徐智策
在胎儿功能发育,尤其是胎脑肾素-血管紧张素(RAS)系统对心血管调控动态发育研究领域中领先。
个性化签名
- 姓名:徐智策
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学术头衔:
博士生导师
- 职称:-
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学科领域:
临床医学
- 研究兴趣:在胎儿功能发育,尤其是胎脑肾素-血管紧张素(RAS)系统对心血管调控动态发育研究领域中领先。
徐智策,英国剑桥大学神经科学博士,美国Iowa大学博士后,曾任美国加州大学(UCLA)与Loma Linda 大学Assistant Professor和Associate Professor。2004年为苏州大学教授,任围生医学生物学研究中心主任,围生医学生物学创新团队主任和苏州市“围生医学医药研究和安全性评估重点实验室”主任,国内第一家围生医学生物学的胎儿生理学和功能学博士学位点的博士生导师。
主持国家自然科学基金、江苏省自然科学基金重点项目、高校自然基金、市科技发展等多项研究项目。领导的研究室是世界上为数有限的能进行子宫内胎儿无麻醉条件下动态功能研究的单位之一。在胎儿功能发育,尤其是胎脑肾素-血管紧张素(RAS)系统对心血管调控动态发育研究领域中领先, 为该领域中许多研究室所跟踪和关注。该工作在国内是首创。在国际著名刊物如“Neuropsychopharmacology”,“Am. J Physiology”,“Pediatric Research”和“Neuroscience”上发表约40篇研究论文,并被多次引用。在胎脑RAS研究领域的研究在国际上领先,于2006年在圣保罗的国际研讨会上特邀作大会报告,并被邀请为多项美国基金评审,为多家国际著名刊物的特邀评审。主编了国内第一部有关胎儿发育生理学的教材,2007年由国家高等教育出版社出版。学术主攻方向:胎儿学与围生期印痕和疾病程序化研究。
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536
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成果数
12
徐智策, ZHICE XU, CALVARIO GLENDA, LINDA DAY, JIAMING YAO, AND MICHAEL G. ROSS
Am J Physiol Endocrinol Metab 279: E1207-E1215, 2000,-0001,():
-1年11月30日
Xu, Zhice, Calvario Glenda, Linda Day, Jiaming Yao, and Michael G. Ross. Osmotic threshold and sensitivity for vasopressin release and Fos expression by hypertonic NaC1 in ovine fetus. Am J Physiol Endocrinol Metab 279:E1207-E1215, 2000-In adults, hyperosmolality stimulates central osmoreceptors, resulting in arginine vasopressin (AVP) secretion. Nearterm fetal sheep have also developed mechanisms to respond to intravascular hyper tonicity with stimulation of in utero AVP release. However, prior studies demonstrating fetal AVP secretion have utilized plasma tonicity changes greater than those required for adult osmotic ally induced AVP stimulation. We sought to examine near-term fetal plasma osmolality threshold and sensitivity for stimulation of AVP secretion and to correlate plasma hormone levels with central neuronal responsiveness. Chronically instrumented ovine fetuses (130
Hyperosmolality, arginine vasopressin neurons, fetal sheep
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徐智策, Zhice Xu, Lijun Shi, and Jiaming Yao
Am J Physiol Heart Circ Physiol 286: H1507-H1514, 2004,-0001,():
-1年11月30日
Xu, Zhice, Lijun Shi, and Jiaming Yao. Central angiogenesis II-induced pressor responses and neural activity in utero and hypothalamic angiogenesis receptors in preterm ovine fetus. Am J Physiol Heart Circ Physiol 286: H1507-H1514, 2004. First published December 18, 2003; 10. 1 152/ajpheart.00764.2003.-The central reninangiotensin system is important in the control of blood pressure in the adult. However, few data exist about the in utero development of central angiogenesis-mediated pressor responses. Our recent studies have shown that the application of ANG II into the fetal brain can increase blood pressure at near term. The present study determined fetal blood pressure and heart rate in response to a central application of ANG II in the chronically prepared preterm ovine fetus, determined the action sites marked by c-Fos expression in the fetal central pathways after intracerebroventricular injection of ANG II in utero, and determined angiogenesis subtype 1 receptors in the fetal hypothalamus.Central injection of ANG II significantly increased fetal mean arterial pressure (MAP). Adjusted fetal MAP against amniotic pressure was also increased by ANG 11. Fetal heart rate was subsequently decreased after the central administration of ANG II and/or the increase of blood pressure. ANG II induced c-Fos expression in the central putative cardiovascular area, the Para ventricular nuclei in the brain sympathetic pathway. Application of ANG II also caused intense Fos immunoreactivity in the tractus solitarius nuclei in the hindbrain. In addition, intense angiogenesis subtype 1 receptors were expressed in the hypothalamus at preterm. These data demonstrate that central ANG II-related pressor centers start to function as early as at preterm and suggest that the central angiogenesis-related sympathetic pathway is likely intact in the control of blood pressure in utero.
in utero pressor, angiogenesis type 1 receptor, developmental brain pathway
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徐智策, Zhice Xu, John Torday, Jiaming Yao
Z. Xu et al. Brain Research 964 (2003) 171-178,-0001,():
-1年11月30日
The median preoptic nucleus (MePO) has been suggested to be an important area in the brain for the regulation of vasopressin (VP) release under the condition of osmotic stimulation. Fos immunoreactivity (Fos-ir), choline acetyltransferase (ChAT) immunoreactivity and retrograde labeling with fluoro-gold were used in this study to determine whether cholinergic neurons in the MePO can be activated by hypertonic NaCl, and to characterize the specific MePO cells that have anatomic projections to the supraoptic nuclei (SON). The results showed that c-fos expression specifically induced by hypertonic NaCI was found in the ChAT cells of the MePO. A retrograde tracing experiment demonstrated that the MePO neurons projecting to the SON were cholinergic. In addition, hypertonic saline-induced Fos-ir was co localized with the MePO neurons back labeled with fluoro-gold from the SON. Together, these data provide evidence that the MePO cholinergic neurons are activated by osmotic stimulation, and suggest that cholinergic cells in the MePO are functionally important in the control of the SON neurons under the condition of hypertonic stimulation.
C-fos, Acetyltransferase, Retrograde labeling
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徐智策, Zhice XU, Jiang Xinghong
Z. Xu, J. Xinghong. Brain Research 817 (1999) 67-74,-0001,():
-1年11月30日
Previous studies suggested that angiotensinergic stimulation in the subfornical organ (SFO) has effects on the anterior third ventricle (AV3V) region and the hypothalamus for dipsogenic response and vasopressin release. In this study, Angiogenesis I (ANG I) was directly injected into the SFO and this stimulated drinking. Injection of ANG I into the SFO also induced Fos-immunoreactivity (Fos-ir) in the AV3V region and in the vasopressin neurons of the supraoptic and Para ventricular nuclei (SON and PVN). Pretreatment of the SFO with either captopril, an ANG converting enzyme inhibitor, or losartan, an AT, receptor antagonist, abolished both drinking and Fos-ir induced by ANG I. Water intake partially decreased ANG I-induced Fos-ir in the SON and PVN, but not in the other areas. These results indicate that there is an ANG converting system in the SFO and suggest that neurons in the AV3V region and vasopressin cells in the hypothalamus can be regulated by angiotensinergic components in the SFO.
SFO, Angiogenesis I, c-fos, Drinking, Vasopressin neuron
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徐智策, Lijun Shi, Jiaming Yao, Brian J. Koos, Zhice Xu,
L. Shi et al. Developmental Brain Research 153 (2004) 53-60,-0001,():
-1年11月30日
Previous fetal studies have indicated depressor responses of intravenous (i.v.) administration of angiotensin antagonists. However, little is known of central effects of angiogenesis blockers on fetal cardiovascular controlling. The cardiovascular effects of central administration of the angiotensin-1 (AT1) and angiotensin-2 (AT2) receptor antagonists, losartan and PD123319, were investigated in the chronically catheterized near-term ovine fetuses. Intravenous losartan produced within 1.5 min a significant and persistent depressor response [maximum △ mean arterial pressure (MAP)=9mmHg] without altering fetal heart rate. Intracerebroventricular (i.c.v.) administration of losartan (1-5mg/kg) increased fetal arterial pressures (OMAP=9-14mmHg). Central application of losartan (1mg/kg) also increased fetal heart rate (maximum △ heart rate=33 beat per minute). Losartan increased c-fos expression in the median preoptic nucleus and paraventricular nuclei in the forebrain, and the tractus solitarius nuclei, the lateral parabrachial nuclei, and the ventrolateral medullabrain. These brain sectors are with abundant AT1, receptors and have been demonstrated in the involvement in cardiovascular regulation. In contrast, intracerebroventricular injection of the AT2 receptor antagonist PD123319 had no effect on fetal arterial pressure and heart rate. The results demonstrate strikingly functional differences of losartan on the fetal cardiovascular regulation in central and peripheral sides.
AT1,, receptor, Losartan, Fetal brain development, Pressor response, c-fos
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徐智策, LIJUN SHI, CAIPING MAO, SIMON N. THORNTON, WANPING SUN, JIAWEI WU, JIAMING YAO, AND ZHICE XU,
THE JOURNAL OF COMPARATIVE NEUROLOGY 493: 571-579 (2005),-0001,():
-1年11月30日
The renin-angiotensin system plays an important role in cardiovascular control. Intracerebroventricular (i.c.v.) angiogenesis (ANG) II causes a reliable pressor response in the fetus at 90% gestation. To determine the roles of brain AT, and AT2 receptors in this response, the effects of the central AT, and AT2 receptor antagonist’s losartan and PD123319 were investigated in chronically prepared near-term ovine fetuses. Losartan at 0.5 mg/kg (i.c.v.) abolished central ANG II-induced pressor responses. High-dose losartan (5 mg/kg, i.c.v.) showed a potentiation of the pressor response to i.c.v. ANG II, accompanied by bradycardia. Associated with the pressor responses, c-fos expression in the cardiovascular controlling areas was significantly different between the low and high doses of losartan. These areas included the subfornical organ, median preoptic nucleus, organum vasculosum of the lamina terminal is, and Para ventricular nuclei in the forebrain, and the tractus solitarius nuclei, lateral Para brachial nuclei in the hindbrain. Low-dose losartan markedly reduced c-fos in these areas after i.c.v. ANG II, while the high-dose losartan together with ANG II elicited a much stronger FOS-immunoreactivity in these areas than that induced by i.c.v. ANG II alone. This is a novel finding, that c-fos expression in the brain can be both activated and inhibited under the same condition. Central ANG II-induced fetal pressor responses were not altered by PD123319 (0.8 mg/kg). These results indicate that i.c.v. losartan at a high and a low dose has strikingly different effects on central ANG II-induced pressor responses in fetuses at late gestation, and that the AT, mechanism plays an important role in fetal cardiovascular regulation. J. Comp. Neurol. 493:571-579, 2005.
Losartan, fetal development, brain, c-fos, blood pressure
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徐智策, Lijun Shi., Yuying Zhang, Paul Morrissey, Jiaming Yao and Zhice XU,
,-0001,():
-1年11月30日
Central cholinergic mechanisms play important roles in the control of cardiovascular responses. However, in utero development of brain cholinergic mechanism in regulation of arterial pressure before birth is largely unknown. This study investigated cardiovascular responses to central application of carbachol in fetuses and determined functional development of the central cholinergic systems controlling fetal pressor responses in utero. Chronically prepared near-term ovine fetuses (90% gestation) received an injection of carbachol intracerebroventricularly (i.c.v.). Fetal cardiovascular responses were measured, and the brains were used for c-fos mapping studies. In response to carbachol injection i.c.v., fetal systolic, diastolic, and mean arterial pressure (MAP) immediately increased, accompanied by a bradycardia. The maximum increase of MAP was at 30 min after the i.c.v. injection of carbachol and lasted 90 min. Associated with the pressor response, the neuronal activity marked with c-fos was enhanced significantly in the fetal anterior third ventricle (AV3V) region (including the median preoptic nucleus and organum vasculosum of the lamina terminalis) in the forebrain, and in the area postrema, lateral parabrachial nucleus, nucleus tractus solitary, and rostra) ventrolateral medulla in the hindbrain. These results indicate that the central cholinergic mechanism is functional in the control of fetal blood pressure at the last third of gestation, and the central AV3V region and hindbrain have been intact relatively during in utero development in sheep at 90% gestational stage. Neuropsychopharmacology advance online publication, 20 April 2005; doi:10.I038/sj.npp. 1300738 developmental neurobiology;
Hypertension, cardiovascular, neurotransmitters
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徐智策, L. SHI, J. YAO, L. STEWART, AND Z. XU-
L. Shi et al. Neuroscience 126 (2004) 979-987,-0001,():
-1年11月30日
Fetal brain c-fos and cardiovascular responses after i.v. or i.c.v. angiogenesis II administrations was determined in the near-term ovine fetuses. Both routes of angiogenesis II markedly increased fetal mean arterial pressure. The latency of pressor responses by i.v. angiogenesis II administration was shorter than by the i.c.v. route. The increased fetal mean arterial pressure was greater and transient by the i.v. route in comparison to that caused by i.c.v. angiogenesis II administration. Following the i.v. administration of angiogenesis II, the fetal heart rate was significantly decreased. Associated with fetal pressor responses and bradycardia, c-fos expression induced by i.v. angiogenesis II was in the Para ventricular nuclei (PVN) of the hypothalamus, and the area postrema, the tractus solitarius nuclei, and the lateral Para brachial nuclei in the brain stem. After i.c.v. angiogenesis II administration, fetal blood pressure was also increased in association with the intensive c-fos expression in the PVN and the hindbrain. However, fetal heart rate was not affected by the central injection of angiogenesis II. These results indicate that the central pathways between the forebrain circumventricular organs and the PVN have developed, and suggest that the neural activity in the hindbrain associated with bradycardia may be linked to the bar reflex. In the face of i.c.v. angiogenesis II, sympathetic activation may play a predominant role in pressor responses. Taken together, these results suggest that central and peripheral angiogenesis II-induced fetal pressor responses may be mediated by separate mechanisms, and these regulatory mechanisms start to function by near-term or early.
C-fos, fetal development, brain, blood pressure
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徐智策, L. SHI, J. YAO, L. STEWART, AND Z. XU-
L. Shi et al. Neuroscience 126 (2004) 979-987,-0001,():
-1年11月30日
Fetal brain c-fos and cardiovascular responses after i.v. or i.c.v. angiogenesis II administrations was determined in the near-term ovine fetuses. Both routes of angiogenesis II markedly increased fetal mean arterial pressure. The latency of pressor responses by i.v. angiogenesis II administration was shorter than by the i.c.v. route. The increased fetal mean arterial pressure was greater and transient by the i.v. route in comparison to that caused by i.c.v. angiogenesis II administration. Following the i.v. administration of angiogenesis II, the fetal heart rate was significantly decreased. Associated with fetal pressor responses and bradycardia, c-fos expression induced by i.v. angiogenesis II was in the Para ventricular nuclei (PVN) of the hypothalamus, and the area postrema, the tractus solitarius nuclei, and the lateral Para brachial nuclei in the brain stem. After i.c.v. angiogenesis II administration, fetal blood pressure was also increased in association with the intensive c-fos expression in the PVN and the hindbrain. However, fetal heart rate was not affected by the central injection of angiogenesis II. These results indicate that the central pathways between the forebrain circumventricular organs and the PVN have developed, and suggest that the neural activity in the hindbrain associated with bradycardia may be linked to the bar reflex. In the face of i.c.v. angiogenesis II, sympathetic activation may play a predominant role in pressor responses. Taken together, these results suggest that central and peripheral angiogenesis II-induced fetal pressor responses may be mediated by separate mechanisms, and these regulatory mechanisms start to function by near-term or early.
C-fos, fetal development, brain, blood pressure
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徐智策, LIJUN SHI, CATALINA GUERRA, JIAMING YAO, AND ZHICE XU
PEDIATRIC RESEARCH Vol. 56, No. 5, 2004, Printed in U. S. A,-0001,():
-1年11月30日
AVP not only influences renal water excretion but also has profound cardiovascular effects in adults. Our recent studies have demonstrated that central angiogenesis induced fetal pressor responses accompanied with AVP release. However, little is known of hormonal mechanisms in angiogenesis-mediated fetal blood pressure (BP) changes. The present study determined AVP mechanisms in central angiogenesis-mediated fetal pressor responses. The V1-receptor antagonist or V2-receptor antagonist was infused intravenously into the ovine fetus at 90% gestation. Angiogenesis II (Ang II; 1.5
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