Who benefit from adjuvant chemotherapy in stage I lung adenocarcinoma? A multi-dimensional model for candidate selection.

BACKGROUND: Despite promising overall survival of stage I lung adenocarcinoma (LUAD) patients, 10-25 % of them still went through recurrence after surgery. [1] While it is still disputable whether adjuvant chemotherapy is necessary for stage I patients. [2] IASLC grading system for non-mucinous LUAD shows that minor high-grade patterns are significant indicator of poor prognosis. [3] Other risk factors, such as, pleura invasion, lympho-vascular invasion, STAS, etc. are also related to poor prognosis. [4-6] There still lack evidence whether IASLC grade itself or together with other risk factors can guide the use of adjuvant therapy in stage I patients. In this article, we tried to establish a multi-variable recurrence prediction model for stage I LUAD patients that is able to identify candidates of adjuvant chemotherapy. METHODS: We retrospectively collected patients who underwent lung surgery from 2018.8.1 to 2018.12.31 at our institution and diagnosed with lung adenocarcinoma pT1-2aN0M0 (stage I). Clinical data, manifestation on CT scan, pathologic features, driver gene mutations and follow-up information were collected. Cox proportional hazards regression analyses were performed utilizing the non-adjuvant cohort to predict disease free survival (DFS) and a nomogram was constructed and applied to the total cohort. Kaplan-Meier method was used to compare DFS between groups. Statistical analysis was conducted by R version 3.6.3. FINDINGS: A total of 913 stage I LUAD patients were included in this study. Median follow-up time is 48.1 months.4-year and 5-year DFS are 92.9 % and 89.6 % for the total cohort. 65 patient experienced recurrence or death. 4-year DFS are 97.0 %,94.6 % and 76.2 %, and 5-year DFS are 95.5 %, 90.0 % and 74.1 % in IASLC Grade1, 2 and 3, respectively(p < 0.0001). High-risk patients defined by single risk factors, such as, IASLC grade 3, pleura invasion, STAS, less LN resected could not benefit from adjuvant therapy. A LASSO-COX regression model was built and patients are divided into high-risk and low-risk groups. In the high-risk group, patients underwent adjuvant chemotherapy have longer DFS than those who did not (p = 0.024), while in the low-risk group, patients underwent adjuvant chemotherapy have inferior DFS than those who did not (p < 0.001). INTERPRETATION: IASLC grading is a significant indicator of DFS, however it could not guide adjuvant therapy in our stage I LUAD cohort. Growth patterns and T indicators together with other risk factors could identify high-risk patients that are potential candidate of adjuvant therapy, including some stage IA LUAD patients.

Ginsenoside Rh2 Ameliorates Neuropathic Pain by inhibition of the miRNA21-TLR8-mitogen-activated protein kinase axis.

Ginsenoside Rh2 is one of the major bioactive ginsenosides in Panax ginseng. Although Rh2 is known to enhance immune cells activity for treatment of cancer, its anti-inflammatory and neuroprotective effects have yet to be determined. In this study, we investigated the effects of Rh2 on spared nerve injury (SNI)-induced neuropathic pain and elucidated the potential mechanisms. We found that various doses of Rh2 intrathecal injection dose-dependently attenuated SNI-induced mechanical allodynia and thermal hyperalgesia. Rh2 also inhibited microglia and astrocyte activation in the spinal cord of a murine SNI model. Rh2 treatment inhibited SNI-induced increase of proinflammatory cytokines, including tumor necrosis factor-α, interleukin (IL)-1 and IL-6. Expression of miRNA-21, an endogenous ligand of Toll like receptor (TLR)8 was also decreased. Rh2 treatment blocked the mitogen-activated protein kinase (MAPK) signaling pathway by inhibiting of phosphorylated extracellular signal-regulated kinase expression. Finally, intrathecal injection of TLR8 agonist VTX-2337 reversed the analgesic effect of Rh2. These results indicated that Rh2 relieved SNI-induced neuropathic pain via inhibiting the miRNA-21-TLR8-MAPK signaling pathway, thus providing a potential application of Rh2 in pain therapy.

Phospholipid peroxidation inhibits autophagy via stimulating the delipidation of oxidized LC3-PE.

Phospholipid peroxidation of polyunsaturated fatty acids at the bis-allylic position drives ferroptosis. Here we identify a novel role for phospholipid peroxidation in the inhibition of autophagy. Using in vitro and in vivo models, we report that phospholipid peroxidation induced by glutathione peroxidase-4 inhibition and arachidonate 15-lipoxygenase overexpression leads to overload of peroxidized phospholipids and culminate in inhibition of autophagy. Functional and lipidomics analysis further demonstrated that inhibition of autophagy was associated with an increase of peroxidized phosphatidylethanolamine (PE) conjugated LC3. We further demonstrate that autophagy inhibition occurred due to preferential cleavage of peroxidized LC3-PE by ATG4B to yield delipidated LC3. Mouse models of phospholipid peroxidation and autophagy additionally supported a role for peroxidized PE in autophagy inhibition. Our results agree with the recognized role of endoplasmic reticulum as the primary source for autophagosomal membranes. In summary, our studies demonstrated that phospholipid peroxidation inhibited autophagy via stimulating the ATG4B-mediated delipidation of peroxidized LC3-PE.

A-Lipoic Acid Alleviates Folic Acid-Induced Renal Damage Through Inhibition of Ferroptosis.

Folic acid (FA)-induced acute kidney injury (AKI) is characterized by the disturbance of redox homeostasis, resulting in massive tubular necrosis and inflammation. Α-lipoic acid (LA), as an antioxidant, has been reported to play an important role in renal protection, but the underlying mechanism remains poorly explored. The aim of this study is to investigate the protective effect of LA on FA-induced renal damage. Our findings showed that LA could ameliorate renal dysfunction and histopathologic damage induced by FA overdose injection. Moreover, FA injection induced severe inflammation, indicated by increased release of pro-inflammatory cytokines tumor necrosis factor (TNF)-α and IL-1ß, as well as infiltration of macrophage, which can be alleviated by LA supplementation. In addition, LA not only reduced the cellular iron overload by upregulating the expressions of Ferritin and ferroportin (FPN), but also mitigated reactive oxygen species (ROS) accumulation and lipid peroxidation by increasing the levels of antioxidant glutathione (GSH) and glutathione peroxidase-4 (GPX4). More importantly, we found that LA supplementation could reduce the number of Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive tubular cells caused by FA, indicating that the tubular cell death mediated by ferroptosis may be inhibited. Further study demonstrated that LA supplementation could reverse the decreased expression of cystine/glutamate antiporter xCT (SLC7A11), which mediated GSH synthesis. What is more, mechanistic study indicated that p53 activation was involved in the inhibitory effect of SLC7A11 induced by FA administration, which could be suppressed by LA supplementation. Taken together, our findings indicated that LA played the protective effect on FA-induced renal damage mainly by inhibiting ferroptosis.

Prognostic Value of Inflammatory Biomarkers in Patients With Stage I Lung Adenocarcinoma Treated With Surgical Dissection.

OBJECTIVE: Inflammation plays a crucial role in tumorigenesis and progression. Our purpose was to investigate the prognostic value of neutrophil-to-lymphocyte ratio (NLR), systemic inflammation response index (SIRI) and systemic immune-inflammation index (SII), and develop a nomogram to predict the cancer-specific survival (CSS) and disease-free survival (DFS) of stage I lung adenocarcinoma patients. METHODS: 1431 patients undergoing surgical resection with pathologically confirmed stage I lung adenocarcinoma were reviewed. The optimal cut-off values for NLR, SII, and SIRI were defined by the receiver operating characteristic (ROC) curve. Cox proportional hazards regression analyses were performed to recognize factors significantly correlated with CSS and DFS to construct the nomogram. The value of adjuvant chemotherapy on model-defined high-risk and low-risk patients was further explored. RESULTS: The cohort had a median follow-up time of 63 months. Multivariate analysis revealed that higher NLR (≥2.606), higher SIRI (≥0.705), higher SII (≥580.671), later T stage, histological pattern with solid or micropapillary components and radiologic features with solid nodules were significantly associated with worse CSS and DFS. The concordance index (C-index) of the nomogram established by all these factors was higher than that of the TNM staging system both in CSS (validation set 0.778 vs 0.652) and DFS (validation set 0.758 vs 0.695). Furthermore, the value of the established nomogram on risk stratification in stage I lung adenocarcinoma patients was validated. CONCLUSIONS: Higher NLR, SII and SIRI pretreatment were associated with worse survival outcomes. A practical nomogram based on these three inflammatory biomarkers may help clinicians to precisely stratify stage I lung adenocarcinoma patients into high- and low-risk and implement individualized treatment.

Pretreatment with Roxadustat (FG-4592) Attenuates Folic Acid-Induced Kidney Injury through Antiferroptosis via Akt/GSK-3ß/Nrf2 Pathway.

Folic acid- (FA-) induced kidney injury is characterized by the tubule damage due to the disturbance of the antioxidant system and subsequent interstitial fibrosis. FG-4592 is an inhibitor of prolyl hydroxylase of hypoxia-inducible factor (HIF), an antioxidant factor. The present study investigated the protective role of FG-4592 pretreatment at the early stage of the kidney injury and long-term impact on the progression of renal fibrosis. FG-4592 was administrated two days before FA injection in mice. On the second day after FA injection, the mice with FG-4592 pretreatment showed an improved renal function, compared with those without FG-4592 pretreatment, indicated by biochemical and histological parameters; meanwhile, the cellular content of iron, malondialdehyde, and 4-hydroxynonenal histologically decreased, implying the suppression of iron accumulation and lipid peroxidation. Simultaneously, upregulation of HIF-1α was found, along with Nrf2 activation, which was reflected by increased nuclear translocation and high-expression of downstream proteins, including heme-oxygenase1, glutathione peroxidase4, and cystine/glutamate transporter, as well as ferroportin. Correspondingly, the elevated levels of antioxidative enzymes and glutathione, as well as reduced iron accumulation, were observed, suggesting a lower risk of occurrence of ferroptosis with FG-4592 pretreatment. This was confirmed by reversed pathological parameters and improved renal function in FA-treated mice with the administration of ferrostatin-1, a specific ferroptosis inhibitor. Furthermore, a signal pathway study indicated that Nrf2 activation was associated with increased phosphorylation of Akt and GSK-3ß, verified by the use of an inhibitor of the PI3K that phosphorylates Akt. Moreover, FG-4592 pretreatment also decreased macrophage infiltration and expression of inflammatory factors TNF-α and IL-1ß. On the 14th day after FA injection, FG-4592 pretreatment decreased collagen deposition and expression of fibrosis biomarkers. These findings suggest that the protective role of FG-4592 pretreatment is achieved mainly by decreasing ferroptosis at the early stage of FA-induced kidney injury via Akt/GSK-3ß-mediated Nrf2 activation, which retards the fibrosis progression.

Human colorectal cancer antigen GA733-2-Fc fused to endoplasmic reticulum retention motif KDEL enhances its immunotherapeutic effects.

OBJECTIVE: The aim of this is to compare the immunotherapeutic effects of human colorectal cancer antigen GA733-2 fused to the Fc fragment of antibody (GA733-2-Fc) and to Fc and endoplasmic reticulum (ER) retention motif KDEL (GA733-2-Fc-KDEL). MATERIALS AND METHODS: Recombinant GA733-2-Fc and GA733-2-Fc-KDEL were produced from infiltrated Nicotiana benthamiana leaves and purified by affinity chromatography. Glycan structures were determined by matrix-assisted laser desorption/ionization-time-of-flight mass spectrometry. The allergic and immunogenic responses of recombinant GA733-2-Fc and GA733-2-Fc-KDEL were estimated in an intraperitoneally immunized mouse. The tumor regression effect of recombinant GA733-2-Fc and GA733-2-Fc-KDEL was examined using a colorectal carcinoma CT-26 animal model. RESULTS: Recombinant GA733-2-Fc contained plant-specific glycan structures including ß(1,2)-xylose and α(1,3)-fucose whereas recombinant GA733-2-Fc-KDEL contained oligomannose type glycan structures. Mice immunized intraperitoneally with recombinant GA733-2-Fc and GA733-2-Fc-KDEL elicited strong GA733-2-Fc-specific immunoglobulin G (IgG) and IgA serum antibody responses. Recombinant GA733-2-Fc-KDEL reduced the production of GA733-2-Fc-specific IgE. Recombinant GA733-2-Fc-KDEL increased the production of interferon-γ. Intraperitoneal preimmunization with recombinant GA733-2-Fc and GA733-2-Fc-KDEL regressed tumor growth in a colorectal carcinoma CT-26 animal model. The tumor regression effect induced by recombinant GA733-2-Fc-KDEL was greater than that induced by recombinant GA733-2-Fc. The human and mouse colorectal carcinoma cell binding activities of recombinant GA733-2-Fc-KDEL-immunized sera were higher than those of recombinant GA733-2-Fc. CONCLUSIONS: Our results suggest that GA733-2-Fc conjugated to ER-retention motif KDEL is a more efficient antigen to prevent tumor growth induced by colorectal carcinoma and minimize an allergic response.

[Spatiotemporal variation of vegetation phenology in the Daxing'an Mountains stratified by eco-geographical regions.] / åŸºäºŽç”Ÿæ€åœ°ç†åˆ†åŒºçš„å¤§å ´å®‰å²­æ¤è¢«ç‰©å€™æ—¶ç©ºå˜åŒ–.

Vegetation phenology is a good indicator of climate change, because of the close correlation between vegetation and climate. The Daxing'an Mountains, located in Chinese northernmost region, are more sensitive to climate change. Researching the spatio-temporal variation of vegetation phenology in this region is of great significance for assessing the influence of global change on terrestrial ecosystem. According to the eco-geographical zoning of China, the Daxing'an Mountains can be divided into for four eco-geographical regions. In this study, the spatial distribution and dynamics of vegetation phenology in the Daxing'an Mountains were analyzed using 8-km resolution GIMMS NDVI 3g dataset from 1982 to 2012. Results showed that the start of growing season in all partitions exhibited an advancing trend, and the end of growing season in all partitions had an extending trend. Vegetation phenology which was sensitive to the change of meteorological factors had a stronger correlation with temperature than with precipitation for all four eco-geographical regions. There was a significant negative correlation between the start of growing season in the northern region and spring temperature. Except for the south of the Daxing'an Mountains, the ending days of growing season in the other three eco-geographical regions had significant negative correlations with summer precipitation. The change of vegetation phenology in the whole study was obvious along with altitude and latitude.

Hypericin-photodynamic therapy induces human umbilical vein endothelial cell apoptosis.

The conventional photosensitizers used in photodynamic therapy (PDT), such as haematoporphyrin (HP), have not yet reached satisfactory therapeutic effects on port-wine stains (PWSs), due largely to the long-term dark toxicity. Previously we have showed that hypericin exhibited potent photocytotoxic effects on Roman chicken cockscomb model of PWSs. However, the molecular mechanism of hypericin-mediated photocytotoxicity remains unclear. In this study, we employed human umbilical vein endothelial cells (HUVECs) to investigate the hypericin-photolytic mechanism. Our study showed that hypericin-PDT induced reactive oxygen species (ROS), resulting in cell killings and an activation of the inflammatory response. Importantly, we have also discovered that photoactivated hypericin induced apoptosis by activating the mitochondrial caspase pathway and inhibiting the activation of the vascular endothelial growth factor-A (VEGF-A)-mediated PI3K/Akt pathway. Notably, we found that hypericin exhibited a more potent photocytotoxic effect than HP, and largely addressed the inconvenience issue associated with the use of HP. Thereby, hypericin may be a better alternative to HP in treating PWSs.

Pomolic acid induces apoptosis in SK-OV-3 human ovarian adenocarcinoma cells through the mitochondrial-mediated intrinsic and death receptor-induced extrinsic pathways.

The cytotoxic effect of pomolic acid (PA), a pentacyclic triterpene isolated from flowers of Osmanthus fragrans var. aurantiacus Makino, was investigated in SK-OV-3 human ovarian adenocarcinoma cells. PA dose-dependently inhibited the viability of SK-OV-3 cells. PA-induced apoptosis was further characterized by detection of cell surface annexin V and sub-G1 apoptotic cell populations. The number of cells immunostained with annexin V-fluorescein isothiocyanate (FITC) increased following treatment with PA. The sub-G1 cell populations also increased in PA-treated SK-OV-3 cells. PA induced the activation of caspase-8, -9 and -3, critical mediators of apoptosis signaling. PA decreased the mitochondrial transmembrane potential (ΔΨ(m)), resulting in the activation of caspase-9. In addition, PA increased the expression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis signaling-related death receptor 5 (DR5), mediating caspase-8-involved extrinsic pathway. Taken together, our results indicate that PA induces apoptosis in SK-OV-3 cells, which is mediated by the mitochondrial-mediated intrinsic and death receptor-induced extrinsic pathways.

[Relationship and interactions between elevated fasting glucose and hypertension for cardiocerebral vascular disease].

OBJECTIVE: To explore the relationship and interaction of elevated fasting glucose and hypertension on cardiocerebral vascular disease. METHODS: 10 054 males and females were recruited for our cross-sectional study during May 2007 to August 2007. Unconditional logistic regression was used to analysis the relationship between fasting glucose and hypertension on cardiocerebral vascular disease. A product of fasting glucose and hypertension was added to the logistic regression model to evaluate the multiplicative interaction and relative excess risk of interaction (RERI), attributable proportion (AP) of interaction and synergy index (S) was applied to evaluate the additive interaction of the two factors. Bootstrap was used to calculate 95% confidence intervals (CI) of RERI, AP and S. RESULTS: After adjusting age, gender, smoking, drinking, body mass index (BMI) and region, the product of fasting glucose and hypertension was not statistically significant, which means there was no multiplicative interaction between the two. But the additive indexes RERI, AP and S with 95%CI of diabetes and hypertension were 0.64 (0.03, 1.25), 0.27 (0.01, 0.47) and 1.83 (1.02, 5.13) respectively, which means significant additive interaction was shown between the two on cardiovascular disease but not no stroke. And there were no additive interaction between impaired fasting glucose on cardiovascular disease or stroke. CONCLUSIONS: Hypertension was independently related to cardiovascular disease and stroke in Beijing citizens, and diabetes were independently related to stroke. There was additive interaction between diabetes and hypertension on cardiovascular disease.

[Impact of acute smoking on artery function in healthy chronic smokers].

OBJECTIVES: To explore the effect of acute smoking on vascular endothelial function, arterial stiffness and the possible underlying mechanisms. METHODS: We measured the endothelial function and arterial stiffness in 50 healthy chronic smokers before and after acute smoking with EndoPAT2000. The test was carried out on two separate finger tips. The endothelial function was evaluated by PAT ratio of the finger tip and systemic arterial stiffness was evaluated by augmentation index (AI). Plasma soluble intercellular adhesion molecule-1 (sICAM-1) and tissue plasminogen activator (tPA) before and 20 min after acute smoking were measured with enzyme linked immuno sorbent assay. RESULTS: The PAT ratio was decreased (1.87 ± 0.40 vs. 1.73 ± 0.28, P = 0.004) while AI was significantly increased after acute smoking (2.94% ± 21.77% vs. 7.11% ± 20.65%, P = 0.01). There was no significant changes in sICAM [(306.5 ± 76.1) µg/L vs. (315.7 ± 90.9) µg/L, P = 0.402], but tPA [7.87 (5.41 - 10.08) µg/L vs. 5.77 (3.77 - 9.68) µg/L, P < 0.01] was significantly decreased after smoking. CONCLUSIONS: Smoking could acutely affect endothelia function, arterial stiffness and deteriorate the activity of fibrinolytic system which could lead to coronary thrombosis in smokers.

[Association between marital status and prevalence of peripheral arterial disease among Beijing residents: a cross-sectional study].

OBJECTIVE: To investigate the relationship between marital status and prevalence of peripheral arterial disease (PAD) among Beijing residents. METHODS: From May to August 2007, 10 054 residents were interviewed to collect demographic and biochemistry information. Generalized linear mixed model was used to determine the relationship between marital status and prevalence of PAD in terms of OR and corresponding 95% confidence intervals. RESULTS: After adjusting the traditional risk factors including age, area, lipid, serum glucose, blood pressure, central obesity, smoking, drinking and physical activities for PAD, relationship between marital status and prevalence of PAD was found both at the female and male groups of those with 45 years or older. Compared with married men, OR and 95% confidence interval of PAD for unmarried men were 1.56 (0.39 - 6.35) and 1.61 (0.77 - 3.35) for those with 45 years younger and older respectively, while compared with married women, OR and 95% confidence interval of PAD for unmarried women were 0.75 (0.22 - 2.57) and 1.78 (1.23 - 2.58) for those with 45 years younger and older respectively. Significant differences (all P < 0.01) were found between married and unmarried women of 45 years or older in terms of age, waist circumstances, systolic blood pressure, fasting glucose, total cholesterol, low-density lipoprotein and smoking. CONCLUSIONS: Peripheral arterial disease was related to marital status for women of 45 years or older among Beijing residents. Estrogen level and the distribution of other PAD risk factors might contribute to the observed finding.

[Prevalence of dyslipidemia and borderline dyslipidemia and other risk factors of coronary heart disease in residents from Beijing communities].

OBJECTIVE: To investigate the prevalence of dyslipidemia and borderline dyslipidemia and other coronary heart disease (CHD) risk factors in residents from Beijing communities. METHODS: Resident samples were selected by random cluster multistage method. Serum lipid level and CHD factors were obtained through questionnaire, physical examination and biochemical analysis during June 2007 to August 2007 from 10 054 residents. RESULTS: Age- and sex-adjusted standardized prevalence of hypercholesterolemia, high low-density lipoprotein cholesterolemia, low high-density lipoprotein cholesterolemia, and triglyceridemia were 9.3%, 2.56%, 18.79% and 16.84%, respectively. Incidence of borderline hypercholesterolemia was 23.96%. Incidence of dyslipidemia and borderline dyslipidemia was 31.23% and 23.30% respectively, 71.17% residents have at least 1 CHD major risk factor and 20.23% residents were in borderline CHD risks. Prevalence of hypertension, diabetes, smoking and obese was 41.57%, 11.08%, 35.81% and 22.89%, respectively. The odds ratio for dyslipidemia (95% confidence interval) in residents having 1 borderline CHD risk factor (RF), 2 RF, and 3 RF versus none RF was 1.668, (95%CI: 1.319 - 2.110), 2.537 (95%CI: 1.989 - 3.235), and 3.203 (95%CI: 2.007 - 5.114). CONCLUSIONS: The prevalence of dyslipidemia of residents from Beijing communities is higher the average level of China (25.1%). Over 1 out of 5 residents were in increased risk for borderline dyslipidemia or CHD risks. Intensive control of dyslipidemia and CHD risk factors are warranted in Beijing residents.

[The smoking status of patients with acute coronary syndrome and effect of simple intervention on smoking cessation.].

OBJECTIVE: To evaluate the abstinence rate and relapse rate of smoker with ACS after discharged from hospital, to evaluate the effect of simple smoking cessation interventions. METHODS: 150 smokers with ACS were collected and was divided into simple intervention group (n = 87) and control group (n = 63), respectively, followed up for 6 months. 2 months, 6 months abstinence rate, relapse rate were compared between two groups, logistic regression model was used to analyzed the relevant factors for relapse. RESULTS: The smoking rate in patients with ACS was 31.14%, 6-month continuous abstinence rate and 6-month relapse rate was 64.6%, 36.4%, respectively. 6-month continuous abstinence rate and relapse rate between simple quit-smoking intervention group and control group showed no difference. Nicotine dependence score more than 4 points can be used as predictor of relapse. CONCLUSIONS: The smoking rate and the abstinence rate of smoker with ACS is higher than the general population, simple quit-smoking intervention do not increase the success rate of quit-smoking, indicated the need to strengthen the intervention in patients with ACS and smoking.

[Epidemiologic characteristics of major risk factors of coronary heart disease in residents from Beijing communities in different age groups].

OBJECTIVE: To study the difference in prevalence of major risk factors of coronary heart disease (CHD) in resident from Beijing communities in different age groups so as to offer suggestions for prevention of CHD in Beijing. METHODS: The samples were selected by random cluster multistage method. Serum lipid level and CHD factors were determined through questionnaire, physical examination and biochemical detection for 10 054 subjects in Beijing communities during June 2007 to August 2007. According to age, the subjects were divided into 3 groups: 20 - 44 yr group, 45 - 59 yr group and > or = 60 yr group. RESULTS: After age and sex standardization the prevalence of hypercholesterolemia, hypertension, diabetes, smoking and obesity was 9.30%, 41.57%, 10.18%, 35.81% and 22.89% respectively. The prevalence of hypercholesterolemia, hypertension and diabetes showed an rising trend with advancing age (trend chi(2): 15.6, 31.7 and 18.0, all P < 0.001). The group of 45 - 59 yr had the highest prevalence in smoking and obesity 28% and 25.27% respectively. Over 30% in the groups of 45 - 59 yr and > or = 60 yr were in the borderline of hypercholesterolemia and hypertension and over 40% were overweight. After age and sex standardization, 67.15% of community residents had at least 1 CHD risk factor, 21.37% and 8.50% 2 or over 3 CHD risk factors. As compared with group 20 - 44 yr, the odds ratio (95%CI) for clustering of CHD risk factors in groups 45 - 59 yr and > or = 60 yr were 2.63 (95%CI 2.371 - 2.924) and 4.3 (95%CI 3.764 - 4.913) respectively. The odds ratio (95%CI) for clustering of CHD risk factors for male vs female was 4.392 (95%CI 3.938 - 4.899). CONCLUSION: The prevalence of CHD major risk factors of Beijing community residents is high. Groups of 45 - 59 yr and > or = 60 yr have a higher prevalence and clustering of CHD major risk factors than 20 - 44 yr group. So these age groups deserve a higher priority of comprehensive prevention and control strategies of CHD.