EFFECTS OF PULSE MAGNETIC FIELD ON CHANGES OF RHEOLOGICAL PROPERTY

ＥＦＦＥＣＴＳＯＦＰＵＬＳＥＭＡＧＮＥＴＩＣＦＩＥＬＤＯＮＣＨＡＮＧＥＳＯＦＲＨＥＯＬＯＧＩＣＡＬＰＲＯＰＥＲＴＹＥＦＦＥＣＴＳＯＦＰＵＬＳＥＭＡＧＮＥＴＩＣＦＩＥＬＤＯＮＣＨＡＮＧＥＳＯＦＲＨＥＯＬＯＧＩＣＡＬＰＲＯＰＥＲＴＹＷａｎｇＴｉａｎｙｏｕ...     

STUDY ON MECHANISM OF THE BIOEFFECTS OF TRANSIENT ELECTROMAGNETIC PULSE

ＳＴＵＤＹＯＮＭＥＣＨＡＮＩＳＭＯＦＴＨＥＢＩＯＥＦＦＥＣＴＳＯＦＴＲＡＮＳＩＥＮＴＥＬＥＣＴＲＯＭＡＧＮＥＴＩＣＰＵＬＳＥＳＴＵＤＹＯＮＭＥＣＨＡＮＩＳＭＯＦＴＨＥＢＩＯＥＦＦＥＣＴＳＯＦＴＲＡＮＳＩＥＮＴＥＬＥＣＴＲＯＭＡＧＮＥＴＩＣＰＵＬＳＥＷ...     

THE FEATURES OF THE COMMON THERAPEUTIC LASERS USED IN OPTHALMOLOGY AND THEIR CLINICAL APPLICATIONS

ＴＨＥＦＥＡＴＵＲＥＳＯＦＴＨＥＣＯＭＭＯＮＴＨＥＲＡＰＥＵＴＩＣＬＡＳＥＲＳＵＳＥＤＩＮＯＰＴＨＡＬＭＯＬＯＧＹＡＮＤＴＨＥＩＲＣＬＩＮＩＣＡＬＡＰＰＬＩＣＡＴＩＯＮＳＴＨＥＦＥＡＴＵＲＥＳＯＦＴＨＥＣＯＭＭＯＮＴＨＥＲＡＰＥＵＴＩＣＬＡＳＥＲＳＵ...     

CHANGES OF 6-K-PGF_(1a) RELEASE FROM THE LUMINAL SURFACE OF DACRON SEEDED WITH AUTOLOOUS VENOUS TISSUE FRAGMENTS

ＣＨＡＮＧＥＳＯＦ６－Ｋ－ＰＧＦ１ａＲＥＬＥＡＳＥＦＲＯＭＴＨＥＬＵＭＩＮＡＬＳＵＲＦＡＣＥＯＦＤＡＣＲＯＮＳＥＥＤＥＤＷＩＴＨＡＵＴＯＬＯＯＵＳＶＥＮＯＵＳＴＩＳＳＵＥＦＲＡＧＭＥＮＴＳＣＨＡＮＧＥＳＯＦ６－Ｋ－ＰＧＦ１ａＲＥＬＥＡＳＥＦＲＯＭＴＨ...     

ADULT HUMAN ENDOTHELIAL CELL LINING PREVENTS EARLY PLATELET DEPOSITION ON VASCULAR GRAFTS IN VITRO

ＡＤＵＬＴＨＵＭＡＮＥＮＤＯＴＨＥＬＩＡＬＣＥＬＬＬＩＮＩＮＧＰＲＥＶＥＮＴＳＥＡＲＬＹＰＬＡＴＥＬＥＴＤＥＰＯＳＩＴＩＯＮＯＮＶＡＳＣＵＬＡＲＧＲＡＦＴＳＩＮＶＩＴＲＯＡＤＵＬＴＨＵＭＡＮＥＮＤＯＴＨＥＬＩＡＬＣＥＬＬＬＩＮＩＮＧＰＲＥＶＥＮＴＳＥ...     

THE SOFTWARE SIMULTION SYSTEM OF ELECTRICAL IMPEDANCE TOMOGRAPHY RECONSTRUCTION ALGORITHM USING AUTOMATIC MESHES GENERATION

ＴＨＥＳＯＦＴＷＡＲＥＳＩＭＵＬＴＩＯＮＳＹＳＴＥＭＯＦＥＬＥＣＴＲＩＣＡＬＩＭＰＥＤＡＮＣＥＴＯＭＯＧＲＡＰＨＹ　ＲＥＣＯＮＳＴＲＵＣＴＩＯＮＡＬＧＯＲＩＴＨＭＵＳＩＮＧＡＵＴＯＭＡＴＩＣＭＥＳＨＥＳＧＥＮＥＲＡＴＩＯＮＴＨＥＳＯＦＴＷＡＲＥＳＩＭ...     

PREPARATION OF COLLAGEN/HYDROXYLAPATITE COMPOSITE FILLING PLASTIC MATERIAL AND ANIMAL EXPERIMENT STUDY

ＰＲＥＰＡＲＡＴＩＯＮＯＦＣＯＬＬＡＧＥＮ／ＨＹＤＲＯＸＹＬＡＰＡＴＩＴＥＣＯＭＰＯＳＩＴＥＦＩＬＬＩＮＧＰＬＡＳＴＩＣＭＡＴＥＲＩＡＬＡＮＤＡＮＩＭＡＬＥＸＰＥＲＩＭＥＮＴＳＴＵＤＹＰＲＥＰＡＲＡＴＩＯＮＯＦＣＯＬＬＡＧＥＮ／ＨＹＤＲＯＸＹＬＡＰＡ...     

A COMPUTERIZED SYSTEM FOR ANALYSING CHAOTIC CHARACTERISTICS OF HEART PERIOD SIGNAL

ＡＣＯＭＰＵＴＥＲＩＺＥＤＳＹＳＴＥＭＦＯＲＡＮＡＬＹＳＩＮＧＣＨＡＯＴＩＣＣＨＡＲＡＣＴＥＲＩＳＴＩＣＳＯＦＨＥＡＲＴＰＥＲＩＯＤＳＩＧＮＡＬＡＣＯＭＰＵＴＥＲＩＺＥＤＳＹＳＴＥＭＦＯＲＡＮＡＬＹＳＩＮＧＣＨＡＯＴＩＣＣＨＡＲＡＣＴＥＲＩＳＴＩＣＳ...     

AN ALGORITHM OF EDGE DETECTION IN ULTRASONEC MEDICINE IMAGING BASED ON ENTROPY OPERATOR

ＡＮＡＬＧＯＲＩＴＨＭＯＦＥＤＧＥＤＥＴＥＣＴＩＯＮＩＮＵＬＴＲＡＳＯＮＥＣＭＥＤＩＣＩＮＥＩＭＡＧＩＮＧＢＡＳＥＤＯＮＥＮＴＲＯＰＹＯＰＥＲＡＴＯＲＡＮＡＬＧＯＲＩＴＨＭＯＦＥＤＧＥＤＥＴＥＣＴＩＯＮＩＮＵＬＴＲＡＳＯＮＥＣＭＥＤＩＣＩＮＥＩＭＡＧ...     

医用磁性纳米材料的制备───制备条件对有效粒径的影响

医用磁性纳米材料的制备＊制备条件对有效粒径的影响常津（天津大学生物工程研究中心，天津３０００７２）ＰＲＥＰＡＲＡＴＩＯＮＯＦＭＥＤＩＣＡＬＭＡＧＮＥＴＩＣＤＥＸＴＲＡＮＮＡＮＯＰＡＲＴＩＣＬＥＳＩＮＦＬＵＥＮＣＥＯＦＰＲＥＰＡＲＡＴＩＯＮＣＯＮＤＩＴ...     

大鼠创伤性脑损伤后细胞凋亡及NOS阳性细胞的变化

目的：探讨大鼠创伤性脑损伤后不同时相皮质、海马、隔区细胞凋亡及NOS、ChAT阳性细胞的变化。方法：采用大鼠自由落体脑损伤模型，伤后1、2、3、4、5、7、10d取脑切片，经Nissl染色，用TUNEL法检测细胞凋亡，NADPH—d组化染色观察NOS阳性细胞，ChAT免疫组化染色观察隔区ChAT阳性细胞。结果：Nissl染色可见损伤侧海马CA2、CA3区锥体细胞层细胞消失或紊乱。损伤区周围皮质凋亡细胞伤后3d达到高峰；损伤侧海马凋亡细胞伤后5d达到高峰；损伤侧隔区凋亡细胞7d达到高峰。正常侧上述脑区各时相点均未见到凋亡细胞。损伤区周围皮质、损伤侧海马和隔区iNOS阳性细胞数量明显增加。损伤侧隔区ChAT阳性神经元也明显减少。结论：大鼠创伤性脑损伤后损伤区周围皮质和损伤侧海马、隔区细胞凋亡数量的变化与伤后时程有关。伤后细胞iNOS表达增加是导致细胞凋亡的因素。     

bFGF对胚胎神经干细胞分化为神经元及神经胶质细胞的影响

本研究观察了碱性成纤维生长因子对胚胎神经干细胞生长和分化的影响。从孕 12 d大鼠胚胎神经管分离神经干细胞 ,进行体外培养 ,分为碱性成纤维生长因子组及对照组。培养过程中观察神经干细胞的生长 ,于培养第 3、5、10 d用免疫组化方法检测培养细胞神经元特异烯醇化酶和胶质纤维酸性蛋白的表达 ,以观察神经干细胞分化为神经元及神经胶质细胞的状况。碱性成纤维生长因子可明显地促进培养细胞的生长和分化。免疫组化细胞计数显示 ,培养第 3 d,特异烯醇化酶、胶质纤维酸性蛋白阳性细胞数均明显增加 ;培养第 5 d,特异烯醇化酶阳性细胞数是对照组的 1.9倍 ,胶质纤维酸性蛋白阳性细胞数为对照组的 1.6倍 ,前者表达增加明显 ;培养第 10 d,两者的阳性细胞数仍高于对照组 ,但增加不明显。不同培养时间的胞体最长突起长度也均高于对照组 ;胞体直径及表面积随培养时间延长而增大。说明 ,碱性成纤维生长因子既能促进胚胎神经干细胞的生长 ,也可促使其分化为神经元及神经胶质细胞 ,尤以神经元为明显     

体外原代培养大鼠胚胎脊髓神经细胞机械损伤后的凋亡与caspase-3的表达

为了研究体外培养大鼠胚胎脊髓神经细胞损伤前后的凋亡变化及caspase-3的表达情况,本实验建立了一个模拟脊髓横断损伤后脊髓组分-原代培养的脊髓神经细胞机械损伤模型,并用Hoechst33342/PI双染法检测脊髓神经细胞的凋亡变化,用免疫荧光染色方法检测caspase-3的表达。结果显示:(1)损伤前几乎未见凋亡的神经细胞,损伤后6 h凋亡细胞开始出现,损伤后12 h明显增多,1 d时达高峰,但损伤后3 d凋亡细胞开始呈明显下降的趋势,至损伤后7 d又开始增加,一直持续到损伤后14d;(2)相应时刻caspase-3表达趋势的改变与脊髓神经细胞凋亡趋势的变化基本相同;(3)经过caspase-3抑制剂Ac-DEVD-CHO干预后,凋亡细胞的数量与caspase-3的表达均减少,并呈剂量依赖性。以上结果提示,机械损伤可以诱发体外培养的脊髓神经细胞凋亡,且此凋亡的发生可能与caspase-3的表达有关。     

大鼠急性脊髓损伤后神经细胞凋亡及Fas和Cathepsin D的表达

目的探讨大鼠急性脊髓损伤后神经细胞凋亡及Fas、Cathepsin D的表达。方法 78只成年健康Sprague-Dawley(SD)大鼠,使用改良Allen氏法制作急性脊髓损伤模型,采用HE染色、原位末端脱氧核糖核酸转移酶介导DUTP标记法(TUNEL)对损伤脊髓组织进行标记;免疫组化方法测定Fas、Cathepsin D的表达变化。结果正常组、假手术组TUNEL、Fas、Cathepsin D阳性细胞较少见,损伤组TUNEL阳性细胞8 h明显增多,3 d达到高峰,7 d明显降低。Fas阳性表达的细胞也在8 h开始增高,3 d达到高峰,7 d下降。Cathepsin D阳性细胞数则在脊髓损伤后3 d明显增多,5 d达高峰,至观察时间点结束,未有明显衰减。结论 Fas、Cathepsin D均参与了脊髓继发性损伤的调节。     

大鼠视网膜不完全性缺血引起细胞凋亡及bcl-2表达的研究

目的 :通过结扎双侧颈总动脉造成大鼠视网膜不完全性缺血 ,用 TUNEL及免疫组化方法观察视网膜细胞凋亡和 bcl- 2的表达。结果 :缺血 1天即见节细胞层和内核层出现凋亡细胞 ,7天在外核层也出现 ;高峰时间是缺血 14天 ,术后 6 0天仍可见凋亡细胞。缺血 1天 Mul　¨ le's细胞内侧部 bcl- 2表达明显 ,7天着色区域扩大至Mul　¨ le's细胞外侧部 ,14天阳性反应局限于 Mul　¨ le's细胞内侧部 ,并且着色明显 ,持续至缺血 30天。缺血 6 0天bcl- 2表达明显减弱。结论 :细胞凋亡参与视网膜缺血损伤 ,缺血后 bcl- 2表达增强是细胞防御功能增强的体现     

Reduced redox state allows prolonged survival of axotomized neonatal retinal ganglion cells

Axonal injury to CNS neurons results in apoptotic cell death. The processes by which axotomy signals apoptosis are diverse, and may include deprivation of target-derived factors, induction of injury factors, bursts of reactive oxygen species (ROS), and other mechanisms. Our previous studies demonstrated that death of a dissociated retinal ganglion cell, an identified CNS neuron, is ROS-dependent. To better define the mechanisms by which ROS induce retinal ganglion cell death after axotomy, we studied their effects in dissociated neonatal rat retinal cultures. Postnatal day 2-4 Long-Evans rat retinal ganglion cells were retrogradely labeled with the fluorescent tracer 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine (DiI). Postnatal day 7-9 retinas were dissociated and cultured in the presence of specific ROS generating systems, scavengers, or redox modulators. Retinal ganglion cells were identified by DiI positivity and viability determined by metabolism of calcein-acetoxymethyl ester.We found that ROS scavengers protected against retinal ganglion cell death after acute dissociation, and the effects of ROS appeared to be due to shifts in the redox potential, as retinal ganglion cell survival was critically dependent on redox state, with greatest survival under mildly reducing conditions. Culture of retinal ganglion cell with the non-thiol-containing reducing agent tris(carboxyethyl)phosphine resulted in long-term survival equivalent to or better than with neurotrophic factors.Our data suggest that axotomy-associated neuronal death induced by acute dissociation may be partly dependent on ROS production, acting to shift the redox state and oxidize one or more key thiols. Understanding the mechanisms by which ROS signal neuronal death could result in strategies for increasing their long-term survival after axonal injury.     

Naturally occurring and induced ganglion cell death

Summary The retina in frogs grows continuously throughout the whole life of the animal by the addition of rings of cells at the ciliary margin. Naturally occurring neuron death cannot, consequently, be established by counting surviving neurons. A new approach, retinal wholemount autoradiography was introduced in this study to estimate cell loss occurring in the ganglion cell layer over a long period of time. ³H-thymidine injection at stage 53 (midlarval stage) labels a ring of cells, thereby marking the extent of retina formed up to the time of isotope administration. In the present study the number of neurons in the ganglion cell layer within the autoradiographically identified central retinal sector was estimated from midlarval stage to 6 months after metamorphosis in Xenopus laevis.The mean neuron number in the central retinal sector formed up to stage 53 was 17,420 and this was reduced by 20% to 13,515 by 6 months after metamorphosis. Optic nerve section at the time of isotope injection and subsequent regeneration brought about a reduction of the number of surviving neurons in the part of the retina formed up to stage 53 to 7,720, or to about 57% of the normal neuron number in an equivalent retinal area of an intact eye of the same age. A further reduction to 20% of normal neuron population was observed in retinae where the optic nerve failed to regenerate. The surviving neurons are assumed to be amacrine cells.The bulk of natural neuron loss in the retinal centre occurs during premetamorphic stages while little further loss takes place in the next 6 months suggesting that the underlying mechanism is a fine tuning of the developing retinal projections.     

The role of nitric oxide in the apoptosis of neurons in the retina of the human fetal eye

The locations of NADPH-diaphorase (NADPH-d), inducible NO synthase (iNOS), and TUNEL-immunoreactive neurons in the retina of human fetuses collected during the first to third trimesters of pregnancy were studied. High levels of NADPH-d activity were seen in the inner segments of light-sensitive cells, amacrine cells, and ganglion cells. The population of NADPH-d-positive amacrine cells included three types of neuron. Type 1 neurons were large and had sparse dendritic fields occupying the inner nuclear and outer retinal layers. Small type 2 neurons were located in the inner retinal layer. Ectopic amacrine cells, type 3, were located in the outer part of the ganglion layer. A high density of NADPH-d-positive neurons was seen in the central part of the retina, surrounding the central fovea and optic disk area. NADPH-d activity increased progressively during ontogenesis and correlated with the appearance of immunoreactive iNOS in neurons. iNOS labeled a subpopulation of amacrine and ganglion cells, which appeared at 20–21 weeks of development and reached a peak of immunoreactivity by the end of the third trimester. TUNEL-immunopositive neuron nuclei with signs of apoptotic destruction were seen at 30–31 weeks of pregnancy. The greatest apoptotic index was seen in the ganglion and amacrine cell populations. These data identify NO as a factor mediating apoptosis of neurons during the critical period of differentiation of interneuronal connections in the human retina. Director: Doctor of Biological Sciences M. A. Vashchenko Director: Doctor of Biological Sciences S. L. Kondrashov __________ Translated from Morfologiya, Vol. 129, No. 1, pp. 42–49, January–February, 2006.     

Glutathione depletion induces differential apoptosis in cells of mouse retina, in vivo

Oxidative stress affects numerous intracellular macromolecules, and may result in cell death unless precisely regulated. Unregulated oxidative stress can be controlled by various cellular defense mechanisms such as glutathione (GSH) which can critically counteract the damaging effects of oxidative stress in mammalian cells. We determined the effects of unregulated oxidative stress induced by GSH depletion on cells in mouse retina. Mice were intraperitoneally injected with buthionine sulphoximine (BSO) at 1.5 g/kg. After 0, 1, 4, and 7 days of BSO administration, retinas were excised and sections were subjected to GSH assay and terminal uridine deoxynucleotidyl nick end labeling (TUNEL) analysis. After 4 days of BSO administration, the number of TUNEL positive cells was significantly increased. However, after 7 days, TUNEL positive cells returned to the basal level. The retinal region most affected by the BSO treatment appeared to be the outer nuclear layer where the photoreceptor cells reside. Different from cells in other regions, retinal cells in the inner nuclear layer increased in their apoptosis even after the first day of BSO injection, and the increase was further potentiated after 4 days. Taken together, our studies suggested that GSH depletion may cause unregulated oxidative stress to the cells in the retina and indeed increased cell death in the retina. The cells in the inner nuclear layer seemed to be affected earlier than the cells in other layers of the retina. The GSH level in the retina may be a crucial therapeutic target in preventing blindness.     

Effect of FGFs on adult bovine Muller cells: proliferation, binding and internalization.

A new method for culturing retinal Muller cells from adult bovine tissue is described. The identification of these glial cells was based on immunocytochemical analysis of specific Muller cell markers. Cultured cells from fourth to ninth passage showed positive labelling for S 100 protein, carbonic anydrase (CAA), glutamine synthetase (GS), alpha cristallin (alpha C) and polyclonal glial fibrillary acidic protein (GFAP) antibody, but were negative for both monoclonal GFAP antibody and also for Muller cells in the retina. Investigation of the effect of acidic fibroblast growth factor (aFGF), basic fibroblast growth factor (bFGF), and epithelial growth factor (EGF) on the proliferation of the Muller cells revealed that bFGF was the most potent mitogen (EC50 = 14 pM). Binding data revealed the presence of two classes of binding sites for aFGF and bFGF: (1) a high affinity binding site (Kd of 14 pM and 27 pM for aFGF and bFGF respectively); (2) a low affinity binding site (Kd of 3.2 nM and 0.6 nM for aFGF and bFGF respectively with great variability in the number of binding sites). In addition, the cross-linking experiments revealed the presence of high molecular weight FGF receptors (110-140 kDa). After aFGF or bFGF binding to Muller cells, aFGF and bFGF-cell surface receptors were rapidly downregulated with a half-life for disappearance of 35-50 min. Internalization and degradation of 125I-bFGF bound to the Muller cell receptors did not occur at 4 degrees C. At 37 degrees C, however, there was a rapid decrease in receptor-bound 125I-bFGF due to the downregulation of bFGF receptors. Concomitantly 125I-bFGF appeared inside the Muller cells. After 2 h, 125I-bFGF began to be degraded and after 6 h three fragments of 16 kDa, 8 kDa and 5.5 kDa were discernible. Degradation of bFGF appeared to occur in the lysosomal compartment since it was inhibited by chloroquine, an inhibitor of lysosomal proteases; aFGF internalization and degradation followed the same kinetics as bFGF with the appearance of 7 kDa and 5 kDa fragments. These results suggest that Muller cells may be the target for aFGF and bFGF contained in other cells of the retina. The fact that aFGF could be released from rod outer segment by a phosphorylation-dependent mechanism, and that apical prolongation of the Muller cells is connected with the photoreceptor cells suggest that these factors may be the mediators involved in the communication between glial cells and neurons.