目的:探讨甲状腺功能低下的早产儿血清游离三碘甲状腺原氨酸(Free trilute,FT3)、游离甲状腺激素(Free thyroxin,FT4)、促甲状腺激素(Thyroid stimulation hormone,TSH)水平进行动态态变化及临床意义。方法:我院在2007年11月至2008年4月住院的32例诊断为甲状腺功能低下的早产儿为研究对象,应用放射免疫法检测生后第1天,第7天,第15天,1月和2月血清FT3、FT4、TSH水平。结果:32例诊断为甲状腺功能低下的早产儿中,有窒息史的22例,呼吸窘迫综合症(Respiratory distress syndrome,RDS)10例,单纯性早产5例;出现少吃少动临床症状6例;生后各时期的TSH变化没有统计学差异,生后1、5天与生后1、2月FT3、FT4则可见Plt;0.05具有统计学差异。结论:有窒息和RDS的早产儿中,容易发生甲状腺功能降低,以低甲状腺素血症最为常见,使用左旋甲状腺素后,FT-3、FT-4水平可迅速恢复正常。如果同时存在TSH增高,则TSH水平恢复较慢。
摘要:目的:探讨卡配因抑制剂3（MDL28170）对新生大鼠缺氧缺血性脑损伤(HIBD)神经细胞凋亡的影响。方法:建立新生SD大鼠HIBD模型,治疗组于缺养缺血后即刻、2 h、4 h腹腔内注射MDL28170,对照组及手术组同时予生理盐水。缺氧缺血后24 h用免疫组化方法观察大脑皮质及海马CA1区Caspase3 蛋白表达、TUNEL法检测细胞凋亡,观察组织病理改变并计算海马神经元死亡数,透射电镜观察细胞超微结构。结果:缺氧缺血后24 h缺血侧大脑皮质及海马CA1区Caspase3和TUNEL阳性细胞数较对照组明显增加,透射电镜证实有凋亡细胞;MDL28170可减少阳性细胞数量,抑制神经元死亡,差异有显著性(Plt;0.05)。结论:MDL28170可通过抑制神经凋亡而对新生大鼠HIBD具有一定保护作用。Abstract: Objective: To investigate the effect of (Calpain inhibitor3) MDL28170 on neural apoptosis in a neonatal model of hypoxicischemic brain damage (HIBD). Methods: A neonatal model of HIBD was established, 7dayold SD rats were divided into three groups. The treatment group received MDL28170(ip) at 0 h,2 h,4 h after HI, whereas the other two groups were administered normal saline simultaneously. The expression of caspase3 (by immunohistochemistry), neural apoptosis (by TUNEL) in cortex and hippocampus ipsilateral to the insult were observed 24 h after HI; hippocampal CA1 neural loss and electromicroscopic changes were assessed at the same time. Results: Apoptotic body was observed by electromicroscopy. Caspase3 positive cells and apoptotic cells increased significantly in the ipsilateral cortex and hippocampal CA1 region compared to the control, and MDL28170 reduced the number of positive cells, attenuated CA1 neural loss with significance (Plt;0.05). Conclusion: It is suggested that MDL28170 may protect the brain of neonatal rats after HIBD by suppressing neural apoptosis.
ObjectiveTo observe the effect of integrin β8 on the neuronal apoptosis after hypoxia ischemia (HI) in astrocyte/neuron co-culture system. MethodsAstrocytes and neurons were cultured in vitro from cerebral cortex of the P1-3 days Sprague Dawley rats and E16 days fetal rats, respectively. Immunocytochemistry staining was used to identify the purity of cells. Integrin β8 mRNA expression was qualified in the astrocytes at 12 hours, 1 day, and 2 days after HI and reoxygenation (experimental group) and in normal astrocytes (control group) by RT-PCR. Integrin β8 small interering RNA (siRNA) system was established to specifically block astrocyte β8 expression, the efficiency of integrin β8 inhibition was detected by real-time fluorescent PCR. The astrocytes and neurons were co-cultured to established the astrocyte/neuron co-culture system. The neuronal apoptosis was detected with TUNEL in the normal neurons/astrocytes group (co-cultured HI group), the astrocytes infected by integrin β8 siRNA for 2 days/normal neurons group (β8 RNA interference group), and normal neurons in vitro with HI treatment group (HI group) at 1 day after HI and reoxygenation. The normal neurons without treatment as control (control group). ResultsGlial fibrillary acidic protein and neuronal nuclei staining suggested a purity of more than 90% in cultured cells. HI resulted in an increase of integrin β8 mRNA expression at 12 hours after reoxygenation in astrocytes, which peaked at 1 day after reoxygenation, then slowly decreased and remained higher at 2 days, showing significant differences between control group and experimental group and among different time points in experimental group (P<0.05). RNA interference efficiency was most significant at 2 days after astrocytes infected with integrin β8 siRNA (P<0.05). The neuronal apoptosis was significantly increased in HI group, co-cultured HI group, and β8 RNA interference group when compared with control group (P<0.05). But neuronal apoptosis index (AI) was significantly decreased in co-cultured HI group and β8 RNA interference group when compared with HI group (P<0.05). The significant difference of AI was found between co-cultured HI group and β8 RNA interference group (P<0.05). ConclusionIntegrin β8 expression can be induced with hypoxic-ischemic brain damage, leading to decreased AI of neurons and obvious protective effect.
ObjectiveTo analysis the fundus characteristics of fundus fluorescein angiography (FFA) of retinopathy of prematurity (ROP). MethodsEighty-four cases (168 eyes) who were diagnosed with ROP by a binocular indirect ophthalmoscope were included in the study. Among the 84 cases, there were 2 cases (4 eyes) of stage 1 ROP, 26 cases (52 eyes) of stage 2 ROP, 40 cases (80 eyes) of stage 3 ROP, 4 cases (8 eyes) of stage 4 ROP, and 4 cases (8 eyes) of stage 5 ROP, 9 cases (18 eyes) of plus disease, 8 cases (16 eyes) of aggressive posterior ROP (APROP). All infants received FFA with RetCam Ⅱ under general anesthesia and mydriasis. The retinal vein morphology, capillary filling state, neovascularization morphology and fluorescein leakage were observed. ResultsFFA revealed increased branching, expansion and tortuous peripheral retinal capillaries, increased capillary permeability with a small amount of fluorescein leakage in stage 1 ROP. There was a clear dividing line between the vascular area and the remote avascular area. In stage 2, the peripheral branches of temporal retinal blood vessels increased, and parallel distributed like a broom. The capillary end anastomosed with each other to form a loop. The fibrous tissues at the lesion edge proliferated as a ridge, with popcorn phenomenon. In stage 3, the ridge continued broadening, and the neovascular fibrous membrane formed breakthrough internal limiting membrane, stretched into the vitreous with a lot of fluorescein leakage. The ridge and remote avascular zone demarcated clearly. In stage 4 and 5, the vessel changes had similar phenomenon with the stage 2 and 3 in undetached retina, but the vessels in the detached retina expanded with fluorescein leakage. As for plus disease, the retinal arterioles in the posterior pole were tortuous, there were a large number of non-perfusion area in the peripheral retina with hemorrhage and obscured fluorescence. The retinal vessels in posterior pole in AP-ROP were also tortuous, and the capillaries were extreme expanded, while there were very few tortuous vessels and no capillary formation in the other part of retina.At the avascular zone boundaries, there were a large group of neovascularization with fluorescein leakage. ConclusionsThe demarcation line separating the avascular from the vascularized retinal regions is formed in stage 1, 2 and 3, and the amount of fluorescein leakage gradually increase from stage 1 to stage 3 ROP. The detached retina of stage 4 and stage 5 has an unclear focal length in the FFA. The plus disease mainly has arteriolar tortuosity in the posterior pole retina. In the AP-ROP cases, both of the arterioles and venules in posterior pole of retina are tortuous and expanding with neovascularization leakage of fluorescein.