How do navy escorts influence piracy risk in East Africa? A Bayesian network approach.

Navy escorts are considered crucial in countering illegal piracy attacks. In this paper, a novel approach is developed to investigate the effect of navy escorts on piracy incidents by models based on two enhanced Tree-Augmented Naïve (TAN) Bayesian networks. This approach offers a systematic investigation into the various factors that influence pirate activities, and helps to identify changes in piracy attack behaviors when confronted by navy escorts and assess the effectiveness of anti-piracy measures. An empirical study is conducted utilizing a unique data set compiled from multiple sources from 2000 to 2019. The empirical evidence shows that there was a gradual reduction in the incidence of piracy attacks in East Africa following the implementation of navy escorts in 2009, but with a surge in 2010 and 2011. The data set is, thus, divided into two time periods at the point of 2009 to facilitate a robust and comprehensive analysis, resulting in the development of two TAN models. Meanwhile, the geographical distribution of pirate attacks has shifted from international waters to port areas and territorial waters. We argue that the surge and geographical shift could be attributed to the calculating behavior of pirates when they encounter external pressures. Finally, a Shapely approach is introduced to evaluate the potential effectiveness of the implemented risk management strategies from a Game Theory perspective. This study offers new insights into the promotion of navy escorts and contributes to the development of a framework for assessing piracy risks in uncertain and dynamic anti-piracy environments.

A pan-cancer analysis revealing the role of LFNG, MFNG and RFNG in tumor prognosis and microenvironment.

BACKGROUND: Fringe is a glycosyltransferase involved in tumor occurrence and metastasis. However, a comprehensive analysis of the Fringe family members lunatic fringe (LFNG), manic fringe (MFNG), radical fringe (RFNG) in human cancers is lacking. METHODS: In this study, we performed a pan-cancer analysis of Fringe family members in 33 cancer types with transcriptomic, genomic, methylation data from The Cancer Genome Atlas (TCGA) project. The correlation between Fringe family member expression and patient overall survival, copy number variation, methylation, Gene Ontology enrichment, and tumor-infiltrating lymphocytes (TILs) was investigated by using multiple databases, such as cBioPortal, Human Protein Atlas, GeneCards, STRING, MSigDB, TISIDB, and TIMER2. In vitro experiments and immunohistochemical assays were performed to validate our findings. RESULTS: High expression levels of LFNG, MFNG, RFNG were closely associated with poor overall survival in multiple cancers, particularly in pancreatic adenocarcinoma (PAAD), uveal melanoma (UVM), and brain lower-grade glioma (LGG). Copy number variation analysis revealed that diploid and gain mutations of LFNG was significantly increased in PAAD and stomach adenocarcinoma (STAD), and significantly associated with the methylation levels in promoter regions. Significant differential genes between high and low expression groups of these Fringe family members were found to be consistently enriched in immune response and T cell activation pathway, extracellular matrix adhesion pathway, RNA splicing and ion transport pathways. Correlation between the abundance of tumor-infiltrating lymphocytes (TILs) and LFNG, MFNG, and RFNG expression showed that high LFNG expression was associated with lower TIL levels, particularly in PAAD. In vitro experiment by using pancreatic cancer PANC1 cells showed that LFNG overexpression promoted cell proliferation and invasion. Immunohistochemical assay in 90 PAAD patients verified the expression level of LFNG and its relationship with the prognosis. CONCLUSIONS: Our study provides a relatively comprehensive understanding of the expression, mutation, copy number, promoter methylation level changes along with prognosis values of LFNG, MFNG, and RFNG in different tumors. High LFNG expression may serve as a poor prognosis molecular marker for PAAD.

Analysis of Clinical Efficacy and Influencing Factors of Nerve Growth Factor (NGF) Treatment for Sudden Sensorineural Hearing Loss.

Objective: This study aims to examine the clinical efficacy and prognostic factors associated with nerve growth factor (NGF) treatment for sudden sensorineural hearing loss (SSHL). Materials and methods: A retrospective analysis was conducted on the clinical data of 101 patients with moderate or more severe SSHL who underwent secondary treatment at Sun Yat-sen Memorial Hospital of Sun Yat-sen University between January 2019 and July 2020. Prior to treatment, all patients were assessed using Pure Tone Audiometry (PTA), auditory brainstem response, otoacoustic emission, temporal bone computed tomography, or inner ear magnetic resonance imaging. Fifty-seven patients received conventional systemic treatment and served as the control group, while 44 patients received NGF in conjunction with conventional systemic treatment, forming the experimental group. PTA results were compared between the two groups before treatment and at 1 week, 2 weeks, and 1 month post-treatment. Additionally, the impact of age, sex, affected side, hypertension, and other factors on patient prognosis was analyzed. Results: Both groups demonstrated significant PTA improvements following treatment, with a statistically significant difference (P < .05). The hearing recovery effective rate in the control group was 42.1%, while that of the experimental group reached 70.5%, with a statistically significant difference between the groups (P < .05). Most patients experienced notable hearing improvements 1 week after treatment, with some patients still showing progress 2 weeks post-treatment. Multifactor analysis revealed that hypertension and onset days were associated with treatment outcomes. Conclusion: Secondary treatment remains clinically significant for patients with SSHL who have not achieved a satisfactory response or show no clear improvement following initial treatment. The presence of hypertension and delayed treatment are negative factors related to treatment efficacy.

Chronic Remote Ischemic Conditioning on Mild Hypertension in the Absence of Antihypertensive Medication: A Multicenter, Randomized, Double-Blind, Proof-of-Concept Clinical Trial.

BACKGROUND: Exploratory studies have shown that remote ischemic conditioning (RIC) has the potential to lower blood pressure (BP). We investigated whether chronic RIC reduces BP for hypertension. METHODS: This is a multicenter, randomized, double-blind, parallel-controlled trial. Patients with an office BP of 130/80 to 160/100 mm Hg and a 24-hour average BP ≥125/75 mm Hg not on antihypertensive medications were recruited. After a 1-week compliance screening phase, they were randomly assigned in a 1:1 ratio to receive RIC or sham RIC twice daily for 4 weeks. The primary efficacy outcome was the change in 24-hour average systolic BP from baseline to 4 weeks. Safety events were assessed over the study period. RESULTS: Ninety-five participants were randomly allocated to the RIC (n=49) and sham RIC (n=46) groups. In the intention-to-treat analysis, the reduction in 24-hour average systolic BP was greater in the RIC group than the sham RIC group (-4.6±9.5 versus -0.9±6.8 mm Hg; baseline-adjusted between-group mean difference: -3.6 mm Hg [95% CI, -6.9 to -0.3 mm Hg]; adjusted P=0.035). The per-protocol analysis showed that 24-hour average systolic BP reduced -5.9±8.6 mm Hg in the RIC group and -0.7±6.7 mm Hg in the sham RIC group (baseline-adjusted between-group mean difference: -5.2 mm Hg [95% CI, -8.5 to -1.9 mm Hg]; adjusted P=0.002). No major adverse events were reported in both groups. CONCLUSIONS: RIC is safe in patients with mild hypertension and may lower BP in the absence of antihypertensive medications. However, the effects of RIC on clinical outcomes in these patients require further investigation. REGISTRATION: URL: https://www. CLINICALTRIALS: gov; Unique identifier: NCT04915313.

miR-34a/DRP-1-mediated mitophagy participated in cisplatin-induced ototoxicity via increasing oxidative stress.

PURPOSE: Cisplatin is a widely used and effective chemotherapeutic agent for most solid malignant tumors. However, cisplatin-induced ototoxicity is a common adverse effect that limits the therapeutic efficacy of tumors in the clinic. To date, the specific mechanism of ototoxicity has not been fully elucidated, and the management of cisplatin-induced ototoxicity is also an urgent challenge. Recently, some authors believed that miR34a and mitophagy played a role in age-related and drug-induced hearing loss. Our study aimed to explore the involvement of miR-34a/DRP-1-mediated mitophagy in cisplatin-induced ototoxicity. METHODS: In this study, C57BL/6 mice and HEI-OC1 cells were treated with cisplatin. MiR-34a and DRP-1 levels were analyzed by qRT‒PCR and western blotting, and mitochondrial function was assessed via oxidative stress, JC-1 and ATP content. Subsequently, we detected DRP-1 levels and observed mitochondrial function by modulating miR-34a expression in HEI-OC1 cells to determine the effect of miR-34a on DRP-1-mediated mitophagy. RESULTS: MiR-34a expression increased and DRP-1 levels decreased in C57BL/6 mice and HEI-OC1 cells treated with cisplatin, and mitochondrial dysfunction was involved in this process. Furthermore, the miR-34a mimic decreased DRP-1 expression, enhanced cisplatin-induced ototoxicity and aggravated mitochondrial dysfunction. We further verified that the miR-34a inhibitor increased DRP-1 expression, partially protected against cisplatin-induced ototoxicity and improved mitochondrial function. CONCLUSION: MiR-34a/DRP-1-mediated mitophagy was related to cisplatin-induced ototoxicity and might be a novel target for investigating the treatment and protection of cisplatin-induced ototoxicity.

Alterations of gut microbiota and cytokines in elevated serum diamine oxidase disorder.

The present study aimed to explore gut microbiota alterations and host cytokine responses in a population with elevated serum diamine oxidase (DAO) disorder. A total of 53 study participants were included in this study, segregated into 2 groups: subjects with high-level DAO (DAO-H, n = 22) subjects with normal DAO level (DAO-N, n = 31). We investigated the clinical and demographic parameters of study participants. The fecal bacterial communities and serum cytokines in 2 groups were assessed by 16S ribosomal RNA gene sequencing and immunoassay. High-pressure liquid chromatography was used to determine hemoglobin Alc. Flow cytometry was used to find the cytokine level in the blood serum. There is no difference in age, total cholesterol (TCHO), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), hemoglobin Alc, fasting plasma glucose (FPG) and homocysteine between the 2 groups. No significant difference were found in α-diversity between the 2 groups, however, the gut microbiota of subjects in DAO-H were characterized by marked interindividual differences, decreased abundance of Phocaeicola, Lachnospira, Bacteroides, Alistipes, Agathobacter, Lachnospira and Bactetoides and increased abundances of Mediterraneibacter, Blautia, Faecallibacterium, Agathobacter, and Parasutterella. Furthermore, the cytokines were no related to the DAO level in both groups and exhibited no significant differences between DAO-H and DAO-N. This study adds a new dimension to our understanding of the DAO and gut microbiota, and revealed that an increase in the DAO level in the intestinal mucosa could alter the gut microbiota composition, which can cause gut-related complications. Research is needed to extensively evaluate downstream pathways and provide possible protective or treatment measures pertaining to relevant disorders.

Correlation of Job stress and self-control through various dimensions in Beijing Hospital staff.

BACKGROUND: Mental, emotional and physical exhaustion has been increasing in humans due to work related stress. Many studies have been conducted on various variables contributing to and counteracting job stress. In our study, we aimed to examine the effect of different demographic and personal variables on job stress and its correlation with self-control in a hospital setting. METHOD: Our cross-sectional study involved 220 healthy staff members from Beijing hospital. Job stress and self-control were measured via the Chinese versions of the House and Rizzo Work Scale and the Self-Control Scale, respectively. RESULT: Participants with male gender and those with leading positions of authority reported higher job stress and poorer self-control (P < 0.01). Smokers also showed poorer self-control (P < 0.05, Bonferroni corrected P > 0.05). Poor physical and mental health conditions were observed to be significantly related to poor self-control (Bonferroni corrected P < 0.01) and higher job stress (Bonferroni corrected P < 0.05). Moreover, negative correlation was found between job stress and self-control and its dimensions (P < 0.001). Furthermore, job stress group and leadership position could interact to influence self-control, healthy habit, and resistance to temptation. CONCLUSION: We concluded that gender difference, leadership position, physical and mental health conditions all can affect work stress and an individual's self-control. Moreover, self-control dimensions like impulse control and attention to work correlated to job stress. Furthermore, the interaction between job stress and leadership could affect self-control and its dimensions. Future studies can be focused on using these variables to cope up with the ever increasing work related stress in the modern world.

The relationship between job stress and job burnout moderated by BDNF rs6265 polymorphism.

RATIONALE: Job stress can lead to job burnout, and BDNF polymorphism has been found to be involved in its psychopathological mechanism. Research needs a better understanding of the important role of gene × environment (i.e., BDNF polymorphism × job stress) interaction on job burnout. OBJECTIVE: This study aimed to explore how BDNF rs6265 polymorphism may moderate the relationship between job stress and job burnout. METHODS: Three hundred forty-one healthy participants (187 males and 154 females) from a Chinese university were included. The present study used a standardized questionnaire including demographic characteristics, job stress assessed by the House and Rizzo's Work Stress Scale, and job burnout assessed by the Maslach Burnout Inventory-General Survey. The BDNF rs6265 polymorphism was genotyped. RESULTS: Job stress showed a positive correlation with emotional exhaustion (p < 0.001), cynicism (p < 0.001), and reduced personal accomplishment (p < 0.01). The main effects of BDNF rs6265 polymorphism on emotional exhaustion and cynicism were significant [F(1,333) = 5.136, p = 0.024; F(1,333) = 4.175, p = 0.042, respectively]. The interaction between job stress and BDNF rs6265 on cynicism was significant (△ R2 = 0.013, p = 0.014) after controlling for age, sex, education, and position, indicating that individuals with BDNF rs6265 TT genotype showed higher level of cynicism when in high job stress. CONCLUSIONS: The results provided evidence for the association of BDNF gene rs6265 polymorphism, job stress, and their interaction with job burnout. Individuals with TT genotype in BDNF rs6265 might be susceptible to stressful situations, which would lead to cynicism.

Metformin alleviates cisplatin-induced ototoxicity by autophagy induction possibly via the AMPK/FOXO3a pathway.

Cisplatin is an antitumor drug that is widely used for the treatment of various solid tumors. Unfortunately, patients are often troubled by serious side effects, especially hearing loss. Up to now, there have been no clear and effective measures to prevent cisplatin-induced ototoxicity in clinical use. We explored the role of autophagy and the efficacy of metformin in cisplatin-induced ototoxicity in cells, zebrafish, and mice. Furthermore, the underlying molecular mechanism of how metformin affects cisplatin-induced ototoxicity was examined. In in vitro experiments, autophagy levels in HEI-OC1 cells were assessed using fluorescence and Western blot analyses. In in vivo experiments, whether metformin had a protective effect against cisplatin ototoxicity was validated in zebrafish and C57BL/6 mice. The results showed that cisplatin induced autophagy activation in HEI-OC1 cells. Metformin exerted antagonistic effects against cisplatin ototoxicity in HEI-OC1 cells, zebrafish, and mice. Notably, metformin activated autophagy and increased the expression levels of the adenosine monophosphate-activated protein kinase (AMPK) and the transcription factor Forkhead box protein O3 (FOXO3a), whereas cells with AMPK silencing displayed otherwise. Our findings indicate that metformin alleviates cisplatin-induced ototoxicity possibly through AMPK/FOXO3a-mediated autophagy machinery. This study underpins further researches on the prevention and treatment of cisplatin ototoxicity.NEW & NOTEWORTHY Cisplatin is an antitumor drug that is widely used for the treatment of various solid tumors. Up to now, there have been no clear and effective measures to prevent cisplatin-induced ototoxicity in clinical use. We investigated the protective effect of metformin on cisplatin ototoxicity in vitro and in vivo. Our findings indicate that metformin alleviates cisplatin-induced ototoxicity possibly through AMPK/FOXO3a-mediated autophagy machinery. This study underpins further researches on the prevention and treatment of cisplatin ototoxicity.

Repetitive transcranial magnetic stimulation on chronic tinnitus: a systematic review and meta-analysis.

BACKGROUND: Although the clinical efficacy and safety of repetitive transcranial magnetic stimulation (rTMS) in the treatment of chronic tinnitus have been frequently examined, the results remain contradictory. Therefore, we performed a systematic review and meta-analysed clinical trials examining the effects of rTMS to evaluate its clinical efficacy and safety. METHODS: Studies of rTMS for chronic tinnitus were retrieved from PubMed, Embase, and Cochrane Library through April 2020. Review Manager 5.3 software was employed for data synthesis, and Stata 13.0 software was used for analyses of publication bias and sensitivity. RESULTS: Twenty-nine randomized studies involving 1228 chronic tinnitus patients were included. Compared with sham-rTMS, rTMS exhibited significant improvements in the tinnitus handicap inventory (THI) scores at 1 week (mean difference [MD]: - 7.92, 95% confidence interval [CI]: - 14.18, - 1.66), 1 month (MD: -8.52, 95% CI: - 12.49, - 4.55), and 6 months (MD: -6.53, 95% CI: - 11.406, - 1.66) post intervention; there were significant mean changes in THI scores at 1 month (MD: -14.86, 95% CI: - 21.42, - 8.29) and 6 months (MD: -16.37, 95% CI: - 20.64, - 12.11) post intervention, and the tinnitus questionnaire (TQ) score at 1 week post intervention (MD: -8.54, 95% CI: - 15.56, - 1.52). Nonsignificant efficacy of rTMS was found regarding the THI score 2 weeks post intervention (MD: -1.51, 95% CI: - 13.42, - 10.40); the mean change in TQ scores 1 month post intervention (MD: -3.67, 95% CI: - 8.56, 1.22); TQ scores 1 (MD: -8.97, 95% CI: - 20.41, 2.48) and 6 months (MD: -7.02, 95% CI: - 18.18, 4.13) post intervention; and adverse events (odds ratios [OR]: 1.11, 95% CI: 0.51, 2.42). Egger's and Begg's tests indicated no publication bias (P = 0.925). CONCLUSION: This meta-analysis demonstrated that rTMS is effective for chronic tinnitus; however, its safety needs more validation. Restrained by the insufficient number of included studies and the small sample size, more large randomized double-blind multi-centre trials are needed for further verification.

[Research progress on the relationship between cisplatin ototoxicity and autophagy].

Cisplatin is an anti-tumor drug which is widely used for the treatment of various solid tumors. Unfortunately, seriousside-effects have affected patients, such as hearing loss. Up to now, there is no clear and effective measure to protect the cisplatin-induced ototoxicity in the clinical use of cisplatin studies indicated that autophagy may be involved in the whole process of cisplatin-induced hearing loss. In this review, the relationship between cisplatin ototoxicity and autophagy was reviewed. It is hoped that this study can provide reference for further study of cisplatin ototoxicity and intervention of autophagy with autophagy activator or inhibitor.

Mitochondrial ROS activate interleukin-1ß expression in allergic rhinitis.

Allergic rhinitis (AR) is the most common cause of inflammation of the nasal mucosa. It is also the most common form of non-infectious rhinitis associated with an immunoglobulin E (IgE)-mediated immune response against allergens. Previous studies have indicated that interleukin-1ß (IL-1ß) has a pathological role in the development of allergic asthma. The present study was designed to assess whether IL-1ß participates in the pathogenesis of AR. A total of 45 patients with AR were enrolled in the present study and were identified to have increased IL-1ß expression expressed by peripheral blood mononuclear cells (PBMCs), and the mitochondrial reactive oxygen species (ROS) and NLRP3 are required for IL-1ß synthesis in monocytes/macrophages and PBMCs from patients with AR. The levels of IL-1ß and interleukin-17 (IL-17) were increased in patients with AR and were positively correlated with each other. The results of the present study suggested that patients with AR have raised mitochondrial ROS levels, which may upregulate the expression of IL-1ß, affecting IL-17-production and serving a role in the pathogenesis of AR.

Sirtuin 1 and Autophagy Attenuate Cisplatin-Induced Hair Cell Death in the Mouse Cochlea and Zebrafish Lateral Line.

Cisplatin-induced ototoxicity is one of the major adverse effects in cisplatin chemotherapy, and hearing protective approaches are unavailable in clinical practice. Recent work unveiled a critical role of autophagy in cell survival in various types of hearing loss. Since the excessive activation of autophagy can contribute to apoptotic cell death, whether the activation of autophagy increases or decreases the rate of cell death in CDDP ototoxicity is still being debated. In this study, we showed that CDDP induced activation of autophagy in the auditory cell HEI-OC1 at the early stage. We then used rapamycin, an autophagy activator, to increase the autophagy activity, and found that the cell death significantly decreased after CDDP injury. In contrast, treatment with the autophagy inhibitor 3-methyladenine (3-MA) significantly increased cell death. In accordance with in vitro results, rapamycin alleviated CDDP-induced death of hair cells in zebrafish lateral line and cochlear hair cells in mice. Notably, we found that CDDP-induced increase of Sirtuin 1 (SIRT1) in the HEI-OC1 cells modulated the autophagy function. The specific SIRT1 activator SRT1720 could successfully protect against CDDP-induced cell loss in HEI-OC1 cells, zebrafish lateral line, and mice cochlea. These findings suggest that SIRT1 and autophagy activation can be suggested as potential therapeutic strategies for the treatment of CDDP-induced ototoxicity.

The Associations of Serum Lipids with Vitamin D Status.

AIMS: Vitamin D deficiency has been associated with some disorders including cardiovascular diseases. Dyslipidemia is a major risk factor for cardiovascular diseases. However, data about the relationships between vitamin D and lipids are inconsistent. The relationship of vitamin D and Atherogenic Index of Plasma (AIP), as an excellent predictor of level of small and dense LDL, has not been reported. The objective of this study was to investigate the effects of vitamin D status on serum lipids in Chinese adults. METHODS: The study was carried out using 1475 participants from the Center for Physical Examination, 306 Hospital of PLA in Beijing, China. Fasting blood samples were collected and serum concentrations of 25(OH)D, total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C) and low density lipoprotein cholesterol (LDL-C) were measured. AIP was calculated based on the formula: log [TG/HDL-C]. Multiple linear regression analysis was used to estimate the associations between serum 25(OH)D and lipids. The association between the occurrences of dyslipidemias and vitamin D levels was assessed by multiple logistic regression analysis. Confounding factors, age and BMI, were used for the adjustment. RESULTS: The median of serum 25(OH)D concentration was 47 (27-92.25) nmol/L in all subjects. The overall percentage of 25(OH)D ≦ 50 nmol/L was 58.5% (males 54.4%, females 63.7%). The serum 25(OH)D levels were inversely associated with TG (ß coefficient = -0.24, p < 0.001) and LDL-C (ß coefficient = -0.34, p < 0.001) and positively associated with TC (ß coefficient = 0.35, p < 0.002) in men. The associations between serum 25(OH)D and LDL-C (ß coefficient = -0.25, p = 0.01) and TC (ß coefficient = 0.39, p = 0.001) also existed in women. The serum 25(OH)D concentrations were negatively associated with AIP in men (r = -0.111, p < 0.01) but not in women. In addition, vitamin D deficient men had higher AIP values than vitamin D sufficient men. Furthermore, the occurrences of dyslipidemias (reduced HDL-C, elevated TG and elevated AIP) correlated with lower 25(OH)D levels in men, whereas the higher TC and LDL-C associated with higher 25(OH)D levels in women. CONCLUSION: It seems that the serum 25(OH)D levels are closely associated with the serum lipids and AIP. Vitamin D deficiency may be associated with the increased risk of dyslipidemias, especially in men. The association between vitamin D status and serum lipids may differ by genders.

Cloning and characterization of TaMBD6 homeologues encoding methyl-CpG-binding domain proteins in wheat.

DNA methylation is a major epigenetic marker in plants that plays a crucial role in transcriptional and developmental regulation. The DNA methylation 'code' is thought to be 'read' by a set of proteins containing methyl-CpG-binding domain (MBD). However, little is known about MBD genes in common wheat (Triticum aestivum L.). Here, we report the isolation and characterization of TaMBD6 and its homeologues (TaMBD6_A, TaMBD6_B, and TaMBD6_D) in hexaploid wheat. The cDNA was quite different among the three homeologues and InDel mutations were detected in 5'-UTR and coding region. Two types of TRs (tandem repeats) -- TR1 (57 bp) and TR2 (39 bp) -- occurred in the coding region. TaMBD6_B harbored five copies of TR1 and two copies of TR2. In contrast, TaMBD6_A lacked 30 bp between the 2nd and 3rd copy of TR1, while TaMBD6_D was missing two copies of TR1 but had three copies of TR2. TaMBD6_A, TaMBD6_B, and TaMBD6_D encoded 435, 446, and 420 amino acids, respectively. Structural analysis of TaMBD6 protein indicated that each of the three homeologues had an identical MBD domain at the N-terminal, as well as a typical nuclear localization signal. Although genomics analysis showed that two introns were included, the length of the first intron varied from 3100 bp to 3471 bp and their sequences were very different. Expression analysis demonstrated that the transcription level of TaMBD6 began to increase gradually in developing grains at 15 days after pollination while decreasing significantly in endosperm and embryo tissues during germination. Expression of TaMBD6 appeared to be positively correlated with starch metabolism in the endosperm but was negatively correlated with embryo formation and sprouting. We were also interested to learn that TaMBD6 homeologues were differentially expressed in developing wheat plants and that their expression patterns were variously affected by vernalization treatment. Further investigation revealed that TaMBD6 was induced by prolonged chilling, indicating that the protein is potentially involved in regulating the developmental transition from vegetative to reproductive stages. Although the homeologues generally showed similar differential expression patterns, TaMBD6_D and TaMBD6_B contribute more to the processes of grain development and germination while TaMBD6_A is predominant in mature plants.

[Radiation injury of interstitial implantation 125I seeds on normal trachea tissue of rabbits].

OBJECTIVE: To study the radition injury of tracheal mucous membrane tissue after interstitial implanted radioactive 125I in normal rabbit,improve the safety of clinical application. METHOD: Sixty New Zealand rabbits, weighing 2.15-2.30 kg, were randomly divided into 1 w, 1 m, 2 m, 4 m and the control group, the control group was further divided into four subgroups. The 0.8mCi 125I seeds were implanted into the tissue by the first tracheal ring in the treatment groups and nonradioactive seeds were implanted in the control group. Taking the tracheal mucous membrane tissue for pathological examination by HE staining to observe the mucosal injury and VEGF, Pan-Cadherin immunohistochemical staining to observe the expression in differernt time. RESULT: Immunohistochemical staining: VEGF and Pan-Cadherin have statistically significant differences in the expression on different time, the expression is dynamic. CONCLUSION: The expression of VEGF and Pan-Cadherin reflect the radioactive 125I seed has little influence on normal trachea tissue and the damage can be repaired by the regeneration of the basal cell.

[Numerical Study on the Characteristics of Regional Transport of PM2.5 in Shandong Province During Spring in 2014].

In this paper, spatial and temporal distribution, transportation and deposition of PM2.5 in Shandong Province in Spring, 2014 were all analyzed by applying PSAT of CAMx model and we also developed a transport matrix of PM2.5 between different cities in Shandong. The results showed that ρ(PM2.5) presented obvious spatial distribution characteristics; ρ(PM2.5) was higher in the western part compared to that in peninsula and ρ(PM2.5) was mainly concentrated below 2 000 m in vertical direction. Simulated horizontal transport flux of PM2.5 was up to 110 µg.(m2.s)-1 and the total deposition amount of PM2.5 was 23. 05 x 10(4) t in Shandong during Spring, 2014. Analysis of regional contribution found that the pollutants mainly came from local districts and the average external transport contribution to the whole Shandong province was about 21. 08% ± 3. 83% while it was 40. 45% ± 5. 96% between different cities; the contribution rates of Jinjinji distrcit, background and boundary conditions gradually increased by 7. 56% and 6. 18% respectively as the altitude increased.

[Relationship between job burnout and cognitive function and influencing factors of job burn out among medical staff].

OBJECTIVE: To explore the relationship between job burnout and cognitive function and the influencing factors of job burnout among medical staff. METHODS: Questionnaire survey was conducted for 197 medical workers in a grade-three general hospital in Beijing. Maslach Burnout Inventory-General Survey (MBI-GS) was carried out to assess the degree of job burnout among medical staff; Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) was used to evaluate the overall cognitive function and cognitive situations of different dimensions. RESULTS: (1) There was a certain level of job burnout among medical staff, especially for the emotional exhaustion dimension (13.29 ± 7.67). (2) High level job burnout group (81.08 ± 12.34) scored lower on visual span than low level job burnout group (92.48 ± 19.62), P<0.05. Overall, job burnout had a negative influence on the general cognitive function (P<0.05). (3) The results of regression analysis indicated that, inefficacy was negatively correlated with age (r=-0.162, P<0.05). Job burnout was positively correlated with level of education (r=0.234, P<0.05) as well as exercise frequency (r=0.320, P< 0.001), and emotional exhaustion was correlated with overtime work (r=0.135, P<0.05); Level of job burnout stayed higher among doctors and nurses, compared with administration staff in hospitals (t=2.966, P<0.05). CONCLUSION: Job burnout of medical staff was relatively in high level; influenced by age, education level, overtime work, exercise frequency and occupational type, job burnout affected the visual span and general cognitive function.

Long-range PCR in next-generation sequencing: comparison of six enzymes and evaluation on the MiSeq sequencer.

Long-range PCR remains a flexible, fast, efficient and cost-effective choice for sequencing candidate genomic regions in a small number of samples, especially when combined with next-generation sequencing (NGS) platforms. Several long-range DNA polymerases are advertised as being able to amplify up to 15 kb or longer genomic DNA. However, their real-world performance characteristics and their suitability for NGS remain unclear. We evaluated six long-range DNA polymerases (Invitrogen SequalPrep, Invitrogen AccuPrime, TaKaRa PrimeSTAR GXL, TaKaRa LA Taq Hot Start, KAPA Long Range HotStart and QIAGEN LongRange PCR Polymerase) to amplify three amplicons, with sizes of 12.9 kb, 9.7 kb, and 5.8 kb, respectively. Subsequently, we used the PrimeSTAR enzyme to amplify entire BRCA1 (83.2 kb) and BRCA2 (84.2 kb) genes from nine subjects and sequenced them on an Illumina MiSeq sequencer. We found that the TaKaRa PrimeSTAR GXL DNA polymerase can amplify almost all amplicons with different sizes and Tm values under identical PCR conditions. Other enzymes require alteration of PCR conditions to obtain optimal performance. From the MiSeq run, we identified multiple intronic and exonic single-nucleotide variations (SNVs), including one mutation (c.5946delT in BRCA2) in a positive control. Our study provided useful results for sequencing research focused on large genomic regions.