A review of the system background for the multi-institution physician practice in China,and an analysis for the specific constraints for physicians of public hospitals to embrace such a practice On this basis, the paper probed into the measures to encourage the physicians for doing so. The measures recommended include advanced design, improvement of the quality of care and safety mechanism,incentives mechanism, mandatory enforcement of medical liability insurance to minimize risk exposure of such a practice, aiming at advancement of this practice.

As introduced in the paper,Australian government subsidize the public hospitals with all their budget needs as compensation,with the two levels of governments constituting the largest buyer of health products and services in the country.In addition,the government supports the hospitals with their facilities.A rational government investment mechanism is proposed with reference to such a model for the ongoing reform of public hospitals in China.

Adult ; Aged ; Breast Neoplasms ; genetics ; metabolism ; pathology ; surgery ; Female ; Gene Amplification ; Genital Neoplasms, Male ; genetics ; metabolism ; pathology ; surgery ; Humans ; Male ; Middle Aged ; Paget Disease, Extramammary ; genetics ; metabolism ; pathology ; surgery ; Paget's Disease, Mammary ; genetics ; metabolism ; pathology ; surgery ; Penile Neoplasms ; genetics ; metabolism ; pathology ; surgery ; Receptor, ErbB-2 ; genetics ; metabolism ; Scrotum ; Vulvar Neoplasms ; genetics ; metabolism ; pathology ; surgery

Objective　To explore the effect of hypoxia on the apoptosis of cultured human umbilical vein endothelial cells（HUVECs） and the role of vascular endothelial growth factor（VEGF） in inhibition of apoptosis． Methods　①Culture and identification of HUVECs．②Establishment of hypoxic model（0，12，24，48 h）in HUVECs．③Incubation of HUVECs with VEGF(0 ng, 100 ng) under hypoxic condition for 24 h. ④Detection of apoptosis of HUVECs with TUNEL method． Results　The percentages of apoptosis were different under different hypoxic conditions． The longer hypoxic time was，the higher apoptosis percentage was．VEGF reduced the apoptosis of HUVECs induced by hepoxia． Conclusion　Over-apoptosis EVCs in one of the important factors for the impairment of endothelial function. HEGF inhibits the apoptosis of HVCs and having a pretive function on them.

AIM:To determine the relationship between ischemia,hypoxia and the production of vascular endothelial growth factor in rat myocardium and its basic mechanism. METHODS:(1) 28 Wistar rats were randomly divided into 4 groups: group A,normal control;group B,1 day's acute myocardial infarction;group C,3 day's acute myocardial infarction;group D, 7 day's acute myocardial infarction. (2) Rat cardiac myocytes cultured were primarily divided into some groups, hypoxia incubated 24 hours; PMA groups, hypoxia incubated 24 hours with PKC activator (PMA), A 0 ng/mL; B 10 ng/mL; C 100 ng/mL; D 1 000 ng/mL; Chelerythrine groups, hypoxia incubated 24 hours with PKC inhibitor (chelerythrine), A 0 nmol/L; B 10 nmol/L. (3) By computer scanned and quantitated, vascular endothelial growth factor (VEGF) protein was detected with immunohistochemical technique. RESULTS: The longer time of ischemia and hypoxia was, the higher the VEGF production. The relationship was found between the time of ischemia or hypoxia and the production of VEGF. The production of VEGF protein was further promoted by PMA with different concentration, decreased by chelerythrine.CONCLUSION:Ischemia or hypoxia strongly stimulated the production of VEGF in myocardium, which played an important role in autoprotecting of ischemic or hypoxic myocardium. Hypoxia-induced PKC activation is one kind of basic mechanisms in this course.

French hospital administrators have undergone several changes to meet the needs of economic and social development,resulting in the pattern of hospital administration by both the central government and regional organizations.This paper made descriptions and analysis of the French hospital administrators and came up with the following insights:Making public hospitals as the main health service provider benefits provision of public services; public and private hospitals can jointly meet public service needs under government regulation; the government should focus on controlling health care resources;medical service system needs an overall policy guidance; hospital management organizations should streamline in the reform.

This paper overviewed typical government compensation sources and practices for public hospitals in the world.Government compensation should be made based on regional health planning,while the central government shoulders greater compensation responsibility.The fee-for-case mix is found to be the best incentive The government adjusts its funding baselines for different hospitals to adjust the compensation.In view of the compensation for public hospitals in China,the paper analyzed the enlightenments and lessons from international experiences The authors recommend an evolution from the pattern of compensation per person/per bed,to payment by service unit or volume(for example,per outpatient or emergency visit and days of stay),and in the end to that of payment per disease.

AIM To explore the effect of hypoxia on apoptosis in human umbilical vein endothelial cells(HUVECs) and the role of ecdysterone(EDS)in inhibition of apoptosis. METHODS ① Culture and identification of HUVECs;② Hypoxic model(0,12,24,48 h) in HUVECs was established. While HUVECs was incubated 24 h with EDS(100 mg?L -1 ) under hypoxic condition. Apoptosis in HUVECs was detected by TUNEL;③ HUVECs received EDS 100 mg?L -1 in normal and hypoxic condition. After 24 h, vascular endothelial growth factor (VEGF) was detected with immunohistochemical technique. RESULTS The apoptosis percentages are different under different hypoxic condition. The longer hypotic the time was, the higher the apoptosis percentage was. EDS reduced apoptosis of HUVECs. EDS could enhance expression of VEGF protein in cardiac myocytes of rat in normal and hypoxic condition. CONCLUSION The role of hypoxia in HUVECs apoptosis is more significant along with prolonging of hypoxic time. VEGF play an important role in protective effect of EDS on endothelial cell apoptosis.

Objective To observe the estrogenic activity of octylphenol(OP) in vitro and to conduct a preliminary study of its mechanism. Methods The estrogenic activity of OP was detected by cell proliferation test of MCF 7 cells in vitro and the mechanism was preliminarily studied by growth curve analysis, cell cycle analysis, tamoxifen(Tam) antagonistic test and apoptosis detection. Results OP was found to have estrogenic activity to stimulate the proliferation of MCF 7 cells. Cell cycle analysis revealed that the cell proliferation indexes of OP and 17? estradiol(E 2) were higher than those of alcohol. The estrogenic activities of OP and E 2 to stimulate the proliferation of MCR 7 could be antagonized by Tam. Both OP and E 2 could inhibit the cell apoptosis of MCF 7 cells. Conclusion OP possesses estrogenic activity to stimulate the proliferation of MCF 7 cells. The mechanism may be due to binding to the estrogen receptor, which may have effect on cell proliferation and apoptosis.

OBJECTIVETo observe the effect of β₃adrenoceptors (β₃-AR) activation on rat thoracic aorta smooth muscle contractility and the possible related mechanism.

METHODSThe endothelium removed thoracic aorta was pre-contracted with 30 mmol/L KCl physiological saline solution (PSS). Then the tension of the thoracic aorta was recorded in presence of BRL37344 (BRL) to determine the action of β₃-AR. The tension of the thoracic aorta was also recorded in the presence of Propranolol (PRA), SR59230A (SR), L-NNA, H-89 and Iberiotoxin (IBTX) respectively to reveal the underling mechanism of β₃-AR activation on rat vascular smooth muscle. Immunohistochemistry was adopted to confirm the existence and the distribution of β₃-AR in rat thoracic aorta.

RESULTSThe results showed that: (1) The thoracic aorta was relaxed by β₃-AR activation, with a relaxation percentage of (10.59 ± 0.79). (2) β₃-AR was expressed in both endothelial and smooth muscle layer in thoracic aorta sections of rats. (3) PRA did not block the effect of BRL on the thoracic aorta. The relaxation actions of BRL could be antagonized by pre-incubating the thoracic aorta with SR. (4) L-NNA (a NOS inhibitor) and H-89 (a PKA inhibitor) reversed the relaxation effect of BRL on vascular smooth muscle. (5) The effect of BRL was decreased after application of Ibriotoxin (IBTX), a large conductance calcium dependent potassium channel blocker.

CONCLUSIONThe results confirmed that activation of β₃-AR led to relaxation of thoracic aorta smooth muscle. The relaxation action of β₃-AR on smooth muscle of rat thoracic aorta was related to activation of NOS and PKA signaling pathway. Large conductance Ca²⁺-K⁺ channels were involved in the relaxation action of β₃-AR activation on rat thoracic aorta smooth muscle.

Animals ; Aorta, Thoracic ; physiology ; In Vitro Techniques ; Isoquinolines ; Large-Conductance Calcium-Activated Potassium Channels ; physiology ; Muscle Contraction ; Muscle Relaxation ; Muscle, Smooth, Vascular ; physiology ; Nitroarginine ; Peptides ; Propanolamines ; Propranolol ; Rats ; Receptors, Adrenergic, beta-3 ; physiology ; Signal Transduction ; Sulfonamides