2,3,4',5-Tetrahydroxystilbene-2-O-ß-d-glucoside attenuates atherosclerotic progression by inhibiting inflammation via downregulation of TNF receptor-associated factor 6 expression.

OBJECTIVE: Atherosclerosis (As) is an inflammatory disease, and 2,3,4',5-tetrahydroxystilbene-2-O-ß-d-glucoside (TSG) has been shown to suppress inflammation. However, it is still unclear if TSG alleviates As by inhibiting inflammation. MATERIALS AND METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to assess the mRNA levels of tumor necrosis factor (TNF) receptor-associated factor 6 (TRAF6), TNF-α and interleukin-6 (IL-6) in lipoprotein E knockout (ApoE -/-) mice with As. Hematoxylin-eosin (H&E) staining was performed to examine the atherosclerotic plaques in the aortic sinus. QRT-PCR and western blotting were used to measure the expression levels of TRAF6, TNF-α, and IL-6 in human umbilical vein endothelial cells (HUVECs), and enzyme-linked immunosorbent assays (ELISAs) were performed to monitor the levels of TNF-α and IL-6 in serum and cell culture medium. RESULTS: TSG inhibited subendothelial plaques formation in the aortic sinus and inhibited the levels of total cholesterol (TCHO), low-density lipoprotein (LDL), TRAF6, TNF-α and IL-6 in AS mice in a dose-dependent manner. Moreover, TSG attenuated the oxidatively modified LDL (ox-LDL)-induced increases in TRAF6, TNF-α and IL-6 expression, whereas TRAF6 overexpression reversed the TSG-induced decreases in TRAF6, TNF-α, and IL-6 expression in HUVECs. CONCLUSIONS: TSG attenuates atherosclerotic progression by inhibiting inflammation via the downregulation of TRAF6 in ApoE-/- mice and HUVECs.

[Analysis on the proportion of men who have sex with men and related factors among male over 15 years old in Kunming].

Objectives: To investigate the proportion of MSM among males over 15 years old and analyze its related factors to provide a reference for estimation of MSM size. Methods: Using cross-sectional survey design, multi-stage sampling method, and street interception survey method, a survey was conducted on males over 15 years old in Kunming from October to December 2019, with an estimated sample size of 9 908. Results: Totally, 10 707 males were recruited from 30 sites in 5 counties, and 10 283 were effectively surveyed with a response rate of 96.0%. Respondents aged 16 to 40 accounted for 75.3% (7 748), senior high school or above 71.1% (7 312), and unmarried 49.8% (5 121). The proportion of homosexual behavior in the past half-year was 1.06% (95%CI: 0.86%-1.26%), and the age-adjusted rate was 0.97% (95%CI: 0.78%-1.16%). And multivariate logistic regression showed the associated factors for homosexual behavior as following: proportion of main urban area was 2.217 times (95%CI:1.004-4.895) that of the outer suburbs, registered residence outside Kunming was 0.421 times (95%CI:0.260-0.682) that of in Kunming, having been in Kunming ≤6 months was 2.282 times (95%CI:1.262-4.126) that of >6 months, senior middle school or above was 0.336 times (95%CI:0.228-0.495) that of junior middle school and below, and being married was 0.462 times (95%CI:0.303-0.705) that of unmarried. Conclusions: The proportion of over 15-year-old males who have recently practiced male-male behavior was close to 1.00% in Kunming. The relevant factors included survey areas with a permanent residency of Kumming, short-time residency, education level, and marital status. This study obtained the data and related factors, which provided a reference for estimating MSM size in Yunnan province.

[Features and clinical significance of gene mutations in patients with myelodysplastic syndromes with ring sideroblasts].

Objective: To explore the features and clinical significance of gene mutations in patients with myelodysplastic syndromes with ring sideroblasts (MDS-RS) . Methods: A total of 255 newly diagnosed primary MDS-RS patients were retrospectively reviewed from our center from January2001 to June 2019. SF3B1 gene mutations were detected by Sanger sequencing in 129 patients, and next generation sequencing (NGS) was performed in the other 126 patients using a set of selected 112-genes. Results: A total of 193 (75.7%) patients presented with SF3B1 mutation, predominantly mutant at amino acid position 700 (K700E) (n=147, 76.2%) . Non-SF3B1 gene mutations were TET2 (16.7%) , ASXL1 (14.3%) , U2AF1 (11.1%) , TP53 (7.9%) , SETBP1 (6.3%) , and RUNX1 (6.3%) . RS 5%-<15% patients had a higher SETBP1 mutation frequency than RS≥15% patients (21.4% vs 4.5%, P=0.044) . Mutation frequencies of other genes were similar in both groups (all P>0.05) . SF3B1 variant allele frequencies (VAF) had positive correlation with marrow RS percentage but without statistical significance in RS 5%-<15% group (P=0.078, r=0.486) . SF3B1 mutant patients presented with higher marrow RS percentage compared with wild-type patients[40.0% (15.0%-80.0%) vs 25.5% (15.0%-82.0%) , P<0.001], and SF3B1 VAF positively correlated with RS percentage (P=0.009, rs=0.261) in RS≥15% group. Age, ANC, PLT, mean RBC corpuscular volume, RS percentage, IPSS-R cytogenetics, and IPSS-R risk score were significantly different between patients with SF3B1 mutations and wild-type SF3B1 (all P<0.05) . Multivariable survival analyses adjusted by age and IPSS-R cytogenetics revealed that SF3B1 mutation was an independent favorable prognostic factor (HR=0.265, 95% CI 0.077-0.917, P=0.036) , and TP53 mutation was an adverse variable independent of SF3B1 mutation (HR=6.272, 95% CI 1.725-22.809, P=0.005) . According to the mutant status of SF3B1 and TP53, MDS-RS patients were categorized into 4 groups, namely, with SF3B1 and TP53 mutation, with wild-type SF3B1 and TP53, with wild-type SF3B1 but TP53 mutation, and with SF3B1 mutation but wild-type TP53. There was a significant difference for OS among these 4 groups (P<0.001) . The former 3 groups showed no significant difference in OS in multiple comparisons. However, the SF3B1 mutation but wild-type TP53 group had a better OS than wild-type SF3B1 but TP53 mutation group and wild-type SF3B1 and TP53 group, whereas a similar OS compared with SF3B1 and TP53 mutation group. Conclusion: SF3B1 mutations were prevalent in MDS-RS patients with the most common mutation at amino acid position 700 (K700E) . SF3B1 mutation was an independent favorable prognostic variable, whereas TP53 mutation was an independent adverse variable. SF3B1 mutation could coordinate with TP53 mutation for more sophisticated prognosis stratification in MDS-RS patients.

[Mean corpuscular volume ≤100 fl was an independent prognostic factor in patients with myelodysplastic syndrome and bone marrow blast<5 percent].

Objective: To explore the prognostic effects of mean corpuscular volume (MCV) in patients with myelodysplastic syndromes (MDS) . Methods: 321 newly diagnosed, untransfused primary MDS patients who administered from December 2009 to December 2017 were enrolled. The association of MCV with prognosis and several clinical features and genetic mutations were analyzed. Results: Patients were divided into MCV≤100 fl (n=148) and MCV>100 fl (n=173) cohorts. Median overall survival of patients with MCV≤100 fl was shorter than their counterparts (27 months vs 72 months, P<0.001) . In subgroup analysis, MCV≤100 fl patients had worse survivals in bone marrow blast <5% cohort (34 months vs not reached, P=0.002) , but not so in ≥5 % cohort (17 months vs 20 months, P=0.078) . MCV≤100 fl was still an independent adverse variable (HR=1.890, 95%CI 1.007-3.548, P=0.048) after adjusting for clinical and laboratory variables and mutation topography in bone marrow blasts<5% cohort. In bone marrow blasts<5% cohort, patients with MCV≤100 fl had higher hemoglobin levels [90 (42-153) g/L vs 78.5 (28-146) g/L, P=0.015].The proportions of Revised International Prognostic Scoring System (IPSS-R) high/very high risks and poor/very poor IPSS-R karyotypes were higher in MCV≤100 fl cohort (28.8% vs 10.8%, P=0.003; 24.7% vs 12.9%, P=0.049) . MCV≤100 fl cohort had more genetic mutations than those with MCV>100 fl though without significance (0.988 vs 0.769, P=0.064) . Mutated SF3B1 was less frequently in MCV≤100 fl cohort (4.7% vs 15.4%, P=0.018) . Conclusion: MCV≤100 fl was an independent adverse variable after adjusting for clinical and laboratory variables and mutation topography in MDS patients with bone marrow blasts<5%.

Population Structure and Genetic Diversity of Fungi Causing Rice Seedling Blight in Northeast China Based on Microsatellite Markers.

Rice seedling blight, which is caused by diverse pathogenic microorganisms, occurs worldwide and is the most important seedling disease affecting rice production in Northeast China. To further characterize the population structure and genetic diversity of the fungi responsible for rice seedling blight in Northeast China, 225 fungal strains were isolated from diseased rice seedlings collected from various rice-producing areas. The isolated strains included Fusarium oxysporum (48.0%), F. verticillioides (11.6%), F. tricinctum (8.0%), F. redolens (6.7%), F. equiseti (6.2%), F. solani (6.2%), Rhizoctonia solani (6.7%), Alternaria alternata (4.0%), and Curvularia coatesiae (2.7%). F. oxysporum was the dominant fungal species causing rice seedling blight, with most isolates exhibiting moderate pathogenicity. Moreover, to our knowledge, this is the first study to identify A. alternata and C. coatesiae as causal agents of rice seedling blight in Northeast China. None of the F. oxysporum isolates were sensitive to 10 µg/ml of carbendazim, implying that carbendazim is ineffective for controlling rice seedling blight in Northeast China. The F. oxysporum isolates were divided into nine groups based on a simple sequence repeat analysis involving 14 primer pairs. In addition, an analysis of molecular variance revealed a significant correlation between the F. oxysporum population and geographical location, which had a significant effect on the differentiation of the dominant isolate population. The results of this study provide insights into the genetic diversity of F. oxysporum strains causing rice seedling blight and may be useful for selecting isolates to screen for disease-resistant rice varieties, evaluating fungicide efficacy, and developing effective disease management strategies.

[Fibrosis-driving cells in patients with primary myelofibrosis and myelodysplastic syndromes with myelofibrosis].

Objective: To compare fibrosis-driving cells in patients with primary myelofibrosis (PMF) and patients with myelodysplastic syndromes (MDS) with myelofibrosis (MF) (MDS-MF) . Methods: Bone marrow biopsy sections of patients with newly diagnosed PMF and MDS (10 each randomly selected for MF-0/1, MF-2, and MF-3) were stained with specific immunofluorescence antibodies to label Gli1, LeptinR, alpha smooth muscle actin (α-SMA) , CD45, and ProcollagenⅠ. Images captured by confocal microscopy were analyzed by Fiji-ImageJ to calculate the cell counts of Gli1(+), LeptinR(+) cells, and fibrosis-driving cells including α-SMA(+), α-SMA(+)/Gli1(+), α-SMA(+)/LeptinR(+), and ProcollagenⅠ(+)/CD45(+) cells. Results: Patients with PMF and MDS with MF-2/3 had higher LeptinR(+), α-SMA(+), α-SMA(+)/Gli1(+), and Procollagen Ⅰ(+)/CD45(+) cell counts compared with those with MF-0/1 (all P values<0.05) . However, patients with PMF with MF-2/3 presented with higher Gli1(+) and α-SMA(+)/LeptinR(+) cell counts than those with MF-0/1 (P=0.001 and 0.006) , whereas these cells were similar between patients with MDS with MF-0/1 and MF-2/3 (P=0.169 and 0.067) . In patients with MF-0/1, all fibrosis-driving cells did not differ between PMF and MDS (all P>0.05) . However, in patients with MF-2/3, Procollagen Ⅰ(+)/CD45(+) cell counts were higher in patients with PMF compared with those with MDS (P=0.007) , while other fibrosis-driving cell counts were similar between these two groups (all P>0.05) . MF grade and fibrosis-driving cell counts were not correlated with overall survival in patients with either PMF or MDS. Conclusion: α-SMA(+) cells in patients with PMF originated from both Gli1(+) and LeptinR(+) cells, whereas α-SMA(+) cells in patients with MDS-MF only originated from Gli1(+) cells; patients with PMF had higher ProcollagenⅠ(+)/CD45(+) cell counts than those with MDS-MF.

[Spatial-temporal cluster of hemorrhagic fever with renal syndrome in Hebei province, 2005-2016].

Objective: To explore the spatial-temporal distribution and epidemic characteristics of hemorrhagic fever with renal syndrome (HFRS) in Hebei province from 2005 to 2016. Methods: Records of HFRS cases reported from each county in Hebei during January 2005 to December 2016 were collected from National Notifiable Disease Surveillance System (NNDSS). Global and local spatial association statistics were used to measure the spatial autocorrelation and software GeoDa 1.2.0. Software SaTScan 9.4.1 was used to analyze spatiotemporal clusters. Software ArcGIS 10.2 was used to visualize the yearly scan results. Results: In Hebei province, a total of 8 437 human HFRS cases reported from 170 counties with an annual incidence rate of 0.99/100 000 population during 2005-2016. The peak incidence season was spring. Global spatial autocorrelation analysis on the incidence of HFRS at county-level showed that the value of Moran's I were all above 0 (P<0.05), indicating that the significant spatial cluster. The result of local indicators on spatial association (LISA) analysis revealed that identified hot spots were mainly in northeastern area, while cold spots were found in some counties of central and southern areas. Spatial-temporal scan detected that the primary cluster of HFRS incidence was mainly distributed in Qinhuangdao city and Tangshan city, including 11 counties (city/district): Beidaihe district, Haigang district, Funing district, Shanhaiguan district, Changli county, Lulong county and Qinglong Manchu autonomous county in Qinhuangdao city, and Qian'an city, Laoting county, Luanzhou city and Luannan county in Tangshan city (RR=39.64, P<0.001), during January-July in 2005. Conclusions: There were significant spatial-temporal cluster of HFRS in Hebei from 2005 to 2016. The cluster areas of HFRS were mainly in northeastern Hebei, it is necessary to strengthen the prevention and control programs of HFRS in these areas.

[Clinical implications and prognostic value of TP53 gene mutation and deletion in patients with myelodysplastic syndromes].

Objective: To explore the clinical implications and prognostic value of TP53 gene mutation and deletion in patients with myelodysplastic syndromes (MDS) . Methods: 112-gene targeted sequencing and interphase fluorescence in situ hybridization (FISH) were used to detect TP53 mutation and deletion in 584 patients with newly diagnosed primary MDS who were admitted from October 2009 to December 2017. The association of TP53 mutation and deletion with several clinical features and their prognostic significance were analyzed. Results: Alterations in TP53 were found in 42 (7.2%) cases. Of these, 31 (5.3%) cases showed TP53 mutation only, 8 (1.4%) cases in TP53 deletion only, 3 (0.5%) cases harboring both mutation and deletion. A total of 37 mutations were detected in 34 patients, most of them (94.6%) were located in the DNA binding domain (exon5-8) , the remaining 2 were located in exon 10 and splice site respectively. Patients with TP53 alterations harbored significantly more mutations than whom without alterations (z=-2.418, P=0.016) . The median age of patients with TP53 alterations was higher than their counterparts[60 (21-78) years old vs 52 (14-83) years old, z=-2.188, P=0.029]. TP53 alterations correlated with complex karyotype and International prognostic scoring system intermediate-2/high significantly (P<0.001) . Median overall survival of patients with TP53 alterations was shorter than the others[13 (95%CI 7.57-18.43) months vs not reached, χ(2)=12.342, P<0.001], while the significance was lost during complex karyotype adjusted analysis in multivariable model. Conclusion: TP53 mutation was more common than deletion in MDS patients. The majority of mutations were located in the DNA binding domain. TP53 alterations were strongly associated with complex karyotype and always coexisted with other gene mutations. TP53 alteration was no longer an independent prognostic factor when complex karyotype were occurred in MDS.

[Prognostic implication of alterations in epidermal growth factor receptor and MGMT in glioblastoma].

Objective: To investigate the prognostic impact of alterations of epidermal growth factor receptor(EGFR) and MGMT in glioblastoma. Methods: The retrospective study included 161 supratentorial glioblastomas diagnosed in the Department of Pathology, Xuanwu Hospital, Capital Medical University from 2009 to 2015. EGFR and EGFRvⅢ protein expression was detected by immunohistochemistry; EGFR amplification was detected by fluorescence in situ hybridization; MGMT promoter methylation was detected by pyrosequencing. The change of molecular genetics EGFR and MGMT and outcome were assessed statistically. Results: There were 161 patients, including 85 (52.8%) males and 76 (47.2%) females. The mean age was 53 years, and the median overall survival was 13 months. The integrated classification of glioblastoma included 16 IDH-mutant, 134 wild type, and 11 NOS. The rate of overexpression of EGFR protein was 32.9%(53/161), and that of EGFR amplification was 37.5%(18/48). There was high concordance between immunohistochemistry and FISH(85.4%, Kappa=0.475, P<0.01) and between the level of EGFR protein and EGFR amplification (P<0.01). Twelve cases showed EGFRvⅢ expression, and all also showed EGFR protein overexpression; 149 cases were EGFRv Ⅲ wild type, and EGFR protein overexpression was seen in 27.5%(41/149) of cases. There was no correlation between EGFR and EGFRv Ⅲ expression. Of all cases, 70.2%(106/151) showed MGMT promoter methylation by pyrosequencing. The changes of molecular genetics of EGFR and MGMT were not related. EGFR amplification and protein overexpression had no significant relationship with prognosis. Patients with EGFRv Ⅲ-mutant had shorter survival time than the EGFRv Ⅲ-wild type(P=0.014); patients with MGMT promoter methylation had better prognosis than without (PFS:P=0.002,OS:P=0.006),and MGMT promoter methylation was an independent predictor for overall survival (HR=0.269, 95%CI 0.124-0.583, P=0.001). Conclusions: EGFR protein expression by immunohistochemistry correlates with the status of EGFR amplification. Patients with EGFRv Ⅲ-mutant tumors have poorer prognosis than that with EGFRv Ⅲ-wild type tumors. MGMT promoter methylation is closely associated with prognosis and an independent predictor for overall survival.

[A study of clinical characteristics and prognosis of primary myelofibrosis patients with thrombocytopenia in varied degrees].

Objective: To evaluate clinical characteristics and prognosis of primary myelofibrosis (PMF) patients with thrombocytopenia in varied degrees. Methods: Clinical features and survival data of 1 305 Chinese patients with PMF were retrospectively analyzed. The prognostic value of thrombocytopenia in patients with PMF was evaluated. Results: 320 subjects (47%) presented severe thrombocytopenia (PLT<50×10(9)/L), 198 ones (15.2%) mild thrombocytopenia [PLT (50-99)×10(9)/L] and 787 ones (60.3%) without thrombocytopenia (PLT ≥ 100×10(9)/L). The more severe the thrombocytopenia, the higher the proportions of HGB<100 g/L, WBC<4×10(9)/L, circulating blasts ≥ 3%, abnormal karyotype and unfavourable cytogenetics (P<0.001, P<0.001, P=0.004, P<0.001 and P<0.001, respectively) were observed in this cohort of patients. The more severe the thrombocytopenia, the lower the proportion of JAK2V617F positive (P<0.001) was also noticed. Platelet count was positively correlated with splenomegaly, HGB and WBC (P<0.001, correlation coefficients were 0.131, 0.445 and 0.156, respectively). Platelet count was negative correlated with constitutional symptoms and circulating blasts (P=0.009, P=0.045, respectively; correlation coefficients were -0.096 and -0.056, respectively). The median survival of patients with severe thrombocytopenia, mild thrombocytopenia and without thrombocytopenia were 32, 67 and 89 months, respectively (P<0.001). Multivariate analysis identified thrombocytopenia in varied degrees (HR=1.693, 95%CI 1.320-2.173, P<0.001) and Dynamic Internation Prognostic Scoring System(DIPSS) prognostic model (HR=2.051, 95%CI 1.511-2.784, P<0.001) as independent risk factors for survival. Conclusion: PMF patients with severe thrombocytopenia frequently displayed anemia, leucopenia, circulating blasts and short survival, so active treatment measures should be taken especially in these patients.

[The anti-proliferative and anti-inflammatory mechanisms of JAK1 inhibitor SHR0302 versus Ruxolitinib in SET2 cell line and primary cells].

Objective: To explore the effects and molecular mechanism of the selective JAK1inhibitor SHR0302 and Ruxolitinib on myeloproliterative neoplasms (MPN) cell line SET2 and primary cells in vitro. Methods: Cell proliferation was detected by CCK8 kit. Colony forming experiment was conducted to evaluate erythroid burst colony formation unit (BFU-E) of primary cells from MPN patients. Multi-factor kits were used to detect six inflammatory cytokines. Phosphorylated proteins of Jak-Stat signaling pathway were tested by Western blot. Results: At different time points after treated with SHR0302 and Ruxolitinib, the inhibition of cell proliferation was dose dependent by both drugs (P<0.01) . The inhibitory rates of 2.5 µmol/L SHR0302 and 0.1 µmol/L Ruxolitinib on SET2 cells for 72 h were comparable, i.e. (59.94±0.60) % and (64.00±0.66) %, respectively, suggesting that the inhibitory effect of SHR0302 was weaker than that of Ruxolitinib. Similarly, both SHR0302 and Ruxolitinib inhibited BFU-E in primary marrow cells from MPN patients in a dose-dependent manner. SHR0302 1.0 µmol/L produced similar degree of inhibition compared to Ruxolitinib 0.2 µmol/L. Except IL-12, the expression of other 5 cytokines (IL-6, TNF-α, IL-1ß, IL-2, IL-8) was significantly inhibited by 1.6 µmol/L SHR0302 in SET2 cells at 24 h (P<0.01) , while Ruxolitinib 1.0 µmol/L had the same effect. Several phosphorylated molecules of Jak-Stat signaling pathway were significantly inhibited by SHR0302 in SET2 cells only for 3 h. P-stat1 (Tyr701) , p-stat3 (Tyr705) were down-regulated when treated with SHR0302 1.0 µmol/L (P<0.05) , p-jak1 (tyr1022/1023) and p-stat5 (Tyr694) were inhibited at 5.0 µmol/L (P<0.05) . Ruxolitinib significantly inhibited the downstream STAT protein at 0.1 µmol/L. Again, the inhibitory effect of SHR0302 on protein expression was weaker than that of Ruxolitinib. Conclusion: SHR0302 can effectively inhibit the proliferation of MPN cell line and patients' primary cells, as well as the expression of inflammatory factors. The molecular mechanism is possibly related to the down-regulation of phosphorylated proteins of Jak-Stat signaling pathway. Overall, the anti-proliferative and anti-inflammatory effects of SHR0302 are weaker than those of Ruxolitinib.

[Using the sequenced sample cluster analysis to study the body mass index distribution characteristics of adults in different age groups and genders].

Objective: To explore the characteristics of distribution on Chinese adult body mass index (BMI) in different age groups and genders and to provide reference related to obesity and related chronic diseases. Methods: Data from the China Health and Nutrition Survey in 2009 were used. Sequential sample cluster method was used to analyze the characteristics of BMI distribution in different age groups and genders by SAS. Results: Our results showed that the adult BMI in China should be divided into 3 groups according to their age, as 20 to 40 years old, 40 to 65 years old, and> 65 years old, in females or in total when grouped by difference of 5 years. For groupings in male, the three groups should be as 20 to 40, 40 to 60 years old and>60 years old. There were differences on distribution between the male and female groups. When grouped by difference of 10 years, all of the clusters for male, female and total groups as 20-40, 40-60 and>60 years old, became similar for the three classes, respectively, with no differences of distribution between gender, suggesting that the 5-years grouping was more accurate than the 10-years one, and BMI showing gender differences. Conclusions: BMI of the Chinese adults should be divided into 3 categories according to the characteristics of their age. Our results showed that BMI was increasing with age in youths and adolescents, remained unchanged in the middle-aged but decreasing in the elderly.

[Knowledge, related behavior and on AIDS/HIV infection among rural adults with Derung minority, in Yunnan province, 2016].

Objective: To understand the related risk behaviors, knowledge and status of HIV/AIDS infection among rural adults of Derung minority, to provide relevant messages for the development of HIV/AIDS intervention strategy in this minority group. Methods: We used system sampling method to conduct a cross-sectional survey in 6 administration villages of Derung Township, Gongshan Derung and Nu Autonomous County in Nujiang Lisu Autonomous Prefecture of Yunnan Province, with a sample size estimated as 383. Adult residents with Derung minority in six villages of Gongshan County were involved, with relevant information collected through door-to-door visit. HIV antibody was tested and SPSS 17.0 was used for statistical analysis. Results: Information on 394 valid respondents was collected, with age as between 18 and 65 (34.39±9.74), 80.7% (318/394) as married, 54.0% (213/394) having had primary school education, 13.2% (52/394) as migrant workers. In this population, the overall HIV infection rate appeared as 0.5% (2/400), mainly through sexually transmission. The rate of awareness on HIV/AIDS was 69.8% (275/394), mainly through free publicized materials 50.0% (197/394). Rates on premarital sexual behavior on multiple sexual partners in the past year, on temporary sexual partners in the past year, having commercial sexual experiences in the past year and ever used condoms when engaging in casual sex, were 6.4% (60/366), 18.0%(66/366), 5.7%(21/366), 1.9%(7/366) and 8.0%(25/311), respectively. Conclusions: Few numbers of HIV infections were identified among the migrating workers with Derung minority, with sexual transmission as the major route, along with the increased number of rural migrant workers and the low rates both on AIDS knowledge and condom use, accompanied by the high risk sexual behavior appeared in this rural adult residents of Derung minority. Relative strategies on HIV/AIDS intervention and control should be developed.

[Diagnostic and prognostic roles of loss of CIC protein expression in oligodendroglial tumors].

Objective: To investigate the usefulness of loss of CIC expression as the prescreening detection of 1p/19q co-deletion in the diagnosis of oligodendroglial tumors and its prognostic implication. Methods: The retrospective study included 113 oligodendroglial tumors diagnosed in the Department of Pathology, Xuanwu Hospital, Capital Medical University. Expression of CIC protein was detected by immunohistochemistry, and the 1p/19q co-deletion by fluorescence in situ hybridization in all the tumors; and the correlation of the loss of protein and 1p/19q co-deletion with prognosis was assessed. Results: The rate of negative CIC protein expression was 59.3% (67/113) in 113 oligodendroglial tumors. CIC protein expression was differentially lost in various gliomas, 85.7% (42/49) in pure oligodendrogliomas and 39.1% (25/64) in mixed oligodendroglial tumors (P<0.01). The loss of CIC protein expression showed a sensitivity of 76.1% (54/71), specificity 71.1% (27/38), false positive rate of 16.9% (11/65), and a false negative rate of 38.6% (17/44). In 63 cases integrated diagnosis as oligodendroglial tumors with mutant IDH and 1p/19q co-deletion, the loss of CIC protein expression was 81.0% (51/63); the sensitivity and specificity were increased to 81.0% (51/63) and 76.9% (20/26), and the false positive rate and false negative rate decreased to 10.5% (6/57) and 37.5% (12/32), respectively. By using Kaplan-Meier analysis, the CIC negative group showed a trend towards better outcome than the CIC positive group, but there was no statistical difference (overall survival: P=0.218; progression free survival: P=0.249). Conclusions: Detection of the lost CIC protein expression can predict the chromosome 1p/19q co-deletion. In oligodendroglial tumors with IDH mutant and 1p/19q co-deletion, there is no relation between prognosis and CIC protein expression.

[Application of ATRX in diagnosis and prognostic evaluation of glioma].

Objective: To investigate the diagnostic and prognostic implications of ATRX mutation and p53 mutation in patients with glioma. Methods: The clinicopathologic and molecular features of Chinese adult glioma patients, including diffuse and anaplastic astroastrocytoma with IDH mutation, oligodendroglioma and anaplastic oligodendroglioma with IDH mutation and 1p/19q co-deletion and diffuse astroastrocytoma with IDH wild type were reviewed and tested for ATRX loss expression and p53 overexpression. Results: Loss of ATRX expression was seen in 85.19% (23/27) diffuse and anaplastic astroastrocytoma with IDH mutation, higher than that of oligodendroglial tumors (0/53; P<0.01). Loss of ATRX expression was strongly linked to p53 overexpression(69.57%, 16/23). The patients who lost ATRX expression combined with normal p53 expression survived longer(P=0.013). Conclusions: ATRX mutation is a molecular marker for astrocytic tumors. ATRX mutation combined with p53 mutation can predict prognosis of patients with glioma.

Gene expression profiling of somatic and pluripotent cells reveals novel pathways involved in reprogramming.

We investigated gene expression in embryonic stem (ES) cells, induced pluripotent stem (iPS) cells, and fibroblasts. Microarray expression data sets obtained from the Gene Expression Omnibus were analyzed using the Partek software. Human genes from ES cells, iPS cells, and fibroblasts were ranked from low to high according to their expression levels. The gene expression mode in iPS cells was much more like the mode in ES cells, and the expression levels of fibroblast genes fluctuated more dramatically than those of iPS and ES cells. The number of genes with significantly different expression was lower in the iPS and ES cells. Several genes with the expression levels that were significantly different between ES and iPS cells were found, including LEFTY2, DLK1, and NLRP2. Four genes belonged to the low expression category in fibroblasts with the high expression category occurring in ES cells, i.e., HESRG, PROM1, NTS, and LRRN1. Analyzing the expression of these genes is helpful to elucidate the mechanisms of cell fate regulation and efficiently obtain iPS cells.

Genome-scale meta-analysis of DNA methylation during progression of lung adenocarcinoma.

Identification of epigenetic alterations in tumors has become a common method for identifying genes critical to cancer development and progression. Thus, we identified DNA methylation alterations on the genome scale during lung adenocarcinoma (LADC) progression to understand the carcinogenic process and identify clinically relevant biomarkers. We found that epigenetic alterations in LADC mainly occur during the early stage of LADC progression, and there are no significant methylation differences between early-stage and late-stage LADCs. This suggests that DNA methylation alterations characterize a turning point of early events in LADC progression. By comparing DNA methylation between early-stage LADCs and normal lung tissues, we further identified 940 genes with significant alterations in DNA methylation. Sixty-seven genes were found to exhibit strong correlation between methylation alterations and expression changes, based on associated gene expression data. According to gene ontology analysis, these genes are involved in lung development, respiratory system development, cell cycle, histidine metabolism, the Wnt signaling pathway, and the p53 signaling pathway. We also found that genes on chromosome 18 most frequently showed promoter hypermethylation. Moreover, we found that LADC-associated DNA hypomethylation occurred preferentially at neither histone H3 lysine 4 nor histone H3 lysine 27 mark domains in human embryonic stem cells (NMDs) and that hypomethylation of NMDs was associated with a poor prognostic signature in LADC. Our findings have important implications for LADC progression because of the identification of novel epigenetic biomarkers potentially involved in early-stage LADC and for establishing the importance of NMD DNA hypomethylation for predicting prognosis in LADC.

The determinations of nucleosome positioning.

OBJECTIVE: Nucleosomes are the basic packaging units of chromatin, determinants of nucleosome organization playing a major role in genome packaging. Although a wide variety of nucleosome organization factors have been considered separately across the whole or partial human genomic regions, it is unclarified that what the major determinants and their roles in scale are when being put all together. And it is also unknown that what the similarities and differences of determinants between different genomic features such as genes of different expression levels or genomic regions with different functions. MATERIALS AND METHODS: We detected commonalities and characteristics of nucleosome positioning determinants in different genes and regions with 1591486 nucleosomes identified by ourselves in human CD4+ cell. RESULTS: It was found that a distinct linear combination of about 20 nucleosome-positioning factors explained nucleosome occupancy for each genomic feature. In those linear combinations, 6 DNA sequence attributes (Roll stiffness and Twist stiffness, CT and AG, CG and shift stiffness) and a histone modification (H4R3me2) are shared. And other factors are varied. Roll stiffness and Twist stiffness are the most important features. They are dominant, alone explaining 96.61-98.45% of the positioning weight in each genomic feature. The characteristic factors in each combination are larger in number, but weaker in power. Numerous histone modifications play a subtle role for nucleosome positioning. CONCLUSIONS: The present study provides a more accurate positioning nucleosome-map with higher resolution and a dramatically simplified means to predict and understand intrinsic nucleosome occupancy in different genomic features in human CD4+ cell. Roll stiffness and Twist stiffness are the two most important determinants in all genomic features. They may dominate because they both determine the degree of DNA bending and correlates with many other DNA structural characteristics. Histone modifications play a role of subtle allocation for nucleosome occupancy.

Seroprevalence of Toxoplasma gondii infection in pigs in Jilin Province, Northeastern China.

In the present study, a total of 1,235 porcine serum samples were collected from 9 counties in Jilin Province (40°52'~46°18'N,121°38'~131°19'E), northeastern China from August to October 2013, and the seroprevalence of Toxoplasma gondii infection was tested by indirect haemagglutination assay (IHA). The results showed that antibodies to T. gondii were found in 19.1% (95% confidence interval [CI], 16.9% to 21.3%), with higher seroprevalence in the breeding boars (28.6%, 95% CI, 20.0% to 37.2%), and breeding sows (32.0%, 95% CI, 25.2% to 38.9%). No significant difference was found among the slaughter pigs, fattening pigs and the piglets. These results indicated that infection with T. gondii in pigs is widespread in Jilin province, and is of public health concern.

Tissue-specific modification of clock methylation in aging mice.

BACKGROUND: Circadian rhythms tend to change as animals age; however, the molecular mechanisms underlying these are not yet fully understood. OBJECTIVE: To investigate whether the DNA methylation of clock genes changes with age and contributes to circadian dysfunction in aged animals. METHODS: We examined the methylation of clock promoters in the stomach, kidney, striatum, and spleen by using a methylation-specific polymerase chain reaction (MSP) assay. RESULTS: Our results show that different tissues exhibit specific patterns of clock methylation. Additionally, methylation frequency decreased significantly in older mice at the Per1 promoter in the stomach, but it was significantly increased in older mice at the Cry1, Bmal2, and Npas2 promoters in the spleen. CONCLUSION: The findings from our study suggest that DNA methylation contribute to age-related changes in circadian rhythms in certain slave oscillators.