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Objective: To investigate the levels of cardiovascular disease risk factors and their relations to clinical phenotype associated with coronary artery disease (CAD)., Methods: The subjects were recruited from five independent cardiovascular centers. Coronary angiography was employed to define the CAD with stenosis in each major vessel > or = 70% and control with stenosis < 10% in every lesion. The classic risk factors including family history, body mass index, smoking habits, hypertension, diabetes mellitus, and serum lipid levels were surveyed according to established criteria. Associations between risk levels and clinical phenotypes were assessed by case control and correlation analysis., Results: A total of 762 individuals were collected, including 481 men and 281 women, aged from 17 to 81 (mean 60 +/- 10) years. The patients with CAD accounted for 55.5% of all participants, and controls 44.5%, respectively. Compared with the pattern in published data, our study showed that mean serum high density lipoprotein cholesterol (HDL-C) level was significantly lower (P < 0.001) and triglycerides was significantly higher (P < 0.001), while total cholesterol (TC) and low density lipoprotein cholesterol levels were comparative (both P > 0.05). The prevalence of low HDL-C (< 40 g/L) and hypertriglyceridemia (> 150 g/L) were 27.2% and 41.4%, respectively. Mean serum levels of HDL-C and apolipoprotein A1 were significantly higher in female subjects than in male (P < 0.001). Lower HDL-C functioned as an independent risk factor for CAD only in men (RR = 2.8, 95% CI: 1.5-4. 2, P < 0.001), yet increased non-HDL cholesterol combined with diabetes mellitus and obesity seemed to play a key role in the development of CAD in women. Similarity in risk association with CAD was found for hypertension and TC/HDL ratio in male and female subjects, while family history had no relationship with the presence of CAD., Conclusion: It is remarkable that emphasis of intervention in future should be given on the prevalent low serum HDL-C and its strong risk correlation with the presence of CAD in male subjects of Chinese Han population.

Objective: To investigate the changes in plasma levels of vascular endothelial growth factor (VEGF) and stromal cell-derived factor-1 (SDF-1) and in peripheral CD34(+) cells in patients with acute myocardial infarction (AMI), and explore their role in AMI., Methods: Enzyme-linked immunoassay (ELISA) was employed for measuring the levels of VEGF and SDF-1 in AMI patients on days 1, 3, 7, 10, and 14 of onset and in normal control subjects. The absolute counts of CD34(+) in the peripheral blood were measured on days 1, 7, and 14 by flow cytometry in AMI patients, with their myocardial enzyme and troponin I detected and electrocardiography (ECG) and echocardiography (UCG) recorded., Results: Peripheral CD34(+) cells obviously increased on day 7 after AMI onset (2.35-/+0.72/microl vs 1.48-/+0.49/micro, P<0.05). VEGF levels were significantly higher in AMI patients than in the control subjects, reaching the peak level and on day 14 (197.56-/+39.87 vs 53.79-/+18.12 pg/ml, P<0.01). SDF-1 level obviously decreased on day 1 after AMI onset (1683.12-/+224.79 vs 2178.67-/+265.34 pg/ml, P<0.01), followed by gradually increased to the control level. Obvious correlation was noted between the level of VEGF on day 7 and the peak level of peripheral CD34(+) cells, and the peak plasma VEGF level was obviously associated with the peak serum CK-MB and troponin I levels., Conclusion: The stem cells are mobilized into the peripheral blood in the event of AMI. Obviously increased VEGF level following AMI may persist for at least 2 weeks, whereas SDF-1 level undergoes temporary decrement after AMI. The dynamic changes of VEGF and SDF-1 can be related to the mobilization and homing of the stem cells to the injured myocardium.

Objective: To study the clinicopathologic features of myeloid sarcoma and to evaluate the role of immunohistochemical study in diagnosis of this entity., Methods: Eighty-two cases of myeloid sarcoma were retrieved from the archives of Department of Pathology, West China Hospital of Sichuan University during the period from January, 1990 to February, 2005. The morphologic features were reviewed and classified according to the 2001 WHO classification for hematopoietic and lymphoid tissue tumors. Immunohistochemical study using a panel of 11 antibodies was performed on 73 cases. The survival data were collected and analyzed by SPSS 10.0., Results: The median age of patients was 35.5 years. The male-to-female ratio was 1.4:1. The sites of occurrence included lymph node (43.1%), skin (16.7%), nose (7.8%), soft tissue (7.8%) and bone (6.9%). Fifty-one cases (62.2%) represented myeloid sarcoma associated with an underlying myeloproliferative disorder and 25 cases (30.5%) represented solitary myeloid sarcoma. As for the morphology, 79 cases (96.3%) were granulocytic sarcoma, including 41 cases (51.9%) blastic type, 25 cases (31.6%) immature type and 13 cases (16.5%) differentiated type. The other 3 cases (3.7%) were monoblastic sarcoma. Immature eosinophils were found in 51 cases (64.6%) of granulocytic sarcoma, among which 13 cases (31.7%) were of blastic type. Immunohistochemical study showed that 95.9% cases (70/73) were positive for myeloperoxidase, 95.5% (63/66) for lysozyme, 95.2% (60/63) for CD68 (KP1), 90.8% (59/65) for leukocyte common antigen, 85.7% (54/63) for CD43, 77.8% (49/63) for CD117, 58.7% (37/63) for CD99, 54.0% (34/63) for CD15, 22.2% (14/63) for CD34, and 4.7% (3/64) for CD68 (PG-M1). Proliferation index, as demonstrated by Ki-67 positivity, was 0.49+/-0.22. Follow-up data was obtained in 59 of the 82 patients. The two- and five-year survival rates were 36.1% and 17.3% respectively. No significant prognostic factors were found in the survival analysis., Conclusions: Myeloid sarcoma may precede, develop in a background of myeloproliferative disorder or even after remission of the disease. The presence of immature eosinophils is an important morphologic clue and immunohistochemical study plays an essential role in arriving at a correct diagnosis. Immunopositivity for myeloperoxidase is specific for granulocytic differentiation, while CD68 (PG-M1)-positivity suggests monocytic differentiation. Detailed clinicopathologic correlation is also helpful.

Objective: To investigate the effects and mechanisms of sodium ferutate (SF) in treating diabetic nephropathy (DN)., Methods: Eighty patients of diabetes mellitus type 2 with DN were randomly divided into two groups, 40 cases in each group. The routine group treated with conventional treatment including dietary therapy and hypodermic injection of insulin, and the SF group treated with intravenous dripping of SF 300 mg/d additionally besides the conventional therapy, the therapeutic course for both groups was 4 weeks. And 40 healthy volunteers were allocated in a group for normal control. Before and after therapy, levels of fasting blood glucose (FBG), hemoglobin A1c(HbA1c), triglyceride (TG), total cholesterol (TC), high-density lipoprotein (HDL-C), serum creatinine (SCr), blood urea nitrogen (BUN), mean arterial pressure (MAP), urinary albumin excretion rate (UAER), serum collagen type IV (CIV) and endothelin (ET) were detected., Results: After 4 weeks of treatment, FBG and HbA1c reduced obviously in both groups with insignificant difference in comparison of them (P > 0.05). Before treatment, TG, TC, MAP, SCr, BUN, UAER, CIV and ET were markedly higher in DN patients than those in the health control (P < 0.05), these criteria decreased significantly in the SF group (P < 0.05) but insignificantly in the routine group (P > 0.05) after treatment, showing difference between the two groups (P < 0.05)., Conclusion: Sodium ferulate could ameliorate lipid metabolic disorder, reduce blood pressure, lower UAER and CIV level, and improve renal function in DN patients, the mechanism might be through decreasing ET production and inhibiting the combining of ET with its receptor.

Objective: To investigate whether intrapericardial urokinase irrigation along with pericardiocentesis could prevent pericardial constriction in patients with infectious exudative pericarditis., Methods: A total of 94 patients diagnosed as infectious exudative pericarditis (34 patients with purulent pericarditis and 60 with tuberculous pericarditis, the disease courses of all patients were less than 1 month), 44 males and 50 females, aged from 9 to 66 years (mean 45.4 +/- 14.7 years), were consecutively recruited from 1993 to 2002. All individuals were randomly given either intrapericardial urokinase along with conventional treatment in study group, or conventional treatment alone (including pericardiocentesis and drainage) in control group. The dosage of urokinase ranged from 200000 to 600000 U (mean 320000 +/- 70000 U). The immediate effects were detected by pericardiography with sterilized air and diatrizoate meglumine as contrast media. The long-term investigation depended on the telephonic survey and echocardiographic examination. The duration of following-up ranged from 8 to 120 months (mean 56.8 +/- 29.0 months)., Results: Percutaneous intrapericardial urokinase irrigation promoted complete drainage of pericardial effusion, significantly reduced the thickness of pericardium (from 3.1 +/- 1.6 mm to 1.6 +/- 1.0 mm in study group, P < 0.001; from 3.4 +/- 1.6 mm to 3.2 +/- 1.8 mm in control group, P > 0.05, respectively), and alleviated the adhesion. Intrapericardial bleeding related to fibrinolysis was found in 6 of 47 patients with non-blood pericardial effusion and no systemic bleeding and severe puncture-related complication was observed. In follow-up, there was no cardiac death, and pericardial constriction events were observed in 9 (19.1%) of study group and 27 (57.4%) of control group. Cox analysis illustrated that urokinase could significantly reduce the occurrence of pericardial constriction (relative hazard coefficient = 0.185, P < 0.0001)., Conclusion: The early employment of intrapericardial fibrinolysis with urokinase and pericardiocentesis appears to be safe and effective in preventing the development of pericardial constriction in patients with infectious exudative pericarditis.

Experiments were performed to investigate the effects of long-term treatment with adrenergic receptor antagonist on electrical remodeling of the left ventricle with chronic pressure-overload. New Zealand rabbits underwent subtotal banding of superrenal abdominal aorta. At 10 weeks after surgery, echocardiography examination was performed, then action potential (AP), inward rectifier potassium current (I(Ki)), delayed rectifier potassium current (I(K)) and Na(+)/Ca(2+) exchanger current (I(Na(+)/Ca(2+))) were recorded in midmyocardial cells isolated from left ventricle of abdominal aorta banded group (banded group), abdominal aorta banding plus Carvedilol intervention group (Carvedilol group), and normal control group rabbits by using the whole-cell patch-clamp techniques. The results showed that left ventricular mass index in control, banded, and Carvedilol groups were 1.78+/-0.06 (n=7), 2.33+/-0.11 (n=7), and 1.87+/-0.08 (n=7), respectively (banded vs control and Carvedilol, P<0.01). At basic cycle length of 2 s, AP duration (measured at 90% repolarization, APD(90), ms) in control, banded, and Carvedilol groups were 522.0+/-19.5 (n=6), 664.7+/-46.2 (n=7), 567.8+/-14.3 (n=8) respectively (banded vs control, P<0.01; Carvedilol vs banded, P<0.05). At test potential of -100 mV, inward I(Ki) density (pA/pF) in control, banded, and Carvedilol groups were -11.8+/-0.50 (n=8), -8.07+/-0.28 (n=8), -10.69+/-0.35 (n=8) respectively (banded vs control and Carvedilol, P<0.01). At test potential of +50 mV, I(K) tail current density (pA/pF) in control, banded, and Carvedilol groups were 0.59+/-0.04 (n=8), 0.40+/-0.02 (n=9), 0.51+/-0.02 (n=8) respectively (banded vs control, P<0.01; Carvedilol vs banded, P<0.05). At test potential of +60 mV, outward I(Na(+)/Ca(2+)) density (pA/pF) in control, banded, and Carvedilol groups were 1.06+/-0.11 (n=8), 1.54+/-0.10 (n=9), 1.24+/-0.07 (n=8), respectively (banded vs control and Carvedilol, P<0.01). At test potential of -120 mV, inward I(Na(+)/Ca(2+)) density (pA/pF) in control, banded, and Carvedilol groups were -0.54+/-0.06 (n =8), -0.75+/-0.04 (n=9), -0.60+/-0.03 (n=8), respectively (banded vs control, P<0.01; Carvedilol vs banded, P<0.05). It is shown that long-term treatment with Carvedilol not only prevents development of cardiac hypertrophy, but also improves the electrophysiological alterations in rabbit hearts with chronic pressure-overload. This finding may add new electrophysiological evidence for the treatment of heart failure and hypertension with adrenergic receptor antagonist.

Objective: To investigate the distribution characteristics of Na+/Ca2+ exchanger current (I(Na+/Ca2+)) across the left ventricular wall of rabbit and the relationship between I(Na+/Ca2+) and transmural depolarization heterogeneity., Methods: By using whole-cell patch clamp techniques, action potentials (AP), I(Na+/Ca2+), and both rapid and slow components of delayed rectifier potassium current (I(Kr) and I(Ka)) were recorded in subendocardial (Endo), midmyocardial (M), and subepicardial (Epi) cells of the left ventricular wall of rabbit., Results: AP duration in M cells was longer than that in Epi cells, P<0.01. At the test potential of +40 mV, outward I(Na+/Ca2+) in M cells was larger than that in Epi and Endo cells, P<0.01, P<0.05, respectively. At the test potential of -100 mV, inward I(Na+/Ca2+) in M cells was larger than that in Epi cells, P<0.05. At the test potential of +50 mV, the tail current density of I(Ka) in M cells was smaller than that in Epi cells, P<0.05, and there was no significant difference among the tail current densities of I(Kr) in Endo, M, and Epi cells., Conclusion: The distribution of I(Na+/Ca2+) and I(Ka) across the left ventricular wall of rabbit is unequal, which contributes to the transmural depolarization heterogeneity.

Purpose: To review the diagnosis and management of injury of the major cervical vessels., Methods: The clinical data of 12 cases with injury of the major cervical vessels were analyzed retrospectively. The causes of injury, emergency management, outcomes and complications were investigated., Results: Among 12 cases, no death and no severe complications developed through appropriate management., Conclusions: For patients with cervical injury, the possibility of vascular injury should be considered. The key to salvage on spot is hemostasis by local compression with rapid filling. Complete exposure of the vessels is the key to success of surgical salvage. Anti-shock measures, endotracheal intubation general anesthesia and immediate operation are mandatory to improvement of treatment outcomes.

Multidrug resistance (MDR) is an important biological behavior of tumor cells in chemotherapy. And it is also one of the major causes of clinical chemotherapy failure. According to the literature at home and abroad, and combining with the results of authors' investigations, this paper mainly discusses the mechanism of tumor cells' MDR and its reversion by Chinese herbs.

This article reviewed information related to the apoptosis of breast cancer cells. Breast cancer is a common malignant tumor in women. Apoptosis is related to the response and resistance to treatment in breast cancer. Here we summarized and integrated the data on apoptosis and its role in the development, prognosis, and treatment of breast cancer. Further study on apoptosis in breast cancer can help find more candidates for predictors and indices of response. Such study will also develop treatment regimens that are tailored to individual tumors and thereby maximize survival.

Aim: To investigate the mechanism of rhubarb protection of the gut barrier., Methods: The gut barrier damage models caused by hemorrhagic shock and intraperitoneal endotoxin were used to study the protective effect of rhubarb on the intestinal mucosal barrier. Rats were randomly divided into four groups, as follows: treatment (rhubarb) group; Positive control group; Negative control group; Placebo treatment group. Plasma endotoxin, tissue superoxidedismutase (SOD) and lipoperoxide (LPO) concentrations were measured and histological analysis was performed. Rhubarb was observed to have a protective effect on the gut., Results: Rhubarb decreased intestinal permeability, attenuated endotoxin absorption (endotoxin serum levels: shock group 0.557 EU/mL ± 0.069 EU/mL vs rhubarb group 0.345 EU/mL ± 0.055 EU/mL), and decreased tissue SOD and tissue LPO levels (SOD serum, intestine and liver levels: endotoxin group 122.92 NU/mL ± 43.19 NU/mL, 292.24 NU/mL ± 88.76 NU/mL, 272.70 NU/mL ± 85.79 NU/mL vs rhubarb group 312.23 NU/mL ± 54.93 NU/mL, 391.09 NU/mg ± 98.16 NU/mg, 542.86 NU/mg ± 119.93 NU/mg; LPO content in the intestine and liver: endotoxin group 8.57 μmol/L ± 2.58 μmol/L, 86.97 μmol/L ± 46.54 μmol/L vs rhubarb group 3.05 μmol/L ± 1.13 μmol/L, 13.18 μmol/L ± 19.64 μmol/L). Gut histopathology revealed that rhubarb promoted goblet cell proliferation, increased mucus secretion and protected intestinal mucosa in the hemorrhagic shock model., Conclusion: Rhubarb may protect the gut barrier by decreasing intestinal permeability, scavenging oxygen free radicals, and promoting goblet cell proliferation within the intestinal mucosa.