雌激素类似药NH1996对去卵巢大鼠海马突触素和钙结合蛋白表达的影响

采用大鼠卵巢切除 ( OVX)动物模型 ,用免疫组织化学方法结合图象分析 ,探讨雌激素、NH 1996对大鼠海马突触素及钙结合蛋白 ( Ca BP及 PV)的调节作用。图像分析表明 OVX组海马 CA1区及齿状回突触素、PV、Ca BP平均光密度及面积密度均显著低于对照组 ( P<0 .0 1) ,补充雌激素和 NH19963 5 d,这三项指标的平均光密度及面积密度均恢复至正常水平 ,与 OVX组相比 ,有显著性差异 ( P<0 .0 1)。推测雌激素、NH1996可能通过调节海马、齿状回神经元突触密度 ,改善学习记忆功能 ,缓解老年性痴呆病人的症状 ,并通过维持胞内 Ca2 + 的恒定达到保护神经元的目的。     

铁蓄积小鼠去势前后骨吸收活性的差异

目的了解小鼠在去势前与去势后,铁对骨吸收影响的差异。方法建立高铁小鼠模型,将小鼠随机分为假手术组(SHAM组)、高铁去势组(F+OVX组)、去势组(OVX组)。铁剂干预两周后去势。在去势前(雌激素存在)与去势7周后(雌激素缺乏)检测小鼠体重,血清铁蛋白;反转录聚合酶链反应(RT-PCR)检测胫骨内抗酒石酸酸性磷酸酶(TRAP)、降钙素受体(CTR)、基质金属蛋白酶9(MMP9)、组织蛋白酶K(cathepsin K)、雌激素受体α(ERα)、雌激素受体β(ERβ)表达情况,股骨远端Micro-CT三维分析,提取各组小鼠股骨骨髓细胞进行破骨细胞培养,抗酒石酸酸性磷酸酶(TRAP)染色观察破骨细胞分化情况。结果各组小鼠体重无明显差异。F+OVX组铁蛋白含量明显升高(P<0.05)。Micro-CT分析表明:雌激素存在时,正常组与铁干预组骨密度及相关指标无明显差异(P>0.05);雌激素缺乏时,与OVX组比较,F+OVX组骨量下降更为严重(P<0.05)。半定量PCR结果显示:雌激素存在时,两组TRAP、CTR、MMP9、cathepsin K基因表达无统计学差异;雌激素缺乏时,F+OVX组各基因表达水平较OVX组显著升高(P<0.05)。去势后ERβ表达下降(P<0.05),ERα无明显差异。TRAP染色显示去势前各组小鼠破骨细胞数无明显差异(P>0.05);而去势后,F+OVX组破骨细胞数明显高于OVX组(P<0.05)。结论未去势时(有雌激素),FAC对骨吸收影响甚微;去势后(无雌激素),FAC能显著增强破骨活性。     

雌激素对去卵巢大鼠脑黑质-纹状体多巴胺系统的影响

目的 :观察去卵巢 ( OVX)大鼠纹状体多巴胺 ( DA)神经递质的含量、释放及其受体活性的变化 ,并于体外进一步观察雌二醇对纹状体脑片释放 DA的作用特点。方法 :DA含量采用高效液相电化学检测器检测 ,其他采用同位素标记法。结果 :OVX鼠纹状体 DA含量明显低于正常组 ;纹状体脑片 DA释放显著减少 ;DA摄取未见改变 ;纹状体 DA受体活性在 OVX鼠是对照组的 2倍 ,在下丘脑无明显改变。体外观察到雌二醇对纹状体 DA释放作用的剂量 -效应曲线呈钟形。结论 :雌激素对脑内纹状体 DA功能有明显调节作用 ,并存在部位、剂量依赖性     

卵巢去势对骨折愈合超微结构和BMP-4基因表达的影响

目的:探索雌激素对骨折愈合超微结构和骨形态发生蛋白-4(BMP-4)基因的定位分布的影响.方法:选用健康SD大鼠,随机分为卵巢切除(OVX)组和假手术对照(S)组.制成胫骨骨折愈合模型并分别于骨折后不同时间点处死取材.通过电镜观察超微结构变化;采用原位杂交方法研究卵巢去势对BMP-4基因表达影响.结果:(1)OVX组在骨痂形态及成骨细胞和破骨细胞活性与S组比较有明显差异;(2)骨折后1～3d BMP-4m RNA表达强度:S组＜OVX组.结论:雌激素缺乏时,骨转换加快,从而BMP-4表达增多.雌激素在骨折愈合过程中起重要作用.     

围术期诱发中枢胆碱能系统功能减退的相关因素

围术期神经认知紊乱(perioperative neurocognitive disorders,PND)是指在围术期发生的神经认知功能的减退,主要表现为学习记忆等认知能力的下降[1]。大脑多个脑区广泛分布中枢胆碱能系统,不同脑区的胆碱能系统功能与学习和记忆等认知功能存在着密切联系[2]。中枢胆碱能系统功能受到围术期多种因素的损害,可能导致PND的发生。本文对围术期诱发中枢胆碱能系统功能减退的相关因素研究进展作一综述,为临床预防PND的发生提供参考。     

重组人甲状旁腺素（1-34)与雌激素对去卵巢大鼠骨代谢的影响

目的观察重组人甲状旁腺素(1-34)与雌激素单用和联用对去卵巢大鼠骨代谢的影响。方法选用雌性4月龄SD大鼠45只,随机分为5组:①假手术(Sham)8只;②去卵巢(OVX)9只;③雌激素治疗组(OVX E)10只:OVX2个月后给予苯甲酸雌二醇治疗6w;④PTH治疗组(OVX PTH)9只:OVX2个月后给予rhPTH(1-34)治疗6w;⑤雌激素与PTH联合治疗组(OVX E PTH)9只:OVX2个月后给予rhPTH(1-34)和E2联合治疗6w。观察各组大鼠胫骨近端松质骨骨小梁形态计量学参数,椎体生物力学指标及部分血清骨生化代谢指标。结果雌激素治疗组和PTH治疗组的骨静态参数均表现为骨量增加;雌激素治疗组的骨形成参数和骨吸收参数降低;PTH治疗组的骨形成指标明显升高,而骨吸收指标虽较Sham高,但较OVX组有所降低;E2与PTH联合治疗组与单用E2组和单用PTH组比较,骨量明显提高,骨转换率参数介于单用E2和单用PTH组之间。3个治疗组的生物力学指标较OVX组均有明显提高,其中E2与PTH联合治疗组改善最明显。结论雌激素和PTH可使去卵巢大鼠松质骨骨量增加和改善生物力学性能,两者联合治疗有协同作用。     

普萘洛尔对去卵巢大鼠骨密度及血清IL-6的影响

目的 探讨普萘洛尔对去卵巢大鼠骨密度及对血清IL-6水平的影响。方法 50只健康雌性未交配6个月龄SD大鼠随机分为5组,每组10只:①假手术组(sham);②去卵巢(PVX)后雌激素治疗组(O E);③OVX后普萘洛尔治疗组(O p);①OVX后雌激素 普萘洛尔治疗组(O E P);⑤OVX后安慰剂组(OVX);OVX后1周开始经灌胃给予普萘洛尔8 mg·kg-1·d-1、皮下注射17β-雌二醇20μg·kg-1·d-1,共12周。动物处死时留取第3,4,5腰椎、血清标本,进行骨密度分析及血清IL-6水平测定。结果 O P、O E P、O E组的骨密度较手术组(OVX)明显增高(P<0.05),血清IL-6较OVX组明显下降(P<0.01)。结论 普萘洛尔能有效地预防OVX大鼠的骨丢失,同时降低血清IL-6水平。     

雌激素对骨髓细胞白细胞介素-6及骨髓源性破骨细胞形成的影响

目的 观察雌激素对骨髓细胞白细胞介素-6(IL-6)及骨髓源性破骨细胞的影响.方法 将90只雌性SD大鼠均分为3组:对照组(N组)、去卵巢组(OVX组)及雌激素组(OVX+ E2组).OVX组与OVX+ E2组大鼠行双侧卵巢切除术.术后OVX+ E2组按照0.02 ml/kg的剂量每周肌肉注射苯甲酸雌二醇1次.术后第1、3、5周取骨组织培养骨髓细胞,检测骨组织培养液及血清中IL-6含量,对破骨细胞进行计数.结果 (1)术后第1、3、5周OVX组骨组织培养液IL-6含量分别为(62.01±12.38)、(95.63±16.79)、(139.00±20.11) ng/L,OVX+E2组分别为(27.99±9.59)、(30.74±10.17)、(36.29±11.28) ng/L,两组含量均高于N组(P＜0.05),且两组含量随时间逐渐增加(P＜0.05);(2)各组各时间点血清中IL-6含量差异无统计学意义(P＞0.05);(3)术后第1、3、5周OVX组破骨细胞数分别为(16.55±1.78)、(28.02±3.99)、(29.57±2.86)个/高倍视野,OVX+ E2组分别为(10.99±1.52)、(20.02±3.52)、(18.01±2.17)个/高倍视野,OVX+ E2组各时间点破骨细胞数均小于OVX组(P＜0.05),但均大于N组(P＜0.05).结论 雌激素对骨髓细胞IL-6具有一定抑制作用,但对血清中IL-6无明显影响;雌激素对骨髓源性破骨细胞形成具有一定抑制作用.     

骨质疏松发生一氧化氮机制及雌激素调控作用研究

目的　研究骨质疏松发生的一氧化氮机制及雌激素防治骨质疏松作用的一氧化氮通路 ,深入理解骨质疏松症病理过程中一氧化氮作用环节。方法　 45只SD雌性大鼠分为①假手术组(Sham组 ) ;②卵巢切除组 (OVX组 ) ;③OVX +倍美力治疗 (Premarin组 )。进行iNOS原位杂交及iNOS、eNOS免疫组化研究 ,测定其平均灰度值及平均积分光密度 (ODI)作统计指标。结果　iNOS原位杂交实验结果显示 :正常大鼠去卵巢后 ,骨髓腔内及骨小梁表面iNOSmRNA有强阳性表达 ,差异有非常显著性 (P <0 0 1) ,iNOS免疫组化实验结果也显示OVX组iNOS阳性表达明显较Sham组增加 ;而Pre marin组iNOS表达强度较OVX组明显降低 (P <0 0 5 )。OVX组与Sham组eNOS表达差异无显著性 ,Premarin组较OVX组eNOS表达强度则明显增加 (P <0 0 5 )。结论　NO是调节OB、OC功能活动的一种重要效应因子 ,NO导致细胞因子诱导性骨吸收增强与绝经后雌激素缺乏OP密切相关。雌激素可下调iNOSmRNA表达 ,抑制iNOS蛋白合成 ,从而减轻功能亢进的OC性骨吸收 ,而对骨组织正常生理活动中的eNOS合成 ,有适度促进作用 ,有利于骨组织的重建及骨量的恢复 ,从而重建骨形成 吸收新平衡偶联     

雌激素促进小儿血管瘤血管生成的体外实验研究

目的论证雌激素促进小儿血管瘤血管生成的作用。方法应用已建立的三维血管瘤血管生成体外培养模型,以雌激素及雌激素受体竞争性抑制剂三苯氧胺分组干预小儿血管瘤体外血管生成过程。实验分为四组:①组1对照组;②组2雌激素组(50pg/ml);③组3三苯氧胺组(10-6mol/L);④组4雌激素(50pg/ml) 三苯氧胺组(10-6mol/L)。比较各时间点各组间新生血管区面积的差异。结果三维血管生成模型中对照组培养2～3d后组织块芽生出细小血管,至第8～9天长成树枝状血管。培养后第3、6、9天组织块新生血管区面积组2均大组1,组4及组3均小于组2及组1(P<0.05)。结论雌激素能促进小儿血管瘤血管生成,从而促进血管瘤增殖,该过程能被三苯氧胺所阻滞。     

Changes in muscarinic cholinergic receptor and choline acetyltransferase in experimental ischemic brain

Acetylcholine (ACh) is the neurotransmitter related to learning and memory. The activity of its metabolic enzyme - choline acetyltransferase (CAT) is found to be remarkably decreased at autopsy. We consider that there is some relationship between ACh and cerebrovascular dementia such as dementia in ischemia and forgetfulness after ischemia. So we studied the relationship between ischemia and cholinergic neuron. We examined changes of muscarinic cholinergic receptor (m-ChR) in experimental ischemia by binding assay and autoradiography, and performed immunohistochemical study of CAT that is, acetylcholine synthetase, by PAP method. We also studied delayed neuronal death from the aspect of cholinergic system because the hippocampus receives ACh pathway arising from the basal nucleus. Materials used include: Pulsinelli's 4 vessel occluded rats, Tamura's MCA occluded rats and forebrain ischemia mongolian gerbils. In ischemia, the number of m-ChR decreased and binding affinity of m-ChR increased, and recirculation caused increased the number of m-ChR. While m-ChR changed immediately after ischemia, it was not until the fourth day that CAT positive cells decreased in hippocampus. In other words, at first m-ChR in postsynaptic membrane changed in ischemia, and with the progress of neuronal damage, CAT also changed. After m-ChR decreased in the thalamus, stria terminalis and Meynert nucleus 1 day following ischemia, it decreased in hippocampus after 7 days. We can consider receptor changed corresponding to the pathway of cholinergic neuron. Our study suggested that the receptor change in cholinergic system plays some role in the delayed neuronal death in the hippocampus.     

Association of learning and memory impairments with changes in the septohippocampal cholinergic system in rats with kaolin-induced hydrocephalus

OBJECTIVE: The septohippocampal cholinergic (SHC) system plays an important role in the maintenance of normal memory and learning. However, the fact that memory and learning impairments under hydrocephalic conditions are directly related to the SHC system is less well known. We investigated the relationships between pathological changes in SHC neurons and impairments in memory and learning among hydrocephalic rats. METHODS: Rats with kaolin-induced hydrocephalus were prepared with injections of kaolin suspension into the cisterna magna. Learning and memory performance was assessed with the passive avoidance and Morris water maze tests. Ventricular sizes were measured for the lateral and third ventricles. Acetylcholinesterase and choline acetyltransferase immunostaining was performed to investigate degenerative changes in cholinergic neurons in the medial septum and hippocampus. RESULTS: Hydrocephalic rats demonstrated significant learning and memory impairments in the passive avoidance and Morris water maze tests. Decreased hesitation times in the passive avoidance test and markedly increased acquisition times and decreased retention times in the Morris water maze test indicated learning and memory dysfunction among the hydrocephalic rats. The numbers of cholinergic neurons in the medial septum and hippocampus were decreased in the hydrocephalic rats. The decreases in choline acetyltransferase and acetylcholinesterase immunoreactivity were significantly correlated with enlargement of the ventricles. CONCLUSION: Impairment of spatial memory and learning may be attributable to degeneration of SHC neurons. These results suggest that learning and memory impairments in rats with kaolin-induced hydrocephalus are associated with the dysfunction of the SHC system induced by ventricular dilation.     

Human neural stem cells overexpressing choline acetyltransferase restore cognitive function of kainic acid-induced learning and memory deficit animals

Alzheimer disease (AD) is a progressive neurodegenerative disease, which is characterized by loss of memory and cognitive function. In AD patients dysfunction of the cholinergic system is the main cause of cognitive disorders, and decreased activity of choline acetyltransferase (ChAT), an enzyme responsible for acetylcholine (ACh) synthesis, is observed. In the present study we investigated if brain transplantation of human neural stem cells (NSCs) genetically modified to encode ChAT gene improves cognitive function of kainic acid (KA)-induced learning deficit rats. Intrahippocampal injection of KA to hippocampal CA3 region caused severe neuronal loss, resulting in profound learning and memory deficit. F3.ChAT human NSCs transplanted intracerebroventricularly improved fully the learning and memory function of KA-induced learning deficit animals, in parallel with the elevation of ACh levels in cerebrospinal fluid. F3.ChAT human NSCs migrated to the KA-induced injury site (CA3) and differentiated into neurons and astrocytes. The present study demonstrates that human NSCs expressing ChAT have lesion-tropic property and improve cognitive function of learning deficit model rats with hippocampal injury by increasing ACh level.     

Opposing roles for dopamine and serotonin in the modulation of human spatial working memory functions

Neurocognitive research has focused on monoaminergic influences over broad behavior patterns. For example, dopamine (DA) generally facilitates informational transfer within limbic and cortical networks to promote reward-seeking behavior. Specifically, DA activity in prefrontal cortex modulates the ability for nonhuman primates and humans to perform spatial working memory tasks. Serotonin (5HT) constrains the activity of DA, resulting in an opposing relationship between DA and 5HT with respect to emotional and motor behaviors. A role for 5HT in constraining prefrontally guided spatial working memory (WM) processes in humans has not been empirically demonstrated but is a logical avenue for study if these principles of neurotransmitter activity hold within cortical networks. In this study, normal humans completed a visuospatial WM task under pharmacological challenge with (i) bromocriptine, a DA agonist and (ii) fenfluramine, a serotonin agonist, in a double-blind, repeated-measures, placebo-controlled design. Findings indicate that bromocriptine facilitated spatial delayed, but not immediate, memory performance. Fenfluramine resulted in impaired delayed spatial memory. These effects were not due to nonspecific arousal, attentional, sensorimotor or perceptual changes. These findings suggest that monoaminergic neurotransmitters (DA and 5HT) may interact within cortical networks to modulate the expression of specific cognitive behaviors, particularly effortful processes associated with goal-directed activity.      

右美托咪定对反复缺血-再灌注脑损伤小鼠学习记忆能力的影响

目的探讨右美托咪定对反复缺血-再灌注(IR)脑损伤小鼠学习记忆能力的影响。方法无特定病原体(SPF)级成年C57BL/6J小鼠60只,按照随机数字表法分为四组:右美托咪定25μg/kg组(L组)、右美托咪定50μg/kg组(H组)、缺血-再灌注组(IR组)和假手术组(Sham组),每组15只。L组和H组小鼠分别经腹腔注射右美托咪定25μg/kg、50μg/kg,30min后采用双侧颈总动脉夹闭术,建立反复IR脑损伤模型;IR组小鼠建立反复IR脑损伤模型;Sham组小鼠只分离双侧颈总动脉,但不夹闭。Sham组和IR组小鼠于缺血前30min分别经腹腔注射等容量的生理盐水。采用Morris水迷宫试验测试小鼠术前及术后的学习记忆能力,随后处死小鼠,留取海马组织并测定其湿/干重比(W/D)和总含水量(TCW),采用伊文斯蓝(EB)法检测血脑屏障的通透性。采用逆转录-聚合酶链式反应(RT-PCR)测定海马组织Toll样受体4(TLR4)、核调节因子-κB(NF-κB)mRNA表达水平,采用Western blot测定海马组织TLR4、NF-κB蛋白含量。结果术后3、7dIR组小鼠逃避潜伏期及游泳距离均明显长于Sham组,L组和H组小鼠的逃避潜伏期及游泳距离明显短于IR组(P0.05)。IR组小鼠海马组织W/D、TCW和脑组织EB含量明显高于Sham组,L组和H组小鼠海马组织W/D、TCW和脑组织EB含量明显低于IR组(P0.05)。IR组小鼠海马组织NF-κB mRNA、TLR4mRNA和蛋白表达水平明显高于Sham组,L组和H组小鼠海马组织NF-κB mRNA、TLR4mRNA和蛋白表达水平明显低于IR组,H组小鼠海马组织NF-κB mRNA、TLR4mRNA和蛋白表达水平明显低于L组(P0.05)。结论腹腔注射25μg/kg、50μg/kg的右美托咪定均可改善反复IR脑损伤小鼠的学习记忆能力,其机制可能与其抑制海马组织TLR4和NF-κB表达、减轻脑损伤有关。     

Intraretrosplenial cortical grafts of fetal cholinergic neurons and the restoration of spatial memory function

The retrosplenial cortex (RSC) receives cholinergic afferent fibers from the medial septal nucleus and diagonal band of Broca (DBB) by way of the cingulate bundle and the fornix. Bilateral lesions of both the cingulate and fornix pathways result in a complete depletion of cholinergic input to the RSC. In the present study we have examined the effects of transplanting cholinergic neurons from fetal rat pups to the RSC of adult rats following lesions of the cingulate bundle and fornix. The animals with lesions exhibited severe spatial memory impairments with a complete loss of extrinsic cholinergic afferents to the RSC. Animals with intraretrosplenial cortical transplants exhibited significant improvements in learning and memory performance as revealed by decreased escape latencies in spatial reference memory tests, increased numbers of platform crossings in spatial navigation tests, and a higher percentage of correct choices in a spatial working memory task. These improvements appeared to be cholinergically mediated because atropine administration significantly disrupted spatial navigation performance. The survival of the transplanted cholinergic neurons and their innervation of the RSC were characterized using a monoclonal antibody to choline acetyltransferase (ChAT). The staining of graft-derived ChAT-positive fibers also revealed a pattern of innervation that mimicked that of the cholinergic input in normal animals. These results indicate that intraretrosplenial cortical transplants of cholinergic neurons can rectify spatial memory deficits produced by the loss of intrinsic cholinergic afferents from the medial septal nucleus.     

远端缺血后处理对大鼠全脑缺血再灌注损伤的影响

目的 探讨远端缺血后处理对大鼠全脑缺血再灌注损伤的影响.方法 健康成年雄性SD大鼠128只,体重为200～ 250 g,采用随机数字表法,将其随机分为4组(n=32):假手术组(S组)、缺血再灌注组(I/R组)、I/R+远端缺血后处理组(I/R+ RIPoC组)以及远端缺血再灌注组(RI/R组).采用改良的Pulsinelli四动脉阻断法建立大鼠全脑缺血再灌注模型.S组不制备全脑缺血再灌注模型;I/R+ RIPoC组于再灌注开始行双侧股动脉缺血15 min,再灌注15 min,共计3个循环;RI/R组仅行双侧股动脉缺血15 min,再灌注15 min,共计3个循环.于再灌注24、48 h时取脑组织,行海马CA1区和额叶皮层凋亡细胞计数,测定海马CA1区Bcl-2和Bax的表达水平,并于再灌注48 h测定超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的活性及丙二醛(MDA)的含量;再灌注4d时行Morris水迷宫实验;再灌注7d时取脑组织,计算海马CA1区和额叶皮层神经元密度.结果 与S组比较,I/R组再灌注时凋亡细胞计数升高,Bcl-2和Bax表达上调,神经元密度、SOD和CAT活性降低,MDA含量升高,逃避潜伏期明显延长,穿越原平台次数与第2象限停留时间百分比降低(P≤0.Ol),RI/R组上述指标差异无统计学意义(P＞0.05);与I/R组比较,I/R+ RIPoC组再灌注时凋亡细胞计数降低,Bcl-2表达上调,Bax表达下调,神经元密度、SOD和CAT活性升高,MDA含量降低,逃避潜伏期缩短,穿越原平台次数与第2象限停留时间百分比升高(P＜0.01).结论 远端缺血后处理可减轻大鼠全脑缺血再灌注损伤,其机制与抑制脂质过氧化反应,调节Bcl-2与Bax的平衡抑制细胞凋亡有关.     

Secreted Tartrate-Resistant Acid Phosphatase 5b is a Marker of Osteoclast Number in Human Osteoclast Cultures and the Rat Ovariectomy Model

Purpose: To study the effects of estrogen withdrawal on osteoclast number and osteoclast activity in the rat ovariectomy (OVX) model. Methods: We first cultured human CD34+ osteoclast precursor cells on bovine bone slices, allowing them to differentiate into mature resorbing osteoclasts. Secreted tartrate-resistant acid phosphatase 5b (TRACP 5b) and C-terminal cross-linked telopeptides of type I collagen (CTX) were determined from the culture medium. TRACP 5b correlated strongly with osteoclast number and CTX with osteoclast activity, facilitating their subsequent use in the rat OVX model. An 8 week OVX study was then performed including sham-operated rats receiving vehicle, OVX rats receiving vehicle, and OVX rats receiving 10 μg/kg/day 17β-estradiol (E2). Trabecular bone parameters were determined from the tibial metaphysis using peripheral quantitative computed tomography and histomorphometry. Osteoclast number was normalized with bone perimeter (N.Oc/B.Pm) and tissue area (N.Oc/T.Ar, indicating absolute number of osteoclasts). TRACP 5b and CTX were determined from fasting serum samples. Results: Trabecular bone parameters indicated substantial bone loss after OVX that was prevented by E2. N.Oc/B.Pm increased after OVX, while N.Oc/T.Ar and TRACP 5b decreased, and TRACP 5b correlated strongly with N.Oc/T.Ar. However, CTX values increased after OVX, and the “resorption index” CTX/TRACP 5b showed more substantial changes than either CTX or TRACP 5b alone. Conclusion: These results show that TRACP 5b is a reliable marker of osteoclast number, and the index CTX/TRACP 5b is a useful parameter in rat OVX model. The high elevation of CTX/TRACP 5b values by OVX demonstrates that estrogen withdrawal generates high activity of osteoclasts in the rat OVX model. Disclosure statement: Jukka Rissanen, Mari Suominen, and Zhiqi Peng have nothing to disclose; Jussi Halleen receives royalties from and works as a consultant of SBA Sciences, a company owned by IDS Ltd.