The clinic main application of medical ultrasonic techniques are introduced,including ophthalmology,neurology,angiology,cardiopathy,digestive system,urology,gynaecology and obstetrics,and surgery. Four kinds of medical ultrasonic techniques in the value on the clinic diagnosis are important,namely transcranial color -coded duplex sonography(TCCD),tissue harmonic imaging(THI),three dimensional imaging(3D),and extended field Of view(EFV).

We found previously that water soluble extract of Liriope spicata Lour (SanMaiDong) possesses cardioprotective action. The paper reported that effects of total aminoacid ex- traded from Liriope spicata Lour (Tal) on experimental myocardial ischemia in rats. The results indicate that Tal (5 mg?kg-1 ,ip) obviously antagonized ischemic ECG changes induced by pituitrin in rats. In myocardial ischemic rats caused by isoprenaline (8 mg?kg-1) Tal 15 mg? kg-1ip significantly reduced ST and decreased CPK release and lowered the content of MDA. In a myocardial ischemic mode) induced by ligat-ing the left anterior descending coronary artery in rats, Tal 15 mg?kg-1ip remarkably decreased plasma CPK and FFA levels and was found todiminish the infarct size. The ratio of its infarct size (5. 80%) is similar to that of propranolol (5. 41%),but apparently smaller than that of ligated group (18.55%). The results suggest that Tal can protect ischemic myocardium and this action may relate to the prevention of my-ocardial lipid peroxication and improvement of myocardial metabolism.

BACKGROUND:Many animal experiments and clinical observation proved that dispeling turbid phlegm herb has good adjustment function on serum lipid, lipoprotein and liver lipid. OBJECTIVE: To observe the effects of dispeling turbid phlegm herb on monocyte chemotactic factor-1, C-reactive protein and serum lipids in rabbits with dietary atherosclerosis. METHODS: A total of 50 New Zealand white rabbits were randomly divided into five groups. Rabbits in the blank control group were fed with basic feed, and simultaneously intragastricaly administrated physiological saline 10 mL/kg per day, for 10 consecutive weeks. Rabbits in the model group were given high-fat diet to prepare atherosclerosis models, and simultaneously intragastricaly administrated physiological saline 10 mL/kg per day, for 10 consecutive weeks. Rabbits in the phlegm turbidity treatment group were given high-fat diet to prepare atherosclerosis models, and simultaneously intragastricaly administrated dispeling turbid phlegm herb 10 mL/kg per day, for 10 consecutive weeks. Rabbits in theXuezhikang group were given high-fat diet to prepare atherosclerosis models, and simultaneously administratedXuezhikang 10 mL/kg per day, for 10 consecutive days. Rabbits in the phlegm turbidity treatment group were given high-fat diet for 10 weeks to prepare atherosclerosis models, and intragastricaly administered physiological saline 10 mL/kg per day for 6 weeks, and then given dispeling turbid phlegm herb 10 mL/kg per day for 4 weeks. At 10 weeks, serum lipid, C-reactive protein, and monocyte chemokine 1 mRNA expressions were detected, and pathological observation of the aorta was performed. RESULTS AND CONCLUSION:Xuezhikang and dispeling turbid phlegm herb could decrease serum total cholesterol, triglyceride, low density lipoprotein cholesterol, high density lipid protein cholesterol, C-reactive protein and monocyte chemokine 1 mRNA expression level, and apparently inhibited atherosclerotic changes. The preventive effect of dispeling turbid phlegm herb was better that its therapeutic effect.

Objective To investigate the effect of active vitamin D (VD) on macrophage M1 and M2 phenotype and its role in protecting podocyte impairment in diabetic nephropathy (DN).Methods Diabetes mellitus rats were established by intraperitoneal injection with streptozocin.Rats were randomly divided into four groups:normal-1 (NC-1,n=8),normal-2 (NC-2,n=8,normal rats treated with calcitriol 0.1 μg· kg-1 · d-1 by gavages),DN (n=24) and VD (n=24,DN+calcitriol 0.1 μg· kg-1 · d-1 by gavages).Blood glucose and body weight were assessed,and 24-hour urine was collected regularly.Blood and urine samples were taken for biochemical study,and kidney tissues were used for PAS staining to assess histological changes.Immunohistochemical staining was used to detect number of CD68 + macrophage.Western blotting was used to detect protein expressions of nephrin,podocin,CD68,M1 specific marker of inducible nitric oxide synthase (iNOS),TNF-α and M2 specific marker of CD163,arginase 1 (Arg-1),mannose receptor (MR).Results (1) In DN group,levels of BUN,Scr,urinary protein and glomerular mesangial matrix proliferation were significantly higher (P ＜ 0.05),and the expressions of nephrin,podocin were significantly decreased compared with NC groups (P ＜ 0.05).These above changes were significantly improved in VD group (P ＜ 0.05).(2)Number of CD68 + macrophage infiltration in DN group was increased in a time dependent manner compared with NC groups,which was significantly reduced in VD group (P ＜ 0.05).(3)To further definite M1 and M2 macrophage activation phenotype,the protein expressions of iNOS and TNF-α was increased in DN group at 8th,14th,18th weeks compared with NC groups (P ＜ 0.05),which were significantly decreased in VD group (P ＜ 0.05).Although,there were no significant difference of protein expressions of CD163,Arg-1 and MR between VD and DN group at both 8th and 14th week (P ＞ 0.05),the protein expressions of CD163,Arg-1 and MR were higher in VD group at 18th week than that in DN group (P ＜ 0.05),and the ratio of CD163/CD68 was also enhanced in VD group (P ＜0.05).(4)Moreover,the protein expression of iNOS was negatively correlated with expression of either nephrin or podocin (r =-0.707,P ＜ 0.01; r =-0.712,P ＜ 0.01),whereas the protein expression of CD163 was positively correlated with expression of either nephrin or podocin (r =0.627,P＜ 0.01; r=0.613,P ＜ 0.01).Conclusion Vitamin D can regulate macrophage phenotype,via inhibiting M 1 macrophage activation and enhancing M2 macrophage activation to protect podocyte impairment.

Objective To investigate the effect of 1,25(OH)2D3 on high glucose induced podocyte injury and its signal transduction mechanism.Methods Differentiated mouse podocytes were exposed to normal glucose,high glucose,and different concentrations of 1,25(OH)2D3 or LY294002 (a selective PI3K inhibitor) for 24 h.PCR and immunofluorescent staining were used to detect nephrin,podocin,and desmin.Western blotting was used to detect protein expression of nephrin,podocin,desmin,PI3K,Akt and p-Akt.Results Compared with high glucose group,1,25(OH)2D3 (100 nmol/L and 1000 nmol/L) significantly up-regulated the expression of podocin and nephrin in podocytes induced by high glucose (P ＜ 0.05).Meanwhile,1,25(OH)2D3 (100 nmol/L) significantly reduced the expression of desmin (P ＜ 0.05).PI3K and p-Akt were obviously reduced in high glucose group.In the presence of 1,25(OH)2D3,the trends were reversed.However the above effects of 1,25(OH)2D3 were abolished when p-Akt was blocked by the PI3K inhibitor LY294002.Conclusions 1,25 (OH)2D3 can inhibit high glucose-induced pedocyte injury through PI3K/p-Akt signaling pathway.

Objective To investigate the effects and underlying mechanism of calcitriol on ameliorating podocytes impairment in DN rats.Methods SD rats were randomly divided into four groups:normal control (NC) group,calcitriol treatment (VD) group:calcitriol 0.1μg· kg--1 d-1,diabetic nephropathy (DN) group:streptozocin (STZ) 58 mg/kg,DN treated with calcitriol (DN + VD) group:calcitriol 0.1 μg · kg-1 · d-1 + STZ 58 mg/kg.Rats were sacrificed at the end of 18 weeks.Results Compared with the DN group,the DN + VD group exhibited significantly lower proteinuria by 36％,improved renal histology at the end of the experiment (P ＜ 0.05),and similar levels of blood glucose,serum urea nitrogen as well as body weight (P ＞ 0.05).There were no significant differences in the serum concentrations of creatinine,calcium and phosphorus among the four groups (P ＞ 0.05).In DN group,the expressions of nephrin,podocin,VDR,PI3K-p85 and p-Akt were significantly decreased and the expression of desmin was increased compared to NC group.Calcitriol treatment could attenuate the above changes.Additionally,a positive correlation was observed between the expressions of nephrin and VDR (r=0.776,P ＜ 0.05).Likewise,the expression of nephrin was positively correlated with either PI3K -p85 or p-Akt (r=-0.736,r=0.855,all P ＜ 0.05).Conclusion Calcitriol can ameliorate podocytes injury in DN rats,which might be related with the further up-regulation of PI3K/p-Akt signaling pathway.

Objective To investigate the effect of 1,25(OH)2D3 on high glucose induced macrophage activation and its underlying signal transduction mechanism.Methods RAW 264.7 cells were used to perform cell culture,the activity of intracellular iNOS was measured.VDR siRNA and PPARγ antagonist pre-treatment with macrophages were done before using 10-8 mol/L1,25(OH)2D3 to intervene high glucose pre-incubated macrophages.M1 markers including iNOS,TNF-α,IL-12,M2 markers including MR,Arg-1,IL-10 and nuclear receptors VDR and PPARγ were separately examined.Results The iNOS activity was increased in a glucose-dose and time dependent manner.Particularly,25 mmol/L glucose at 24 h gave the maximum response.After being treated with 25 mmol/L glucose for 24 h,not only inflammatory cytokines of TNF-α,IL-12 in the supernatant were increased,but quantitative real-time PCR and Western blotting analysis showed iNOS was also up-regulated (P ＜ 0.05).However,M2 markers,i.e.MR and Arg-l were significantly decreased (P ＜ 0.05).When in the presence of 1,25(OH),D3,the trends were reversed:the markers of M1,including TNF-α,IL-12 and iNOS were obviously reduced (P ＜ 0.05),while M2 markers,IL-10,Arg-1 and MR were increased (P ＜ 0.05).In addition,VDR and PPARγ were also increased (P ＜ 0.05).However,the above effects of 1,25 (OH)2D3 were abolished when further inhibited the expression of VDR and PPARγby VDR siRNA and PPARγ antagonist.Besides,accompanied by VDR,PPARγwas also decreased upon the treatment with VDR siRNA (P ＜ 0.05).Conclusion 1,25(OH)2D3 can promote high glucose induced classically activated macrophages (M1) converting to alternatively activated macrophages (M2) and this is achieved through VDR-PPARγ pathway.

Objective To evaluate the role of protein kinase C (PKC ) in reduction of mitochondrial injury during myocardial ischemia-reperfusion (I/R) by ischemic preconditioning in rats .Methods Forty male Sprague-Dawley rats ,aged 12-13 weeks ,weighing 280-320 g ,were randomly divided into 4 groups ( n=10 each) using a random number table:sham operation group (S group) ,I/R group ,ischemic preconditioning group (IP group) and PKC inhibitor chelerythrine group (C group) .Myocardial I/R was produced by 35 min occlusion of left anterior descending branch of coronary artery followed by 120 min reperfusion .Ischemic preconditioning was induced by 3 episodes of 5 min occlusion of left anterior descending branch at 5 min intervals before myocardial ischemia . Chelerythrine 1 mg/kg was injected intravenously via the caudal vein before ischemic preconditioning in group C . At 120 min of reperfusion ,the animals were sacrificed and the hearts were immediately removed .Mitochondrial suspension was prepared for determination of activities of succinate dehydrogenase (SDH ) , xanthine oxidase (XOD ) , glutathione peroxidase (GSH-Px ) and Ca2+-ATPase , content of Ca2+ , myocardial mitochonerial permeability transition pore (mPTP) opening and membrane potential (Δψm ) .Results Compared with S group , the activities of XOD and Ca2+-ATPase ,content of Ca2+ and mPTP opening were significantly increased ,and the activities of SDH and GSH-Px and Δψm were decreased in I/R group ( P<0.05) .Compared with I/R group ,the activities of XOD and Ca2+-ATPase , content of Ca2+ and mPTP opening were significantly decreased , and the activities of SDH and GSH-Px and Δψm were increased in IP group ( P<0.05) .Compared with IP group ,the activities of XOD and Ca2+-ATPase , content of Ca2+ and mPTP opening were significantly increased , and the activities of SDH and GSH-Px and Δψm were decreased in C group ( P<0.05) .Conclusion PKC is involved in reduction of mitochondrial injury during myocardial I/R by ischemic preconditioning in rats .

[ ABSTRACT] AIM:To investigate the effect of polysaccharide from Fructus corni ( PFC) on cardiomyocytes against hypoxia/reoxygenation ( H/R) injury and its possible relationship with ROS/PKC/p38 MAPK pathway.METHODS:Prima-ry cardiomyocytes were isolated from neonatal SD rats and randomly divided into normal group, H/R group, PFC (20 mg/L, 100 mg/L and 200 mg/L) preconditioning+H/R groups, chelerythrine+PFC (100 mg/L)+H/R group and SB203580+PFC (100 mg/L)+H/R group.The cell viability was measured by inverted microscopic observation.Apoptosis in the car-diomyocytes was detected by Hoechst 33258 staining and fluorescence microscopy.The levels of lactate dehydrogenase ( LDH) and superoxide dismutase ( SOD) in the cell culture supernatants, and the reactive oxygen species ( ROS) in the cells were also measured by microplate reader.The protein levels of PKC, p-p38 MAPK and HSP70 in the cells were detec-ted by Western blotting.RESULTS:Compared with normal group, the cell viability and beating frequency were decreased in H/R group.LDH and ROS contents, apoptotic rate and p-p38 MAPK level increased significantly (P<0.01).Compared with H/R group, PFC preconditioning increased beating frequency, SOD activity and the protein level of PKC and HSP70, and decreased ROS production, the protein level of p-p38 MAPK and cell apoptotic rate.However, the effect of PFC was in-hibited by chelerythrine or SB203580.CONCLUSION:PFC may protect cardiomyocytes from hypoxia/reoxygenation injury. Its mechanism is possibly involved in the inhibition of ROS via increasing the activity of SOD and the activation of PKC, and suppression of excessive activation of p38 MAPK.

BACKGROUND:Femoral offset reconstruction is significant for recovering strength of abductor and the balance of soft tissue tension surrounding hip joint, maintaining joint stabilization, restoring joint function, reducing limping after replacement, decreasing prosthetic abrasion, and the incidence of joint prosthesis dislocation.
OBJECTIVE:To discuss effect of femoral offset reconstruction on hip joint function in total hip arthroplasty.
METHODS:We comparatively analyzed 20 patients (20 hips) undergoing the modular prosthesis (S-ROM) total hip arthroplasty and 19 patients (20 hips) undergoing the one modular prosthesis (Corail) total hip arthroplasty at the same time. According to Harris hip score and radiography results, hip joint function and femoral offset reconstruction rate were comparatively studied in both groups.
RESULTS AND CONCLUSION:No infection, fracture, dislocation, deep venous thrombosis or neurovascular injury occurred in either group. Clinical fol ow-up results:In the modular prosthesis and one modular prosthesis groups, there was no significant difference in preoperative Harris hip score between the femoral offset reconstruction and non-reconstruction groups (P>0.05). At 12 months and the latest fol ow-up, the Harris hip score was higher in the patients with femoral offset reconstruction than those with femoral offset non-reconstruction (P<0.05). The range of abduction of hip joint was larger in patients with femoral offset reconstruction than those with femoral offset non-reconstruction (P<0.05). Radiographic fol ow-up results:significant differences in the rate of femoral offset reconstruction were detected between the modular prosthesis and one modular prosthesis groups (χ2=3.956, P<0.05). 39 (98%) femoral stems were in neutral position and one (2.5%) was in mild valgus. There was no significant difference in the abduction angle and the anteversion angle between patients with and without femoral offset reconstruction (P>0.05). These results indicated that functional recovery and the range of abduction were better in patients with femoral offset reconstruction than those without femoral offset reconstruction. Modular prosthesis has a high rate of femoral offset reconstruction.