OBJECTIVE:To explore the effects of short-term application of atorvastatin combined with ezetimibe on efficacy and related indicators of patients with primary nephrotic syndrome with hyperlipidemia. METHODS:Data of 50 patients with prima-ry nephrotic syndrome with hyperlipidemia were retrospectively collected and divided into combination group and control group ac-cording different treatment,25 cases in each group. All patients received low-salt,low-fat ,high-quality protein,giving prednisone 1 mg/(kg·d),po,qd,combined with anticoagulation,diuretic,anti-infection,taking cytotoxic drugs if necessary. Based on it, control group received Atorvastatin calcium tablet 20 mg before going to bed,qd;combination group received Atorvastatin calcium tablet(the same dosage and usage with control group)+Ezetimibe tablet 10 mg,qd. They were treated for 2 weeks. Lipid-lowering efficacy and low-density lipoprotein(LDL-C),triglyceride(TG),cholesterol(TC),high-density lipoprotein(HDL-C),24 h uri-nary protein (M-TP),serum albumin,alanine aminotransferase (ALT),aspartate aminotransferase (AST),serum creatinine and blood urea nitrogen before and after treatment in 2 groups were observed and the incidence of adverse reaction was recorded. RE-SULTS:There was no significant differences in the total effective rate of Lipid-lowering in 2 groups(P>0.05). After treatment, LDL-C,TC and HDL-C in 2 groups were significantly lower than before,Alb in combination group and ALT in 2 groups were sig-nificantly higher than before,with statistical significance(P<0.05),while there were no significant difference in 2 groups(P>0.05). And there was no significant difference in the TG,M-TP,AST,serum creatinine and blood urea nitrogen before and after treatment(P>0.05). CONCLUSIONS:Atorvastatin combined with ezetimibe can improve the blood lipid of patients with primary nephrotic syndrome with hyperlipidemia,while showing similar efficacy and safety with atorvastatin alone in a short term.

Aim To establish phlegm and blood stasis, qi-stag-nation and blood stasis, phlegm turbid+qi-stagnation and blood stasis model in rats and to study the characteristics of animal models with different blood stasis. Methods SD rats were ran-domly divided into normal group, high fat diet group, chronic unpredictable mild stress group ( CUMS ) and high fat diet +chronic unpredictable mild stress group. Different states of blood stasis rat models were established by corresponding factors for 6 weeks. Indexes of weight, open field behavior, serum lipids and corticosterone were monitored dynamically at the 2 nd, 4 th, 6 th weeks. At the end of the experiment(6th week), the heart func-tion was detected by small animal ultrasound and the left ventric-ular intubation. The blood rheology indexes were detected by the viscosity tester and red blood cell deformation/aggregation test instrument. Results Compared with the normal group, blood stasis could be induced by high fat diet and chronic unpredicta-ble mild stress, introducing the influence of different degree on animal behavior, blood lipids, heart function and blood viscosi-ty. When the two factors were superimposed, the changes of the indexes about blood stasis were the most significant. Perform-ance as: compared with normal control group, a significant re-duction was observed in body weight ( P < 0. 01 ); horizontal movement, vertical movement and movement time were reduced (P<0. 01 or P<0. 05) at the 2 nd week;at the 2 nd and 4 th week, serum corticosterone was increased ( P <0. 01 or P <0. 05) as well as TG at the 4 th and 6 th week (P<0. 01); at the 6 th week, velocity of blood was slowed down ( P<0. 01 );left ventricular anterior wall and posterior wall thickness at end-systolic was increased ( P<0. 01 or P<0. 05 ); left ventricular diastolic index was increased ( P<0. 01 ); the maximum rate of myocardial contraction was decreased ( P < 0. 05 ); the whole blood viscosity was increased ( P<0. 01 ) . Conclusions Blood stasis could be formed by high fat diet and chronic unpredictable mild stress, which has different characteristics. When the two factors are superimposed, the abnormal behavior, blood viscosi-ty, heart function, blood lipid and other indexes of the animal could obviously appear, which can provide the basis for the stud-y of blood stasis syndrome and related drugs.

Glomerular disease refers to a class of diseases in which the lesions are mainly located in the glomerulus,and the clinical manifestations are mainly hematuria,proteinuria,edema,hypertension and renal dysfunction.In recent years,it has been found that the urokinase-type plasminogen activator (uPA) of the plasminogen activator family,urokinase-type plasminogen activator receptor (uPAR) and its soluble form have been up-regulated in the pathogenesis of certain glomerular diseases.The combination with integrin affects signaling pathways and changes the morphology and function of podocytes to promote disease progression.In this paper,the relevant research progress is summarized as follows.

Periodontitis is a chronic infectious disease in which periodontal tissue loss is caused by dental plaque biofilm. Atherosclerosis is a chronic inflammatory disease that occurs in the walls of arteries and is characterized by lipid accumulation. Recently, many studies have suggested that there is a certain relationship between periodontitis and atherosclerosis. From an epidemiological perspective, a previous literature review indicated that patients with periodontitis have a higher incidence of atherosclerosis. IL-17 secreted by Th17 cells may aggravate the progression of the two diseases by elevating the levels of matrix metalloproteinases, which may damage the connective tissue. Treg cells reduce the activation of T cells and limit the development of inflammation by secreting anti-inflammatory factors and expressing coinhibitory molecules. Periodontal intervention may contribute to the treatment of atherosclerosis by reducing inflammatory markers in atherosclerosis. Many studies have shown that periodontitis and atherosclerosis may interact with each other, but further studies are needed to explore the concrete mechanism of the interaction between periodontitis and atherosclerosis.