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1.
目的分析化学发光免疫法检验原发性肝癌肿瘤生物标志物[糖类抗原199(CA199)、甲胎蛋白(AFP)、癌胚抗原(CEA)、γ-谷氨酰转肽酶(γ-GT)]的应用价值。方法选择68例原发性肝癌患者作为观察组,另选取68例健康者作为对照组,所有研究人员均实施化学发光免疫法检验。观察比较两组肿瘤生物标志物CA199、AFP、CEA、γ-GT水平以及其阳性检出率,统计观察组肿瘤生物标志物联合阳性检出率。结果观察组患者肿瘤生物标志物CA19-9(53.52±10.37)U/ml、AFP(157.54±137.85)ng/ml、CEA(30.36±6.73)ng/ml、γ-GT(273.67±124.65)U/L均高于对照组的(4.63±0.68)U/ml、(1.67±0.25)ng/ml、(2.46±0.46)ng/ml、(32.58±11.78)U/L,差异均有统计学意义(P<0.05)。观察组患者的CA19-9、AFP、CEA、γ-GT阳性检出率分别为67.65%、47.06%、58.82%、80.88%,均高于对照组的0、0、0、0,差异均有统计学意义(P<0.05)。观察组患者肿瘤生物标志物CA19-9、AFP、CEA、γ-GT联合阳性检出61例,阳性检出率为89.71%,高于单独检测的阳性检出率,差异均有统计学意义(P<0.05)。结论原发性肝癌患者采用化学发光免疫法进行检验后能够取得较高的检验效果,可以为患者的后续治疗提供可靠的依据,值得大力推广。  相似文献   
2.
Alcohol consumption causes significant liver damage, including hepatitis, fibrosis, cirrhosis, and even primary liver carcinoma. Metadoxine (MTDX) is considered to be a beneficial treatment for alcoholic liver disease (ALD) because it accelerates the metabolism and elimination of ethanol. However, the underlying mechanism is not well understood. Here, the rat model of ALD was developed by feeding with 50% ethanol at the dose of 5 g/kg, and samples of serum and liver tissue were collected to test the levels of liver injury and inflammation and evaluate the hepatoprotective function of MTDX in alcohol-induced liver injury. Further investigation on the infiltration of immune cells was performed to understand the potential hepatoprotective mechanism of MTDX in the ALD model. The results showed that MTDX attenuated liver injury, evidenced by decreased levels of alanine transaminase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP). Meanwhile, the liver proinflammatory environment was improved after MTDX treatment, evidenced by decreased levels of TNF-α, IL-6, and NLRP3 in the liver tissue. Furthermore, inhibited infiltrations of macrophages and neutrophils were observed in MTDX-treated ALD rats compared with the untreated ALD rats. Our results indicated that MTDX played an important role in preventing the progression of ALD, and the underlying mechanisms might be related to its function of attenuating liver inflammation by inhibiting immune cell infiltration.  相似文献   
3.
4.
目的评价新型定量超声(QUS)技术诊断家兔肝纤维化和肝细胞气球样变的价值。方法将30只新西兰大白兔随机分为实验A组(n=12)、实验B组(n=12)及对照组(n=6),以高脂饲料喂养建立兔肝细胞脂肪变性模型;采用剪切波弹性成像(SWE)、剪切波频散成像(SWD)及声衰减成像技术测量相关参数,根据病理学结果判断家兔肝纤维化分期及肝细胞气球样变程度,与超声参数进行比较并分析其相关性。结果实验B组2只家兔死亡,22只模型建立成功,实验A组及B组肝脏均发生不同程度纤维化和肝细胞气球样变。肝纤维化分期是SWV的独立影响因素(P<0.05);F1~3期与F0期家兔剪切波速度(SWV)差异有统计学意义(P<0.05),而F1~2期与F3期差异无统计学意义(P>0.05);肝纤维化分期与SWV呈正相关(r=0.74,P<0.05)。肝细胞气球样变分级是频散值的独立影响因素(P<0.01);B0、B1、B2级肝细胞气球样变家兔频散值两两比较差异均有统计学意义(P均<0.05);肝细胞气球样变分级与频散值呈正相关(r=0.76,P<0.05)。声衰减系数与肝纤维化分期及肝细胞气球样变分级均无显著相关(P均>0.05)。以SWV诊断轻度(≥F1期)和重度纤维化(≥F3期)的曲线下面积(AUC)分别为0.95及0.84;以频散值诊断轻度(≥B1级)和重度肝细胞气球样变(B2级)的AUC分别为0.94及0.87。结论SWE判断家兔肝纤维化分期价值较高;SWE可更好地评估肝细胞气球样变程度。  相似文献   
5.
国医大师徐经世教授在60余年的临床实践中总结提出肝癌的病机为正虚为本,邪实为标;早期多表现为正虚邪实,木旺土虚;病延日久累及下元,则出现水不涵木的病理表现。正虚是该病的病机关键,治疗应遵循“扶正祛邪,分期论治”的治疗原则,病初应“调和中州,培土达木”为主,病至后期则累及下元,治疗则应“滋水涵木,濡养下元”;同时强调饮食生活起居和情志调护,做到精神内守,从而使邪去正安。  相似文献   
6.
The microvascular anatomy of the non-lobulated liver of adult Xenopus laevis was studied by scanning electron microscopy of vascular corrosion casts. Hepatic portal veins and hepatic arteries entered hepatic lobes at the hiluses, hepatic veins left at these sites. Intraparenchymal, hepatic portal veins branched up to 10 times before terminal portal venules supplied liver sinusoids. Hepatic arteries closely followed portal vessels. Arteriolar side branches formed anastomoses with close by portal venules (arteriolar-portal anastomoses; APAs), liver sinusoids (arteriolar-sinusoidal anastomoses; ASAs), and peribiliary plexus vessels. Distally, hepatic arteries anastomosed with terminal portal venules having >100 μm in diameter. Liver sinusoids formed a dense three-dimensional network displaying signs of non-sprouting and sprouting angiogenesis evidenced by “holes” and blind ending tapering cast vascular structures (sprouts), respectively. Sinusoids drained via efferent hepatic veins. Right and left hepatic veins drained into the posterior caval vein. Locally, a dense honeycomb-like 3D-meshwork of resin structures was found around terminal portal venules and hepatic arteries. These networks were fed by hepatic arterioles and drained into adjacent terminal portal venules. As their morphologies differed significantly from sinusoids and they were found at sites where diffuse lymphoid tissue is described, we are convinced that they represent the vasculature of diffuse lymphoid tissue areas. Frequencies and diameter ratios of hepatic portal venules versus hepatic arterioles anastomosing with the former (APAs) implicate that the arterial supply contributes to the oxygenation of parenchymal and stromal cells rather than to a significant increase in blood flow towards hepatic sinusoids.  相似文献   
7.
Valproic acid (VPA) is an anti-seizure drug that causes idiosyncratic liver injury. 2-propyl-4-pentenoic acid (Δ4VPA), a metabolite of VPA, has been implicated in VPA-induced hepatotoxicity. This review summarizes the pathogenesis involved in VPA-induced liver injury. The VPA induce liver injury mainly by i) liberation of Δ4VPA metabolites; ii) decrease in glutathione stores and antioxidants, resulting in oxidative stress; iii) inhibition of fatty acid β-oxidation, inducing mitochondrial DNA depletion and hypermethylation; a decrease in proton leak; oxidative phosphorylation impairment and ATP synthesis decrease; iv) induction of fatty liver via inhibition of carnitine palmitoyltransferase I, enhancing nuclear receptor peroxisome proliferator-activated receptor-gamma and acyl-CoA thioesterase 1, and inducing long-chain fatty acid uptake and triglyceride synthesis. VPA administration aggravates liver injury in individuals with metabolic syndromes. Therapeutic drug monitoring, routine serum levels of transaminases, ammonia, and lipid parameters during VPA therapy may thus be beneficial in improving the safety profile or preventing the progression of DILI.  相似文献   
8.
胰岛素抵抗(insulin resistance,IR)是因肝脏等靶组织对胰岛素敏感下降导致高胰岛素血症、糖耐量受损的一种病理性反应。IR作为2型糖尿病典型的病理特征,其发病机制是抗糖尿病研究的焦点。本文就糖尿病状态下的糖代谢、脂代谢、氧化应激、线粒体功能障碍、内质网应激、炎症与肝脏胰岛素抵抗相关信号通路的分子生物学机制进行综述,为糖尿病治疗提供新思路及理论指导。  相似文献   
9.
Transfusion-associated graft-versus-host disease (TA-GVHD) is a rare life-threatening complication of blood transfusion caused by donor T cells that escape rejection by the recipient immune system. These donor T cells drive recipient tissue damage in response to host antigens. On the other hand, GVHD occurring after allogeneic hematopoietic cell transplantation (HCT-GVHD) is also caused by donor T cells, but its pathophysiology is more complex and differs due to the effects of tissue damage caused by pre?HCT conditioning and profound immunosuppression. Both TA-GVHD and HCT-GVHD can be fatal; however, mortality is higher with TA-GVHD due to the paucity of treatment options. Here, we compare and summarize the presentation, diagnosis, pathophysiology, prevention, and treatment of TA-GVHD and HCT-GVHD.  相似文献   
10.
目的探讨乙肝相关性肝癌临床病理学特征与溶血磷脂酸(LPA)和高敏C反应蛋白(hs-CRP)表达的相关性。方法选取2019年1月至2020年1月间河南省驻马店市中心医院收治的198例乙肝相关性肝癌患者作为乙肝组,198例酒精相关性肝癌患者作为酒精组。两组患者都进行血清hs-CRP和LPA表达检测,调查患者的病理学特征并进行相关性分析。结果乙肝组患者血清hs-CRP和LPA含量均高于酒精组,差异均有统计学意义(均P <0.05)。两组患者血清ALP、AFP、ALT、AST和GGT含量比较,差异均无统计学意义(P> 0.05)。乙肝组不同临床分期和组织学分化患者的血清hs-CRP和LPA含量比较,差异均有统计学意义(均P <0.05)。乙肝组患者的临床分期和组织学分化与血清hs-CRP和LPA表达均存在相关性,差异均有统计学意义(均P <0.05)。患者的临床分期和组织学分化均为影响hs-CRP和LPA表达的重要因素,差异均有统计学意义(均P <0.05)。结论相对于酒精相关性肝癌,乙肝相关性肝癌的血清hs-CRP和LPA呈现高表达,与患者的临床病理学特征存在相关性。  相似文献   
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