OBJECTIVETo explore the associations between fasting serum lipids and high-sensitivity C-reactive protein (hsCRP).

METHODSSerum triglyceride (TG), high-density lipoprotein cholesterol (HDL-C) and hsCRP were measured in residents of Chengdu, China. Subjects with potential factors which might influence lipids and hsCRP were excluded, 580 subjects [mean age (62.3 ± 6.6) years; male: 58.7%] were finally recruited by random sampling methods.

RESULTSThere was a weak positive relationship between TG and hsCRP (r = 0.108, P = 0.01) and a weak negative relationship between HDL-C and hsCRP (r = -0.197, P < 0.001), this was also true in the sub-group with BMI < 24 kg/m(2) (r = 0.236, -0.140 respectively, all P < 0.001). In subjects with BMI < 24 kg/m(2), the hsCRP concentration was significantly higher in subjects with higher TG or lower HDL-C (all P < 0.05). hsCRP increased in proportion with the degree of dyslipidemia. After adjusting for gender, age, TC, LDL-C, fasting blood glucose, systolic blood pressure, diastolic blood pressure, history of hypertension and diabetes, smoking and alcohol drinking, logistic regression analysis showed that the odds ratio for increased hsCRP was 1.970 in subjects with either increased TG or lower HDL-C (P = 0.105) and 9.098 in subjects with both higher TG or lower HDL-C levels (P = 0.031). However, the observed relationship between TG, HDL-C and hsCRP in subjects with BMI < 24 kg/m(2) could not be observed in subjects with subjects with BMI > 24 kg/m(2) despite significant more cardiovascular risk factors in these subjects.

CONCLUSIONSA weak positive correlation between TG and hsCRP as well as a weak negative correlation between HDL-C and hsCRP was evidenced in the whole cohort suggesting dyslipidemia might be related to enhanced inflammatory status. However, this relationship is not observed in subjects with BMI > 24 kg/m(2) despite existence of more cardiovascular risk factors in these subjects.

Aged ; Alcohol Drinking ; C-Reactive Protein ; analysis ; Cardiovascular Diseases ; blood ; epidemiology ; China ; epidemiology ; Cholesterol, HDL ; blood ; Cholesterol, LDL ; blood ; Dyslipidemias ; epidemiology ; Female ; Humans ; Inflammation ; Male ; Middle Aged ; Smoking ; Triglycerides ; blood

OBJECTIVETo analyze the influence of benign prostatic hyperplasia (BPH) drugs on incidence and pathology grading of prostate cancer in China.

METHODSRetrospectively investigated the history of drug treatment in 1029 cases of BPH in patients from February 1998 to December 2004. According to the history of drug use, the patients were divided into 4 groups: finasteride group, alpha-receptor inhibitor group, finasteride and alpha-receptor inhibitor combination group and control group (untreated group). We gathered pathology sections of patients in all groups, and gave Gleason Score to each. The difference of incidence and pathology grading of prostate cancer were analyzed by Stata 7.0.

RESULTSThe incidence of prostate cancer in the population of our study was 13.5%; The incidence in finasteride group, alpha-receptor inhibitor group, combination group and control group was 9.8%, 16.0%, 10.3% and 18.6%, respectively. There was significant difference between the two groups with the use of finasteride and the two groups without it (P < 0.05). In our study, the ratio of middle or high level pathology grading (Gleason ≥ 7) in prostate cancer patients was 58.3%, the ratio of middle or high level pathology grading prostate cancer patients in the four groups was 71.4%, 59.6%, 67.7% and 40.0%, respectively. In the comparison of composition ratio of middle or high level prostate cancer, there was significant difference between the two groups with the use of finasteride and the two groups without it (P < 0.05).

CONCLUSIONSFinasteride can lower the risk of prostate cancer, but increase the pathology grade of the prostate cancer which has occurred in the same time. The alpha-receptor inhibitor does not have the same effect.

Adrenergic alpha-Antagonists ; therapeutic use ; Aged ; Aged, 80 and over ; Finasteride ; therapeutic use ; Humans ; Incidence ; Male ; Middle Aged ; Prostatic Hyperplasia ; drug therapy ; Prostatic Neoplasms ; epidemiology ; pathology ; Retrospective Studies

OBJECTIVETo develop thrombus-targeted urokinase immune liposome through incorporating D-dimer monoclonal antibody (DDmAb) to liposome and observe the thrombolytic efficiency in a rabbit pulmonary thromboembolism (PE) model.

METHODSReverse-phase evaporation method was used to develop targeted urokinase immune liposome by coupling DDmAb to urokinase liposome (liposomal-encapsulated urokinase) with glutaraldehyde. The PE models were induced by injecting 4 autologous emboli (2 mm x 5 mm) through jugular vein catheter into pulmonary arteries. New Zealand white rabbits (n = 32) were randomized into four groups: A group (TBS), B group (150 000 IU/kg UK), C group (30 000 IU/kg urokinase liposome) and D group (30 000 IU/kg urokinase immune liposome). The right ventricular pressure and the emboli size in pulmonary arteries were determined.

RESULTSThe right ventricular pressure increased significantly in PE rabbits (P < 0.01), the average value is (6.75 +/- 6.82) mm Hg (1 mm Hg = 0.133 kPa). Eighty minutes post various treatments, right ventricular pressure remained unchanged as post PE in group A [(40.15 +/- 11.22) mm Hg vs. (41.67 +/- 14.23) mm Hg], decreased to baseline level in group B and D [(34.71 +/- 8.67) mm Hg vs. (33.98 +/- 9.32) mm Hg, (30.65 +/- 6.67) mm Hg vs. (30.77 +/- 6.85) mm Hg, all P > 0.05], decreased but not returned to normal value in group C. Residual emboli size remained unchanged in group A and partly reduced in group C and more significantly reduced in group B and D. Hemorrhage of heart, kidney and liver was evidenced in group A but not in other groups.

CONCLUSIONAcute PE could be successfully treated by the thrombus-targeted urokinase immune liposome with D-dimer monoclonal antibody.

Animals ; Antibodies, Monoclonal ; administration & dosage ; Blood Pressure ; Disease Models, Animal ; Fibrin Fibrinogen Degradation Products ; immunology ; Fibrinolytic Agents ; therapeutic use ; Liposomes ; Pulmonary Embolism ; drug therapy ; physiopathology ; Rabbits ; Thrombolytic Therapy ; methods ; Urokinase-Type Plasminogen Activator ; administration & dosage

OBJECTIVETo observe the exercise single photon emission computed tomography (SPECT) myocardial perfusion imaging of patients with myocardial bridge and assess the association between myocardial ischemia and extent of myocardial systolic compression.

METHODSSeventeen patients with myocardial bridge diagnosed by coronary angiogram were included and underwent exercise SPECT myocardial perfusion imaging.

RESULTSAbnormal SPECT perfusion imaging was evidenced in 12 out of 17 patients with myocardial bridge (2 out of 6 patients with systolic compression induced stenosis < 50%, 3 out of 4 patients with systolic compression induced stenosis between 50% - 75% and 7 out of 7 patients with the systolic compression induced stenosis between 75% - 100%).

CONCLUSIONExercise stress SPECT myocardial perfusion imaging could detect myocardial ischemia in patients with myocardial bridge and abnormal perfusion is positively related to the extent of systolic compression induced stenosis.

Adult ; Aged ; Coronary Angiography ; Exercise Test ; Female ; Heart ; diagnostic imaging ; Humans ; Male ; Middle Aged ; Myocardial Bridging ; diagnostic imaging ; Myocardium ; Technetium Tc 99m Sestamibi ; Tomography, Emission-Computed, Single-Photon ; methods

To study the methylation in the promoter of LRP15 gene and its relationship with gene expression and to explore the possible mechanism of regulating LRP15 gene methylation, the methylation in the promoter of LRP15 gene in K562 cell line was detected by MS-PCR. Then K562 was exposed to 5-aza-2'-deoxycytidine (CdR) and trichostatin (TSA), to determine whether the silencing of LRP15 gene by de novo methylation could be reversed. As a result, it was confirmed by MS-PCR that the promoter of LRP15 was hypermathylated in K562 cell line, and lost its transcription activity. After CdR, with or without TSA, the silencing of LRP15 gene by de novo methylation can be reversed. Observation demonstrated that the expression of LRP15 was controlled by methylation in its promoter in K562. It is suggested that methyltransferase inhibitor and deacetylase inhibitor may be effective agents in leukemia therapy.
Azacitidine ; analogs & derivatives ; pharmacology ; DNA Methylation ; DNA Modification Methylases ; antagonists & inhibitors ; Enzyme Inhibitors ; pharmacology ; Gene Expression Regulation ; drug effects ; Histone Deacetylase Inhibitors ; Humans ; Hydroxamic Acids ; pharmacology ; K562 Cells ; Neoplasm Proteins ; biosynthesis ; genetics ; Polymerase Chain Reaction ; methods ; Promoter Regions, Genetic ; genetics

Adult ; Aged ; Angina, Unstable ; blood ; diagnostic imaging ; Antigens, CD ; blood ; Coronary Artery Disease ; diagnostic imaging ; Endoglin ; Female ; Humans ; Male ; Middle Aged ; Receptors, Cell Surface ; blood ; Ultrasonography, Interventional

BACKGROUNDRupture of unstable plaque with subsequent thrombus formation is the common pathophysiological substrate of acute coronary syndrome (ACS). It is of potential significance to explore the blood indexes predicting plaque characteristics. We investigated the relationship among soluble CD105, hypersensitive C-reactive protein (hs-CRP), and coronary plaque morphology.

METHODSA clinical study from April 2004 to December 2006 was conducted in 130 patients who were divided into 3 groups: 56 patients (43.1%) in stable angina (SA) group, 52 patients (40.0%) in unstable angina (UA) group and 22 patients (16.9%) in acute myocardial infarction group. The concentrations of soluble CD105 and hs-CRP were measured in all of the patients by cardioangiography (CAG). Plasma samples of arterial blood were collected prior to the procedure. The levels of soluble CD105 and hs-CRP were measured by enzyme-linked immunosorbent assay (ELISA).

RESULTSUnstable and ruptured plaque was found more frequently in patients with acute myocardial infarction and UA. External elastic membrane cross-sectional area (EEM CSA), plaque area, lipid pool area and plaque burden were significantly larger in the ruptured and unstable plaque group. Positive remodeling, thinner fabric-cap, smaller minimal lumen cross-sectional area (MLA), dissection and thrombus were significantly more frequent in the ruptured and unstable plaque group. Remodeling index (RI) was positively correlated with the levels of soluble CD105 in the UA group (r = 0.628, P < 0.01) and the acute myocardial infarction group (r = 0.639, P < 0.01). The levels of soluble CD105 and hs-CRP were higher in the ruptured plaque group. Soluble CD105 > 4.3 ng/ml was used to predict ruptured plaque with a receiver operating characteristic (ROC) curve area of 0.77 (95% confidence interval (CI), 66.8% - 87.2%), a sensitivity of 72.8%, a specificity of 78.0% and an accuracy of 70.2% (P < 0.01), similarly for hs-CRP > 5.0 mg/ml with a ROC curve area of 0.70 (95% CI, 59.2% - 80.2%), a sensitivity of 70.2%, a specificity of 76.2% and an accuracy of 67.2% (P < 0.01).

CONCLUSIONSThe plaque characteristics correlate with the clinical presentation. The elevation of soluble CD105 and hs-CRP is related to the plaque instability and rupture.

Aged ; Angina Pectoris ; blood ; pathology ; Antigens, CD ; blood ; C-Reactive Protein ; analysis ; Coronary Vessels ; diagnostic imaging ; pathology ; Endoglin ; Female ; Humans ; Male ; Middle Aged ; Myocardial Infarction ; blood ; pathology ; Receptors, Cell Surface ; blood ; Ultrasonography, Interventional ; methods

Among the types of lung cancer, lung adenocarcinoma accounts for the majority, and its overall survival rate is poor. B-cell translocation gene 2 (BTG2) is a member of the antiproliferative gene family, belonging to the BTG/TOB family. Many studies have shown that BTG2 was abnormally expressed in many types of tumors, but its regulatory role in the radiosensitivity of lung adenocarcinoma remained unclear. In this study, we explored the expression level of BTG2 in patients with lung adenocarcinoma and its correlation with clinical prognosis through online database and tissue samples of lung adenocarcinoma patient. The results indicated that the expression level of BTG2 decreased significantly in lung adenocarcinoma patient with radiation resistance. Bioinformatics analysis confirmed that BTG2 could respond to radiotherapy in lung adenocarcinoma cell lines, and its low expression in lung adenocarcinoma patients was associated with poor prognosis (P < 0.05). The lentivirus overexpressing BTG2 (OE-BTG2) was transfected into human lung adenocarcinoma cell lines to increase the expression level of BTG2 including A549 and H1299. And the effect of BTG2 overexpression on the radiosensitivity of lung adenocarcinoma cell lines was detected by clone formation assay. Clone formation experiment confirmed that overexpression of BTG2 could significantly enhance the radiosensitivity of A549 and H1299 cell lines (P < 0.05). The expression levels of BTG2 and apoptosis related protein-Bax were detected by Western blotting (WB) and immunohistochemistry (IHC). The effect of BTG2 on radiation sensitivity of lung adenocarcinoma was further detected via nude mouse in vivo. WB experiment confirmed that BTG2 upregulation could significantly increase the apoptosis level of A549 and H1299 cells after radiation. Moreover, BTG2 overexpression can markedly enhance the radiosensitivity of lung adenocarcinoma (P < 0.05) and increase the protein level of Bax after radiation in vivo. In conclusion, BTG2 had low expression in lung adenocarcinoma patients and its low expression level was closely related to the poor clinical prognosis. Overexpression of BTG2 can increase the radiosensitivity of lung adenocarcinoma cell lines and promote the process of apoptosis after radiation, indicating a new target for overcoming the radiation resistance of lung adenocarcinoma.

Repetitive transcranial magnetic stimulation (rTMS), a noninvasive and painless brain stimulation technique, can improve cognition and alleviate behavioral and psychological symptoms in patients with Alzheimer's disease through several mechanisms associated with neuronal plasticity, brain network, neurotransmitter, neurotrophic factors, and so on.

Oral squamous cell carcinoma (OSCC) has a high incidence of metastasis. Tumour immunotherapy targeting PD-L1 or PD-1 has been revolutionary; however, only a few patients with OSCC respond to this treatment. Therefore, it is essential to gain insights into the molecular mechanisms underlying the growth and metastasis of OSCC. In this study, we analysed the expression levels of protein kinase D3 (PKD3) and PD-L1 and their correlation with the expression of mesenchymal and epithelial markers. We found that the expression of PKD3 and PD-L1 in OSCC cells and tissues was significantly increased, which correlated positively with that of mesenchymal markers but negatively with that of epithelial markers. Silencing PKD3 significantly inhibited the growth, metastasis and invasion of OSCC cells, while its overexpression promoted these processes. Our further analyses revealed that there was positive feedback regulation between PKD3 and PD-L1, which could drive EMT of OSCC cells via the ERK/STAT1/3 pathway, thereby promoting tumour growth and metastasis. Furthermore, silencing PKD3 significantly inhibited the expression of PD-L1, and lymph node metastasis of OSCC was investigated with a mouse footpad xenograft model. Thus, our findings provide a theoretical basis for targeting PKD3 as an alternative method to block EMT for regulating PD-L1 expression and inhibiting OSCC growth and metastasis.
Animals ; B7-H1 Antigen/metabolism* ; Carcinoma, Squamous Cell ; Cell Line, Tumor ; Feedback ; Head and Neck Neoplasms ; Humans ; Mice ; Mouth Neoplasms ; Protein Kinase C ; STAT1 Transcription Factor ; Squamous Cell Carcinoma of Head and Neck