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Objective:To investigate the serum levels of myonectin, corticostatin and Delta like ligand 4 (DLL4) in patients with type 2 diabetes mellitus (T2DM) diabetes retinopathy (DR) and their clinical significance.Methods:A prospective selection of 341 T2DM patients admitted to Beijing Hospital of Traditional Chinese Medicine, Huairou Hospital from May 2020 to March 2022 was conducted. The patients underwent fundus examination and were divided into a non DR group ( n=85 cases) and a DR group ( n=256 cases) based on DR diagnostic criteria. The DR group was divided into non proliferative and proliferative types according to the staging criteria in China′s DR clinical diagnosis and treatment guidelines, with 142 cases and 114 cases, respectively; 190 healthy individuals who underwent physical examinations in our hospital during the same period were selected as the control group. Enzyme linked immunosorbent assay was used to detect the levels of serum sarconectin, corticostatin, and DLL4 in three groups, collect patient data, and detect biochemical indicators. Logistic regression analysis was used to analyze the influencing factors of DR, and Pearson correlation analysis was used to investigate the relationship between serum sarconectin, corticostatin, DLL4, glucose and lipid metabolism, and insulin resistance; Logistic regression analysis was used to analyze the influencing factors of DR, and Pearson correlation analysis was used to investigate the relationship between serum sarconectin, corticostatin, DLL4, glucose and lipid metabolism, and insulin resistance; The receiver operating characteristic (ROC) curve was used to analyze the diagnostic value of serum sarconectin, corticostatin, and DLL4 in DR. Results:The levels of serum sarconectin and DLL4 in the DR group and non DR group were higher than those in the control group, while the levels of corticostatin were lower than those in the control group (all P<0.05); The levels of sarconectin and DLL4 in the DR group were higher than those in the non DR group, while the levels of corticostatin were lower than those in the non DR group (all P<0.05). The serum levels of sarconectin and DLL4 in proliferative DR patients were higher than those in non proliferative DR patients, while the levels of corticostatin were lower than those in non proliferative DR patients (all P<0.05). The duration of T2DM in the DR group was longer than that in the non DR group, with smoking and alcohol consumption, systolic blood pressure, fasting blood glucose, glycated hemoglobin, triglyceride and insulin resistance index (HOMA-IR) were higher than those in non DR group (all P<0.05). Logistic regression analysis showed that the course of T2DM, systolic blood pressure, smoking and alcohol consumption, glycated hemoglobin, triglycerides, myonectin, corticostatin and DLL4 were the influencing factors of DR (all P<0.05). Pearson correlation analysis results showed that serum sarconectin, DLL4, and fasting blood glucose, glycated hemoglobin, fasting insulin and HOMA-IR were positively correlated (all P<0.05), while cortisol was negatively correlated with fasting blood glucose, glycated hemoglobin and HOMA-IR (all P<0.05). The ROC analysis results showed that the area under the curve (AUC) for the diagnosis of DR was 0.691, 0.745, 0.749, and 0.861 for sarconectin, corticostatin, and DLL4 alone and in combination, respectively. The combined application had higher diagnostic value. Conclusions:Patients with T2DM complicated with DR have elevated levels of serum sarconectin and DLL4, while decreased levels of corticostatin, which are closely related to glucose and lipid metabolism and insulin resistance, and are influencing factors for the occurrence of DR. Combined detection of the three can improve the value of predicting DR.
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Objective To investigate the surgical method of treating the third ventricle cysticercosis with neuroendoscopy and to discuss the related problems. Methods Clinical data of 7 cases of the third ventricle cysticercosis from July 2009 to December 2014 were retrospectively analyzed. Patients aged from 12 to 49 and all of them received endoscopic resection of the third ventricle cysticercosis and orally taken Albendazole after surgery. Results The symptoms of high intracranial pressure in patients show different levels of releasing, except 1 case with postoperative fever symptoms, the other patients had no other palpable complications. After rechecked by CT and MRI, the size and shape of ventricle of all patients improved to varying degrees and hydrocephalus symptoms was relieved that all cases were satisfactory. Conclusions The treatment of neuroendoscopy aimed to the third ventricle cysticercosis is simple, safe and with less postoperative complications, which should be the preferred treatmnt to the third ventricle.
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BACKGROUND:Colagen hydrogel provides good matrix support for hepatocyte growth and tissue reconstruction, and the colagen-based engineered tissue is easy to merge the growth and form integrated tissue. OBJECTIVE:To improve the thickness of engineered hepatic tissue by dissociating hepatocytes/colagen hydrogel composite into smal hepatic units that accumulate in the subcutaneous cavity. METHODS:Freshly isolated hepatocytes from rats were mixed with colagen hydrogel to establish hepatocytes/colagen hydrogel composite. The hepatocytes/colagen hydrogel composite was dissociated into smal hepatic units after being cured. The undissociated hepatocytes/colagen hydrogel composite was taken as a control. Six Spraque-Dawley rats were enroled. Three of them were subjected to a two-thirds partial hepatectomy to induce liver regeneration. Dissociated and undissociated hepatocytes/colagen hydrogel composites were implanted into the bilateral inguinal subcutaneous cavity. Dissociated and undissociated hepatocytes/colagen hydrogel composites were implanted into the bilateral inguinal subcutaneous cavity of the other three rats. At the 7th day after transplantation, engineered hepatic tissue formation was evaluated using hematoxylin-eosin staining, immunohistochemical staining and India ink perfusion methods. RESULTS AND CONCLUSION:The grafts in these two groups al formed vascular engineered hepatic tissue in the subcutaneous cavity, but after the smal hepatic units merged, a large piece of vascular engineered hepatic tissue formed. The hepatic tissue thickness was up to 4 mm. The whole piece of implanted liver grafts only formed smal pieces of hepatic tissues, with only several layers of cels. Immunohistochemistry staining confirmed that the hepatocytes in vascular engineered hepatic tissue had the characteristics and functions of natural hepatocytes. Partial hepatectomy experiment showed that engineered hepatic tissue had the ability to respond to regenerative stimulus of partial hepatectomy. These results show that dissociating the hepatocytes/colagen hydrogel grafts into smal units that accumlate in the subcutaneous cavity can increase the thickness of the engineered hepatic tissue.
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<p><b>OBJECTIVE</b>To investigate the effect of intensive rosuvastatin therapy on adhesion molecules in patients with peripheral atherosclerosis and explore the possible upstream mechanism.</p><p><b>METHODS</b>Twenty asymptomatic patients with peripheral atherosclerosis were enrolled and given 5-20 mg/day rosuvastatin for 3 months. Before and after the treatment, the lipid profile and plasma vascular cell adhesion molecule-1 (VCAM-1) levels were examined. The expression of intercellular adhesion molecule-1 (ICAM-1) in the mononuclear cells was measured using flow cytometry, and the mRNA and protein expressions of peroxisome proliferator-activated receptor γ (PPARγ) were detected using RT-PCR and Western blotting, respectively.</p><p><b>RESULTS</b>Compared with the baseline levels, ICAM-1 expression decreased and PPARγ protein expression increased in the lymphocytes. Rosuvastatin therapy did not produce obvious effects on plasma VCAM-1 level or ICAM-1 expression in the monocytes in these patients.</p><p><b>CONCLUSION</b>Rosuvastatin produces anti-inflammatory effects by decreasing the expression of ICAM-1 in mononuclear cells, and its upstream mechanism may involve the PPARγ pathway.</p>