目的 探討18氟-脫氧葡萄糖（18F-FDG）雙探頭符合線路對非小細胞肺癌胸內淋巴結轉移的診斷價值，并分析其假陽性、假陰性診斷的原因。 方法 回顧性分析2010年12月－2012年6月非小細胞肺癌患者161例的臨床資料，其中腺癌122例，鱗癌23例，其他類型16例。分析患者術前18F-FDG雙探頭符合線路顯像對肺門、縱膈淋巴結的診斷結果（其中陽性53例，陰性108例），以術后病理診斷為金標準，評價其診斷價值。分析9例假陽性、26例假陰性診斷患者的吸煙史、慢性支氣管炎肺氣腫、肺結核病史、局限性肺炎、腫瘤標志物、淋巴結短徑、腫瘤原發灶T/N比值、外周血白細胞等指標。 結果 18F-FDG雙探頭符合線路單光子發射計算機斷層成像（SPECT）診斷非小細胞肺癌淋巴結轉移的靈敏度、特異性、準確性、陽性預測值、陰性預測值分別是62.9%、90.1%、78.3%、83%、75.9%。假陽性組患者慢支炎肺氣腫、局限性肺炎者高于真陽性組。假陰性組的淋巴結短徑、原發灶T/N比值小于真陽性組。 結論 18F-FDG雙探頭符合線路SPECT是術前診斷肺癌淋巴結轉移的有效手段；假陽性淋巴結與慢支炎肺氣腫、局限性肺炎有關；假陰性淋巴結與淋巴結短短徑小、原發腫瘤攝取18F-FDG低有關。
Objective To investigate different gases and hematocrits on cerebral injury during deep hypothermic circulatory arrest (DHCA) in a piglet model including monitoring by near-infrared spectroscopy (NIRS). Methods Twenty-four piglets were assigned to 4 groups with respect to different blood gas and hematocrit during DHCA. Group A: hematocrit was maintained between 0.25 to 0.30, pH-stat strategy during cooling phases and alpha stat strategy in other phases; group B: hematocrit was maintained between 0.25 to 0.30 and alpha stat strategy; group C: hematocrit was maintained between 0.20 to 0.25, pH-stat strategy during cooling phases and alpha stat strategy in other phases; group D: hematocrit was maintained between 0.20 to 0.25 and alpha stat strategy. Cerebral oxygenations of piglets were monitored continuously by NIRS. The brain was fixed in situ at 6 hours after operation and a histological score for neurological injury was assessed. Results Oxygenated hemoglobin (HbO2) and total hemoglobin (HbT) signals detected by NIRS were significantly lower in group D than those in group A and group B during cooling (Plt;0.05). Oxygenated hemoglobin nadir time was significantly shorter in group A(Plt;0.05). All piglets with oxygenated hemoglobin signal nadir time less than 25 minutes were free from histological evidence of brain injury. Conclusion Combination of pH-stat strategy and higher hematocrit reduces neurological injury after DHCA.
【摘要】 目的 觀察百草枯中毒大鼠腎組織中血紅素氧合酶1(HO1)的表達,探討其病理生理機制。 方法 SD大鼠126只隨機分為空白對照組、中毒組和褪黑素組,各42只。中毒組、褪黑素組予以百草枯(25 mg/kg)腹腔注射染毒,對照組予以等量生理鹽水腹腔注射,15 min后褪黑素組予以褪黑素(10 mg/kg)腹腔注射,對照組、中毒組予以等量生理鹽水腹腔注射。于1、3、6、12 h,1、2、3、5 d時各組隨機取6只處死。蘇木精〖CD3/5〗伊紅（HE）染色觀察各組腎組織病理學變化,采用免疫組識化學和RTPCR觀察腎組織HO1蛋白和mRNA表達。 結果 ①與對照組相比,中毒組染毒后3 h即可見充血、水腫及空泡變性等病理變化,1 d達頂峰,病理損傷評分3.30±0.31(Plt;0.05),其后緩解趨勢不明顯；而褪黑素組病理變化明顯減輕且緩解趨勢明顯,1 d時病理損傷評分2.70±0.26,與中毒組相比差異有統計學意義(Plt;0.05)。②與對照組相比,中毒組染毒3 h在皮質部腎小管上皮細胞的細胞膜及細胞漿HO1呈陽性表達,免疫組識化學評分(IHS)3.33±1.75,HO1 mRNA表達增強,與對照組相比差異有統計學意義(Plt;0.05),1 d達頂峰,HIS為7.00±2.00,之后減弱,5 d仍有陽性表達,但與對照組相比差異無統計學意義(Pgt;0.05)；褪黑素組HO1表達較中毒組明顯增強,IHS評分6 h~3 d差異具有統計學意義(Plt;0.05),5 d不再有統計學意義(Pgt;005)。 結論 HO1在百草枯中毒大鼠腎組織中呈高表達,褪黑素能明顯改善百草枯中毒腎臟病理損傷,增強HO1表達可能是其作用途徑之一,而氧化損傷可能是百草枯中毒腎損傷病理生理機制之一。【Abstract】 Objective To investigate the expression of heme oxygenase1 (HO1) in paraquartinduced renal injury in rats and the protective effects of melatonin, and explore possible mechanism of paraquartinduced renal injury. Methods One hundred and twentysix adult healthy SpragneDawley rats were randomly divided into three groups and 42 in each group: control group (A), paraquart group (B), and melatonin group (C). The rats in group B and group C were treated with paraquart (25 mg/kg) intraperitoneally, the rats in group A were treated with the same dose of normal saline. In 15 minutes, the rats in group C were given melatonin intraperitoneally at a dose of 10 mg/(kg·d) and the rats in group A and B were treated intraperitoneally with the same dose of normal saline. Six rats in each group were randomly sacrificed at one, three, 12 hours and one, tou, three, five days respectively. Renal histopathological changes were observed under light microscope by HE staining. The protein and mRNA expressions of HO1 were evaluated by immunohistochemical staining and RTPCR respectively. Results ①In group B, there were obvious lesions in the renal tubule of cortical part, including edema, congestion and vacuolar degeneration. These pathologic changes gradually reached the peak on the first day and did not relieved till the end of this study, the pathologic injury score was 3.30±0.31, and there was a statistical significance between group B and group A (Plt;0.05). The aforementioned pathological lesion was more palliative in group C, the pathologic injury score was 2.70±0.26 at the first day; Compared with group B, there was a statistical significance. ②In group A, there was no or weak expression of HO1 and HO1 mRNA. At the third hour, the expression of HO1 in group B was observed in the membrane and cytoplasm of renal tubular epithelial cell of cortical part. Immunohistochemistry score (IHS) was 3.33±1.75 and the expression of HO1 mRNA increased, there was a statistical significance between group B and group A (Plt;0.05). It reached the peak on the first day, IHS was 7.00±2.00, but there was no statistical difference between group B and group A on the fifth day (Pgt;0.05); Compared with group B, the expression in group C was enhanced obviously, IHS were higher obviously on the six hour till to the third day (Plt;0.05), but there were no statistical differences on the fifth day (Pgt;0.05). Conclusion The expression of HO1 in the paraquartdamaged kidney increases and melatonin surely has an protective effect by increasing the expression of HO1, which suggests that oxidative injury might be the main mechanism of paraquartinduced renal injury.
摘要:目的:探討卡配因抑制劑3（MDL28170）對新生大鼠缺氧缺血性腦損傷(HIBD)神經細胞凋亡的影響。方法:建立新生SD大鼠HIBD模型,治療組于缺養缺血后即刻、2 h、4 h腹腔內注射MDL28170,對照組及手術組同時予生理鹽水。缺氧缺血后24 h用免疫組化方法觀察大腦皮質及海馬CA1區Caspase3 蛋白表達、TUNEL法檢測細胞凋亡,觀察組織病理改變并計算海馬神經元死亡數,透射電鏡觀察細胞超微結構。結果:缺氧缺血后24 h缺血側大腦皮質及海馬CA1區Caspase3和TUNEL陽性細胞數較對照組明顯增加,透射電鏡證實有凋亡細胞;MDL28170可減少陽性細胞數量,抑制神經元死亡,差異有顯著性(Plt;0.05)。結論:MDL28170可通過抑制神經凋亡而對新生大鼠HIBD具有一定保護作用。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 understand the effect of nitric oxide (NO) on the formation of hyperdynamic circulatory syndrome (HCS) and the influence of level of NO on HCS. MethodsAfter establishment of stable HCS in partial portal vein ligated rats,the quantity of NO in blood of portal vein and the activity of nitric oxide synthase (NOS) in liver were determined by pre and post injection of inhabitor of NOS (NGmethylLarginine) and hemodynamics was supervised simultaneously.ResultsThe quantity of NO was paralleled with the activity of NOS and was elevated markedly by 24 hours after operation and reached the top by 48 hours after surgery. These sequential changes were coincided with the dilation of general vascularture. There was a close relation between this changes and the formation of HCS.The quantity of NO and the activity of NOS were decreased significantly to the level of the control group after injection of NGmethylLarginine (LNMMA). LNMMA inhabited the activity of NOS and blocked the production of NO. HCS ameliorated obviously. ConclusionNO plays an important role in initiating the dilation of general vascularture and plays a critical role in the formation of HCS. HCS will be ameliorated obviously or be blocked completely by eliminating the effect of NO and the portal pressure will decreased significantly or recover to normal range.
ObjectiveTo investigate the effects of short-time hyperoxia ventilation on lung tissue and pulmonary surfactant proteins C and D (SP-C and SP-D) in rats.MethodsSixteen male Sprague-Dawley rats were randomly divided into two groups (n=8): hyperoxia group (FiO2=0.90), air group (FiO2=0.21). Tracheal intubations were administrated after anesthesia, and rats in two groups were exposed hyperoxia or air ventilation for 4 h. At the same time, carotid artery blood gas was analyzed after 2 h and 4 h of ventilation, then oxygenation index (OI) was calculated. Four hours later, the anterior lobe of right lung was taken to observe the pathological change and the injury level was scored. The middle lobe of right lung was prepared for making tissue homogenate, and the remaining part of the lung was used to measure the wet/dry weight (W/D) ratio. The bronchoalveolar lavage fluid (BALF) was prepared in left lung. The content of SP-C and SP-D were detected in lung tissue homogenate and BALF by ELISA.ResultsComparing with hyperoxia group, the arterial partial pressure of oxygen, lung histopathology score and lung W/D ratio in air group were significantly increased (P<0.05), but OI, the content of SP-C and SP-D in lung tissue homogenate and BALF were significantly decreased (P<0.05).ConclusionHyperoxia ventilation for 4 h in rats can cause lung injury histologically, and reduce the concentration of SP-C and SP-D apparently in the lungs.
目的 探討HIF-1α和BAK蛋白在胃癌中的表達情況，以及二者在胃癌中的相互關系及作用。方法 應用免疫組化SABC染色法檢測80例胃癌組織和20例正常胃組織中的HIF-1α和BAK蛋白的表達情況。結果 胃癌中HIF-lα和BAK蛋白的表達陽性率分別為56.3%（45/80）和67.5%（54/80），而在胃正常組織中分別為5.0%（1/20）和20.0%（4/20），二者在胃癌中的表達顯著高于胃正常組織，其差異有統計學意義（P＜0.05）。HIF-1α蛋白表達與胃癌組織的浸潤范圍、分化程度及淋巴結轉移有關（P＜0.05），與臨床分期、年齡及性別無關（P＞0.05）；BAK蛋白表達與胃癌浸潤及分化程度相關（P＜0.05），與淋巴結轉移、臨床分期、年齡及性別無關（P＞0.05）。胃癌組織中HIF-1α與BAK蛋白的陽性表達之間呈正相關（列聯系數r=0.056，P＜0.05）。結論 HIF-1α與BAK蛋白在胃癌的臨床分期及浸潤轉移中存在關系，這對于研究胃癌的發生和發展，以及對于探索以二者為靶點的抗腫瘤治療有重要意義。
To investigate the function of nitric oxide (NO) and nitric oxide synthetase (NOS) inhibitor, N-nitro-L-arginine methyl ester (L-NAME), the skin avulsion model was made in the lower extremity of pig. The methods of measurement of size of the survived flap, weighing, immunocytochemistry and hybridization in situ were employed, so that the survival surface area of flaps, tissue wet/dry weight ratio, NO content in the serum, gene expression of NO and NOS content in the flap tissue were determined, respectively. The results showed that the early gene expression of NOS was increased as well as the NO content and tissue wet/dry weight ratio (P lt; 0.01). After L-NAME was applied introvenously, the NO content and tissue wet/dry weight ratio were decreased (P lt; 0.01), and the survival surface area of flaps was enlarged (P lt; 0.01). It could be concluded that the NO might play a role in the development of the pathological changes as early congestion, edema and secondary necrosis in the avulsed skin flaps. The early application of L-NAME could do some good to the avulsed skin flap and protect it from further necrosis owing to the presence of NO.
In order to study effect of endothelin (ET-1) on hepatic blood flow in rats and effect of nitric oxide (NO) and prostacyclin (PGI2) on ET-1 biological function, 20 rats were randomized into control, ET-1, ET-1 plus nitric-Larginine, ET-1 plus prostacyclin and indomethen groups. The result showed that ET-1 decreased hepatic blood flow and lasted for longer time. NO and PGI2 may antagonize the biological action of ET-1 during endotoxemia. Therefore, the endothelium-derived vascular factors may regulate hepatic blood flow.