 0.96–1.02), with moderate of heterogeneity (Q = 16.50, P<0.021, I2 = 57.6%). Similar results were observed among all the subgroup analyses. No evidence of publication bias and significant heterogeneity between subgroups were detected by meta-regression analyses. Conclusion: Results of this dose-response meta-analysis of prospective studies found that there was little evidence of an association between parity and CRC risk. [ABSTRACT FROM AUTHOR]

This study was conducted to determine the ontogenetic development of the digestive tract and its accessory structures (liver, pancreas, and gall bladder) in agastric larval Chinese sucker Myxocyprinus asiaticus with the histological and ultrastructural approaches from hatching to 56 days after hatching ( DAH). On the basis of its feeding mode, and analyzing the main histological features of the digestive system, larval development in Chinese sucker was divided into three stages from hatching: stage 1 (endotrophic period): 1-6 DAH; stage 2 (endoexotrophic period): 7-14 DAH; stage 3 (exclusively exotrophic period): from 15 DAH onward. At hatching, the digestive tract of the larvae consisted of an undifferentiated straight tube. At 4 DAH, the mouth opened, and the digestive tract was differentiated into buccopharyngeal cavity, esophagus and intestine. At 7 DAH, fish started to feed exogenously. Yolk sac was completely exhausted at 15 DAH. Until 56 DAH, the digestive tract of the larvae displayed regularly arranged microvilli, abundant vacuoles, and protein inclusion bodies. The pancreas, liver, and gall bladder were functional from 6 DAH, which enabled larvae to ingest, digest, and assimilate the first exogenous food. In comparison with teleosts that have a stomach, the development of the digestive tract of the agastric Chinese sucker seemed relatively slow. [ABSTRACT FROM AUTHOR]

An 8-wk feeding trial was conducted to evaluate the potential of replacing fish meal with canola meal in experimental diets for genetically improved farmed tilapia (GIFT) strain of Nile tilapia, Oreochromis niloticus (mean initial weight: 20.0 ± 0.62 g, means ± SD), reared in fresh water. Six isonitrogenous (30% crude protein) and isolipidic (10%) diets were formulated with canola meal included at six levels of 0 (control), 11, 22, 33, 44, and 55%, replacing 0, 15, 30, 45, 60, and 75% fish meal, respectively. Growth performance and feed utilization showed no significant differences among the treatments. In general, dietary canola meal supplementation showed significant effect on hepatic composition of tilapia, but not muscle composition. Viscerosomatic index tended to increase with increasing dietary canola meal levels from 0 to 44%, and then declined when dietary canola meal levels further increased from 44 to 55%. Dietary fish meal replacement by canola meal significantly influenced several hepatic enzymatic activities, including succinate dehydrogenase, lactate dehydrogenase, malic dehydrogenase, lipoprotein lipase, and hepatic lipase, suggesting that dietary fish meal replacement by canola meal had significant effects on nutrient metabolism in the liver. Based on the information above, 75% of dietary fish meal could be replaced by canola meal with no effect on growth performance of GIFT strain of Nile tilapia. Use of canola meal in practical diets for GIFT stain of Nile tilapia may allow producers and feed mills to formulate more economical diets. [ABSTRACT FROM AUTHOR]

An 8-week feeding trial was conducted to determine the effect of dietary conjugated linoleic acid ( CLA) on growth performance, muscle fatty acid profile, hepatic intermediary metabolism and antioxidant responses in genetically improved farmed Tilapia ( GIFT) strain of O reochromis niloticus (initial body weight: 42.6 ± 0.4 g, mean ± standard deviation). Three replicated groups of GIFT strain of Nile tilapia were hand-fed to satiation, twice a day, with the diets in which CLA oil, containing mainly the bioactive cis-9, trans-11 and trans-10, cis-12 isomers, was included at 0 (control), 0.5%, 1%, 1.5%, 2% and 2.5%, respectively, at the expense of fish oil to maintain the constant lipid and energy levels. Growth performance and feed utilization showed no significant differences among the treatments ( P > 0.05). The dietary inclusion of CLA modified total percentages of the main groups of fatty acids. Increasing saturated fatty acid content and reduced mono-unsaturated fatty acid contents in muscle were observed with increasing dietary CLA inclusion ( P < 0.05). Total n-3 fatty acids and total polyunsaturated fatty acids tended to decline with increasing dietary CLA levels ( P < 0.05), but n-6 fatty acids showed no significant differences among the treatments ( P > 0.05). Dietary CLA supplementation resulted in the significant increase in the trans-10, cis-12 and cis-9, trans-11 CLA isomers in muscle ( P < 0.05) and also significantly influenced several hepatic enzymatic activities, such as succinate dehydrogenase, lactate dehydrogenase, malic dehydrogenase, lipoprotein lipase and hepatic lipase activities ( P < 0.05). Reduced superoxide dismutase and glutathione peroxidase activities, and the decline in malondialdehyde levels were observed in fish fed the CLA-supplemented diets ( P < 0.05), indicating that dietary CLA supplementation showed a powerful antioxidant effect for this fish species. Our study was the first report involved in the effect of dietary CLA inclusion on hepatic intermediary metabolism and antioxidant responses in fish, which could be used as indicators of nutritional and physiological status of the fish species. [ABSTRACT FROM AUTHOR]