目的 探讨肝外伤的早期诊断与治疗效果。方法 回顾性分析采用不同手段治疗的各种肝外伤52例患者的临床资料。结果 男30例，女22例，腹部开放性伤18例(34.6%)，腹部闭合性伤34例(65.4%)，腹腔穿刺阳性率为92.3%(48/52)，超声检查阳性率为88.9%(40/45),CT检查阳性率为100%(50/50)。非手术治愈16例； 手术治疗36例(包括3例因非手术治疗而中转手术)，手术方式包括单纯缝合止血、大网膜填塞+缝合止血、明胶海绵填塞+缝合止血、清创性肝切除、腹腔镜探查+缝合止血。治愈率为96.2%(50/52)，死亡率为3.8%(2/52)。2例死于肝内血管损伤大出血。结论 CT检查进行肝损伤分级和血流动力学状态是决定治疗方式的关键，腹腔镜探查是明确诊断的良好微创方法。
The experimental models of chronic hepatic lesion of 40 rabbits were made by intra-abdominal injection of thioacetamide.The chronic hepatic lesion was confirmed by pathological examination and hepatectomies were performed in accordance with different measurements on each rabbit.The observations included indocyanine green retention rate,hepatic resection volume,and the outcomes of operations.The results showed that the mortality was correlative with the change of hepatic functions in the background of chronic hepatic lesion.The indocyanine green retention and the level of serum albumin are important parameters to indicate hepatic impairment.When the former was over 40% or the latter below 2.8g% the operative danger was high and the mortality was over 50%.In accordance with the classification of hepatic function,the preoperative functional state of liver were classified:grade A,B and C.the mortality of posthepatectomy were respectively 16.7%,3O%,and 72%.The multiple progressive regression equation is employed for calculating the postoperative outcome.The equation predicted the postoperative outcome with 88.9% accuracy.
【Abstract】Objective To study the expression of cyclooxygenase-2 (COX-2) in hepatic inflammatory reaction of rats with sepsis, and to explore a new way of protecting hepatic cell. Methods Fifty-four Wistar rats were randomly divided into 3 groups: sham operation group, sepsis group and NS398 group. All rats were subjected to cecal ligation and puncture (CLP) or sham operation. RT-PCR was used to determine COX-2 mRNA expression, serum IL-6, TNF-α and IL-10 were determined by ELISA; and ALT and AST and liver pathological changes were determined in 3 groups and at different times (3, 6, 12 and 24 h) respectively. Results ①The expression of COX-2 mRNA of hepatic tissue was low in sham operation group. It obviously enhanced after CLP at 3 h and peaked at 6 h. High expressions were showed at 12 and 24 h. In NS398 group, it was lower than that of sepsis group at the same time, but higher than that of sham operation group. ②Serum ALT, AST and IL-6, TNF-α were increased in sepsis group than those of sham operation and NS398 group (P＜0.05)； Serum IL-10 was higher in NS398 group than that of sham operation and sepsis group (P＜0.05). ③Hepatic pathological injury extenuate after injected with NS398. Conclusion COX-2 may play an important role in hepatic injury with sepsis.
ObjectiveTo understand the latest development in lineage tracing techniques and their applications in the study of liver regeneration mechanisms. MethodA review of domestic and international literature on the application of lineage tracing techniques in liver regeneration was conducted. ResultsA variety of more reliable and advanced lineage tracing techniques had been developed, such as single-cell RNA sequencing, DNA barcode technology, etc., providing powerful tools for a deeper understanding of the mechanisms of liver regeneration. The marked progress had been made in identifying the origins of liver regeneration cells, identifying liver regeneration areas, and studying the mechanisms of liver regeneration after injury. The lineage tracing techniques help to understand the position and function of different types of liver cells within the liver structure, revealing the regenerative potential and contribution of different subpopulations of liver cells. Moreover, these techniques had supported the phenomenon of transdifferentiation between the hepatocytes and the bile duct cells under chronic liver injury conditions, aiding in understanding the specific roles of key signaling pathways in liver regeneration, such as Wnt/β-catenin, Hippo/YAP, and Notch signaling pathways.ConclusionsAlthough lineage tracing techniques have made marked progress in liver regeneration research, liver regeneration is a complex and important physiological process, and the technique still has limitations, such as challenges in marker specificity, longer research cycles and higher costs, potential limitations in translating from animal models to human clinical applications, inability to solve all questions about liver regeneration mechanisms, and ethical and legal issues. Therefore, more in-depth and comprehensive research is still needed to reveal more details of liver regeneration mechanism.
Objective To explore the relationship between the level of serum ferritin (SF) and liver damage in patients with chronic hepatitis B (CHB). Methods The concentration of serum ferritin of 98 patients with CHB from July to October 2014 was measured, and then correlation analysis was performed to analyze the correlation between SF and such indexes as serum tumor marker α-fetoprotein, biochemical markers [alanine amino transferase (ALT), aspartate amino transferase (AST), total protein (TP), albumin and total bilirubin (TBIL)], and hepatitis B serum markers (hepatitis B surface antigen, hepatitis B surface antibody, hepatitis B e antigen, hepatitis B e antibody, and hepatitis B core antigen). Serum hepatitis B virus DNA (HBV-DNA) viral load was also tested, and then the discrepancy of SF levels in the high and low viral load groups was analyzed. Results The average concentration of the abnormally elevated SF was (878.69±837.98) ng/mL. The SF mean difference between low-load HBV-DNA and high-load HBV-DNA was statistically significant (P < 0.05). Serum ferritin levels were independently and positively correlated with ALT, AST, and TBIL (P < 0.01) and inversely correlated with TP and albumin (P < 0.01). Conclusion The rise of SF is associated with liver damage, which can reflect the state of inflammation of patients with CHB.
目的探讨合并肝后静脉损伤的严重肝损伤时损伤静脉的显露和修复的方法。 方法本组肝右叶切除2例，肝右叶切除并直接修补肝后段下腔静脉1例，直接修补肝中静脉和肝正中裂2例，改良式全肝血流阻断修补肝和肝静脉8例，未发现出血部位行盲目修补2例。结果本组合并肝后静脉损伤15例，其中死于术中大出血4例，死于术后不可逆休克1例，痊愈10例。结论合并肝后静脉损伤时术前复苏、术中对损伤静脉的正确显露与修复是治疗的关键，改良式全肝血流阻断对修复肝后静脉损伤是一种有效方法。
Objective To investigate the protective effect of 4-phenylbutyric acid (PBA) on liver injury induced by severe acute pancreatitis (SAP) in rats and its possible mechanism. Methods Twenty-four SPF adult male Sprague Dawley rats were randomly divided into three groups: shame operation group (SO group,n=8), SAP group (n=8), and PBA group (n=8). SAP model was induced by retrograde injection of 5% sodium taurocholate (1 mL/kg) in biliopancreatic duct in SAP group and PBA group. PBA solution (50 mg/kg) was administeredvia intraperitoneal injection for 3 days prior to establishing models in PBA group. Rats were injected equivalent saline solution instead of PBA solution in SAP group and SO group. All rats were sacrificed at 12 h after modeling. Blood samples were collected by inferior vena cava puncture, and serum levels of amylase (AMY), alanine aminotransferase (ALT), and aspartate transaminase (AST) were measured using a fully automatic chemistry analyzer. The head of pancreas and right lobe of hepatic tissues were harvested and pathological examination was observed under the light microscope. Expressions of glucose-regulated protein 78 (GRP78), CCAAT/enhancer binding protein homologous protein (CHOP) and Caspase-3 in hepatic tissues were evaluated by immunohistochemistry assay. Results Compared with SO group, the serum levels of AMY, ALT and AST were significantly increased in SAP group (P＜0.05). The serum levels of ALT and AST in PBA group were significantly lower than those in SAP group (P＜0.05). There was no difference of the serum levels of AMY between in PBA group and SAP group (P＞0.05). Compared with SO group, the damages of the pancreas and liver tissues and the expressions of GRP78, CHOP and Caspase-3 in hepatic tissues were significantly increased in SAP group (P＜0.05). And the above indices in PBA group were significantly decreased when compared with SAP group. Conclusions PBA can alleviate severe acute pancreatitis-induced liver injury, and the mechanism may be associated with inhibition of endoplasmic reticulum stress (ERS) and reduction of hepatocyte apoptosis.
Objective To summarize the role of nuclear factor kappa B (NF-κB) in the occurrence and progression of various sorts of liver injury. Methods Literatures on the structures, property of molecular biology and function of NF-κB, as well as its relationships with liver injury were collected and reviewed. Results NF-κB was an important nuclear factor existed in cells widely distributed in most cell types. The activation of NF-κB was induced by various sorts of liver injury. The activated NF-κB could affect the liver injury by regulating cytokines, adhesion molecules, and activating factor involving in immunologic reaction， inflammatory reaction and the apoptosis. Conclusion NF-κB plays an important role during the occurrence and progression of liver injury， and may become a new target in the treatment of liver injury.
ObjectiveTo summarize the protective effect of peroxisome proliferator-activated receptor-beta (PPAR-β) in sepsis-induced liver injury and the mechanism, and to provide new ideas for the prevention and treatment of sepsis-induced liver injury.MethodRelevant literatures about protective effect of PPAR-β in sepsis-induced liver injury were collected and reviewed.ResultsPPAR-β played an important role in cell survival, anti-inflammatory, and anti-oxidation. It acted on a variety of pathophysiological processes, could reduce the activation of inflammatory factors, reduce the production of oxygen free radicals, and inhibit the expression of apoptotic proteins, as well as played an important role in anti-inflammatory, anti-oxidative, and anti-apoptotic.ConclusionPPAR-β can inhibit the activation of NF-κB, reduce the release of inflammatory factors, reduce apoptosis, and reduce liver injury by antioxidation, thereby reducing the mortality of sepsis-induced liver injury.
Tumor chemotherapy is a treatment method that employs chemotherapeutic drugs to eradicate cancer cells. These drugs are cytotoxic, meaning they can affect both tumor cells and normal cells. In recent years, there has been a gradual increase in chemotherapy-induced liver injury. Chemotherapy-induced parenchymal liver injury often manifests as diffuse lesions, although focal lesions can occasionally be observed. There is a diversity in the pathogenesis and pathological changes of chemotherapy-induced focal liver disease. Radiologically, there is often challenging in differentiating chemotherapy-induced focal liver disease from hepatic metastases. Therefore, early and accurate diagnosis of this condition poses a certain challenge in clinical practice. This article presents the radiological findings of a case of chemotherapy-induced focal liver disease induced by chemotherapy for gastric cancer, and summarizes the radiological features and differential diagnostic points of chemotherapy-induced focal liver disease, aiming to enhance the understanding of this type of lesion among radiologists and clinicians and reduce related missed diagnoses and misdiagnoses.