脑膜血管瘤病1例

患儿男性,12岁。近1个月反复口角抽搐、凝视伴间歇性头痛,拟诊为癫入院。6年前因手外伤曾引发一次口角抽动、口吐白沫、意识丧失约1 min,后未曾发作。CT示左颞叶血管性病变,动静脉畸形可能大(图1)。MRI检查T1W、T2W平扫+T1W增强示左颞后偏下良性占位,海绵状血管瘤可能性大,动静脉畸形不能除外。术中见局部脑膜增厚、脑组织较硬,血管丰富。     

碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

Objective To investigate the influence of iodine excess on expression of TRAIl/TRAIL-sR1 in NOD and Balb/c mice and to study the effect of TRAIl/TRAIL-sR1 on the pathogenesis of experimental autoimmune thyroiditis(EAT). Methods Both Balb/c and NOD mice were divided randomly into control and iodine excess group by feeding with water containing no NaI or 0.05% Nal. The mice were sacrificed after 8 weeks. TRAIL and TRAIL-sR1 mRNA levels were detected by RT-PCR. The function, morphology and apoptosis of thyroids were also observed by ELISA and Tunnel stain. Results Treated by HI, enlarged follicles and flattened epithelium by accumulation of colloid were found in thyroids of both NOD and Balb/c mice. But significant lymphoid cell infiltration and local fibrosis were only found in thyroids of NOD HI group. The relative weight of thyroids of NOD mice in HI group[(104.8±14.5)mg/kg]was heavier than that of control group [(71.8±20.4)mg/kg]. The level of TT4 declined in HI group[(30.77±3.59)mmol/L]compared with control group[(36.43±2.66)mmol/L], meanwhile, the level of TSH was higher in HI group[(6.98±0.66)μg/L]than that in control group [(5.55±0.56)μg/L]. The difference being statistically significant(t=7.773,-9.526,-4.458, all P < 0.05). The relative weight of thyroids of Balb/c mice of HI group[(155.8±20.8)mg/kg]also heavier than that of control group [(105.1±22.0) mg/kg]. The level of TT4 droped in HI group [(19.75±3.32) mmoL/L]was higher than that in control group[(23.46±6.21)mmoL/L], the level of TSH in HI group[(4.14±1.71)μg/L]was higher than that in control group[(3.55±1.41)μg/L], the difference being statistically significant(t=7.554,-7.239,3.140, all P< 0.05). A great deal of apoptotie ceils observed in NOD (3.97±0.91) and Balb/c mice (1.05±0.45) by Tunnel stain were greater than control groups (0.21±0.15, 0.10±0.03), the difference being statistically significant in beth of the two species(t=-7.167,-17.772, both P < 0.05). The apoptosis index of thyroid follicular epithelium in NOD was obviously higher than Balb/c(t=-7.625, P<0.05). The level of TRAIL mRNA did not remarkably change in Balb/c between control group(0.000 59±0.000 39) and HI group(0.001 24±0.000 46, t=-1.940, P>0.05), but it increased apparently in NOD mice HI group(0.018 88±0.005 77) than that of control group(0.009 61± 0.00591, t=-2.71, P<0.05). The level of the expression of TRAIL-sR1 mRNA increased in HI groups of NOD (0.000 53±0.000 15) and Balb/c mice(0.000 42±0.000 09) than that in control groups of NOD(0.000 28± 0.000 05) and Balb/c mice (0.000 17±0.000 06) and the differences were statistically significant between the two species(t=3.050,3.990, all P<0.05). The differences of the expression of TRAIL and TRAIL-sR1 mRNA between the two species were significant(t=-3.37,-4.76, all P<0.05). Conclusions Iodine excess induces colloid goiter in beth species of mice and thyroiditis in NOD mice. The increase of TRAIL and TRAIL-sR1 influenced by iodine excess is one of the molecular bases of follicular epithelium apoptosis and inflammation in thyroids. Genetic factor is a key factor in the pathogenesis of thyroiditis.     

碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

Objective To investigate the influence of iodine excess on expression of TRAIl/TRAIL-sR1 in NOD and Balb/c mice and to study the effect of TRAIl/TRAIL-sR1 on the pathogenesis of experimental autoimmune thyroiditis(EAT). Methods Both Balb/c and NOD mice were divided randomly into control and iodine excess group by feeding with water containing no NaI or 0.05% Nal. The mice were sacrificed after 8 weeks. TRAIL and TRAIL-sR1 mRNA levels were detected by RT-PCR. The function, morphology and apoptosis of thyroids were also observed by ELISA and Tunnel stain. Results Treated by HI, enlarged follicles and flattened epithelium by accumulation of colloid were found in thyroids of both NOD and Balb/c mice. But significant lymphoid cell infiltration and local fibrosis were only found in thyroids of NOD HI group. The relative weight of thyroids of NOD mice in HI group[(104.8±14.5)mg/kg]was heavier than that of control group [(71.8±20.4)mg/kg]. The level of TT4 declined in HI group[(30.77±3.59)mmol/L]compared with control group[(36.43±2.66)mmol/L], meanwhile, the level of TSH was higher in HI group[(6.98±0.66)μg/L]than that in control group [(5.55±0.56)μg/L]. The difference being statistically significant(t=7.773,-9.526,-4.458, all P < 0.05). The relative weight of thyroids of Balb/c mice of HI group[(155.8±20.8)mg/kg]also heavier than that of control group [(105.1±22.0) mg/kg]. The level of TT4 droped in HI group [(19.75±3.32) mmoL/L]was higher than that in control group[(23.46±6.21)mmoL/L], the level of TSH in HI group[(4.14±1.71)μg/L]was higher than that in control group[(3.55±1.41)μg/L], the difference being statistically significant(t=7.554,-7.239,3.140, all P< 0.05). A great deal of apoptotie ceils observed in NOD (3.97±0.91) and Balb/c mice (1.05±0.45) by Tunnel stain were greater than control groups (0.21±0.15, 0.10±0.03), the difference being statistically significant in beth of the two species(t=-7.167,-17.772, both P < 0.05). The apoptosis index of thyroid follicular epithelium in NOD was obviously higher than Balb/c(t=-7.625, P<0.05). The level of TRAIL mRNA did not remarkably change in Balb/c between control group(0.000 59±0.000 39) and HI group(0.001 24±0.000 46, t=-1.940, P>0.05), but it increased apparently in NOD mice HI group(0.018 88±0.005 77) than that of control group(0.009 61± 0.00591, t=-2.71, P<0.05). The level of the expression of TRAIL-sR1 mRNA increased in HI groups of NOD (0.000 53±0.000 15) and Balb/c mice(0.000 42±0.000 09) than that in control groups of NOD(0.000 28± 0.000 05) and Balb/c mice (0.000 17±0.000 06) and the differences were statistically significant between the two species(t=3.050,3.990, all P<0.05). The differences of the expression of TRAIL and TRAIL-sR1 mRNA between the two species were significant(t=-3.37,-4.76, all P<0.05). Conclusions Iodine excess induces colloid goiter in beth species of mice and thyroiditis in NOD mice. The increase of TRAIL and TRAIL-sR1 influenced by iodine excess is one of the molecular bases of follicular epithelium apoptosis and inflammation in thyroids. Genetic factor is a key factor in the pathogenesis of thyroiditis.     

碘过量和甲状腺球蛋白免疫诱发NOD小鼠甲状腺炎的病变特征

Objective To observe the pathological characteristics of thyroiditis induced by iodine excess and thyroglobulin (Tg) immunization and to explore the mechanism of thyroiditis induced by iodine excess. Methods NOD mice were used for intaking 0.05% Nal water and(or) Tg immunization. Morphologic change in thyroid and apoptosis were observed. The levels of serum TT4, TSH, thyroglobulin antibody (TgAb) and thyroid peroxidase antibody (TPOAb) were measured. Responding to Tg, lymphocytic proliferation of lymph node and spleen, interleukin-4(IL-4)and γ-interferon(IFN-γ) levels in culture medium of splenocytes were detected. Real-time PCR Was used to detect mRNA expressions of IL-4, IFN-γ, chemokine ligand 10 (CXCL10) and intercellular adhesion molecular-1(ICAM-1) in thyroid. Results Distended thyroid follicles,colloid accumulation, intense lymphocytic infiltration and disorganization were seen in thyroid of iodine excess group, along with increased apoptosis of thyroid cells(34.66～ 2.78 vs 5.11±0.62 ,P<0.01). The levels of TT4 were lowered while TSH raised ,but no production of thyroid-specific autoantibodies was revealed. Lymph node and spleen cells showed positive respornse under stimulation of Tg. The level of IFN-γ[(1. 272±0.049 vs 1. 139±0. 025)ng/L,P<0. 01] was raised in culture medium of splenocytes but not IL-4. The expression of IFN-γ, CXCLI0 and ICAM-1 mRNA were increased in thyroid. But in Tg group, some lymphocytes were scattered in thyroid, autoantibodies emerged ,and the level of IL-4 was increased in cuhure medium of splenocytes[(18. 508±0. 113 vs 13. 368±0. 016)ng/L, P<0. 01]. ledine excess combined with Tg enhanced these inflammatory reaction. Conclusion Iodine excess induced thyroiditis in NOD mice. The process seems to be Th1 response dominant organ-specific autoimmune diseases. Iodine excess and Tg immunizatiou play a synergistic role in inducing experimental autoimmune thyroiditis.     

活化白细胞黏附分子在肿瘤恶性生物学行为中的作用

肿瘤的发生、发展是一个多因素、多阶段的过程,其中包括原癌基因的活化、抑癌基因失活、凋亡调控基因功能紊乱等多种作用因子综合作用并产生加权效应,最终导致细胞增殖调控异常、恶性转化、侵袭和迁徙等恶性生物学行为。大多数恶性肿瘤存在一个共同特点即原发性肿瘤多局限于某特定器官或组织内。在形成肿块期间肿瘤细胞必然是彼此黏贴,而细胞黏附分子（Adhesion molecule, AM）在维持肿块结构中发挥重要作用。随着肿瘤的生长,原发性肿瘤侵犯邻近组织或向远处转移。肿瘤细胞脱离原发病灶,侵犯血管或淋巴管游走至远处器官或部位,即形成转移（Metasta-sis）。黏附分子参与肿瘤细胞从原发肿块脱离,然后与转移灶内皮细胞进行再黏附的过程。     

碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

Objective To investigate the influence of iodine excess on expression of TRAIl/TRAIL-sR1 in NOD and Balb/c mice and to study the effect of TRAIl/TRAIL-sR1 on the pathogenesis of experimental autoimmune thyroiditis(EAT). Methods Both Balb/c and NOD mice were divided randomly into control and iodine excess group by feeding with water containing no NaI or 0.05% Nal. The mice were sacrificed after 8 weeks. TRAIL and TRAIL-sR1 mRNA levels were detected by RT-PCR. The function, morphology and apoptosis of thyroids were also observed by ELISA and Tunnel stain. Results Treated by HI, enlarged follicles and flattened epithelium by accumulation of colloid were found in thyroids of both NOD and Balb/c mice. But significant lymphoid cell infiltration and local fibrosis were only found in thyroids of NOD HI group. The relative weight of thyroids of NOD mice in HI group[(104.8±14.5)mg/kg]was heavier than that of control group [(71.8±20.4)mg/kg]. The level of TT4 declined in HI group[(30.77±3.59)mmol/L]compared with control group[(36.43±2.66)mmol/L], meanwhile, the level of TSH was higher in HI group[(6.98±0.66)μg/L]than that in control group [(5.55±0.56)μg/L]. The difference being statistically significant(t=7.773,-9.526,-4.458, all P < 0.05). The relative weight of thyroids of Balb/c mice of HI group[(155.8±20.8)mg/kg]also heavier than that of control group [(105.1±22.0) mg/kg]. The level of TT4 droped in HI group [(19.75±3.32) mmoL/L]was higher than that in control group[(23.46±6.21)mmoL/L], the level of TSH in HI group[(4.14±1.71)μg/L]was higher than that in control group[(3.55±1.41)μg/L], the difference being statistically significant(t=7.554,-7.239,3.140, all P< 0.05). A great deal of apoptotie ceils observed in NOD (3.97±0.91) and Balb/c mice (1.05±0.45) by Tunnel stain were greater than control groups (0.21±0.15, 0.10±0.03), the difference being statistically significant in beth of the two species(t=-7.167,-17.772, both P < 0.05). The apoptosis index of thyroid follicular epithelium in NOD was obviously higher than Balb/c(t=-7.625, P<0.05). The level of TRAIL mRNA did not remarkably change in Balb/c between control group(0.000 59±0.000 39) and HI group(0.001 24±0.000 46, t=-1.940, P>0.05), but it increased apparently in NOD mice HI group(0.018 88±0.005 77) than that of control group(0.009 61± 0.00591, t=-2.71, P<0.05). The level of the expression of TRAIL-sR1 mRNA increased in HI groups of NOD (0.000 53±0.000 15) and Balb/c mice(0.000 42±0.000 09) than that in control groups of NOD(0.000 28± 0.000 05) and Balb/c mice (0.000 17±0.000 06) and the differences were statistically significant between the two species(t=3.050,3.990, all P<0.05). The differences of the expression of TRAIL and TRAIL-sR1 mRNA between the two species were significant(t=-3.37,-4.76, all P<0.05). Conclusions Iodine excess induces colloid goiter in beth species of mice and thyroiditis in NOD mice. The increase of TRAIL and TRAIL-sR1 influenced by iodine excess is one of the molecular bases of follicular epithelium apoptosis and inflammation in thyroids. Genetic factor is a key factor in the pathogenesis of thyroiditis.     

碘诱发NOD和Balb/c小鼠甲状腺炎的实验研究

Objective To observe the different effects of iodine excess on inducing two strain mice thyroiditis. Methods NOD and Balb/c mice, each having 14 mice, were divided into NaI and control group. The mice were given 0.05% NaI water for 8 weeks in NaI group. RIA and ELISA were used respectively to detect TT4, TgAb, TPOAb and TSH level in serum. Morphology changes of thyroid and apoptosis of thyrocytes stained by immunohistochemistry were observed under light microscope. Lymphocytic proliferation of cervical lymph node and spleen to responding to Tg were detected by MTr method. Results After intake of iodine water for 8 weeks, NOD and Balb/c mice showed relative quality of thyroid in Nal group[(104.83±14.52), (155.79±20.77)mg/kg]obviously increased compared with control group[(71.80±20.42), (105.15±21.98)mg/kg, t values:-3.293,-4.429, all P< 0.01)], enlarged follicular lumen with colloid accumulation were observed in thyroid. Serum level of TT4 in Nal group [(29.52±4.42), (19.53± 2.35)nmol/L]to control group[33.40±5.38), (23.47±6.22)nmol/L]of NOD and Balb/c mice showed a decreasing tendency(t values: 1.374,1.567, all P > 0.05). TSH of Nal group showed an increasing tendency in Balb/c mice[(4.14±1.71)μg/L, compared with control [(3.55±1.41)μg/L, t values:-0.705, P > 0.05]and obviously increased in NOD mice [(6.98±0.66)μg/L, compared with control[(555±056)μg/L, t values:-3.562, P< 0.01], but no change of TgAb and TPOAb level in Nal group(1281,1364 cpm, 2.50×103, 0.14×103U/L were observed, compared with control(1297,1220 cpm, 3.17×103,0.03×103 U/L; Zvalues:-0.081,-0.703, -0.244,-1.293, all P > 0.05). In NOD mice NaI group, apoptosis of thyrocytes was more intense than Balb/c mice, obvious infiltration of lymphoeytes, disorganization and focus fibrosis was seen in thyroid. The cell amount of NaI group increased in NOD mice lymph node and spleen cells[(1.100±0.014), (1.076±0.033)]were more than that in the control group [(0.993±0.011), (1.005±0.003), t value:-11.672,-4.314, P < 0.01). Conclusions Iodine leads to enlargement of thyroid and malfunction of thyroid in Balb/c mice. Besides, NOD mice have generate inflammatory reaction in thyroid and produced sensitized lymphocytes to Tg. Iodine excess can induce NOD mice to occur autoimmune thyroiditis.     

Poly(I∶C)加重碘过量诱发的NOD鼠慢性淋巴细胞性甲状腺炎

目的:探讨poly(I∶C)作为病毒类似物对碘过量所致NOD鼠慢性淋巴细胞性甲状腺炎的影响。方法:将32只雌性NOD鼠,随机分为4组,每组8只,分别为:(1)对照组;(2)碘过量组;(3)poly(I∶C)组;(4)碘过量联合poly(I∶C)组。作用9周后处死动物:观测体重、甲状腺重量及其解剖形态;采用放射免疫分析法检测血清中甲状腺激素(T4)水平;HE染色观察甲状腺组织形态变化,TUNEL技术检测甲状腺组织细胞凋亡情况,定量PCR法检测凋亡相关基因(TRAIL、TRAIL-sR1)和炎症相关基因(ICAM-1、CXCL10)mRNA表达。结果:碘过量组较对照组、Poly(I∶C)组甲状腺绝对重量及相对重量均明显增加(P0.01);血清总T4水平下降(P0.05);炎症破坏和细胞凋亡明显加强;上调TRAIL、TRAIL-sR1、ICAM-1、CXCL10mRNA表达(P0.05)。碘过量联合poly(I∶C)组较单纯碘过量组甲状腺绝对重量及相对重量均进一步增加;血清总T4水平显著下降(P0.05);炎症进一步加重,破坏程度IV级所占比例升至50.0%;凋亡细胞数量明显增加,进一步上调TRAIL、TRAIL-sR1、ICAM-1、CXCL10mRNA表达(P0.05)。Poly(I∶C)组各值与对照组趋势一致(P0.05)。结论:Poly(I∶C)加重碘过量所致慢性淋巴细胞性甲状腺炎发病程度,其作用途径与增加淋巴细胞浸润和甲状腺细胞凋亡有关。     

肝细胞生长因子受体c-met在甲状腺乳头状癌中的表达

目的探讨肝细胞生长因子受体c-met在甲状腺乳头状癌中的表达及其形成中的作用。方法采用免疫组化EnVision法检测35例甲状腺乳头状癌切除标本中c-met的表达,并分析表达情况与临床病理指标之间的关系。构建c-met-siRNA慢病毒载体感染甲状腺乳头状癌K1细胞,裸鼠移植瘤实验观察肿瘤生长情况。结果 c-met在甲状腺乳头状癌中的阳性表达率为97.1%,与甲状腺腺瘤和结节性甲状腺肿组织中的表达差别有统计学意义(χ2=20.4044,P<0.05)。c-met在甲状腺乳头状癌组织中的表达与患者年龄有关。裸鼠移植瘤实验显示c-met-siRNA组肿瘤体积较对照组显著缩小。结论 c-met可能在甲状腺乳头状癌的发生、发展中发挥作用,抑制其基因表达可以抑制裸鼠K1细胞移植瘤的生长。