甲状腺素及受体与心肌缺血

亚临床甲状腺功能减退被认为与冠心病发病率和心脏疾病死亡密切相关,新近研究发现甲状腺素(tlhryroid hormone,TH)对缺血心肌有保护作用,现从甲状腺素及其受体角度阐述其机制.     

甲状腺素及受体与心肌缺血

亚临床甲状腺功能减退被认为与冠心病发病率和心脏疾病死亡密切相关,新近研究发现甲状腺素(tlhryroid hormone,TH)对缺血心肌有保护作用,现从甲状腺素及其受体角度阐述其机制.     

甲状腺素及促甲状腺素对骨转换作用机制的研究进展

甲状腺功能亢进症是引起继发性骨质疏松症的危险因素。目前关于甲亢导致的骨质疏松机制还不完全明了,但过量甲状腺素会对骨转换产生影响,促甲状腺素水平的降低可能也参与其中。本文综述甲状腺素、促甲状腺素对骨转换作用机制的研究,为以后甲亢性骨质疏松病因机制研究提供新思路。     

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甲状腺素在外科中一直用来治疗慢性淋巴细胞性甲状腺炎 ,还作为甲状腺全切术后的替代治疗或甲状腺癌术后抗复发的重要药物。近年来有许多关于甲状腺素在治疗非甲状腺疾病 (ｎｏｎｔｈｙｒｏｉｄａｌｉｌｌｎｅｓｓ ,ＮＴＩ)中作用的报道 ,如治疗心衰、高脂血症等。本文就甲状腺素在外科中一些新的应用作一总结。1　甲状腺素在外科危重病人中的应用　　我们于 1987年发现急性梗阻性化脓性胆管炎病人Ｔ3水平明显低于胆管结石和胆囊结石病人 ,并且随病情改善而恢复正常[1] 。众所周知 ,老年病人行急症手术的并发症及病死率均高 ,而那些存在低Ｔ…     

局部应用甲状腺素促进周围神经再生的实验研究

在周围神经系统 ,外源性甲状腺素可以增加受损神经元合成蛋白质的数量 ,促进轴突的再生 [1 ]。近年来研究发现 ,在周围神经系统 ,甲状腺素对于相应细胞的作用需要三碘甲状腺原氨核心受体 (NT3 R) [2 ] 。而在坐骨神经损伤时或许旺细胞的体外培养中 ,许旺细胞会表达 NT3 R[3 ] 。因此 ,局部应用的甲状腺素会与损伤局部许旺细胞上的 NT3 R特异性结合 ,从而发挥甲状腺素促进许旺细胞增殖分化的作用。因此 ,本实验设计用硅胶管桥接大鼠周围神经缺损 ,在其中注入一定剂量的甲状腺素 ,观察其能否促进周围神经的再生 ,从而探索一种新的治疗措施…     

靶肌肉注射甲状腺素促进周围神经再生的实验研究

目的研究在靶肌肉注射甲状腺素(T3)对周围神经再生的作用。方法将60只大鼠随机分为实验组和对照组,每组30只。硅胶管桥接大鼠坐骨神经,实验组于术后每周2次将甲状腺素注射于伤侧胫前肌和腓肠肌上,术后1个月和3个月,应用运动神经传导速度(MNCV)、光镜、透射电镜等方法分别从功能和形态方面测定各项指标;对照组注射等量的生理盐水。结果实验组再生神经在功能和形态方面均优于对照组。结论靶肌肉注射甲状腺素能有效促进周围神经再生。     

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目的 探讨Pendred综合征之甲状腺肿的特点及处理。方法 分析三家系5例病人,甲状腺肿的发病特点,5例病人中1例因误诊而手术,所有病例均口服甲状腺素治疗。结果 甲状腺肿多在青春期出现并常结节变,腺肿边界清楚,柔软而无张力,甲状腺素治疗后腺肿缩小,压迫症状缓解。结论 该征宜以甲状腺素终生替代治疗,若出现明显压迫症状可采取手术。过氯酸盐释放试验可筛选出家族成员中本征携带者。     

高甲状腺素血症及其外科干预

早在1835年 Graves 描述了甲状腺中毒症。 后来，将因血中甲状腺素过多引起的一系列高功能 状态称为甲状腺功能亢进(甲亢)。然而甲状腺素的 测定方法是第2次世界大战以后出现的。因而，目 前甲亢所涵盖的疾病种类已多达17种(见表1) 。 真正意义的“甲亢”应指甲状腺素的合成、血中排放     

高浓度甲状腺素对软骨细胞聚集体(pellets)体外形成软骨组织的作用

目的:药物浓度(100nM)甲状腺素对组织工程软骨形成的作用.方法:将软骨细胞聚集体分为常规培养组(DMED+10％FBS)和100nM甲状腺素组(DMED+10％ FBS +100nM甲状腺素),体外培养1、2和3周取材进行大体形态、组织学、二型胶原和十型胶原免疫组化染色和软骨特异基因PCR分析.结果:100nM甲状腺素组形成的软骨细胞聚集体的体积和湿重均明显低于常规培养组,甲苯胺兰、二型胶原(ColⅡ)染色较常规培养组弱,软骨细胞特异基因的表达水平与常规培养组相似,软骨细胞肥大相关基因十型胶原(Col Ⅹ)及基质金属蛋白酶13(MMP13)的表达较对照组减弱,成骨方向分化相关基因(Col Ⅰ,Runx2)的表达与常规培养组相似.结论:高浓度甲状腺素能够抑制软骨细胞肥大,但同时也抑制了软骨细胞增殖和软骨细胞基质分泌.     

甲状腺素与药物性器官缺血预适应

缺血预适应是减轻器官缺血-再灌注损伤地有效措施.甲状腺素预处理可以通过激活信号转导通路的一系列信号分子,诱导效应蛋白的表达,从而模拟缺血预适应现象,增强器官对缺血-再灌注损伤地耐受能力.本文简要综述甲状腺素诱导器官缺血预适应的分子机制.     

Postoperative thyroid hormone supplementation rates following thyroid lobectomy

BackgroundThyroid lobectomy is performed for symptomatic benign nodules, indeterminate nodules, or low-risk well differentiated thyroid cancer. We aimed to determine factors associated with thyroid stimulating hormone over goal (TH) following lobectomy.MethodsWe performed a retrospective single-institution cohort study of patients undergoing thyroid lobectomy from January 2016 to December 2017. TH was defined as need for thyroid hormone in accordance with guidelines. Univariate and multivariate logistic regression analysis was performed.ResultsOne hundred patients were included and 47% developed.TH73% of those with cancer, 38% with benign pathology (p = 0.002). Patients with TH were more likely to have thyroiditis 26% versus 3.8% (p = 0.002); higher preoperativeTSHmean 1.88mIU/L (SD 1.17) versus 1.16mIU/L (SD 0.77) (p = 0.0002), and smaller remnant thyroid lobe adjusted for body surface area 2.99ml/m2 versus 3.72ml/m2 (p = 0.003).ConclusionsAfter thyroid lobectomy, TH is associated with preoperative TSH level, thyroiditis, remnant thyroid volume, and malignancy. The majority of patients with final pathology of carcinoma will require thyroid hormone supplementation to achieve TSH goal.     

Thyroid hormone regulation of Xenopus laevis metamorphosis: functions of thyroid hormone receptors and roles of extracellular matrix remodeling

The regulatory effects of the thyroid hormone on amphibian metamorphosis is mediated by thyroid hormone receptors. Using Xenopus laevis as a model system, we and others have shown that the mRNA levels of thyroid hormone receptors and 9-cis retinoic acid receptors, which form the functional heterodimers with thyroid hormone receptors, are regulated temporally in a tissue-dependent manner so that high levels of their mRNAs are present in an organ when metamorphosis is occurring. By overexpressing thyroid hormone receptors, 9-cis retinoic acid receptors, or both into developing Xenopus embryos, we have shown that both thyroid hormone receptors and 9-cis retinoic acid receptors are required for mediating the effects of thyroid hormone on embryo development and precocious but specific regulation of the genes, which are normally regulated by thyroid hormone during metamorphosis. Analyses of the developmental expression of one class of thyroid hormone response genes, which encode extracellular matrix-degrading metalloproteinases, suggest that extra cellular remodeling plays an important role during tissue remodeling, including cell death (apoptosis) and cell proliferation and differentiation. This effect of extracellular matrix on cell behavior has been supported directly by in vitro primary cell culture experiments, in which intestinal epithelial cells undergo thyroid hormone-induced apoptosis, just like that during natural metamorphosis.     

The effects of fine-needle biopsy on thyroid hormone levels

OBJECTIVE: Our study aim was to investigate the effects of fine-needle biopsy used for thyroid nodules on serum thyroid hormone levels. STUDY DESIGN: A total of 25 patients who had solid nodules of the thyroid gland and normal thyroid hormone levels underwent diagnostic fine-needle biopsy for a nodule of the thyroid gland. METHODS: Venous blood samples were drawn from the cases for measurement of serum total T(3) and T(4), free T(3) and T(4), thyroid-stimulating hormone, and thyroglobulin levels before, immediately after, and 30 minutes after the initial biopsy. RESULTS: Total T(3) and thyroglobulin levels were found to be significantly higher immediately and 30 minutes following fine-needle aspiration biopsy, compared to the baseline levels (P<0.05). CONCLUSION: Preliminary data suggest that thyroid hormone levels show a mean increase of about 20% immediately after fine-needle aspiration. SIGNIFICANCE: The implication of this finding on patient care should be determined on an individual basis.     

Thyroid-stimulating hormone, thyroid hormones, and bone loss

It has become accepted by virtue of rich anecdotal experience and clinical research that thyrotoxicosis is associated with high-turnover osteoporosis. The bone loss, primarily due to accelerated resorption that is not compensated by a coupled increase in bone formation, has been attributed solely to elevated thyroid hormone levels. Evidence using mice lacking the thyroid hormone receptors α and β establishes a role for thyroid hormones in regulating bone remodeling but does not exclude an independent action of thyroid-stimulating hormone (TSH), levels of which are low in hyperthyroid states, even when thyroid hormones are normal, as after thyroxine supplementation and in subclinical hyperthyroidism. We show that TSH directly suppresses bone remodeling and that TSH receptor null mice have profound bone loss, suggesting that reduced TSH signaling contributes to hyperthyroid osteoporosis. TSH and its receptor could become valuable drug targets in treating bone loss.     

Study of hormone replacement therapy following total thyroidectomy in thyroid cancer--with special reference to the analysis of thyroid hormone peripheral effects, using indirect calorimetry]

Peripheral effects of thyroid hormones were examined using an indirect calorimetry in 18 patients with thyroid cancer before and after total thyroidectomy. Peripheral effects of exogenous thyroid hormones in TSH-suppression therapy after thyroidectomy were also studied. The subjects were maintained without hormone replacement for 3 weeks after total thyroidectomy. The ratio of resting energy expenditure to basal energy expenditure (REE/BEE) was determined before operation, before hormone replacement, and 1 and 5 weeks after the beginning of replacement, and the values were compared with changes in the blood thyroid hormone levels. Positive correlations were observed between the changes in endogenous thyroid hormone levels before and after total thyroidectomy and those in REE/BEE (free T3 vs. REE/BEE; r = 0.756, p less than 0.01), suggesting that evaluation of REE/BEE is clinically useful as an index of peripheral effects of thyroid hormones. Five weeks after the beginning of hormone replacement, T4 and free T4 were slightly range, and no enhancement of energy metabolism was noted. From these findings, the post-operative TSH suppression therapy carried out at our department is considered to be justifiable also from the viewpoint of energy metabolism.     

甲状腺癌术后碘131联合甲状腺激素应用效果分析

目的分析甲状腺癌术后碘131联合甲状腺激素应用效果。 方法回顾性分析2016年6月至2019年7月间收治的196例甲状腺癌患者的临床资料。按术后围术期不同治疗方案分为两组，即联合组(n＝98)，采用碘131联合甲状腺激素治疗；常规组(n＝98)，采用甲状腺激素治疗；采用SPSSS23.0统计软件处理数据，两组肿瘤相关因子、乳腺癌转移抑制基因1(BRMSl )和细胞缝隙连接蛋白43(Cx43)阳性表达率等计量资料以( ±s)表示，采取独立t检验；残余甲状腺组织清除率等计数资料采取χ²检验；P<0.05为差异有统计学意义。 结果联合组用药3个月后残余甲状腺组织清除率62.2%高于常规组的46.9%；P53、Fas及TNF-ɑ表达高于常规组(P<0.05)。联合组用药后BRMSl和Cx43阳性表达率分别为92.9%、94.9%高于常规组的81.6%、80.6%(P<0.05)。两组不良反应发生率差异无统计学意义(P>0.05)。 结论甲状腺癌手术患者采用碘131联合甲状腺激素治疗，能够提高BRMS1和Cx43蛋白表达阳性率，促使残余甲状腺组织清除，临床价值高，值得应用。     

Thyroid-stimulating hormone and thyrocalcitonin content in rat thyroid

Thyroid-stimulating hormone (TSH) does not affect the total thyrocalcitonin content of rat thyroid glands. Normal thyroids, thyroids stimulated by endogenous TSH during treatment with propylthiouracil, and thyroids treated with exogenous TSH all exhibited identical hypocalcemic activity in rat bioassays, when the standard of comparison was the fraction of thyroid injected.     

A review of thyroid hormone administration during adult donor care

Serum concentrations of thyroid hormones tetraiodothyronine and triiodothyronine commonly are low after head injury and brain death. Thyroid hormone replacement therapy, however, is a controversial part of donor management. This article reviews publications in which thyroid hormone administration was evaluated in human donors. A classification of the "quality" of study methods used in those publications is presented as part of the data review. No publications support the routine administration of thyroid hormone for all donors. "Rescue" replacement in support of cardiac inotropic function is supported by some studies, but the experimental design of those investigations is not optimal. Thyroid hormone replacement and its dosing should be decided by organ procurement organizations as part of treatment protocols.