甲状腺C细胞腺瘤1例

患者男性 ,34岁。因颈部包块逐渐长大 1年入院。包块不红不痛 ,患者亦无怕热、多汗、心悸及食欲亢进等表现。平时体健 ,无结核病史。血清Ｔ3、Ｔ4 及ＴＳＨ均正常 ,行左侧甲状腺肿瘤切除术。　　病理检查　灰白色卵圆形包块大小 5 5ｃｍ× 5 2ｃｍ× 4ｃｍ ,表面光滑 ,包膜完整。切面为单房囊性 ,囊腔直径约 3ｃｍ ,内含褐色液体 ,囊壁灰白质细 ,均匀一致。镜下见瘤细胞呈卵圆形或类圆形 ,胞质染色浅 ,近透明状 ,均质性。细胞间境界不清 ,胞核淡染 ,与甲状腺滤泡旁细胞 (Ｃ细胞 )相似。瘤细胞被少量纤维组织分割成巢状或片团状。免疫表型 …     

金黄地鼠甲状腺滤泡旁细胞内晶样体的超微结构

在金黄地鼠（包括胎鼠、新生鼠、幼鼠及青年鼠）甲状腺滤泡旁细胞的胞质内发现一种晶样体。其与线粒体膜紧相贴邻，直径０．３～１．０μｍ，长０．５～８．０μｍ。每个晶样体由８～２０条平行且间距相似的纤维样结构组成，其直径为２０～２５ｎｍ。     

甲状腺滤泡旁细胞的研究进展

甲状腺滤泡旁细胞是甲状腺中产生降钙素的细胞。但作为ＡＰＵＤ系的甲状腺滤泡旁细胞也有分泌多种调节肽的功能。本文对甲状腺滤泡旁细胞分泌调节肽的种类，分泌调节肽的基因机制以及调节肽的作用机制的研究进行综述     

松果体切除对金黄地鼠甲状腺滤泡旁细胞超微结构的影响

通过切除金黄地鼠松时体及补充褪黑素的模型观察了甲状腺滤光旁细胞的超微结构变化。与对照组和假手术组相比，切除松果体１ｈ后的甲状腺滤泡旁细胞内有发达的高匀基复合体及粗面内质网，并可见许多分泌前颗粒。补充褪黑素１ｈ后，甲状腺滤泡旁细胞内高尔基复合体发育不良，分泌前颗粒较少。这些结果表明松果体能抑制甲状腺滤泡旁细胞的分泌活动。     

氢化考的松对大鼠甲状腺滤泡上皮细胞的影响—超微结构观察和形…

应用超微结构观察和形态计量学方法对氢化考的松引起大鼠甲状腺滤泡上皮细胞的形态学变化作了研究。发现实验组的甲状腺滤泡细胞中线粒体的体积密度和数目密度均明显减小，微绒毛和胶质颗粒的数目也明显减少。细胞中粗面内质网和高尔基复合体不如对照组中发达。实验结果提示：外源性氢化考的松可以抑制甲状腺滤泡细胞的功能活动。文中对其形态变化和功能之间的关系等问题进行了讨论。     

氢化考的松对大鼠甲状腺滤泡上皮细胞的影响——超微结构观察和形态计量分析

应用超微结构观察和形态计量学方法对氢化考的松引起大鼠甲状腺滤泡上皮细胞的形态学变化作了研究.发现实验组的甲状腺滤泡细胞中线粒体的体积密度和数目密度均明显减小,微绒毛和胶质颗粒的数目也明显减少.细胞中粗面内质网和高尔基复合体不如对照组中发达.实验结果提示:外源性氢化考的松可以抑制甲状腺滤泡细胞的功能活动.文中对其形态变化和功能之间的关系等问题进行了讨论.     

贫铀通过内质网应激诱导甲状腺损伤

目的 探究贫铀(DU)诱导甲状腺损伤的机制,并探索其防治方法。方法 将大鼠甲状腺细胞FRTL-5分别用500μmol/L的贫铀溶液作用不同时间,用CCK-8法检测细胞活力。将FRTL-5细胞暴露于不同浓度的贫铀,用Annexin V-FITC/PI染色法检测细胞凋亡情况,用Western blot检测葡萄糖调节蛋白78(GRP78)的表达,用免疫荧光染色法检测转录激活因子6(ATF6)的表达。将FRTL-5细胞暴露于500μmol/L的4-苯基丁酸(4-PBA),用CCK-8法检测细胞活力。将FRTL-5细胞分为对照组、DU组和4-PBA+DU组,分别进行相应的处理后,用CCK-8法检测细胞活力。结果 贫铀导致了FRTL-5细胞活力下降和细胞凋亡;贫轴诱导FRTL-5细胞GRP78和ATF6表达增加;500μmol/L的4-PBA对FRTL-5细胞的活力没有影响;4-PBA预处理缓解了贫轴诱导的细胞活力的下降。结论 贫铀通过内质网应激诱导甲状腺细胞损伤,靶向内质网应激的治疗可能具有缓解贫铀导致的甲状腺损伤的作用。     

心理应激对大鼠下丘脑室周核生长抑素mRNA神经元的影响

目的：探讨心理应激因素对下丘脑室周核生长抑素ｍＲＮＡ阳性神经元的影响。材料和方法：采用心理应激大鼠模型，以原位杂交组织化学及图像分析技术，检测下丘脑室周核生长抑素ｍＲＮＡ阳性神经元的表达程度和神经元体积密度及单位体积细胞数密度的变化。     

心理应激对脂质代谢影响的研究进展

脂蛋白代谢紊乱引发的高脂血症 ,在动脉粥样硬化 (AS)的发生和发展中发挥重要作用。研究表明 ,无论是急性还是慢性心理应激都可能导致血浆脂质升高 ,出现致AS脂质相改变。应激引起血浆脂质升高的机制尚不十分清楚 ,目前公认的有两种影响机制 ,即脂解模型和血液浓缩假说     

心理应激对血糖及胰岛素分泌的影响

目的了解心理应激对胰岛素分泌及血糖的影响.方法以健康男大学生为研究对象,采用速算作业使学生产生心理应激,测定应激前后空腹血糖及血清胰岛素值.结果心理应激后血糖较应激前明显增加(t=3.81,p<0.001),血清胰岛素浓度及胰岛素敏感指数较应激前降低(t=4.23,p<0.001);肥胖学生应激所致的血糖增加值较体型正常学生大;应激所致的血糖改变量与胰岛素的改变量呈负相关(r=-0.308,p<0.05).结论心理应激可使健康学生血糖增加;肥胖可增大心理应激的升血糖作用.     

Studies on localization of calcitonin gene-related peptide (CGRP) in the thyroid-parathyroid complex

Summary Calcitonin gene-related peptide (CGRP) was localized by an immunocytochemical technique in the thyroid-parathyroid complexes of rat, guinea pig, rabbit, and in normal human thyroids and parathyroids. Human medullary carcinomas and parathyroid adenomas were also studied. In man and all animal species examined CGRP was present in the parafollicular cell, however, in guinea pigs only in small amounts. Except in rabbits, presence of CGRP was demonstrated in nerves of the thyroid and parathyroid capsule as well as in the nerve fibers of the capsular blood vessels. In the thyroid of guinea pigs CGRP was also noted in nerve fibers and in blood vessel walls between follicles. CGRP was also present in the parathyroid glands of rat and man, in nerve fibers localized between parathyroid cells. In rabbit the parafollicular cells between parathyroid cells also expressed CGRP immunoreactivity. No CGRP was noted in the parathyroids of the guinea pig. The proximity of parathyroid cells and CGRP containing tissue structures suggests a role for CGRP in the modulation of parathyroid hormone secretion. The importance of these regulatory mechanisms appear to be different in individual species.M. Dietel is a visiting Professor from the Institute of Pathology, University of Hamburg, Federal Republic of Germany     

Effects of calcitonin on the brain of aged rats

We have recently demonstrated that calcitonin, a putative neuromodulator, may influence extrapyramidal motor system by decreasing nigro-striatal dopaminergic function. Since calcitonin is extensively used in aged patients, we have investigated whether calcitonin might influence extrapyramidal motor behavior (haloperidol-induced catalepsy and apomorphine-induced hyperactivity) in rats of different ages. Intracerebroventricular injection of salmon calcitonin (I μg/kg) prevented apomorphine-induced hyperactivity in 2, 7, 18 or 21 month old rats, but potentiated haloperidol-induced catalepsy only in 2 or 7 month old rats. In addition, in all the animals salmon calcitonin significantly decreased the secretion of prolactin, an anterior pituitary hormone that may act at central level enhancing nigro-striatal dopaminergic activity.     

Oxidative damage and HSP70 expression in masseter muscle induced by psychological stress in rats

Psychological stressors are generally associated with masseter muscle dysfunction and disorders in emotional response. In addition, oxidative states and HSP70 expression, which are involved in the physical and pathological changes of the masseter muscle, could be altered in the stressed tissues and organs. However, the link between psychological stress and the redox homeostasis or the expression of HSP70 in masseter muscles in rats has not been examined. Therefore, we used a communication box paradigm to induce psychological stress in rats. The successful establishment of the animal model was evidenced by an increase in plasma corticosterone and adrenocorticotropic hormone (ACTH). Meanwhile, the stressed rats showed a decrease in the number of entries on open arms, percentage of time spent in open arms, and distance moved in the elevated plus-maze test. The stressed rats also displayed a decrease in the time spent in the center zone, active velocity, and the distance moved in the open-field test. These results demonstrate affective-like behavioral changes in the stressed rats. Moreover, compared with the control rats, a decrease in SOD, GSH-Px and catalase activities and an increase in MDA content were observed in the masseter muscles in stressed rats after 3 weeks and 5 weeks, and the HSP70 expression was elevated in muscles in the rats exposed to stress for 5 weeks. These results indicate that psychological stress induces oxidative damage and up-regulates the expression of HSP70 in masseter muscles in rats, which are associated with behavior resembling anxiety.     

高压氧疗法对大鼠心理应激条件下的牙周炎治疗效果观察

目的:探讨心理应激对大鼠实验性牙周炎的影响,观察高压氧(hyperbaric oxygen,HBO)治疗对心理应激相关牙周炎的疗效。方法:清洁级4周龄雄性Wistar大鼠80只,随机分为4组:(1)正常对照组;(2)牙周炎组:用浸有牙龈卟啉单胞菌株的丝线结扎左侧上颌第2磨牙牙颈部,复制实验性牙周炎模型;(3)单纯应激组;(4)牙周炎+应激组。于实验后第9周停止应激刺激,对除正常对照组外其它各组大鼠每组选取4只进行HBO治疗。于实验后2、4和8周末分批处死动物,每组处死4只,于实验后10周末处死动物,每组处死8只。采血检测血糖浓度、血浆促肾上腺皮质激素(ACTH)、皮质类固醇和肾上腺素含量。测量术区的牙周附着情况,制作牙体牙周联合切片,观察牙周的组织学改变。结果:检测应激标记物的变化可见单纯应激组的血糖及血浆ACTH、皮质类固醇和肾上腺素含量在实验后第2、4周明显高于正常对照组和牙周炎组(P0.01),第8周时血糖降至正常水平,但血浆ACTH、皮质类固醇和肾上腺素含量仍高于正常对照组和牙周炎组(P0.05);牙周炎+应激组在实验后第2、4和8周血糖及血浆ACTH、皮质类固醇和肾上腺素含量均高于正常对照组和牙周炎组(P0.05);HBO治疗组牙周炎+应激组血糖明显低于非治疗组(P0.01),单纯应激组和牙周炎+应激组血浆ACTH、皮质类固醇和肾上腺素水平显著下降(P0.01)。大体观察可见正常对照组及单纯应激组牙周附着位置正常;牙周炎组出现牙龈萎缩,附着丧失明显;牙周炎+应激组附着丧失明显,根分叉暴露,HBO治疗后,牙龈水肿减轻,牙周袋变浅。单纯应激组与正常对照组在各时点的牙周附着水平的差异不显著(P0.05);牙周炎+应激组附着丧失程度在各时点均明显高于牙周炎组(P0.01);HBO治疗结束后牙周炎组及牙周炎+应激组牙周附着丧失程度减轻(P0.01)。组织学观察可见牙周炎+应激组牙周组织破坏程度在各时点均重于牙周炎组;经HBO治疗后,牙周组织炎症程度减轻,炎症细胞浸润减少。结论:心理应激可加重牙周炎进程。HBO对大鼠实验性牙周炎及心理应激相关牙周炎均有治疗效果。     

心理应激后大鼠腺垂体促甲状腺素细胞的定量观察

目的　探讨心理应激对腺垂体促甲状腺素细胞的影响。方法　采用心理应激模型 ,并在不同应激条件下对大鼠腺垂体促甲状腺素细胞进行免疫组织化学和电镜观察 ,并用体视学公式作定量分析。结果　应激大鼠促甲状腺素细胞体积密度 (Vv)和数密度 (Nv)的值均低于正常对照组 ,且在不同应激条件的A、B、C三组存在显著差别。结论　心理应激可不同程度地抑制大鼠腺垂体促甲状腺素细胞合成和分泌促甲状腺素。     

慢性心理应激对大鼠实验性牙周炎及血清乳酸脱氢酶1的影响

目的: 通过建立大鼠实验性牙周炎模型,探讨慢性心理应激影响牙周炎的致病机制。方法: 清洁级4 周龄雌性Wistar大鼠80只,随机分为4组:(1)正常对照组;(2)实验性牙周炎组:用浸有牙周致病菌的丝线结扎左侧上颌第二磨牙牙颈部复制牙周炎模型;(3)单纯应激组:牙周不作特殊处理,给予应激刺激;(4)牙周炎+应激组:按上法复制牙周炎模型,并予以应激刺激。各组动物分别于实验后第2、4、6和8 周分批处死,各时点每组处死动物5只。大鼠处死前尾静脉采血检测血糖浓度、心脏采血检测血清促肾上腺皮质激素(ACTH)、乳酸脱氢酶(LDH)及其同工酶LDH1。制作组织切片,HE染色观察大鼠左侧上颌第二磨牙牙周组织的炎性变化及牙槽骨的吸收情况。结果: (1)单纯应激组及牙周炎+应激组血糖及血清ACTH水平在2和4 周时明显高于正常对照组和实验性牙周炎组(P<0.01),牙周炎+应激组在6和8周时血糖及血清ACTH水平仍较正常对照组和实验性牙周炎组高(P<0.01);(2)牙周炎+应激组血清LDH水平在各时点明显高于正常对照组和实验性牙周炎组(P<0.01),牙周炎+应激组血清LDH1水平在各时点均明显低于正常对照组和实验性牙周炎组(P<0.01);(3)组织学观察显示与正常对照组和单纯应激组牙龈及牙槽骨均无明显改变;牙周炎+应激组牙龈组织的炎症及牙槽骨破坏程度在4、6和8周时明显高于牙周炎组。结论: 应激刺激可能通过降低牙周组织氧代谢水平加重大鼠牙周炎症程度。     

Ultrastructural study of poorly differentiated medullary carcinoma of the thyroid

Summary Five cases of sporadic medullary carcinoma of the thyroid (MTC) with rapidly progressive disease were studied ultrastructurally. The tumour cells had poorly differentiated C cell characteristics. They exhibited smaller secretory granules in their narrow cytoplasm. Morphometric analysis disclosed that the average diameter of the secretory granules of the cases with a poor prognosis was 173.0 nm in comparison with 254.2 nm of well differentiated cases. The granules were fewer in the poor prognostic group (1.31/µ²) than the well differentiated group (2.75/µ²). Increased free ribosomes and polysomes were noted in the cytoplasm and dispersed chromatin in the nuclei. These cases should be therefore classified as poorly differentiated MTC rather than atypical or anaplastic MTC.     

Ultrastructural demonstration of calcitonin in osmium-fixed human medullary carcinoma of thyroid by the protein A-colloidal gold technique

Summary In two medullary carcinomas of the thyroid gland two types of secretory granules were found electron microscopically in the cytoplasm of the tumour cells. The sizes of the granules in one case ranged 103–345 nm in diameter; they were round in shape, and they co-existed in the same tumour cell. They could not, therefore, be distinctively subdivided into two types. In another case, secretory granules in the cytoplasm closely resemble EC granule in morphology. Using the protein A-colloidal gold (PAG) technique the content of secretory granules could be identified as calcitonin irrespective of their sizes or morphology. Immunoreactivity at the ultrastructural level was fairly well preserved even in the osmium-fixed tumour cells. The labelling index, expressed as a mean number of gold particles per unit square area of the secretory granule, was higher in the non-osmium-fixed tumour cells than in the osmium-fixed. Non-osmium-fixed tumour cells embedded either in epoxy or methacryl resin were almost equally labelled with gold particles. The result indicates that the PAG method is practicable to demonstrate the ultrastructural localization of calcitonin even in the osmium-fixed, epoxy resin embedded material.     

海洛因依赖对大鼠甲状腺降钙素阳性细胞及血清FT_3、FT_4、促甲状腺素的影响

目的探讨海洛因依赖对大鼠甲状腺C细胞表达降钙素(CT)及血清FT3、FT4、促甲状腺素(TSH)的影响。方法成年雄性SD大鼠55只,随机分为正常对照组、盐水对照组及海洛因依赖组。皮下注射海洛因建立海洛因依赖大鼠模型,分别于模型建立的第10、17、24、31、38天取甲状腺组织。采用免疫组织化学SABC法、细胞计数、图像分析方法及化学发光法技术进行研究。结果与正常对照组及生理盐水对照组比较,海洛因依赖组大鼠甲状腺内CT阳性细胞免疫染色强度减弱,细胞数量减少(P0.05);平均灰度值显著升高(P0.05),且呈逐渐增高趋势。海洛因依赖期间,血清TSH浓度与正常对照组比较,差异无统计学意义(P0.05)。海洛因依赖10、17d,血清FT3浓度较正常对照组降低(P0.05)。海洛因依赖期间,血清FT4浓度较正常对照组有所升高,在24d和38d增高明显(P0.05)。结论海洛因依赖期间,大鼠甲状腺CT阳性细胞数量减少,分泌功能减退。血清FT3浓度有所降低,FT4浓度有所升高,TSH浓度无明显变化,提示海洛因依赖可能使甲状腺功能受到影响。     

Pathology of the thyroid in severe acute respiratory syndrome

The severe acute respiratory syndrome (SARS) epidemic started in November 2002 and spread worldwide. The pathological changes in several human organs of patients with SARS have been extensively described. However, to date, little has been reported about the effects of this infection on the thyroid gland. Femoral head necrosis and low serum triiodothyronine and thyroxine levels, commonly found in patients with SARS, raise the possibility of thyroid dysfunction. We have undertaken this study to evaluate for any potential injury to the thyroid gland caused by SARS on tissue samples obtained from 5 SARS autopsies. The terminal deoxynucleotidyl transferase-mediated dUPT nick end-labeling assay was performed to identify apoptotic cells. The follicular epithelium was found to be damaged with large numbers of cells exfoliated into the follicle. The terminal deoxynucleotidyl transferase-mediated dUPT nick end-labeling assay demonstrated many cells undergoing apoptosis. Follicular architecture was altered and showed distortion, dilatation, and collapse. No distinct calcitonin-positive cells were detectable in the SARS thyroids. In conclusion, both parafollicular and follicular cells were injured. This may provide an explanation both for low serum triiodothyronine and thyroxine levels and the osteonecrosis of the femoral head associated with patients with SARS. Apoptosis may play a role in the pathogenesis of SARS associated coronavirus infection in the thyroid gland.