Objective To summarize the recent pathogenetic researches on the acute pancreatitis. Methods Relevant references about the pathogenesis of acute pancreatitis, which were published recently domestic and abroad were collected and reviewed. Results Recent experimental data indicated that the synthesis and release of pro-inflammatory cytokines and chemotactic factors were responsible for local injury and systemic dissemination of the inflammatory mediators. Experimental studies also provided evidences implying that the immune system might play a role in the development of pancreatitis, such as the activation of lymphocyte and neutrophil. Additionally, the pancreas may completely recover or become fibrotic after an attack of acute pancreatitis and the presence of pancreatic stellate cell was known as a crucial factor in the fibrogenesis. Conclusion The pathogenesis of acute pancreatitis is very complicated, the factors that determine the ultimate severity of the attack are still unknown.
The synthesis and secretion of inflammatory cytokines in the monocytes of 68 cases of multiple system organ failure (MSOF) patients was investigated by the method of MTT stained in cytokines dependent defferential cell strain. The data showed that the serum levels of tumor necrosis factor, interleukine 1 and interleukine 6 were increased (Ｐ＜0.01) in the monocytes of MSOF patients. The synthesis and secretion of these inflammatory cytokines gradually increased in the monocytes after onset of MSOF. After 5 days of treatment with antibiotics and electrolytes intravenous infusion, the secretion of TNF, IL-1 and IL-6 were decreased respectively. These results suggested that the TNF, IL-1 and IL-6 are integrated into system inflammatory responese and caused the injury to the tissues and organs. The production levels of these cytokines can be regarded as the index of MSOF and its severity.
The study of relation between hepatogenic peptic ulcer and portal hypertension,transmitter metabolic disturbance,hepatic insufficiency and infection;and the therapeutic principles of complications of peptic ulcer are described.Twenty four of 58 patients with hepatogenic peptic ulcer were examined by color Doppler ultrasound.Portal venous flow volume (24 cases) was 1060.9±96ml/min.Portal venous pressure(8 cases)was 3.77±2.51kPa tested during operation.Histamine concentration (8 cases) was 0.70±0.31μmol/L in peripheral blood.The gastrin contents of 9cases tested 3cm,5cm away from the ulcer were 2195.6±1043.89ng/L and 2140.3±978.5ng/L respectively. H pylori positive rate was 80% in 58 cases.The therapeutic results were satisfactory with no death.The results suggest that pathogenesis of hepatogenic peptic ulcer is closely related to these factors foresaid.The treatment is nonsurgical and massive hemorrhage or perforation once occurs,surgical treatment is necessary.
Objective To investigate the expression of high mobility group protein-B1( HMGB1)and α-smooth muscle actin( α-SMA) in Bleomycin induced pulmonary fibrosis in mice. Methods Twenty C57BL/ 6 male mice were randomly divided into a Bleomycin group and a control group. The Bleomycin group was treated with Bleomycin( 3 mg/kg) by endotracheally injection to induce pulmonary fibrosis. The control group were treated with normal saline( NS) . Then they were sacrificed by abdominal aortic bleeding 10 days after the injection. The right lung was stained with hematoxylin-eosin and Masson trichrome respectively for pathological examination. Immunohistochemistry and RT-PCR were performed to identify the protein and mRNA levels of α-SMA and HMGB1 respectively. Results The mRNA( 0. 89 ±0. 12, 0. 61 ±0. 08) and protein( 13. 66 ±1. 01, 13. 12 ±1. 33) expressions of α-SMA and HMGB1 in the Bleomycin group were all significantly higher than those of the control group( mRNA: 0. 60 ±0. 07, 0. 15 ±0. 02; protein: 8. 18 ±1. 33,7. 92 ±1. 10; all P lt; 0. 01) . Conclusions The expressions of HMGB1 and α-SMA are increased in Bleomycin induced pulmonary fibrosis. HMGB1 participates in the pathological process of pulmonary fibrosis probably by activation of the α-SMA expression.
现已认识到免疫反应、转录因子核因子κB( NF-κB) 的激活、细胞因子、中性粒细胞的激活和肺泡渗入、凝血级联反应、肾素-血管紧张素系统等多种因素构成的复杂网络参与急性肺损伤/急性呼吸窘迫综合征( ALI/ARDS) 的发病过程[ 1-5] 。虽然脓毒症、创伤、肺炎等ALI/ARDS诱发因素很常见, 但仅有部分病人发生ALI/ARDS, 并且具有相似临床特征的ALI/ARDS病人可有截然不同的结果, 这种异质性引起研究者对影响ALI/ARDS 易感性和预后的遗传因子进行鉴别的浓厚兴趣[ 6] 。由于数量庞大的表现型变异, 不完全的基因外显率、复杂的基因-环境相互作用及高度可能的基因座不均一性而使ALI 遗传学的研究受到挑战[ 7] 。近年来基因组学技术被应用于ALI/ARDS 发病机制的研究, 加深了人们对ALI/ARDS的认识并有可能发展出新的治疗策略以降低其发病率和病死率。
Objective To review the research progress of alcohol-induced osteonecrosis of the femoral head (ONFH). Methods Recent literature concerning alcohol-induced ONFH was reviewed and summarized. Results Alcohol-induced ONFH accounte for approximately 1/3 of total ONFH. Alcohol intake and the incidence of ONFH has a significant dose-effect relationship. There are some correlations between alcohol-induced ONFH and lipid metabolism, secretion of corticosteroid, and some gene of alcohol or lipid metabolism. Conclusion The relationships between alcohol and lipid metabolism, and between alcohol and steroid are still the main direction of the research of ONFH. Gene level researches can not demonstrate the pathogenesis, therefore further research should be carried on.
Objective To investigate the role of β-catenin in pathogenesis and progression of knee primaryosteoarthritis (OA) by detecting the expression of β-catenin. Methods Between October 2010 and May 2011, 40 cartilagespecimens were collected from adult knee primary OA patients undergoing total knee arthroplasty and 10 cartilage specimensfrom adult patients suffering from amputation and femoral condylar fracture. All cartilage samples were taken out from femoralcondylar. The decalcified paraffin-embedded sections were prepared and stained with fast green-safranin O to observe thedegeneration of cartilage, then the modified Mankin scale was used to classify the degeneration. The expression of β-cateninwas detected by the immunohistochemistry staining and Western blot. Results According to the Mankin scale, 10 caseshad normal cartilage, 12 had mild degenerative cartilage, and 28 had moderate to severe degenerative cartilage. The histologicalobservation showed the mild degenerative cartilage characterized by fissures in the superficial zone of the articular cartilage,decreased chondrocytes, arrangement disorder, and duplicated tidemark; and the moderate to severe degenerative cartilagecharacterized by fissures in the deep zone of the articular cartilage, obviously decreased chondrocytes and cluster, and even fullthicknesscartilage defect. The β-catenin did not expressed in normal articular cartilage; but it expressed in the degenerativecartilage, and the expression was significantly higher in the moderate to severe degenerative cartilage than in mild degenerativecartilage (P lt; 0.05). Conclusion β-catenin plays a significant role in the pathogenesis and progression of knee primary OA,and the mechanism may be the activation of Wnt/β-catenin signaling pathway, which promotes transcri ption of inflammatorygenes and leads to the destruction of articular cartilage.
Objective To explore the difference between bone marrow edema syndrome (BMES) and avascular necrosis of femoral head (ANFH). Methods Recent original articles about BMES and ANFH were extensively reviewed, and were comprehensively analysed. Results The pathology, pathogenesis, clinical features, treatment selection, and prognosis are different between these two diseases. Conclusion BMES and ANFH are two different diseases. Micro-fracture may be the cause of bone marrow edema.
Objective Glucocorticoid is the main cause of non-traumatic avascular necrosis of femoral head. To explore the changes of reactive oxygen species (ROS) in the bone microvascular endothel ial cells treated with glucocorticoid so as to investigate the pathogenesis of steroid-induced avascular necrosis of femoral head. Methods The cancellous bone of femoral head was harvested from voluntary donators undergoing total hip arthroplasty, and then the bone microvascular endothel ial cells were isolated by enzyme digestion. The cells at passage 3 were cocultured with different concentrations of hydrocortisone (0, 0.03, 0.10, 0.30, and 1.00 mg/mL) for 24 hours. MTT assay was used for the inhibitory rate of cell prol iferation, flow cytometry for apoptosis rate, and fluorescence probe for the production of ROS and xanthine oxidase (XOD). Results At 2-3 days primary culture, the cells were spindle and arranged l ike cobbles and they reached confluence after 1 week. The inhibitory rates of cell prol iferation in 0.03, 0.10, 0.30, and 1.00 mg/mL groups were 20.22% ± 2.97%, 22.94% ± 4.52%, 43.98% ± 3.35%, and 78.29% ± 3.85%, respectively; and 2 high-concentration groups (0.30 and 1.00 mg/mL groups) were significantly higher (P lt; 0.05) than 2 low-concentration groups (0.03 and 0.10 mg/mL groups). The apoptosis rates in 0, 0.03, 0.10, 0.30, and 1.00 mg/mL groups were 0.10% ± 0.01%, 0.23% ± 0.02%, 1.83% ± 0.04%, 6.34% ± 0.11%, and 15.33% ± 0.53%, respectively; 2 high-concentration groups (0.30 and 1.00 mg/mL groups) were significantly higher (P lt; 0.05) than 0 mg/mL group. In 0, 0.30, and 1.00 mg/ mL groups, the ROS levels were 57.35 ± 7.11, 120.47 ± 15.68, and 166.15 ± 11.57, respectively, and the XOD levels were 0.017 9 ± 0.000 9, 0.028 3 ± 0.001 7, and 0.067 7 ± 0.004 1, respectively; there were significant differences in the levels of ROS and XOD among 3 groups (P lt; 0.05). Conclusion Increasing of ROS production in bone microvascular endothel ial cells can be induced by high concentration glucocorticoid, and it can result in cell injury
Objective To review the research progress of heterotopic ossification (HO) pathogenesis.Methods Recent articles about HO including the risk factors and pathogenesis were reviewed and comprehensively analyzed. Results The pathogenesis of HO is not completely understood, but the extracellular factors, signaling pathways, and transcription factors in the pathogenesis of HO are understood deeply, such as bone morphogenic protein, Smad signaling, and core binding factor α1/runt-related transcription factor 2, which are probably involved in HO. Furthermore, some related microRNAs are also probably involved in HO. Conclusion The pathogenesis of HO should be further investigated so as to lay a foundation for preventing and treating HO.