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
Diabetic retinopathy (DR) is one of common and specific microvascular complications caused by diabetic mellitus, and remains a serious and common ocular complication leading preventable blindness. At present, the specific pathogenesis of DR is not completely clear, and many factors are involved in its occurrence and development. Adiponectin (APN) is an endogenous cytokine secreted by adipocytes. It is expressed in all layers of retina, especially in the outer layer (rods and cones). It is involved in regulating fatty acid oxidation and glucose metabolism by binding with specific receptors. In recent years, a lot of studies have found that APN can be involved in regulating blood glucose, inhibiting neovascularization, reducing inflammation, dilating blood vessels and improving vascular endothelial function. At present, the specific mechanism of APN in the occurrence and development of DR Remains to be determined. Further research on the level changes and the specific mechanism of action of APN in DR may help to identify the characteristic metabolic changes of DR, thus providing new biomarkers for the diagnosis of DR, while helping to promote the innovation of the treatment of DR.
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.
Hydroxychloroquine is widely used in a variety of autoimmune diseases. However, long-term use of hydroxychloroquine can cause severe retinopathy, which has a complex pathogenic mechanism and diverse clinical manifestations, mainly manifested as photoreceptor and retinal pigment epithelial damage and irreversible vision loss. Identifying damage before retinitis pigment epithelium lesions preserve central vision, so early detection is crucial to slow disease progression and reduce vision loss. The development of multimodal imaging technology and the issuance of the latest treatment guidelines provide a powerful tool for the early screening and treatment of hydroxychloroquine retinopathy. Proficient in the latest guidelines for the treatment of hydroxychloroquine can better guide clinicians to do a good job in disease screening and management, recommend risks, safe dosages and appropriate screening procedures to patients and strengthen the prevention of hydroxychloroquine retinopathy, which will help save the vision of more patients and reduce the waste of medical resources.
【Abstract】ObjectiveTo review the research advance of intestinal barrier changes and its pathogenesis in stress conditions.MethodsThe literatures in recent years on the changes of the intestinal barrier,and its pathogenesis in stress conditions were reviewed.Results In some severe stress conditions, such as trauma, severe inflammation and acute severe pancreatitis, etc, a series of pathophysiologic disorders of intestinal barrier， even systemic inflammatory response syndrome and multiple organ dysfunction syndrome or multiple organ failure were induced. The pathogenesis was a result of a series of neurologic, immunologic and endocrine factors making one another. ConclusionRecognizing the changes and pathogenesis have an important clinical significance for treating and preventing the intestinal barrier dysfunction induced by stress.
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.
ObjectiveTo review the research progress of pathogenesis mechanism of spinal deformity in neurofibromatosis type 1 (NF1). MethodsRecent literature concerning the pathogenesis mechanism of spinal deformity in NF1 was extensively reviewed, and current developments of the correction of spinal deformity and NF1 and the pathogenesis mechanism were summarized. ResultsThe pathogenesis mechanism of spinal deformity in NF1 is not yet clearly known. Current theories include erosion and stress of neurofibromas, melatonin-related decreased contractility of paraspinal muscles, osteopenia and osteoporosis, sexual precocity and mesoderm dysplasia. ConclusionThe clinical manifestations of NF1 may cause the spinal deformities in patients with NF1. The research of pathogenesis mechanism of spinal deformity in NF1 will be conducive to further understanding, diagnosis and treatment of NF1-related spinal deformity.
Progressive ischemic stroke is one of the major diseases damaging the health of Chinese people. Its pathogenesis is complex and there are many influencing factors, but the treatment methods are limited. In recent years, the rapid development of neuroimaging and the results of various clinical trials have been reported in succession, which have made new progress in the clinical diagnosis and treatment of progressive ischemic stroke. This paper summarizes the progress of progressive ischemic stroke, introduces its pathogenesis (including increased intracranial pressure and reduced perfusion pressure, thrombosis progression, hemorrhagic transformation, cerebral edema, and inflammatory response), influencing factors, predictive indicators (including image indicators, biochemical indicators, and molecular biology indicators) and treatment (including admission to “stroke unit”, intravascular treatment, platelet aggregation inhibition treatment, anticoagulation treatment, and general treatment), to provide references for preventing the occurrence and development of progressive ischemic stroke, assessing the condition, guiding treatment and improving the prognosis.
ObjectiveTo summarize basic research progress and current status of clinical diagnosis and therapy for gastroesophageal reflux disease. MethodRelated literatures were collected to review the pathogenesis, clinical manifestations, diagnosis and therapy of gastroesophageal reflux disease. ResultsGastroesophageal reflux disease was caused by many factors, such as hiatus hernia, hypotensive lower esophageal sphincter pressure, acid pocket, prolonged esophageal clearance, and delayed gastric emptying. Extra-esophageal symptoms was a common clinical presentation to gastroesophageal reflux disease. The diagnosis methods for gastroesophageal reflux disease included the symptom observation, gastroscopy examination, 24 h pH monitoring of esophageal, proton pump inhibitor test, questionnaire of gastroesophageal reflux disease and so on. The laparoscopic fundoplication could essentially treat the pathophysiologic abnormalities of gastroesophageal reflux disease, which had an obvious curative effect and wide application prospect. ConclusionPathogenesis, diagnosis, and therapy of gastroesophageal reflux disease are associated with multiple factors, which is still controversial and remains to be further studied.
Bacterial biofilm is the key problem of chronic wound infection and difficult healing. How to prevent and control bacterial biofilm and improve the prognosis of chronic wound has become a research hotspot in the field of wound care. This paper will summarize from the following aspects: four major stages in the process of chronic wound bacteria biofilm formation (surface adhesion, formation of small colonies, biofilm maturation, and dispersion and separation); characteristics of host immune response in the presence of biofilms; morphological, microbiological, and molecular detection methods for biofilms; and progress in in vitro trials, animal trials, clinical trials, and new therapeutic methods of biofilm. The purpose of this review is to provide evidence for the treatment of biofilms for chronic wounds.