BACKGROUND: Critical closing pressure (CCP) is recently thought to play a key role in cerebral blood flow autoregulation as an effective downstream pressure of cerebral circulation and can objectively reflect the cerebrovascular tone, namely the vascular smooth muscle contraction and diastole, which is subjected to dynamic modulation.OBJECTIVE: To dynamically assess the hypertension-induced damage of the contraction function of cerebral microvascular smooth muscles and its correlation with morphological changes based on CCP evaluation.DESIGN: Randomized controlled experiment.SETTING: Institute of Neural Science of Second Hospital Affiliated to Guangzhou Medical College and Department of Neurology, First Hospital Affiliated to Sun Yet-san University.MATERIALS: The experiment was carried out at the Laboratory of Physiological Science of Sun Yet-san University between July 2002 and August 2003. Totally 160 health male SD rats were randomized into control group and hypertension group with 80 rats in each group. METHODS: Stroke-prone renovas cular hyp ortonsive rats were established in rats of the hypertension group by bilateral renal artery occlusion with two clips. The rats in the control group were not subjected to the occlusion with other treatments identical to those of the hypertension group. At the time points of 2, 4, 6, 8, 10, 12, 14 and 16 weeks after operation, respectively, 10 rats were randomly selected from each of the two groups for determination of arterial pressure and CCP. After the measurements the frontal-parietal lobe was obtained from the anaesthetized rats and cut into slices for quantitative analysis of the morphological changes in cerebral microvessels.different postoperative time points.mean arterial pressure in hypertension group obviously increased from the 6th postoperative week with significant difference from that of the control after operation to a level significantly higher than that of the control group at postoperative 14 and 16 weeks [(63.75±7.43) vs (37.28±3.68) mm Hg and (67.37±15.57) vs (38.39t7.41) mm Hg, respectively, P ＜ 0.05].significance from that of the control group at the 8th postoperative week (Paverage arterial pressure and cerebral arteriole tunica media (r=0.906 93,0.811 36, respectively, P ＜ 0.05). The changes in CCP was more obvious in the early and advanced stages of blood pressure elevation, but not so manifest during obvious blood pressure increment, displaying an inverted S-shaped curve of changes (R2=0.996 2, P ＜ 0.05).CONCLUSION: Contraction of the cerebrovascular smooth muscles is enhanced with the dynamic increment of arterial pressure after the development of hypertension. Vascular tone increase is more manifest during the early and advanced stages of hypertension.

AIM:To study the effect of hypertensive arteriosclerosis on cerebral blood flow autoregulation (CBFA), and to introduce a new method to measure the lower limit. METHODS:The blood velocities and blood pressure was recorded simultaneously and the curves of CBFA were analyzed and classified into classical and non-classical pattern. The lower limit were determined by clinical closing pressure (CCP) and the curve CBFA. RESULTS:When the blood pressure was decreasing, the classical and non-classical pattern of the cerebral blood flow autoregulation were 25% and 75% respectively in normal SD rats, while they were 40.55% and 54.45% respectively in renovascular hypertensive rats (RHR). However, when the blood pressure was elevating, the classical and non-classical pattern were 76.47% and 23.53% respectively in SD rats, while they were all classical in RHR. Furthermore, in SD and RHR ras, the lower limits measured by CCP were well in accordance with that measured by CBFA. CONCLUSION:Hypertensive arteriosclerosis could influence the limits and the patterns of cerebral blood flow autoregulation. The lower limit of CBFA can be measured and analyzed by CCP.

Objective 　To establish a new practical method to assess the cerebral blood flow autoregulation. Methods　We assessed the flow velociey of middle cerebral artery with transcranial Doppler and recorded invasively the blood presure simultaneonsly. Then on the basis of critical closing pressure (CCP), the lower limit of cerebral blood flow autoregulation and the blood flow resistance of arterioles were calculated.The data compared with the results generated by routine method. Results　The lower limit of autoregulation working out by CCP was 70.88±24.05 mmHg, which was similar to the result measured by routine method. The lower limit of autoregulation and the arteriole resistance in RHR were significantly higher than those of normal controls, and highly relate to arterial blood pressure significantly, especially pulse pressure. Conclusions　The physiology and pathology of cerebral blood flow can be evaluated conveniently and accurately by assessment of the lower limit of autoregulation and arterioles resistance with CCP.

Objective: To explore the influencing factors of slow blood flow phenomenon after emergency percutaneous coronary intervention (PCI) in patients with acute myocardial infarction (AMI). Methods: Clinical and PCI angiographic data of 488 patients, who were diagnosed as AMI and received primary PCI in our hospital from Jan 2010 to Jun 2011, were retrospectively analyzed. Patients were divided into slow blood flow group (n=51, TIMI flow ≤ grade 2) and normal flow group (n=437, TIMI flow= grade 3). Their clinical characteristics between two groups were compared. Results: Compared with normal flow group, there were significant reductions in percentages of thrombus aspiration (75.3% vs. 60.8%) and application of platelet glycoprotein IIb/IIIa receptor antagonist (81.7% vs. 68.6%) during PCI, and significant rise in total length of implanted stents [(31.8±12.2) mm vs. (35.7±12.0) mm] in slow blood flow group, P<0.05 all. Multi-factor Logistic regression analysis indicated that percentages of thrombus aspiration during PCI and total length of stents were independent influencing factors for slow blood flow (P<0.05 both). Conclusion: Percentages of thrombus aspiration and total length of stents during PCI are independent influencing factors for slow blood flow.

AIM: To study the effect of hypertensive arteriosclerosis on cerebral blood flow autoregulation (CBFA), and to introduce a new method to measure the lower limit. METHODS: The blood velocities and blood pressure was recorded simultaneously and the curves of CBFA were analyzed and classified into classical and non-classical pattern. The lower limit were determined by clinical closing pressure (CCP) and the curve CBFA. RESULTS: When the blood pressure was decreasing, the classical and non-classical pattern of the cerebral blood flow autoregulation were 25% and 75% respectively in normal SD rats, while they were 40.55% and 54.45% respectively in renovascular hypertensive rats (RHR). However, when the blood pressure was elevating, the classical and non-classical pattern were 76.47% and 23.53% respectively in SD rats, while they were all classical in RHR. Furthermore, in SD and RHR ras, the lower limits measured by CCP were well in accordance with that measured by CBFA. CONCLUSION: Hypertensive arteriosclerosis could influence the limits and the patterns of cerebral blood flow autoregulation. The lower limit of CBFA can be measured and analyzed by CCP.

Objective To evaluate the influence of renal insufficiency (RI) on long-term major adverse cardiac events (MACE) of patients with acute myocardial infarction (AMI) plus metabolic syndrome (MetS) and received percutaneous coronary intervention (PCI). Methods This was a retrospective study. From February, 2011 to Octorber, 2013 , we consecutivly enrolled 223 AMI patients with MetS in the First Affiliated Hospital of China Medical University. There were 88 patients with RI in group A, and 135 patients as the control group (group B). Patients were followed up for major adverse cardiac events (MACE) for 1 year. Results Compared with group B, the incidence of 1-year MACE of patients in group A was increased (36.4% vs. 18.5%, P= 0.003). Result of Cox proportional hazard regression analysis showed that RI was a predictive factor for 1-year MACE (HR = 3.56,95%CI 1.004 ~ 4.170, P = 0.002). Conclusion The incidence of 1-year MACE for AMI patients with RI and MetS post-PCI was high. RI was a risk factor for poor prognosis of AMI patients with MetS.

OBJECTIVETo investigate the relationship of telomerase genes and the malignant transformation of atypical mammary ductal hyperplasia.

METHODSTelomerase genes hTR and hTRT in 50 cases of mammary hyperplasia (the cases included 6 benign hyperplasia, 9 mild atypical hyperplasia, 12 medium atypical hyperplasia, 23 severe atypical hyperplasia) and 26 cases of breast carcinoma were detected by in situ hybridization.

RESULTSThe expression of hTR and hTRT mRNA were weak or negative in benign hyperplasia (1/6, 0), weaker in mild-moderate atypical hyperplasia (2/9, 1/9, 4/12, and 3/12), strong in severe atypical hyperplasia (14/23, 60.9% and 12/23, 52.1%), while very strong expression (23/26, 88.5% and 21/25, 80.8%) in carcinoma of the breast. The difference between mild-moderate atypical hyperplasia, invasive ductal carcinoma and severe atypical hyperplasia was significant (P < 0.05) and the difference between severe atypital hyperplasia and intraductal carcinoma was not significant (P > 0.05).

CONCLUSIONSTelmerase genes (hTR, hTRT) expression is closely related to the malignant transformation of atypical hyperplasia. The reactivated telomerase may play a crucial role in the development of breast cancer.

Breast Neoplasms ; enzymology ; pathology ; Carcinoma, Intraductal, Noninfiltrating ; enzymology ; pathology ; DNA-Binding Proteins ; Female ; Gene Expression ; Humans ; RNA, Messenger ; Telomerase ; genetics

OBJECTIVETo investigate telomerase gene expression in precancerous mammary lesion, such as atypical ductal hyperplasia and breast cancer and to study the relationship between expression and malignant transformation.

METHODSExpression of human telomerase genes (hTR) and human reverse transcriptase gene (hTRT) in 76 cases of mammary tissue was evaluated using in situ hybridization and included 50 cases of mammary hyperplasia, 6 of which were benign hyperplasia, 9 were mild atypical hyperplasia, 12 were moderate atypical hyperplasia, 23 were severe atypical hyperplasia and 26 were mammary cancer.

RESULTSThe expressions of hTR and hTRT mRNA were much weaker or negative in benign hyperplasia (16.6%, 0), weak to mild moderate in atypical hyperplasia (22.2%, 11.1%, 33.3%, 25.0%), strong in severe atypical hyperplasia (60.9%, 52.1%), and significantly strong in mammary cancer (88.5%, 80.8%). The difference between mild-moderate atypical hyperplasia, invasive ductal carcinoma and severe atypical hyperplasia was significant (P < 0.05) and the difference between severe atypical hyperplasia and intraductal carcinoma was not significant (P > 0.05).

CONCLUSIONTelomerase genes (hTR and hTRT) expressions are related to the transformation of atypical hyperplasia. Activated telomerase may play a role in mammary cancer development.

Breast ; metabolism ; pathology ; Breast Neoplasms ; genetics ; pathology ; DNA-Binding Proteins ; Female ; Gene Expression ; Humans ; Precancerous Conditions ; genetics ; pathology ; RNA ; genetics ; physiology ; RNA, Messenger ; analysis ; Telomerase ; genetics ; physiology