Distribution of D2S2958, D2S1769, and D18S872 alleles in a Chinese population sample.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Shuang Gao.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The Na(+) receptor that exists in the hepatoportal region plays an important role in postprandial natriuresis and the regulation of Na(+) balance during NaCl load. Thus it would be considered that a dysfunction of the hepatic Na(+) receptor might result in the elevation of arterial pressure under a condition of high NaCl diet. To elucidate this hypothesis, arterial pressure was continuously measured during three weeks of high NaCl diet (8% NaCl) in four groups of rats: (i) intact rats, (ii) rats with hepatic denervation (HD), (iii) rats with sinoaortic denervation (SAD), and (iv) rats with SAD+HD. During a 1-week normal NaCl diet period, there was no difference in arterial pressure among the four groups. A high NaCl diet had no influence on arterial pressure in intact or HD rats; however, it significantly increased by 11 +/- 3 mmHg in SAD rats. The addition of HD to SAD had no synergistic effect on arterial pressure; i.e., in SAD+HD rats, mean arterial pressure increased by 13 +/- 1 mmHg. In conclusion, sinoaortic baroreceptor, but not hepatic Na(+) receptor, has a significant role in the long-term regulation of arterial pressure on a high NaCl diet.
To investigate the mechanism of arterial pressure (AP) regulation during hypergravity, the AP response to gravitational force was examined in conscious rats and the AP was found to increase, depending on the degree of gravity load induced by centrifugation. At 20 s after application of 2, 3, or 5 G, the AP increased by 9+/-2, 20+/-3, or 24+/-3 mm Hg, respectively. The AP increase during first 60 s was suppressed by vestibular lesion or pretreatment with hexamethonium, suggesting that the vestibular system and sympathetic nerve system be involved, respectively, in the afferent and efferent pathways. To further examine the central pathway of this response, Fos expression in the brain was examined after exposure to 5 G for 90 min. Intense Fos expression was seen in the medial vestibular nucleus, paraventricular hypothalamic nucleus, autonomic nuclei in the brain stem in intact rats, but not in rats with vestibular lesion. To examine the involvement of the diencephalic nuclei in this pressor response, AP was measured under hypergravity in rats with midcollicular transection. In these rats, the AP change was minimal at 2, 3, and 5 G, indicating that nuclei rostral to the transection level were involved in the pressor response. These results indicate that output from the vestibular system project to the diencephalon, and activation of diencephalic nuclei is indispensable to the pressor response via the sympathetic nerve system.
To examine acute hemodynamic responses to microgravity (microG) in the head, we measured carotid artery pressure (CAP) and jugular vein pressure (JVP) to calculate cephalic perfusion pressure (CPP = CAP - JVP) and recorded images of microvessels in the iris to evaluate capillary blood flow velocity (CBFV) and capillary diameter (CD) in anesthetized rats during 4.5 s of microG induced by free drop. Rats were placed in 30 degrees head-up whole body-tilted (HU, n = 7) or horizontal (flat, n = 6) position. In the flat group, none of the measured variables was significantly affected by microG, whereas in the HU group, CAP, JVP, and CPP increased, respectively, by 23.4 +/- 2.6, 1.3 +/- 0.2, and 22.9 +/- 3.1 mmHg, and CBFV and CD increased, respectively, by 33 +/- 8 and 9 +/- 3%, showing an increase in capillary blood flow. To further examine the mechanisms underlying these CAP and JVP increases, another experiment was performed in which CAP and JVP were measured in anesthetized rats (n = 6) during a postural change from HU to flat. In these animals, the change in JVP was similar to that observed during actual microG, but no change in CAP was seen, indicating that the JVP increase during actual microG is caused by disappearance of the gravitational pressure gradient in the head-to-foot axis, whereas the CAP increase is not. In conclusion, actual microG elicits an increase in CPP due to a greater increase in CAP than JVP, resulting in increased capillary blood flow. Although the increase in JVP is explained by the disappearance of gravitational pressure gradient in the head-to-foot axis as a result of microG, the larger increase in CAP is not.
A new series of fine-tunable phosphite-pyridine (P,N) ligands derived from (S)-2-amino-2'-hydroxy-6,6'-dimethyl-1,1'-biphenyl and (S)-2-amino-2'-hydroxy-4,4',6,6'-tetramethyl-1,1'-biphenyl was employed in Cu(I)-catalyzed conjugate addition of diethylzinc to acyclic enones. Excellent enantioselectivities (up to 98% ee) and highly catalytic activities were achieved for a variety of acyclic enones.
Gravity acts on the circulatory system to decrease arterial blood pressure (AP) by causing blood redistribution and reduced venous return. To evaluate roles of the baroreflex and vestibulosympathetic reflex (VSR) in maintaining AP during gravitational stress, we measured AP, heart rate (HR), and renal sympathetic nerve activity (RSNA) in four groups of conscious rats, which were either intact or had vestibular lesions (VL), sinoaortic denervation (SAD), or VL plus SAD (VL + SAD). The rats were exposed to 3 G in dorsoventral axis by centrifugation for 3 min. In rats in which neither reflex was functional (VL + SAD group), RSNA did not change, but the AP showed a significant decrease (-8 +/- 1 mmHg vs. baseline). In rats with a functional baroreflex, but no VSR (VL group), the AP did not change and there was a slight increase in RSNA (25 +/- 10% vs. baseline). In rats with a functional VSR, but no baroreflex (SAD group), marked increases in both AP and RSNA were observed (AP 31 +/- 6 mmHg and RSNA 87 +/- 10% vs. baseline), showing that the VSR causes an increase in AP in response to gravitational stress; these marked increases were significantly attenuated by the baroreflex in the intact group (AP 9 +/- 2 mmHg and RSNA 38 +/- 7% vs. baseline). In conclusion, AP is controlled by the combination of the baroreflex and VSR. The VSR elicits a huge pressor response during gravitational stress, preventing hypotension due to blood redistribution. In intact rats, this AP increase is compensated by the baroreflex, resulting in only a slight increase in AP.
To evaluate changes in the cerebral circulation during acute microgravity (microG), we measured intracranial pressure (ICP), aortic pressure at the diaphragm level, and cerebral flow velocity (CFV) in anesthetized rats (n = 5) during 4.5 s of microG induced by free drop, then calculated arterial pressure at the eye level (AP(eye)) and cerebral perfusion pressure (CPP = AP(eye)-ICP), and estimated CPP-CFV relationship. The rats were placed in the flat and the 30 degrees head-up positions. In the head-up position, ICP, AP(eye), and CPP were significantly increased by 2.2 +/- 0.4, 12.3 +/- 2.0, and 10.1 +/- 1.7 mmHg respectively during microG, whereas the CFV did not change significantly. In the flat position, none of these variables were significantly affected by microG. The slope of the CPP-CFV relationship was decreased only in the head-up position, suggesting that the cerebrovascular resistance was increased by microG. These findings indicate that the change in gravitational (hydrostatic) pressure is a key factor in understanding the changes in cerebral circulation during acute microG.
As one of the causes of the space adaptation syndrome, an increased intracranial pressure due to the cephalad fluid shift is suggested. In the present study, we measured intracranial pressure (ICP), aortic pressure and cerebral flow velocity (CFV) in anesthetized rats (n=5) during 4.5 sec of microgravity induced by free drop. The rats were set at horizontal prone (Flat) and 30-degree head-up whole body tilting (HU) positions to examine the effect of gravitational pressure gradient. Then, arterial pressure at the eye level (APeye), cerebral perfusion pressure (CPP; CPP=APeye-ICP), and CPP-CFV relationship was calculated. In HU position, ICP, APeye, and CPP increased by 2.2 +/- 0.4, 12.3 +/- 2.0, and 10.1 +/- 1.7 mmHg respectively. However, CFV did not change significantly. In Flat position, none of these variables did not change significantly. In HU position the slope of CPP-CFV relationship decreased, suggesting the increased cerebral flow resistance. However, it did not change in Flat position. These results can be understood by the disappearance of gravitational pressure gradient by microgravity and the cerebral autoregulation.
Focused Ultrasound Surgery (FUS) is a promising minimally invasive technique in tissue ablation. Because of the high intensity at the ultrasound focus, a precise 3D-localization system is required to determine the site of the treating target in order to increase the efficiency and security of FUS. This paper represents a three dimensional ultrasound (3D US) localization system developed and its workflow. The system is mainly composed of imaging and image processing system, movement device and its controlling circuits, and position feedback device. The system has a maximum scan range of +/- 30 degrees with a resolution of 8 levels from 0.54' to 0.36 degrees. For a spherical shape like target, in theory, the maximum diameter is 160 mm the system can treat. The system can be used to localize precisely the treatment targets with general sizes in the suitable parts of the body in FUS.