0.05) but the score after training was higher than before(P

Adolescent ; Gene Rearrangement ; Humans ; Leukemia, Myeloid, Acute ; etiology ; genetics ; Male ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; complications ; genetics ; Receptor, Platelet-Derived Growth Factor beta ; genetics

Objective To investigate the carotid plaque conditions and clinical commonly used test events in patients with type 2 diabetes mellitus (T2DM) and to explore the risk factors affecting the stability of plaques in carotid artery.Methods According to the results of cervical vascular color Doppler ultrasound examination, 125 patients with type 2 diabetes mellitus were divided into unstable plaque group (n=21), stable plaque group (n =54), and non-plaque group (n =50).Analysis related results including age, gender, systolic blood pressure (SBP), diastolic blood pressure (DBP), intima-media thickness (IMT), fasting blood glucose (FBG), triglycerides (TG), total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), uric acid (UA), fibrinogen (Fbg), D-dimer (D-D), free triiodothyronine (FT3), free thyroxine (FT4), and thyroid stimulating hormone (TSH) were analyzed.Results Age, gender, SBP, DBP, TG, HDL, D-D, and TSH were without significant differences among groups.Glucose and Fbg were significant different (P ＜ 0.05) between unstable plague group and stable plaque group/no plaque group.No significance difference was found between stable and no plaque groups.IMT, TC, LDL, and FT4 were significant different (P ＜ 0.05) between unstable and stable plaque groups, and between stable and no plaque groups.Logistic multiple regression analysis suggested that IMT and TC might be independent risk factors for the stability of plaques in carotid artery of patients with type 2 diabetes mellitus (P ＜ 0.05).Conclusions The factors affecting formation of plaques in carotid artery include glucose level, TC, and LDL in patients with type 2 diabetes mellitus.The factors affecting its stability include thickness of IMT, TC, LDL, and FT4.IMT and TC were the independent risk factors for the stability of plaques in carotid artery.

ObjectiveTo investigate the changes in the expression of transforming growth factor beta-1 (TGF-β1) during differentiation of pulmonary microvascular endothelial ceils (PMVECs) into smooth muscle cells in rats with hepato-pulmonary syndrome (HPS).MethodsPrimary PMVECs were harvested from healthy adult SD rats of both sexes aged 3-4 months and inoculated in low-glucose DMEM culture medium (1(6/cm2 ) and randomly divided into 2 groups ( n =24 dishes each):control group ( group C) and HPS group.HPS was produced by chronic ligation of common bile duct.In group C serum obtained from normal rats was added to PMVECs,while in HPS group serum obtained from rats with HPS was added.The final concentration of serum was 10％.After being incubated for 24,48 and 72 h,the expression of SM-MHC,SM-α-actin and calponin protein and TGF-β1 mRNA and protein in PMVECs was determined by RT-PCR and Western blot analysis.ResultsThe expression of SMMHC,SM-α-actin and calponin protein.was positive in HPS group whereas the expression of SM-α-actin and calponin protein was negative and the expression of SM-MHC protein was barely detectable in group C.The expression of SM-MHC,TGF-β1 mRNA and protein was significantly higher in HPS group than in group C.The expression of SM-MHC,SM-α-actin and calponin protein and TGF-β1 mRNA and protein was increasing with duration of incubation from T1 to T3 in group HPS.ConclusionTGF-β1 plays an important role in the myogenic differentiation of PMVECs in rats with HPS.

Objective To investigate the effect of the serum obtained from rat with hepatopuimonary syndrome (HPS) on Akt mRNA and protein expression in rat pulmonary microvascular endotheliai cells (PMVECs) and the role of Akt signaling pathway in the proliferation of PMVECs in the HPS. Methods Healthy 3-4-month-old SD rats of both sexes were used in this study. HPS was produced by chronic ligation of common bile duct according to the method described by Fallon. liver cirrhosis and pulmonary microvascular proliferation were verified by microscopic examination of the liver and lung tissue 2 weeks after bile duct ligation. Serum was obtained from blood taken from aorta of HPS rats. Primary PMVECs were cultured and randomly divided into 2 groups: control group and HPS group. In HPS group serum was added to cultured PMVECs (final concentration was 10%) and incubated. Akt mRNA and protein expression was determined at 24, 48 and 72 h of incubation by RT-PCR and Western blot. The proliferation of PMVECs was detected by MTT and ~3H-TdR. Results The proliferation of PMVECs was significantly enhanced and the expression of Akt mRNA and protein was significantly increased in HPS group as compared with control group. Conclusion The Akt signaling pathway might play an important role in proliferation of PMVECs in the HPS.

Objective To observe the proliferation and phenotype-switching of pulmonary arterial smooth muscle cell (PASMC) induced by hypoxia and interfered by Ad-PKGIα. And to investigate the potential regulative role of PKGIα gene in the molecule mechanism of hypoxia pulmonary vessel remodeling (HPVR). Methods To establish the pure PASMC cultured by tissue-sticking methods. Semi-quantitative reverse transcription and polymerase chain reaction (RT-PCR) and Western blot were used to examine the PKGIα mRNA and protein expression after PASMC were transfected by Ad-PKG. The mRNA and protein expressive change of smooth muscle α actin(SM-α-actin) determined the degree of cell phenotype-switching. The changes of PASMC proliferation were determined by flow cytometry and ~3H-TdR incorporated way. Results Ad-PKGIα could transfect into PASMC and highly express. Hypoxia down-regulated the expression of SM-α-actin protein (44. 25±5.34 in normoxia, 32. 18±4. 19 in 12 h hypoxia condition, 21.90 ±2. 44 in 24 h hypoxia condition, P < 0. 05), that could be blocked by the transfeetion of Ad-PKGIα. Hypoxia could push PASMC mitosis and proliferating(~3H-TdR incorporated way: 7570 ± 371 in normoxia,12 020± 831 in 12 h hypoxia condition,14 924 ± 1491 in 24 h hypoxia condition, P <0. 05), that could be blocked by the transfection of Ad-PKGIα, too. Conclusions The results suggested that PKGIα signaling pathway might play an important role in the molecule mechanism of HPVR. And PKGIα gene might be a target point of gene therapy.

0.05),but all were lower than those of the control group(P

Background Age-related cataract is the leading cause of visual impairment worldwide.To seek the effective prevention and drugs for management of cataract is important.Naphthalene-induced cataract of rat is an ideal animal model for the research of human age-related cataract,and aspirin has been proven to inhibit the development of human age-related cataract.ObjectiveThe present study is to investigate the role of aspirin on naphthalene-induced cataract.Methods Forty-five 150-160 g female SD rats were divided into three groups randomly.Naphthalene was orally taken with 0.5mg/kg per day for 3 days and then 1mg/kg per day for 70 days,and then 100mg/kg of aspirin was given per day for 70 days following four-day washout period in group A.In group B,the animals was given orally only naphthalene at the same way.No any intervention was used in group C.Naphthalene-induced cataract was examined under the slim lamp every week.The experimental animals were sacrificed and lenses were obtained in 70 days.α-Crystalline was extracted from lens homogenate and purified and identified using High Performance Liquid Chromatography(HPLC),2-dimentional electrophoresis gel and Western blot.Different abilities of α-crystalline to protect β low crystalline from aggregation were observed using ultraviolet spectrophotometer.Results Naphthalene-induced cataract formed at the third week in only naphthalene group but at the sixth week in naphthalene+aspirin group under the slim lamp.No significant difference was found in the degree of lenses opacity in the second week among these three groups(F=0.032,P=0.969).However,a statistically significant difference was seen in the degree of lenses opacity in the fourth,sixth,eighth and tenth week among these three groups(F= 5031.130,P=0.000;F=115964.000,P=0.000;F=169846.500,P=0.000;F= 195431.200,P=0.000).Themolecular chaperone-like activity was significantly higher than that of the naphthalene-induced group.Conclusion Aspirin delays the progression of lens opacification through protecting α-crystalline molecular chaperone-like activity.

Objective To investigate the clinical value of aprotinin blood anesthesia in the radical excision of esophageal carcinoma. Methods A total of 90 patients with esophageal carcinoma undergoing radical excision were divided into two groups according to using aprotinin or not. Patients in experiment group (group A, 40 patients) were injected with 1 112 EPU aprotinin followed by constant pumped infusion of 278 EPU/h until 2 h after operation. Patients in the control group (group B, 50 patients) were treated with constant pumped infusion of 0.9% saline. The venous blood was collected for blood routine examination, thromboelastography(TEG) and normal coagulable function test at the following time points: before induction, at 2 h and 4 h after the beginning of operation, at the end of operation and at 12 h after operation. The changes of TEG and normal coagulable state were monitored during the whole surgical process. The intraoperative volume of hemorrhage, perioperative transfusion rate and average volume of transfusion in the two groups were compared. Results The preoperative coagulable state in experiment group was kept relatively stable during the operation. Volume of intraoperative hemorrhage, perioperative transfusion rate and average volume of blood transfusion in experiment group were significantly lower than those in the control group. Conclusion Aprotinin blood anesthesia can stabilize the coagulable state, reduce the volumes and rates of hemorrhage and transfusion, and hence can find wide application in the radical excision of esophageal carcinoma.

The natriuretic peptide(NP) system is an endocrine system that maintains fluid and pressure homeostasis by modulating cardiac and renal function.NP levels are elevated in patients with heart failure(HF) and other cardiac diseases.They are early warning system to help to identify patients at high risk for cardiac events.Measurement of NPs may be used to aid diagnosis and prognosis.NPs also can exert important anti-proliferative,anti-fibrotic effects to prevent the remodification in the heart with myocardial infarction and advanced HF.Brain natriuretic peptide is an important biomarker in patients with HF and other cardiovascular diseases,such as pulmonary hypertension and atherosclerotic vascular disease.In addition,synthetic NPs such as nesiritide could be used to treat the patients with acutely congestive HF. These Recombinant drugs are also being investigated for myocardial and renal protection in the setting of cardiac surgery and for prevention of cardiac remodeling.