Central serous chorioretinopathy (CSC) is one of the main causes of impaired visual function in middle-aged men. CSC is characterized by a thickening of the choroid and hyperpermeability of the choroidal vessels, resulting in serous subretinal fluid. The pathogenesis of CSC is not fully understood. Since the introduction of indocyanine green angiography, the detection of the influence of the vortex veins in CSC, it has been established that the presence of a thick choroid may be caused by congestion of the vortex vein, resulting in new choroidal drainage through a vortex vein anastomosis. The study of vortex venous blood hemodynamics has elucidated the new concept of the pathogenesis of CSC, deepened our understanding of the disease, and provided a theoretical basis for new treatment methods. With a better understanding of the pathogenesis of CSC, we expect to be able to stratify patients at risk in the clinic and evaluate optimized treatment options for patients with CSC
目的 增加对慢性淋巴细胞白血病合并非霍奇金淋巴瘤临床病例的认识。 方法 通过报道2011年11月和2012年7月入住的2例确诊为慢性淋巴细胞白血病合并非霍奇金淋巴瘤患者的诊治过程，复习文献，讨论其发病机制、治疗及预后。 结果 该2例患者均予以化疗，其中1例浅表淋巴结明显缩小，骨髓涂片基本恢复正常，病情控制较好；另1例合并症多、病情恶化快、肿瘤化疗效果欠佳，最后因呼吸衰竭死亡。 结论 慢性淋巴细胞白血病合并非霍奇金淋巴瘤，治疗上应综合考虑患者年龄、ECOG评分、临床分期、预后指数等因素，原则上以治疗恶性程度更高的非霍奇金淋巴瘤为主，可根据慢性淋巴细胞白血病分期进行观察、随访或积极治疗。
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.
Vaccine-associated uveitis (VAU) usually refers to a rare adverse reaction that occurs after vaccination. The clinical manifestations of VAU are most often anterior with mild symptoms and responded promptly to topical corticosteroids. However, more severe forms of posterior and panuveitis may also occur, such as multiple evanescent white dot syndrome, Vogt-Koyanagi-Harada syndrome, and acute posterior multifocal placoid pigment epitheliopathy. The pathogenesis of VAU is still unclear. Currently, it mainly includes vaccine Shoenfeld syndrome, type Ⅲ hypersensitivity reaction caused by immune complex deposition, direct infection with live attenuated vaccine, and molecular mimicry theory. VAU is self-limiting, and most patients heal without treatment. In the future, it is recommended to ask all patients with uveitis about their recent vaccination history in the clinic. For patients with inactivated vaccine or recombinant/subunit vaccination history, the possibility of developing Shoenfeld syndrome should be considered, and the history, signs and symptoms related to autoimmune diseases should be carefully looked for.
Objective To investigate the role of peroxisome proliferator activated receptor α （PPARα） in the pathogenesis of colorectal cancer. Method The literatures about PPARα and the pathogenesis of colorectal cancer were reviewed and analyzed. Result The relationships of PPARα to the proliferation， apoptosis， and differentiation of colorectal cancer cells in the pathogenesis of colorectal cancer were controversial. Conclusions PPARα might be involved in the regulation of proliferation， differentiation， apoptosis of colorectal cancer cells， but the pathogenesis and the up- and down-stream signal pathways are not elucidated. In additional， PPARα might partly be involved in the mechanism of drug resistance of chemotherapy drugs for colorectal cancer， but the role is not very clear yet. So more research works need to be done about the relationship of PPARα to pathogenesis of colorectal cancer.
ObjectiveTo review the research progress on etiology and pathogenesis of spina bifida. MethodsBy consulting relevant domestic and foreign research literature on spina bifida, the classification, epidemic trend, pathogenesis, etiology, prevention and treatment of it were analyzed and summarized. ResultsSpina bifida, a common phenotype of neural tube defects, is classified based on the degree and pattern of malformation associated with neuroectodermal involvement and is due to the disturbance of neural tube closure 28 days before embryonic development. The prevalence of spina bifida varies greatly among different ethnic groups and regions, and its etiology is complex. Currently, some spina bifida patients can be prevented by folic acid supplements, and with the improvement of treatment technology, the short-term and long-term survival rate of children with spina bifida has improved. ConclusionThe research on the pathogenesis of spina bifida will be based on the refined individual information on exposure, genetics, and complex phenotype, and will provide a theoretical basis for improving prevention and treatment strategies through multidisciplinary cooperation.
With the surged prevalence of myopia, the pathogenic mechanism underlying myopia has attracted attention. At present, it is generally believed in the flied that the reduced blood perfusion in the choroid is crucial for myopigenesis. Then, in the process of myopigenesis, how are the blurred visual signals transmitted to the choroidal blood vessels through the retina and retinal pigment epithelium, leading to the reduced choroidal blood perfusion. The cellular and molecular mechanisms underpinning this process remain elusive. In recent years, the theory of scleral hypoxia has attracted much attention. Popular signaling molecules in current research include dopamine, epidermal growth factor, retinoic acid, cholinergic molecules and adenosine, etc. These factors are likely to participate in signal transduction in retina and RPE, thus causing changes in choroidal blood flow and affecting the occurrence and development of myopia. Therefore, these signaling factors and their downstream pathways may provide new ideas for the prevention and control of myopia targets.
Chronic obstructive pulmonary disease is often accompanied by anxiety or depression. The exacerbation of anxiety and depression can lead to the deterioration of chronic obstructive pulmonary disease, reduce patients’ quality of life, worsen poor prognosis, and increase the risk of death. Anxiety and depression are one of the important causes of death in patients with chronic obstructive pulmonary disease, but the complexity of their risk factors and pathogenesis often lead to clinicians being unable to make accurate diagnosis and treatment in a timely manner. Based on existing research, this article elaborates on the risk factors and pathogenesis of chronic obstructive pulmonary disease complicated with anxiety or depression, aiming to improve the diagnosis and treatment ability of clinical physicians for chronic obstructive pulmonary disease complicated with anxiety or depression, achieve timely diagnosis and treatment, improve patients’ prognosis, and improve quality of life.