目的 探讨体重指数(BMI)对接受免疫治疗的晚期肝细胞癌(HCC)患者预后的影响.方法 回顾性分析2016年11月至2020年1月在哈尔滨医科大学附属肿瘤医院消化内科接受靶向治疗(T队列)、免疫治疗(I队列)或靶向联合免疫治疗(T+I队列)的119例晚期HCC患者的临床资料.收集治疗前BMI,将患者分为两组:非超重组(BMI<23 kg/m2)和超重组(BMI≥23 kg/m2).采用Kaplan-Meier生存曲线计算不同队列下各组患者的中位总生存期(OS)和中位无进展生存期(PFS),采用Logistic回归模型分析疾病控制率(DCR).采用Cox比例风险回归模型分析预后的影响因素.I队列中纳入炎性指标中性粒细胞与淋巴细胞比值(NLR),通过受试者工作特征(ROC)曲线确定NLR的最佳截断值及其评估OS的灵敏度和特异度,比较NLR、BMI联合NLR与预后的关系.结果 共纳入119例患者,按照治疗方式分为3个队列,其中I队列41例,T队列41例,T+I队列37例.Kaplan-Meier分析结果显示,在整体人群中,超重组患者的中位OS和中位PFS依次在T队列、I队列、T+I队列中延长,组间差异有统计学意义(P=0.002,P=0.029);非超重组患者中位OS和中位PFS在I队列、T+I队列中均有延长趋势,但差异均无统计学意义(P>0.05).对整体人群行Cox多因素分析显示,BMI、既往肝切除术、既往肝局部治疗为影响OS的独立因素(P<0.05),性别为影响PFS的独立因素(P<0.05).进一步对BMI在各队列中进行分析,I队列:超重组和非超重组的患者OS之间的差异有统计学意义(HR=0.449,95％CI:0.207～0.970,P=0.041);T+I队列:超重组和非超重组的患者OS之间的差异有统计学意义(HR=0.393,95％CI:0.155～0.998,P=0.049);T队列:超重组和非超重组患者OS之间的差异无统计学意义(HR=1.020,95％CI:0.508～2.049,P=0.953).在3个队列中,超重组和非超重组的患者PFS之间的差异均无统计学意义(P>0.05);I队列和T+I队列中超重组患者的PFS分别延长了2.0个月和5.1个月,疾病进展风险分别降低26.8％和41.0％.I队列中,ROC曲线显示NLR的最佳截断值为2.62,NLR<2.62组的患者中位OS较NLR≥2.62组显著延长(37.5个月vs.14.3个月,P=0.016);进一步分析发现OS在BMI≥23 kg/m2且NLR<2.62组的患者中延长趋势最明显,在BMI<23 kg/m2且NLR≥2.62组中最短(P=0.024).Logistic回归分析显示BMI对各队列患者的DCR无显著影响(P>0.05).结论 BMI对接受系统治疗的晚期HCC预后产生影响,结果可能因治疗方式不同而产生差异.超重组(BMI≥23 kg/m2)中接受含免疫治疗的患者OS改善、死亡风险降低,而患者的PFS、DCR与BMI未见相关性.BMI联合NLR检测更能够揭示与接受免疫治疗的晚期HCC患者预后的关系,即高BMI伴随低NLR预示更长的OS,而低BMI伴随高NLR预示OS更差.

Background: In the past few decades, natural products have become an increasingly important source of potential anti-cancer agents. The green walnut husk(GWH) extracts have been reported to inhibit multiple tumor cells and might be a promising chemopreventive agent in human neoplasia. However, it is not clear whether GWH extracts inhibit gastric cancer. Methods: Proliferation, invasion, and migration of gastric cancer cells were assessed by the CCK-8, wound-healing, and Transwell assay. The apoptotic rate was detected by flow cytometry(FCM). The expressions of Bcl-2, Bax, and Caspase-3 proteins were examined by Western blot. Moreover, the growth of gastric cancer cells was assessed using orthotopic xenograft models, and related proteins expressions were evaluated using immunohistochemistry. Finally, the Gene expression profile of gastric cancer treated with GWH extracts was evaluated by using High-throughput RNA sequencing(RNA-seq). Results: GWH extracts effectively inhibited gastric cancer cell growth in vitro and in vivo. In vivo, GWH extracts inhibited the survival of gastric cancer cells in a dose and time-dependent manner, inhibited the migration and invasion of gastric cancer cells, regulated the expressions of apoptosis-related proteins, and induced apoptosis of gastric cancer cells. In vitro, GWH extracts inhibited the growth of mouse xenografted tumors. A total of differentially expressed genes, of which 41 genes were up-regulated, and 610 genes were down-regulated, were identified by RNA-seq. GO, and KEGG analysis showed that these differentially expressed genes might be related to the mechanism of the anti-gastric cancer effect of GWH extracts. Conclusion: GWH extracts played an anti-gastric cancer effect by inducing apoptosis and inhibiting invasion. Secondly, the differential expression of many genes, multiple signal pathways, and metabolic pathways in gastric cancer play an essential role in the anti-gastric cancer effect of GWH extracts. The results suggested that GWH extracts are expected to be a low toxic drug for the treatment of gastric cancer in the future.

We investigated the allele and genotype frequencies of two common CRTH2 single nucleotide polymorphisms (SNPs) [G1544C and A1651G (rs 545659)] in the 3'-untranslated region and the relationship between these SNPs and serum IL-13 levels in Chinese children patients with asthma. For G1544C and A1651G SNPs, there were significant differences in allele and genotype frequencies between asthma patients and controls. Haplotype analysis yielded additional evidence of linkage disequilibrium for the 1544G-1651G haplotype (P < 0.01). Moreover, serum IL-13 levels were significantly different among genotypes in G1544C, A1651G SNPs. These results suggest that SNPs of G1544C and A1651G might be act as susceptibility genetic factors of asthma.

目的 探讨老年晚期胃癌患者一线化疗后采用卡培他滨片/替吉奥维持治疗的临床疗效及预后影响因素.方法 根据治疗方案的不同将90例老年晚期胃癌患者分为3组,其中,维持治疗组22例,采用紫杉醇/奥沙利铂+卡培他滨片/替吉奥胶囊一线诱导化疗后口服卡培他滨片/替吉奥胶囊维持治疗;两药化疗组53例,采用紫杉醇/奥沙利铂+卡培他滨片/替吉奥胶囊一线化疗至疾病控制后定期随访观察,直至肿瘤进展;单药化疗组15例,采用卡培他滨片/替吉奥胶囊单药化疗至疾病进展.分析老年晚期胃癌患者的无进展生存期(PFS)、总生存期(OS)及预后影响因素.结果 维持治疗组、两药化疗组、单药化疗组患者的中位PFS分别为9.0、5.2和4.9个月,中位OS分别为17.0、12.0和8.1个月.3组患者的中位PFS和中位OS比较,差异均有统计学意义(P﹤0.05).维持治疗组患者的常见不良反应包括血液学毒性、胃肠道反应、乏力,以1～2级为主,无治疗相关性死亡.结论 卡培他滨片/替吉奥作为老年晚期胃癌患者一线化疗后的维持治疗药物,可延长患者的PFS和OS,且患者耐受性良好.

Anti-PD-1 monoclonal antibody is approved as an option for third-line treatment of advanced gastric and gastroesophageal junction (G/GEJ) cancer in several countries, but no anti-PD-1 monoclonal antibody treatment is yet approved for first-line treatment of advanced G/GEJ cancer. We report a phase Ib trial of HX008, a highly selective, humanized anti-programmed death-1 monoclonal antibody, plus oxaliplatin and capecitabine as first-line treatment for advanced G/GEJ cancer. Patients with previously untreated, locally advanced or metastatic G/GEJ cancer were enrolled. All patients received HX008 3 mg/kg intravenously every 3 weeks, oxaliplatin 130 mg/m2 intravenously on day 1 every 3 weeks (up to 6 cycles), and capecitabine 1000 mg/m2 orally twice daily for 14 days continuous dosing followed by a 7-day break. The primary end point was the incidence of adverse events and serious adverse events. In total, 35 patients were enrolled. Median follow-up was 12.7 months. Most frequent (>10%) grade ≥3 treatment-related adverse events were anemia (27.5%), neutropenia (20%), thrombocytopenia (17.1%), leukopenia (17.1%) and fatigue (17.3%). Objective response rate was 60.0% (95% confidence interval [CI] 42.1–76.1%). Disease control rate was 77.1% (95% CI 59.9–89.6). Median time to response and duration of response were 1.4 months (range 1.3–2.9) and 12.3 months (range 1.4–17.9+), respectively. Median PFS was 9.2 months (95% CI 5.4-not reached). These results demonstrated that HX008 combined with oxaliplatin plus capecitabine was well tolerated and demonstrated encouraging efficacy as first-line treatment for advanced G/GEJ cancer. This study was registered in china, register number was CTR20181270.

CDC-like kinase 3 (CLK3) is a dual specificity kinase that functions on substrates containing serine/threonine and tyrosine. But its role in human cancer remains unknown. Herein, we demonstrated that CLK3 was significantly up-regulated in cholangiocarcinoma (CCA) and identified a recurrent Q607R somatic substitution that represented a gain-of-function mutation in the CLK3 kinase domain. Gene ontology term enrichment suggested that high CLK3 expression in CCA patients mainly was associated with nucleotide metabolism reprogramming, which was further confirmed by comparing metabolic profiling of CCA cells. CLK3 directly phosphorylated USP13 at Y708, which promoted its binding to c-Myc, thereby preventing Fbxl14-mediated c-Myc ubiquitination and activating the transcription of purine metabolic genes. Notably, the CCA-associated CLK3-Q607R mutant induced USP13-Y708 phosphorylation and enhanced the activity of c-Myc. In turn, c-Myc transcriptionally up-regulated CLK3. Finally, we identified tacrine hydrochloride as a potential drug to inhibit aberrant CLK3-induced CCA. These findings demonstrate that CLK3 plays a crucial role in CCA purine metabolism, suggesting a potential therapeutic utility.

Annexin A2 (ANXA2) has been well known to associate with the progress of malignant tumor. However, the biological behavior of ANXA2 in gastric cancer (GC) remains unclear. We made a hypothesis in transcriptome level from TCGA datasets. Then, we used immunohistochemical staining to quantify the expression level of ANXA2 protein in GC tissues compared with adjacent tissues. Quantitative real-time PCR and western blot were used for analyzing ANXA2 expression in human GC (SGC-7901, MKN-45, BGC-823, and AGS) cell lines. We investigated the effect of a lentivirus-mediated knock-down of ANXA2 on the proliferation, invasion and migration of gastric cancer AGS cells. Cell proliferation was examined by MTT and colony formation tests. Cell apoptosis and cycle were measured by flow cytometry. Migration and invasion were detected by transwell assay. We found that high expression of ANXA2 can increase the mobility of cancer cells from TCGA datasets. ANXA2 was upregulated in GC tissues compared with adjacent tissues. AGS cell line displayed significantly higher expression of ANXA2 among the four GC cell lines. In addition, ANXA2 silencing led to a weakened ability of proliferation, invasion, and migration in GC cells; targeting of ANXA2 may be a potential therapeutic strategy for GC patients.

免疫治疗是通过机体激发自身T淋巴细胞特异性抗肿瘤反应来抑制肿瘤的发生发展.在T淋巴细胞膜的表面上,存在若干免疫检查点,如程序性细胞死亡蛋白1 (programmed cell death-1 ,PD-1)和细胞毒性T淋巴细胞抗原-4(cytotoxic T lymphocyte-associated antigen-4,CTLA-4),在正常情况下能抑制T细胞的功能.然而,免疫检查点抗体介导阻断了免疫检查点的抑制,从而导致T细胞的激活和增强抗肿瘤活性.多项免疫检查点抑制剂临床研究在胃癌的治疗中也有了相关的阴性或阳性结果,使得正在开展及待开展的临床研究结果备受关注.在免疫抑制剂带来获益的同时也造成了一些不可避免的不良反应,但在接受适当治疗后,大多数不良反应的疗程通常为2～4周转归.全文就免疫治疗在胃癌治疗中的现状和前景予以综述.

Objective To study the influencing factors of chronic diseases among the elderly so as to provide effective advice and measures for their chronic disease prevention and treatment.Methods We sorted the data from the Fifth Health Service Survey in Heilongjiang Province,and then selected the elderly aged 60 years and above to serve as the research subjects.The influencing factors were divided into five dimensions,namely health behavior,physical function,interpersonal network,material condition and social support.Statistical analysis was performed by partial least squares structural equation modeling (PLS-SEM).Results The prevalence rate of chronic diseases in the research subjects was 56.52％.The composite reliability estimates of the measurement models were all more than 0.8,meaning the reliability of the data was good.The estimates of the factor loadings were between 0.56 -0.89,showing the models were acceptable.The average variance extracted (AVE) values were more than 0.5,indicating latent variables could be well explained by the observation variables.Health behavior,physical function,material condition and social support were all negatively correlated with the occurrence of chronic diseases.The path coefficients of health behavior with chronic diseases,physical function with chronic diseases,material condition with chronic diseases,and social support with chronic diseases were-0.395,-0.306,-0.340 and-0.244 respectively.Conclusions Health behavior,physical function,material condition and social support have direct effects on chronic diseases;meanwhile,they interact with interpersonal network to build a complex path and generate the synthetic action on the chronic diseases.Among them,health behavior is the primary factor influencing chronic diseases,and the formation of health behavior is conducive to controlling the occurrence and development of chronic diseases.Degradation of body function of the elderly increases the risk of chronic diseases,but improvement of material condition and social support is helpful for lowering the prevalence rate of chronic diseases and promoting the quality of life in the elderly with chronic diseases.

Background/Aims: Although photodynamic therapy (PDT) can relieve esophageal obstruction and prolong survival time of patients with esophageal cancer, it can induce nuclear factor-kappa B (NF-κB) activation in many cancers, which plays a negative role in PDT. Dihydroartemisinin (DHA), the most potent artemisinin derivative, can enhance the effect of PDT on esophageal cancer cells. However, the mechanism is still unclear. Methods: We generated stable cell lines expressing the super-repressor form of the NF-κB inhibitor IκBα and cell lines with lentivirus vector-mediated silencing of the HIF-1α gene. Esophageal xenograft tumors were created by subcutaneous injection of Eca109 cells into BALB/c nude mice. Four treatment groups were analyzed: a control group, photosensitizer alone group, light alone group, and PDT group. NF-κB expression was detected by an electrophoretic mobility shift assay, hypoxia-inducible factor α (HIF-1α) and vascular endothelial growth factor (VEGF) by real-time PCR, NF-κB, HIF-1α, and VEGF protein by western blot, and Ki-67, HIF-1α, VEGF, and NF-κB protein by immunohistochemistry. Results: PDT increased NF-κB activity and the gene expression of HIF-1α and VEGF in vitro and in vivo. In contrast, the DHA groups, particularly the combined DHA and PDT treatment group, abolished the effect. The combined treatment significantly inhibited tumor growth in vitro and in vivo. NF-κB activity and HIF-1α expression were also reduced in the stable IκBα expression group, whereas the former showed no change in HIF-1α-silenced cells. Conclusion: DHA might increase the sensitivity of esophageal cancer cells to PDT by inhibiting the NF-κB/HIF-1α/VEGF pathway.

In the past few decades,with the rapid development of tumor biology and discovery of molecular markers of gastric tumor,various molecular targeted therapies are used in treatment of advanced gastric cancer.The mechanisms involved in the targeted therapy of gastric cancer include the regulation of epidermal growth factor,angiogenesis,immunocheckpoint blockade,cell cycle,cell apoptosis,key enzymes,c-Met,mTOR signaling and insulin-like growth factor receptors.An in-depth understanding of the mechanisms that underlie molecular targeted therapies will provide new insights into gastric cancer treatment.

[Purpose] To study the correlation between the changes of serum VEGFR-2 concentration and short-term effects of hepatocellular carcinoma after transcatheter arterial chemoembolization.[Methods] Serum VEGF-2 expression level,measured by quatitative sandwich enzyme-linked immunosorbentassay (ELISA),was measured before TACE 1 day and 1 month after TACE in 24 patients with HCC and the correlation between the change of VEGFR-2 concentration and clinical pathological characteristics of patients with advanced hepatocellular carcinoma was analyzed.[Results] The serum VEGFR-2 concentration was significantly correlated with the tumor size and hepatic cirrhosis(P＜0.05).The progress free survival(PFS) was significantly correlated with the tumor size,portal vein invasion,tumer number and hepatic cirrhosis (P＜0.05).There were 5 patients with partial response after one month of treatment,14 patients with stable disease,5 patients with progressive disease.The PFS was 7.84,4.71 and 3.68 months,respectively (P＜0.05).[Conclusion] The change of serum VEGFR-2 concentration in early stage is related to PFS and VEGFR-2 may be a tpotential indicator for predicting the short-term effects of TACE in hepatocellular carcinoma.

BACKGROUND:Major depression (MD) is caused by a combination of genetic and environmental factors. In this study we investigated the interaction of variations in the G-protein beta 3 subunit (GNB3) and cAMP response element binding protein 1 (CREB1) genes with negative life events in the pathogenesis of MD. One GNB3 polymorphism (rs5443) and four CREB1 polymorphisms (rs2253206, rs2551941, rs6740584, rs11904814) were investigated based on known associations with MD.METHODS:512 patients with MD and 513 control subjects were genotyped. The frequency and severity of negative life events were measured by the Life Events Scale (LES). Gene-environment interactions (G×E) were assessed using the generalized multifactor dimensionality reduction (GMDR) method.RESULTS:Differences in GNB3 rs5443 allele frequencies and genotype distributions were observed between MD patients and controls. Significant G×E interactions were detected between negative life events and genotypic variation of all five single nucleotide polymorphisms (SNPs). Individuals carrying the T- allele of rs5443 (CC), A- allele of rs2253206 (GG), T- allele of rs2551941 (AA), C- allele of rs6740584 (TT) or G- allele of rs11904814 (TT) conferred susceptibility to MD in subjects only exposed to high-negative life events. However, individuals with the T+ allele of rs5443 (CT, TT) were susceptible to MD when exposed to low negative life events.CONCLUSIONS:Interactions between GNB3, CREB1 and negative life events were revealed. Further evidence is provided about the role of the environment in genetic vulnerability to MD.

目的 了解哈尔滨市2010-2015年青年学生人群的艾滋病相关知识、行为及HIV、梅毒、丙肝感染情况,为在青年学生中开展艾滋病知识宣教及行为干预工作提供参考依据.方法 按照《全国艾滋病哨点监测实施方案》,于2010-2015年抽取哈尔滨市青年学生4 884名,进行问卷调查和HIV、梅毒、丙肝3项血清学检测.问卷及检测结果数据运用SPSS19.0软件进行统计描述.结果 4 884名调查对象的艾滋病知识总知晓率为84.0％.趋势检验结果表明,年份与青年学生艾滋病知晓率之间,随着年份的增加,知晓率呈线性增加的趋势(Z=2.4219,P=0.0154).青年学生性行为发生率为18.7％,在发生过性行为的男学生中,有男男性行为的占8.8％.趋势性检验结果表明,年份与男男性行为比例之间,随着年份的增加,男男性行为比例呈线性增加的趋势(Z=2.1160,P=0.0343).最近一年接受过有关预防艾滋病的宣传服务的人不足1/3,最近一年参与过有关预防艾滋病的宣传服务的人不足1/5,最近一年做过艾滋病检测的人只有2.9％.检出HIV阳性12人、梅毒阳性17人、丙肝阳性14人.结论 针对青年学生的艾滋病相关宣传服务活动的覆盖面和实效性还存在很多问题,学生咨询检测意识还很低;知识知晓率在普遍达到较高水平后,需要加强行为干预工作,避免“知信行”分离;性行为发生率升高不一定伴随感染率升高,艾滋病感染主要原因是危险性行为.在以后的工作中应通过开展更广泛的艾滋病相关宣传服务活动,加强行为干预质量,提倡主动进行咨询检测,正确引导健康性观念,促进青年学生安全性行为意识等一系列有效措施,来遏制艾滋病在青年学生中蔓延.

Objective To evaluate the dynamic changes of running efficiency and productivity of third-grade first-class comprehensive hospitals in Heilongjiang Province during 2007-2013 so as to provide the management evidence and decision references for the hospitals' managers and policymakers.Methods CCR and BCC models were employed for performing a cross-sectional analysis of annual efficiency of the sample hospitals,and the above-mentioned models combined with the Malmquist index model for assessing the total factor productivity and longitudinal cross-period development.Results The 27 third-grade first-class comprehensive hospitals had been rapidly developing in the capacity and scale during 2007-2013,whereas the hospitals' running efficiency was declined.On average,17.43 hospitals were inefficient,11.15 pure technically inefficient and 17.29 scale inefficient.Among the 27 hospitals,there were 10 (37.04％),11 (40.74％),20 (74.07％),13 (48.15％),5 (18.52％) and 10 (37.04％) hospitals' total factor productivity decreased for two consecutive years in 2007-2013.Conclusions The sample hospitals run inefficiently during the 7-year period;and hence,it is necessary to appropriately adjust the hospitals' scale,improve the utilization efficiency of medical resources and promote the running condition of the hospitals.

Recent reports suggest promises on using oncolytic Newcastle disease viruses (NDV) to treat different cancers, while the effects of a NDV-D90 strain on gastric cancer remain unknown. Here we showed that NDV-D90 induced gastric cancer cell apoptosis in a dose-dependent manner in 3 gastric cancer cell lines BGC-823, SGC-7901 and MKN-28. Pronounced reduction in cell invasion was detected in NDV-D90-treated BGC-823 and SGC-7901 cells, but not in MKN-28 cells. The increases in cell apoptosis and reduction in cell growth in NDV-D90-treated gastric cancer cells seemingly resulted from augmentation of p38 signaling and suppression of ERK1/2 and Akt signaling. In vivo, orthotopic injection of NDV-D90 impaired tumor growth and induced intratumoral necrosis. Tumor cells that had been pre-treated with NDV-D90 showed defect in development of implanted tumor. Moreover, NDV-D90 appeared to reduce gastric tumor vascularization, possibly through suppression of vascular endothelial growth factor A and Matrix Metallopeptidase 2. Together, our data suggest that NDV-D90 may have potential anti-cancer effects on gastric cancer.

Altered expression of microRNA-590-5p (miR-590-5p) is involved in tumorigenesis, however, its role in colorectal cancer (CRC) remains to be determined. In this study, we focused on examining the effects of different expression levels of miR-590-5p in cancer cells and normal cells. Results showed that there are lower expression levels of miR-590-5p in human CRC cells and tissues than in normal control cells and tissues. Similarly, in our xenograft mouse model, knockdown of miR-590-5p promoted the progression of CRC. However, an overexpression of miR-590-5p in the mice inhibited angiogenesis, tumor growth, and lung metastasis. Nuclear factor 90 (NF90), a positive regulator of vascular endothelial growth factor (VEGF) mRNA stability and protein synthesis, was shown to be a direct target of miR-590-5p. The overexpression of NF90 restored VEGFA expression and rescued the loss of tumor angiogenesis caused by miR-590-5p. Conversely, the NF90-shRNA attenuated the increased tumor progression caused by the miR-590-5p inhibitor. Clinically, the levels of miR-590-5p were inversely correlated with those of NF90 and VEGFA in CRC tissues. Furthermore, knockdown of NF90 lead to a reduction of pri-miR-590 and an increase of mature miR-590-5p, suggesting a negative feedback loop between miR-590-5p and NF90. Collectively, these data establish miR-590-5p as an anti-onco-miR that inhibits CRC angiogenesis and metastasis through a new mechanism involving NF90/VEGFA signaling axis, highlighting the potential of miR-590-5p as a target for human CRC therapy.

With the frequent occurrence of campus violence, scholars have devoted increasing attention to college students' aggression. This study aims to estimate the prevalence of aggression in Chinese university students and identify factors that could influence their aggression. We can thus find methods to reduce the incidence of college students' aggression in the future. A multi-stage stratified sampling procedure was used to select university students (N=4565) aged 16-25years in Harbin. The Aggression Questionnaire, the Adolescent Self-Rating Life Events Checklist and the Social Support Revalued Scale were used to collect data. Females reported lower levels of aggression than males (p<.001). A multiple linear regression analysis was conducted to determine the influence of factors of aggression, and the model was highly significant (R-2=.233, Ad R-2=.230, p<.01). The results show that the aggression is affected by gender, family-level and school-level variables. Aggression scores are significantly correlated with not only family-level or school-level variables independently, but their combination as well. We find that the risk factors for aggression include a dissatisfying profession, higher levels of study pressure, poor parental relationships, poor interpersonal relationships, the presence of siblings, punishment, health maladjustment, less subjective support, and lower levels of utilization of social support.

Background Depression is a major health concern for college students due to its substantial morbidity and mortality. Although low parental education has been identified as a factor in depression in college students, the mechanisms through which parental educational achievement affects students’ depression are not well understood. We tested whether adverse family and college environments mediate the relationship between parental educational level and depression among Chinese college students. Methods A total of 5180 respondents were selected using a cross-sectional survey. We examined the association of parental education, adverse family and college environments with depression in college students using the Adolescent Self-Rating Life Events Checklist, Beck Depression Inventory and socio-demographic questionnaires. Results Lower parental educational level is significantly correlated with depression in college students in our sample. Additionally, low family economic status, paternal or maternal unemployment, long periods spent apart from family, family conflicts, having been scolded and beaten by parents, poor or dissatisfying test performance, conflict with friends, heavy course load and failure in selection processes are also associated with parental education. Low family economic status, paternal or maternal unemployment, long periods spent apart from family, family conflicts, poor or dissatisfying test performance, conflict with friends and heavy course load mediated the relationship between parental education and depression in college students. Conclusions Adverse family and college environments could explain the influence of parental educational level on depression in college students.

Objective To explore the distribution and characteristics of health risk behaviors between the male and female college freshmen in the medicine and science,and to provide evidence for appropriate health intervention measures.Methods A questionnaire investigation was performed on college students'health risk behaviors among 1019 freshmen from medical and science college in urban area of Harbin.Results (1)There were statistically significant among the different gender in difference of risky behaviors except playing video games,net surfing,considered suicide,drug abuse and a few activities outside the 60 minutes every day (P ＜ 0.01 ).(2)Medical male risk behavior of the frequency(56.4％,19.2％,12.7％ and 47.1％ )higher than that of science and engineering male(35.6％,5.2％,1.6％ and 17.3％ )in trying to smoking,current smoking,sexual behavior and breakfast skipping.Recent medical males drinking rate was 85.3％ higher than male of science and engineering 72.2％.The incidence of female science and engineering students,respectively( 89.3％,50.8％ and 38.5％ ) than female medical students (72.4％,36.9％ and 8.0％ ) in trying to drinking and recent drinking and breakfast skipping.Conclusion The risk behaviors of college freshmen were prevalent.The frequency of risk behaviors are different among the College Freshmen in different genders and with different major,respectively.Therefore,it is necessary to take measures for intervention.