An Evidence-Based Medical Review on Promoting Gastrointestinal Function Recovery After Colorectal Cancer Surgery.

Objective: The objective of this study was to search for, evaluate, and summarize data related to a faster postoperative recovery in patients with colorectal cancer (CRC) based on literature from China as well as internationally. This will serve as an evidence-based foundation for the clinical implementation of enhanced postoperative recovery of gastrointestinal function in patients with CRC. Methods: Based on the hierarchical "6S" evidence model, we conducted a systematic search of computerized decision-support systems, guideline websites, as well as domestic and international databases for evidence, guidelines, expert consensus statements, clinical decision-making, best practices, evidence summaries, and systematic reviews of interventions focusing on accelerating gastrointestinal function rehabilitation after CRC surgery. The time limit for the search was from the date of creation of the database to January 2023. Two researchers evaluated the quality of the literature that was included, and we extracted data and summarized the evidence from those publications that fulfilled the quality criteria. Results: The review included a total of 21 publications, comprising 6 guidelines, 6 systematic reviews, 3 expert consensus statements, 4 randomized controlled trials, and 2 evidence summaries. We summarized 51 best evidence findings across five areas: organizational management, preoperative risk assessment, education, intraoperative monitoring, and postoperative management. Conclusion: There is a wide variety and wealth of information available on interventions to promote enhanced postoperative recovery of gastrointestinal function in patients with CRC. The use of evidence is discussed, keeping in mind the practical situation in China.

[Retracted] Downregulation of miR­29b targets DNMT3b to suppress cellular apoptosis and enhance proliferation in pancreatic cancer.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the Hoechst staining data shown in Fig. 4E were strikingly similar to data appearing in different form in another article by different authors at a different research institute; moreover, an unexpectedly high degree of similarity was noted with the data featured in a couple of different data panels showing the results of apoptosis experiments in Fig. 4D. Owing to the fact that the contentious data in the above article had already been published prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 17: 2113­2120, 2018; DOI: 10.3892/mmr.2017.8145].

Detecting Single-Molecule Dynamics on Lipid Membranes with Quenchers-in-a-Liposome FRET.

Tracking membrane-interacting molecules and visualizing their conformational dynamics are key to understanding their functions. It is, however, challenging to accurately probe the positions of a molecule relative to a membrane. Herein, a single-molecule method, termed LipoFRET, is reported to assess interplay between molecules and liposomes. It takes advantage of FRET between a single fluorophore attached to a biomolecule and many quenchers in a liposome. This method was used to characterize interactions between α-synuclein (α-syn) and membranes. These results revealed that the N-terminus of α-syn inserts into the membrane and spontaneously transitions between different depths. In contrast, the C-terminal tail of α-syn is regulated by calcium ions and floats in solution in two conformations. LipoFRET is a powerful tool to investigate membrane-interacting biomolecules with sub-nanometer precision at the single-molecule level.

Methods for Expression and Purification of Biologically Active Recombinant Progranulin.

Purifying progranulin may be useful in a variety of situations, for example, after it has been mutated or otherwise modified or when working with a species for which commercially produced progranulin is unavailable. A method to express and purify human progranulin is presented. Progranulin is transiently expressed in mammalian cells and isolated from their conditioned medium before purification by reversed-phase high-performance liquid chromatography (RP-HPLC). Human progranulin is used as an example, but the protocol can be applied to any other progranulin protein. Modifications of the expression-purification strategy for metabolic labeling of progranulin and analytical systems based on heparin-affinity chromatography are presented.

Downregulation of miR­29b targets DNMT3b to suppress cellular apoptosis and enhance proliferation in pancreatic cancer.

As one of the most aggressive types of tumor, pancreatic cancer is a principal cause of tumor­associated mortality. Negative associations between microRNA­29 (miR­29) and DNA methyltransferases (DNMT) 3a and 3b have been demonstrated to be associated with the carcinogenesis of a number of types of cancer; however, this has not been completely elucidated in pancreatic cancer. In the present study, pancreatic cancer tissues (n=15) and corresponding paracancerous tissues (n=15) were obtained and the results of reverse transcription­quantitative polymerase chain reaction analysis indicated decreased expression of miR­29b and enhanced mRNA expression of DNMT3b in pancreatic cancer tissues, compared with the corresponding paracancerous tissues. Increased protein expression of DNMT3b was demonstrated by western blotting and immunohistochemistry. In addition, the negative association between miR­29b and DNMT3b was noted in pancreatic cancer tissues, and luciferase reporter assays confirmed that miR­29b was able to directly target DNMT3b in vitro. Notably, miR­29b overexpression was able to decrease cell viability and to promote the apoptosis by targeting DNMT3b, and the knockdown of DNMT3b exhibited consistent results in vitro and in vivo. The results of the present study suggested that miR­29b, as a tumor suppressor, may be a novel target for the development of treatments for pancreatic cancer.

[Effects of intravenous immunoglobulin and aspirin treatment on the functions of circulating endothelial progenitor cells in children with Kawasaki disease].

OBJECTIVE: To study the effects of intravenous immunoglobulin (IVIG) and aspirin treatment on the functions of circulating endothelial progenitor cells (EPCs) in children with Kawasaki disease (KD) and possible mechanisms. METHODS: Blood samples were obtained in 10 children with KD before and 7 days after the treatment by IVIG and aspirin. MTT method, modified Boyden chamber method and cell culture plate adhesion method were used to assess the functions of EPCs, including proliferation, adhension and migration activities. The plasma levels of tumor necrosis factor-α (TNF-α) and high-sensitivity C reactive protein (hs-CRP) were also measured. RESULTS: The functions of circulating EPCs 7 days after IVIG and aspirin treatment were significantly improved. IVIG and aspirin treatment significantly reduced plasma TNF-α and hs-CRP concentrations. There was a significant linear regression relationship between the reduced plasma TNF-α and hs-CRP levels and the increased functions of circulating EPCs. CONCLUSIONS: IVIG and aspirin treatment can improve the functions of circulating EPCs, possibly through reducing plasma concentrations of TNF-α and hs-CRP.

The functions of endothelial progenitor cells were significantly improved after treatment with intravenous immunoglobulin and aspirin in children with Kawasaki disease.

We sought to determine the effects of treatment with intravenous immunoglobulin (IVIG) and aspirin on the functions of endothelial progenitor cells (EPCs) in patients with Kawasaki disease (KD) as well as its relationship with concentrations of tumor necrosis factor-α (TNF-α) and high-sensitivity C-reactive protein (hs-CRP). Ten KD patients in the acute phase of their disease were recruited. We investigated EPC functions in children with KD before and after treatment with IVIG and aspirin. In vitro assays were used to measure the functions, including proliferation, adhesion, and migration activities, of EPCs. Plasma levels of TNF-α and hs-CRP were also assessed. All of the data were assessed before and at 7 days after treatment initiation. EPC functions after 7 days of treatment with IVIG and aspirin were significantly improved than they were before treatment with IVIG and aspirin. Treatment with IVIG and aspirin significantly decreased TNF-α and hs-CRP concentrations. There was a significant linear regression relationship between decreased plasma TNF-α levels, hs-CRP levels, and increased functions of circulating EPCs. The results of our study indicate that the functions of circulating EPCs improved after treatment with IVIG and aspirin, which may be related to decreased concentrations of TNF-α and hs-CRP.

[Influence of light and temperature factors on biomass accumulation of winter wheat in field].

To explore the influence of light and temperature factors on the biomass accumulation of winter wheat at its development stages and in different organs, this paper analyzed the variation patterns of the biomass accumulation and the influence of TEP (thermal effectiveness photosynthetically active radiation) on the accumulation at each development stage, based on the observation data from the Xifen Agrometeorological Experiment Station in Gansu Province, including winter wheat phenophase and yield factors in 1981-2008, biomass at three-leaf, over-wintering, jointing, heading, milky maturity, and maturity stages in 1995-2008, and meteorological data in 1995-2008. The biomass accumulation of winter wheat in its whole growth period presented "S" curve, with the maximum value at heading-milky maturity stage. Since 1981, the TEP at heading-milky maturity stage increased with a rate of 3. 314 MJ x m(-2) x a(-1), and the TEP at other stages varied as parable curves. The TEP at turning green-jointing and milky maturity-maturity stages had a higher value in the 1990s and a lower value in the 1980s and early 21st century, while that at jointing-heading stage had a lower value in the 1990s but a higher value in the 1980s and early 21st century. There was a significant correlation between the TEP at each development stage and the actual yield. The LAI (leaf area index) at each development stage also had a significant correlation with the utilization rate of TEP at corresponding stage. When the LAI at jointing and heading stages was increased by 1, the utilization rate of TEP was correspondingly increased by 0.049 and 0.259 g x MJ(-1), respectively.

[Decreased circulating endothelial progenitor cell function: relationship with serum concentrations of high-sensitivity C-reactive protein in children with Kawasaki disease].

OBJECTIVE: To study the function of circulating endothelial progenitor cells and its relationship with serum concentrations of high-sensitivity C-reactive protein (Hs-CRP) in children with Kawasaki disease. METHODS: Ten children with Kawasaki disease and ten healthy children as a control group were enrolled. The peripheral mononuclear cells were induced into endothelial progenitor cells using Dulbecco's Modified Eagle Medium containing vascular endothelial growth factor and basic fibroblast growth factor. The proliferative ability, migratory ability and adhesive ability of endothelial progenitor cells were assessed by MTT methods, modified Boyden chamber methods and cell culture plate adhesion method, respectively. The concentrations of serum Hs-CRP were measured by latex enhanced turbidimetric immunoassay. RESULTS: The proliferative ability, migratory ability and adhesive ability of endothelial progenitor cells in the Kawasaki disease group were significantly lower than those in the control group (P<0.01). The serum concentrations of Hs-CRP in the Kawasaki disease group were significantly higher than those in the control group (87.1+/-30.2 mg/L vs 5.3+/-3.4 mg/L; P<0.01). The function of circulating endothelial progenitor cells was negatively correlated with serum concentrations of Hs-CRP in the Kawasaki disease group. CONCLUSIONS: The function of circulating endothelial progenitor cells is decreased in children with Kawasaki disease, which may be associated with the abnormal expression of inflammatory mediators.

The number and function of circulating endothelial progenitor cells in patients with Kawasaki disease.

Kawasaki disease (KD) is associated with coronary artery injury. Studies have shown that the endothelial progenitor cell (EPC) participates in the process of arterial repair. Data have been reported that the number of EPC increased significantly in the subacute phase of KD. However, until now, there are no data about the functions of EPC in KD patients. The present study was designed to further investigate the number and functions of EPC in KD. Ten KD patients in the acute phase and ten healthy volunteers were recruited and attributed to the KD group and control group, respectively. The circulating CD34/kinase insert domain-containing receptor double positive cells were evaluated in the two groups using flow cytometry. In vitro assays were used to measure the functions of EPC, including proliferation, adhesion, and migration activities. The plasma levels of nitric oxide (NO), tumor necrosis factor-alpha (TNF-alpha), and high sensitivity C-reactive protein (hs-CRP) were also assessed in both groups. The number of EPC in the KD group was significantly higher than that of the control group (0.021 +/- 0.007% vs. 0.014 +/- 0.003%, P < 0.05). The migratory response of EPC was significantly decreased in the KD group, compared with that of the control group (5.50 +/- 1.78 vs. 3.40 +/- 1.35 cells/high power field, P < 0.01). Similarly, the proliferative and adhesive activities of EPC in the KD group were also decreased (0.47 +/- 0.08 vs. 0.66 +/- 0.07, P < 0.01; 6.5 +/- 2.12 vs. 11.2 +/- 2.04 cells/high power field, P < 0.01). The plasma NO, TNF-alpha, and hs-CRP levels in the KD group were higher than those of the control group (54.10 +/- 11.78 vs. 38.80 +/- 11.10 mumol/l, P < 0.01; 48.20 +/- 7.42 vs. 37.00 +/- 11.12 pg/ml, P < 0.05; 87.10 +/- 30.18 vs. 5.30 +/- 3.37 mg/l, P < 0.01). The number of circulating EPC positively correlated with the level of NO (r = 0.92, P < 0.001), and the functions of EPC negatively correlated with the levels of TNF-alpha and hs-CRP, respectively. In Kawasaki disease, the number of EPC was enhanced and the functions of EPC were attenuated. The two-way regulation of circulating EPC in KD patients may be associated with the disorders of cytokines or messengers in KD patients.

[Effects of in vivo transfer of human chemokine-like factor 1 gene on cardiac function after acute myocardial infarction in rats].

OBJECTIVE: To study the effects of chemokine-like factor 1(CKLF1)-plasmid transfer on cardiac function in a rat acute myocardial infarction (AMI) model. METHODS: Thirty male SD rats were randomly devided into 3 groups. One hundred micrograms of CKLF1-plasmid, empty plasmid or saline were injected intramuscularly with in vivo electroporation, respectively. Rats were subjected to left coronary artery ligation on the 6th day after gene transfer. Ultrasonic cardiography and hemodynamics were conducted and evaluated on the 22nd day after gene transfer. Then, the animals were sacrificed for determination of percentage of myocardial infarcion. RESULTS: The left ventricular ejection fraction in CKLF1 group (67.02% +/- 12.24%) was significantly higher than that in the saline group (43.64% +/- 7.82%) and empty plasmid group (47.56% +/- 4.10%), P<0.05. Fractional shortening of left ventricle in CKLF1 group (33.83% +/- 10.15%) was higher than that in saline group (18.49% +/- 3.96%) and empty plasmid group (20.85% +/- 2.24%), P<0.05. The maximal velocity of left ventricular pressure ascensus was higher in CKLF1 group [(5 720.01 +/- 826.32) mmHg/s, 1 mmHg=0.133 kPa] than in saline group [(3 955.69 +/- 685.91) mmHg/s] and in empty plasmid group [(4 412.03 +/- 500.74) mmHg/s)], P<0.05. And the maximal velosity of left ventricular pressure descensus was higher in CKLF1 group [(4 636.23 +/- 407.17) mmHg/s] than in saline group [(2 984.82 +/- 615.24) mmHg/s] and in empty plasmid group [(2 963.87 +/- 419.36) mmHg/s], P<0.05. While the percentage of myocardial infarction in CKLF1 group (29.63% +/- 3.93%) was smaller than that in saline group (38.01% +/- 5.48%) and in empty plasmid group (37.50% +/- 6.33%), P<0.05. CONCLUSION: CKLF1 gene transfer can limit the mass of myocardial infarction and improve post-infarction cardiac function.

[Location and expression of apo(a) and apoB in peripheral blood of patients with cardiovascular disease].

OBJECTIVE: To explore the relationship between the severity of cardiovascular disease with the expression of apolipoprotein(a) [apo(a)] and apolipoprotein B (apoB) in peripheral blood and their location in peripheral blood cells. METHODS: In this report, we selected 4 patients with angiography which indicated that three coronary arteries were narrowed and 5 control patients with normal angiography. Arterial blood was collected and analyzed for lipid parameters in plasma. The mRNA expression of apo(a) and apoB in peripheral white blood cells and platelets were determined by RT-PCR and their protein expression by western blot. Moreover, the expression and location of apo(a) and apoB in white blood cells were determined by confocal microscopy and computer 3D analysis. RESULTS: In plasma, levels of high density lipo-protein-cholesterol (HDL-C) and polipoprotein A-I(apoA-I) in cardiovascular disease (CVD) patients were significantly less than those in the control patients[(0.62+/-0.05) mmol/L, (0.78+/-0.08) mmol/L vs (0.81+/-0.15) mmol/L, (0.9+/-0.07) mmol/L, P<0.05], but the concentration of other plasma lipid parameters was not different. The size of apo(a) isoforms was not reversely related to the severity of cardiovascular disease and the most commonly occurring phenotype of apo(a) was S4.The expression of apoB in platelets in cardiovascular disease patients was less than that in the control patients by 25.1% (optical density value 0.67+/-0.18 vs 1.00+/-0.10, P<0.05),but the expression of apo(a) was not different between the two groups (optical density value 0.43+/-0.18 vs 0.61+/-0.40, P>0.05). Studies with confocal microscopy indicated that proteins of apo(a) and apoB were co-expressed by a few cells of leukocytes and the ratio of apoB/apo(a) in cardiovascular disease patients was significantly less than that in the control patients (optical density value 1.60+/-0.12 vs 4.40+/-0.35, P<0.05). In platelets and leukocytes, mRNA of apo(a) or apoB was not detectable. CONCLUSION: Our studies indicate that peripheral blood cells can carry apo(a) and apoB, furthermore the contents of apoB and apo(a) in cells are different between cardiovascular disease patients and patients with normal coronary artery.

3,3'-Bis(4-nitro-phen-yl)-1,1'-(p-phenyl-ene)dithio-urea dimethyl sulfoxide disolvate.

The asymmetric unit of the title compound, C(22)H(16)N(6)O(6)S(2)·2C(2)H(6)OS, consists of one half-mol-ecule of the centrosymmetric thiourea derivative and one molecule of dimethyl sulfoxide (DMSO). The carbonyl group forms an intra-molecular hydrogen bond with the NH group, creating a six-membered (C-N-C-N-H⋯O) ring. Two other N-H⋯O hydro-gen bonds link one mol-ecule of the thio-urea to two mol-ecules of DMSO.

6,6'-Dimeth-oxy-2,2'-[(hexane-1,6-diyldi-oxy)bis-(nitrilo-methyl-idyne)]diphenol.

In the title compound, C(22)H(28)N(2)O(6), strong intra-molecular O-H⋯N hydrogen bonds and weak inter-molecular C-H⋯O hydrogen bonds stabilize the three-dimensional supra-molecular structure.

[Study on polymorphism in the apolipoprotein A5 gene in patients with premature coronary heart disease].

OBJECTIVE: To investigate the association between the apolipoprotein A5(APOA5) -1131T/C polymorphism and premature coronary heart disease in northern Chinese Han population. METHODS: Using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and polyacrylamide gel electrophoresis (PAGE), we analyzed the genotype and allele distribution in 140 patients with premature coronary heart disease diagnosed by coronary angiography and 156 healthy controls. The levels of serum lipid profiles were also studied by biochemical methods. RESULTS: The allele frequency of APOA5-1131T/C polymorphism in the premature coronary heart disease group was significantly higher (43.2% vs. 33.0%, P=0.011) than that in the control group. Compared with TT homozygotes, CC homozygotes exhibited a 2.809-fold (95% CI 1.331-5.927) increased risk of developing premature coronary heart disease. Logistic regression analysis found that this correlation was independent of sex, age, body mass index (BMI), smoking history as well as serum total cholesterol(TC), high density lipoprotein cholesterol (HDL-C) and low density lipoprotein cholesterol (LDL-C) levels; In premature coronary heart disease group, the triglyceride(TG) level in CC homozygotes was significantly higher than those in TC heterozygotes or TT homozygotes. CONCLUSION: The APOA5-1131T/C polymorphism has influence on serum TG level, and the APOA5-1131C allele is associated with the development of premature coronary heart disease in northern Chinese Han population.

[In vivo transfer of human chemokine-like factor 1 gene increases peripheral blood CD34+ stem cells after myocardial infarction in rats].

OBJECTIVE: To assess the influence of different doses of CKLF1 plasmid on the dynamics and magnitude of the mobilization of the mobilization bone of marrow stem cells in a rat AMI model. METHODS: Different doses of plasmid DNA encoding CKLF1 gene, empty plasmid or saline were injected into male SD rats intramuscularly with in vivo electroporation. Rats were subjected to left coronary artery ligation 6 days after gene transfer. Peripheral blood samples were drawn and CD34+ cells were assayed by FACS calibur flow-cytometer. The changes in absolute number of CD34+ cells were evaluated. RESULTS: Expressions of CKLF1 mRNA and protein were detected in the injection site 7 days after gene transfer. Five days after gene transfer, the CD34+ cells numbers in CKLF1 groups were significantly higher than those in empty plasmid group, especially in CKLF1 100 microg group (16.63x10(6)/L vs 4.98x10(6)/L, P<0.01). On the 5-7 days, the CD34+ cell numbers in CKLF1 groups reached the peak and the peak number was 3.88 times that of baseline in CKLF1 100 microg group (P<0.01). After AMI, the cell numbers of 1 day to 7 days were significantly higher than those of the baseline in empty plasmid group and saline group. In comparison to empty plasmid group, CKLF1 groups were associated with still higher numbers of cells 1 day after AMI (P< 0.05), especially in CKLF1 100 microg group (14.61x10(6)/L vs 7.85x10(6)/L, P<0.01). CONCLUSION: CKLF1 gene transfer significantly increases the mobilization of CD34+ stem cells in acute myocardial infarction rats.

[Hypoxia/reoxygenation induced endoplasmic reticulum stress in cultured neonatal rat cardiomyocyte].

OBJECTIVE: To investigate the effect of hypoxia/reoxygenation on endoplasmic reticulum stress in cultured neonatal rat cardiomyocytes. METHODS: Neonatal rat cardiac myocytes in primary culture were exposed to hypoxia for 5.5 hours and subsequently reoxygenation for 2-24 hours. Western blot and RT-PCR were applied to monitor the expression change of GRP78 (glucose regulated protein 78). 2-deoxy-D-glucose (2-DG) was the positive control of this study. Then Western blot and RT-PCR were used to examine the expression of GRP78. RESULTS: Cell viability was decreased obviously after hypoxia/reoxygenation. Compared with untreated cells, the GRP78 content of the cells had increased significantly in the hypoxia/reoxygenation cells. The level of GRP78 protein and mRNA elevated from the points of 2 hours to 24 hours after reoxygenation, and increased most obviously at the point of 4 hours after reoxygenation. (4 hours: protein level 142% of the control, mRNA level 200%). 2-DG could induce the increasing expression of GRP78 in a concentration-dependent manner from 10-50 mmol/L. CONCLUSION: Hypoxia/reperfusion can induce endoplasmic reticulum stress in rat cardiomyocytes.

[Non-dilated coronary artery lesion and myocardial perfusion in children with Kawasaki disease: analysis of 43 cases].

OBJECTIVE: The study was designed to investigate the impact of non-dilated coronary artery wall lesion on myocardial perfusion. METHODS: Doppler tissue image (DTI) was used to measure regional ventricular wall motion in 43 Kawasaki children with non-dilated coronary arterial wall echocardiographic abnormalities (rough intima and arterial wall thickening) detected by two-dimensional echocardiography (2DE) at acute phase. A total of 31 cases who had both non-dilated coronary lesion and lowered ventricular wall motion velocity at subacute and convalescence phase underwent submaximal exercise single photon emitting computerized tomography (SPECT) for the evaluation of myocardial perfusion. RESULTS: In 43 cases of Kawasaki disease with non-dilated coronary arterial wall abnormalities, 36 cases (83.7%) still had such lesions at subacute phase and 32 (74.4%)at convalescence. At the same time, lowered regional ventricular wall motion (RVWM) was found in 34 cases at subacute phase and in 31 cases at convalescence. DTI and 2DE had a very good correlation in the detection of such abnormalities (chi(c)2 = 9.64, P < 0.01 in subacute period, and chi(c)2 = 7.14, P < 0.01 in convalescence). In 31 cases accepting SPECT, 17 were positive. A total of 22 ischemic regions were detected. Eighteen out of 22 cases having ischemic regions had abnormal RVWM on DTI. SPECT ischemic regions were significantly in accordance with lowered RVWM in ventricular septum and anterior wall (chi(c)2=5.07 and 7.48, P < 0.05 and P < 0.01, respectively) noted in DTI. CONCLUSION: Non-dilated coronary arterial wall abnormality is one of the forms of coronary artery wall lesions which could reduce myocardial flow perfusion. Its clinical significance is worthy of attention.

Polymorphism K469E of intercellular adhesion molecule-1 gene and restenosis after coronary stenting in Chinese patients.

BACKGROUND: Inflammation is a major cause of restenosis after coronary stenting. Intercellular adhesion molecule-1 (ICAM-1) is an important adhesion molecule that plays a key role in the tight adhesion between leukocytes and vascular endothelium. The object of this study was to investigate the association between the K469E polymorphism of the ICAM-1 gene and restenosis after coronary stenting in North Chinese population. METHODS: The ICAM-1 K469E polymorphism was genotyped using polymerase chain reaction-restriction fragment length polymorphism method in 124 patients who had undergone coronary stenting and coronary angiography at least 3 months earlier. Information on clinical risk factors and procedure-related data were also collected. RESULTS: Of 124 enrolled patients in total, there were 72 cases of in-stent restenosis. The restenosis rate in this population was 58.1%. The frequencies of the three possible genotypes of the ICAM-1 K469E polymorphism were: KK genotype 50.8%, EE genotype 41.9%, and EK genotype 41.9%. Among restenosis patients, the frequency of the KK genotype was 58.3% and the frequency of E allele carriers was 41.7%. Among non-restenosis patients, the frequency of the KK genotype was 40.4%, and the frequency of E allele carriers was 59.6%. The distribution of these two genotype groups between restenosis and non-restenosis patients was significantly different (P = 0.049). Using multivariate logistic regression, the difference between the two groups was more apparent. The odds ratio of KK homozygotes vs E allele carriers was 2.6, with 95% confidence interval 1.2 - 5.8 (P = 0.018). After grading of risk factors, we found that the KK genotype was a stronger predictor of in-stent restenosis in obesity or hyperlipemia patients, with an odds ratio of 9.3 and 3.7, respectively (P < 0.05). CONCLUSION: In our study population, KK homozygotes of the ICAM-1 codon 469 mutation had a higher risk of restenosis after coronary stenting, especially in the case of obese or hyperlipemia patients.