With the tremendous progress in fundus imaging and histopathology over the past decade, the understanding of age-related macular degeneration (AMD) has taken a qualitative leap. AMD is defined as a progressive neurodegenerative disease of photoreceptors and retinal pigment epithelium (RPE) characterized by extracellular deposits under RPE and the retina, including drusen, basal laminar and linear deposits, and subretinal drusenoid deposits, that can evolve to atrophy of the retina, RPE and choroid and neovascularization in the choroid and/or retina. It is the leading cause of blindness and visual impairment in older populations, despite recent advances in treatments. AMD is a multifactorial disease with genetic and environmental factors including advanced age, smoking, high-fat diet, and cardiovascular disorder to enhance the disease susceptibility. The physiopathologic mechanism includes inflammatory processes (complement pathway dysregulation, inflammasome activation), intrinsic (e.g., photo-oxidation) and extrinsic oxidative insult to the retina, age-related metabolic impairment (mitochondrial, autophagic and endoplasmic reticulum stress). Autophagy dysfunction and local inflammation in aged RPE specially result in the extracellular deposits, cell death and AMD. Further investigation of the pathogenesis of AMD will provide with new therapeutic targets and strategy for prevention and treatment of the disease in the early stages.
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.
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.
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
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.
【Abstract】ObjectiveTo investigate the role of PPARδ in the pathogenesis of colorectal cancer. MethodsLiteratures about PPARδ and the pathogenesis of colorectal cancer were reviewed and analyzed.ResultsPPARδ is expressed in the nucleuses of glandular epithelia lining colon and rectum. It is normally suppressed by wild-type adenomatous polyposis coli (APC) but is up-regulated by enhanced β-catenin/T cell factor-4 (TCF-4) binding to TCF-4-responsive elements in the PPAR promoter when an inactivating APC mutation occurs, which indicates PPAR is a potential downstream target of the APC/β-catenin/TCF-4 signaling pathway in colorectal cancer. Consistent with PPAR’s role as an APC/β-catenin/TCF-4 target, some studies reported that PPAR mRNA is frequently overexpressed in colorectal cancers of both humans and rodent animals, which indicates that PPAR is relevant to the tumorigenesis of colorectal cancer. ConclusionPPARδ is closely related with the pathogenesis of colorectal cancer.
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.
ObjectiveTo explore the pathogenesis of acute pancreatitis during pregnancy, differential diagnosis, and standardized treatment. MethodsThe related literatures at home and abroad in recent years were reviewed, and the progress of pathogenesis and treatment of acute pancreatitis during pregnancy were summarized. ResultsThe common cause of acute pancreatitis during pregnancy include biliary system diseases, hyperlipidemia, hyperparathyroidism, the direct effect of pregnancy on the pancreas, etc. According to the different pathogenic factors of acute pancreatitis during pregnancy, the laparoscopic cholecystectomy (LC), endoscopic retrograde cholangiopancreatography (ERCP), low-fat diet combined with Omega-3 fatty acids, parathyroid adenoma resection, or terminal pregnancy could be use. ConclusionAcute pancreatitis during pregnancy is dangerous, the cause, general condition of patients, and the growth of fetus should be give full consideration, and the diagnosis and treatment are standardized.
Non-alcoholic fatty liver disease (NAFLD) is one of the major chronic liver diseases that endanger human health. It is characterized by hepatic steatosis and absence of other causes of hepatic fat accumulation, such as alcohol abuse. The incidence of NAFLD is increasing year by year. However, the pathogenesis is still undefined. Porphyromonas gingivalis is a major periodontal pathogen of various periodontal disease. Apart from affecting periodontal health, Porphyromonas gingivalis is also related to the incidence of many systemic diseases. In recent years, Porphyromonas gingivalis is considered to be a risk factor of NAFLD. In this paper, the relationship between NAFLD and Porphyromonas gingivalis, as well as the possible pathogenesis are discussed.
Acute carbon monoxide poisoning is a common and frequently occurring disease in winter and spring in China, with high disability and mortality. Delayed encephalopathy is a serious sequela after the pseudo-convalescence. Its mechanism is complex, including environmental and genetic factors, hypoxia and energy metabolism disorder, cytotoxicity and oxygen free radical damage, immune disorder and inflammatory activation, neurotransmitter disorder, brain parenchymal changes, vascular and hemorheological abnormalities, calcium overload, and cell apoptosis. At present, methods for predicting delayed encephalopathy in acute carbon monoxide poisoning include detailed inquiry of medical history, laboratory examination of relevant indicators, electrophysiological examination, brain imaging examination, and evaluation scale prediction. This review summarizes the research status of the pathogenesis and early prediction methods of delayed encephalopathy in acute carbon monoxide poisoning, with a view to providing reference for future research directions.