Impact of Physician-Coordinated Intensive Follow-Up on Long-Term Medical Costs in Patients with Unstable Angina Undergoing Percutaneous Coronary Intervention.

Background: To investigate the impact of professional physician-coordinated intensive follow-up on long-term expenditures after percutaneous coronary intervention (PCI) in unstable angina (UA) patients.

Methods: In this study, there were 669 UA patients who underwent successful PCI and followed up for 3 years, then divided into the intensive follow-up group (N = 337), and the usual follow-up group (N = 332). Patients were provided with detailed discharge information and individualized follow-up schedules.

Association between left ventricular end-diastolic pressure and coronary artery disease as well as its extent and severity.

Patients with myocardial ischemia exhibit increased left ventricular end-diastolic pressure (LVEDP). The study was to evaluate the relationship between LVEDP measured by left cardiac catheterization and coronary artery disease (CAD) as well as its extent and severity evaluated by coronary angiography (CAG). 912 patients who underwent CAG and left cardiac catheterization were enrolled.

[Aldosterone stimulates alpha1-(1) procollagen mRNA expression in HSC via activation of ERK1/2 and AP-1].

Objective: It has been known that the intrahepatic renin-angiotensin-aldosterone system (RAAS) plays a key role in the fibrogenesis in livers. Aldosterone (Aldo), the principal effector molecule of the RAAS, exerts local effects on cell growth and fibrogenesis. However, the signal transduction mechanisms underlying the effects of Aldo on hepatic fibrogenesis remain to be fully elucidated.

[Angiotensin II and aldosterone stimulate alpha1-(I) procollagen mRNA expression in hepatic stellate cells via activation of ERK1/2 and AP-1].

Objective: To investigate the signal transduction mechanism underlying the effects of angiotensin II (Ang II) and aldosterone (Aldo) on the signal passageway of active protein-1 (AP-1).

Methods: In vitro, Hepatic stellate cells (HSCs) of the line HSC-T6 were cultured and treated with Ang II or Aldo, the principal effector molecules of the renin-angiotensin-aldosterone system (RAAS) for 10, 30, 60, 120, and 180 minutes respectively. The protein expression of phospho-P42/44 was detected by Western blotting.

ACEI attenuates the progression of CCl4-induced rat hepatic fibrogenesis by inhibiting TGF-beta1, PDGF-BB, NF-kappaB and MMP-2,9.

Aim: Angiotensin II has pro-fibrotic function in the liver. Blockade of the renin-angiotensin-aldosterone-system (RAAS) attenuates hepatic fibrosis. The aim of the present study was to determine the mechanism of angiotensin-converting enzyme inhibitor (ACEI) on the progression of rat hepatic fibrosis.

[Aldosterone stimulating PDGF-B expression in HSC via activation of EGR-1].

Objective: It is known that intrahepatic renin-angiotensin-aldosterone system (RAAS) plays a key role in liver fibrogenesis. Aldosterone (Aldo), the principal effector molecule of the RAAS, exerts local effects on cell growth and fibrogenesis. However, the signal transduction mechanisms underlying the effects of Aldo on hepatic fibrogenesis remain to be fully elucidated.

[Effects of angiotensin II and aldosterone on NF-kappaB binding activity in hepatic stellate cells].

Objective: To investigate the signal transduction mechanism underlying the effects of angiotensin II (AngII) and aldosterone (Aldo) on nuclear factor-kappaB (NF-kappaB) DNA binding activity.

Methods: Sixty male Wistar rats were randomly divided into 4 groups: model group (Mo group), injected with CCl(4) subcutaneously twice a week to establish a model of hepatic fibrosis; perindopril group (Pe group), injected with CCl(4) subcutaneously twice a week and perfused with perindopril once a day; losartan group (Lo group), injected with CCl(4) subcutaneously twice a week and perfused with losartan once a day; and control group (Nc group), injected with olive oil subcutaneously. The rats were killed in batches respectively 4 and 6 weeks after and their livers were collected to undergo Masson staining and be observed by light microscope.

Changes in the expression of angiotensin II type 1 receptor in the development of liver fibrosis.

Objective: To detect the expression of angiotensin II type 1 receptor (AT1R) in the different stages of human liver fibrosis.

Methods: The morphology and ultrastructure of hepatic stellate cells (HSC) in hepatic sinusoids were studied by transmission electron microscopy, collagen I (col I) was tested by immunohistochemical method, an indirect immunofluorescence labeling method was used to detect AT1R, and semiquantitative RT-PCR was used to detect AT1R mRNA.

Results: Positive expression of AT1R was mainly distributed in the periphery of hepatic lobules and in the cytoplasm of HSC in the sinusoids.

[Perindopril attenuates the progression of CCl4-inducing rat hepatic fibrosis].

Objectives: The aim of the present study was to determine the effects of angiotensin-converting enzyme inhibitor, perindopril, on the progression of rat hepatic fibrosis induced by CCl4.

Methods: Male wistar rats weighting about 250g were treated with perindopril (2mg/kg, daily gavage), except for model group and control group. After 4, 6 weeks, morphological examination was based on microscopy.

[Effect of ACE-I and AT-1 receptor blocker on the progression of CCl(4)-inducing rat hepatic fibrogenesis].

Objective: The aim of the present study was to determine the effects of angiotensin-converting enzyme inhibitor (ACE-I) and angiotensin II type 1 receptor (AT-1 receptor) blocker on the progression of rat hepatic fibrosis induced by CCl4.

Methods: 60 male wistar rats weighting about 250 g were divided into 4 groups. Model group (Mo): The rats were injected with 40% CCl(4) 0.

[Expressions of angiotensin II type 1 receptor mRNA in fibrotic and normal liver tissues].

Objective: To investigate the expression profile of angiotensin type 1 receptor (AT1R) mRNA in fibrotic and normal liver tissues.

Methods: Semi-quantitative RT-PCR was used to detect the expression of AT1R mRNA in 18 specimens of fibrotic liver tissues adjacent to liver cancers and 12 normal liver tissue specimens. Specific AT1R product and GAPDH product used as internal control were both amplified by RT-PCR, and the ratio of their integrated optical densities calculated to estimate the relative quantity of AT1R mRNA expression.

Effects of angiotensin II and losartan on the growth and proliferation of hepatic stellate cells.

Objective: To investigate the effects of angiotensin II (AngII) and AT1a blocker losartan on growth and proliferation of rat hepatic stellate cells (HSCs).

Methods: Rat HSCs were isolated, cultured and identified, followed by incubation with AngII or losartan at different concentrations. The cell growth and proliferation were assessed via cell counting and MTT assay, and the effects of the agents on HSC DNA synthesis evaluated by way of (3)H-thymidine incorporation ((3)H-TDR).

[Endoscopic diagnosis and treatment of the early-stage malignant colorectal polyp and follow-up study].

In the past 20 years we have performed endoscopic removal of colorectal polyps in 4 000 cases, and thorough histological examination of the removed polyps identified 121 cases of early-stage malignant polyp. According to the depth of malignant invasion and whether malignant remnants were present after the initial surgical removal, conservative treatment or radical operation was implemented. During the follow-up study, endoscopy was performed once each year in all the patients with malignancies.

Detection of soluble tumor necrosis factor-p55 levels in the serum and ascitic fluid of patients with hepatocellular carcinoma.

Objective: To examine soluble tumor necrosis factor receptor-p55 (sTNFR-p55) levels in the serum and ascitic fluid and investigate the significance of this examination in assessment of the clinical status of patients with primary hepatocellular carcinoma (HCC).

Methods: Enzyme-linked immunosorbent assay (ELISA) was used to examine sTNFR-p55 levels in the serum and ascitic fluid in 25 patients with HCC and 25 with liver cirrhosis (LC).

Results: sTNFR-p55 levels in the serum and ascitic fluid in patients with HCC were significantly higher than those in patients with LC and controls (P=0.