Objective To transmit and browse DICOM images in HIFU remote diagnosis system in Web.Methods Mix-patterned programming of.NET and VC++ was used to create a multi-layers architecture.Results The online compression and web browsing of DICOM images were realized.Conclusion Treatment can be livingly played back and suggestions were proposed for doctors.Medical service in high quality can be provided for remote patients.[Chinese Medical Equipment Journal,2008,29(3):39-41]

Objective To evaluate the technique and efficacy of minimally invasive percutaneous nephrolithotomy (MPCNL) for renal calculi in pediatric patients. Methods From April 2009 to December 2009, 12 pediatric patients (8 males and 4 females) with renal calculi were treated by MPCNL. The age ranged from 18 to 53 months (mean 32 months). All the 12 cases were diagnosed by KUB+IVU, ultrasonography and CT. The stone had average diameter of 1. 3 cm (ranged from 1. 0 to 1. 8 cm). Seven cases had simple renal pelvis stone and 5 cases had multiple renal calyx stone. UPJ stricture was not found in this series. General anaesthesia was applied. Renal transfixion pin was punctured to select renal calices by monitoring with ultrasonography. 12 - 16 F percutaneous renal access was successfully established in all cases and calculi were fragmented by pneumatic lithotripter. Results The average operative time of MPCNL was 74 min. Phase Ⅰ lithotripsy was underwent in all patients. The phase Ⅰ stone-free rate was 67%(8/12). One cases accepted second MPCNL. The calculus clearance rate reached 75%(9/12). Three cases had residual calculi ranged from 2 to 4 mm. One of whom had ESWL 2 weeks postoperatively. All cases were followed up for 1 - 7 months, all cases were in stone free status. Conclusion Regarding the advantages of less bleeding, high clearance rate, and shorter hospital stay, MPCNL is an effective and safe treatment option for renal calculi in pediatric patients.

Objective To investigate the effects of inhibiting NgR on retinal ganglion cells density and synaptophysin expression of diabetic rat.Methods Thirty-two SD male rats were randomly divided into normal control group,diabetic group,siNgR group and scNgR group,8 rats in each group.Normal control group was given no any treatment.Diabetes model was induced by intraperitoneal injection of 50 mg · kg-1 streptozotocin in diabetic group,siNgR group and scNgR group,and the blood giucose more than 16.7 mmol · L-1 at 72 hours was set as the successfully model.The rats of siNgR group were intravitreally administrated with anti-NgR nucleotide and the rats of scNgR group intravitreally administrated with negative nucleotide.Eight weeks later,HE staining was conducted to detect density of retinal ganglion cell (RGC),immunofluorescence was used to evaluate the expression and distribution of synaptophysin (a marker of synaptic number).Relative expression of NgR and synaptophysin in retina were analyzed by Western blot.Results RGC density in normal control group,diabetes group,siNgR group and scNgR group were (624.33 ± 3.51) mm-2,(420.00 ± 2.65) mm-2,(621.67 ± 1.53) mm-2,(416.67 ± 2.52) mm-2,respectively.There was significant difference among four groups (F =5985.37,P ＜ 0.01).Compared with normal control group,RGC density in diabetes group and scNgR group were obviously decreased (all P ＜0.01),but siNgR group had no obviously change (P ＞ 0.05).The synaptophysin mainly expressed in the inner and outer network layer.Compared with normal control group,the positive expression of synaptophysin in diabetes group and scNgR group were decreased,but siNgR group had no obviously change.The relative expression of NgR in normal control group,diabetes group,siNgR group and scNgR group were (11.26 ±0.02) ％,(19.38 ± 0.10) ％,(11.17 ± 0.02) ％,(19.47 ± 0.31) ％,respectively.There was significant difference among four groups (F =2466.09,P ＜ 0.01).Compared with normal control group,the relative expression of NgR in diabetes group and scNgR group were obviously decreased (all P ＜ 0.01),but siNgR group had no obviously change (P ＞0.05).The relative expression of synaptophysin in normal control group,diabetes group,siNgR group and scNgR group were (35.76 ± 0.15) ％,(25.47 ± 0.36) ％,(35.28 ± 0.12) ％,(25.03 ± 0.75) ％,respectively.There was significant difference among four groups (F =583.70,P ＜ 0.01).Compared with the normal control group,the expression of synaptophysin in diabetic group and scNgR group were decreased increased (all P ＜ 0.01),while there was no significant difference in siNgR group (P ＞ 0.05).Conclusion Inhibiting the expression of NgR in the retina of diabetic rats can help to restore the number of synapses and protect the damaged RGC.

Objective:To evaluate the role of natural killer T cells in renal fibrosis in mice with acute kidney injury (AKI).Methods:Twenty-four clean-grade healthy male C57BL/6 mice, aged 8-10 weeks, weighing 20-30 g, were divided into 4 groups ( n=6 each) using a random number table method: control group (group C), AKI group (group A), control plus CD1d antibody group (group C-MA), and AKI plus CD1d antibody group (group A-MA). The model of renal fibrosis in mice with AKI was established by intraperitoneal injection of folic acid 250 mg/kg.In group C, homotypic control antibody 20 mg/kg was injected via the tail vein.In group AKI, homotypic control antibody 20 mg/kg was injected via the tail vein at 24 h before establishing the model. In group C-MA, anti-CD1d monoclonal antibody 20 mg/kg was injected via the tail vein.In group A-MA, anti-CD1d monoclonal antibody 20 mg/kg was injected via the tail vein at 24 h before establishing the model.On the 14th day after folic acid injection, blood samples were taken from eyeballs to determine the concentrations of blood urea nitrogen (BUN) and creatinine (Cr) in serum.Then the mice were sacrificed, and the renal tissues were taken for Sirius red staining and HE staining to determine the area of renal fibrosis, and renal injury was scored.The expression of fibronectin (FN), type I collagen (Col-Ⅰ) and alpha-smooth muscle actin (α-SMA) in renal tissues was detected by immunofluorescence method.The expression of interleukin (IL)-4, IL-13, arginase-1 (Arg-1) and found in inflammatory zone 1 (FIZZ1) mRNA in renal tissues was detected by real-time polymerase chain reaction. Results:Compared with group C, the concentrations of BUN and Cr in serum, renal injury score, and area of renal fibrosis were significantly increased, the expression of FN, Col-Ⅰ and α-SMA and IL-4, IL-13, Arg-1 and FIZZ1 mRNA was up-regulated in A and A-MA groups ( P<0.05), and no significant change was found in the above indexes in group C-MA ( P>0.05). Compared with group A, the concentrations of BUN and Cr in serum, renal injury score, and area of renal fibrosis were significantly decreased, the expression of FN, Col-Ⅰ and α-SMA and IL-4, IL-13, Arg-1 and FIZZ1 mRNA was down-regulated in group A-MA ( P<0.05). Conclusion:Activation of natural killer T cells is involved in the process of renal fibrosis in mice with AKI, and the mechanism may be related to promoting the release of Th2 cytokines and M2 polarization of macrophages.

Objective To explore the diagnosis rate.pathology types and positive rate of cancer cell in spu-tum of early central pulmonary carcinoma in three obstructive signs on chest X ray screened by fiberbromchoscope.Methods 326 cases of three obstructive signs with high risk of lung cancer were screened for central pulmonarycarcinoma by spiral CT.biopsy by fiberbronchoscope and cytological examination of sputum.Results 32 patients were diagnosed with central pulmonary carcinoma,with morbidity of 9.8%.In these patients,21 were confirmed with obstructive pneumonia(65.6%),7 with obstructive atelectasis(21.9%),4 with obstructive emphysema(12.5%);In terms of pathology type,16 cases were defined as squamous cell carcinoma(50.0%),9 as small cell carcinoma(28.1%).3 were as large cell carcinoma(9.4%).2 were as adenocarcinoma(6.3%),1 as admosquamous carci-noma(3.1%),1 as bronchial gland carcinoma(3.1%);cancer cell could be found in sputum of 5 patients of 32 cases,among them,it was found in 3 of 21 patients with obstructive pneumonia(14.3%),1 in 7 patients with ob-structive atelectasis(14.3%),1 in 4 patients with obstructive emphysema(25.0%).Conclusion The prevelance of early central pulmonary carcinoma in three obstructive signs on chest X-ray is 9.815%,in which squamous carci-noma and small-cell carcinoma are common in pathology type.Screening can increase the detection rate of early pul-monary carcinoma.

Objective To investigate the effect of Dan-Hong injection on peripheral neuropathy in experimental rats with type Ⅰ diabetes.Methods Forty Wistar male rats were chose in our study and divided into Dan-Hong injection group,mecobalamin treatment group,model group and normal control group (n=10);rat models of type Ⅰ diabetes in the first three groups were induced by intraperitoneal injection of streptozotocin.Different drugs were given to these rats,and 12 weeks after model making,the blood glucose level and the body weight were measured;footprints gaits were analyzed;nerve conduction velocity was observed;immumohistochemical staining and HE staining were employed to detect the pathological alterations of intraepidermal nerve fiber and peripheral nerve tissues.Results As compared with model group,rats in Dan-Hong injection group had increased nerve conduction velocity and footprint parameters with statistical differences ([62.05±5.45] m/s vs [37.72±4.06] m/s;[22.00±0.34] mm vs [22.74±0.19] mm;[10.79±0.22] mm vs [11.49±0.14] mm;[17.50±0.16] mm vs [17.67±0.17] mm) (P＜0.05).The number of intraepidermal nerve fiber was increased and the pathological damage of peripheral nerves was obvious improved in the Dan-Hong injection group as compared with those in the model group;the nervous tissues showed edema with myelin fuzzy and swelling of the axon,which had been much improved as compared with those in the model group.Conclusions Dan-Hong injection can prevent and improve peripheral neuropathy of rats with type Ⅰ diabetes.

Objective To investigate the effects of miR-129-5p on the proliferation and migration of osteosarcoma cells and the regulation of HMGB1 gene. Methods The expression of miR-129-5p and HMGB1 in osteosarcoma cell line MG-63, Saos-2 and osteoblast hFOB1.19 were detected by RT-PCR and Western blot. Bioinformatics methods were used to predict whether there were binding sites between mir-129-5p and HMGB1 gene. Double luciferase reporter gene system was used to verify the interaction between miR-129-5p and the target gene HMGB1. miR-129-5p mimic and inhibitor were transfected into osteosarcoma cell lines with low and high miR-129-5p expression, respectively, and the transfection efficiency was detected by RT-PCR. After successful transfection, the proliferation and migration of osteosarcoma cell lines were detected by CCK-8 assay, scratch assay and Transwell migration assay, respectively, and Western blot was used to detect the expression of HMGB1 in the transfected osteosarcoma cell lines. Results Expression of miR-129-5p in osteosarcoma cells was lower than that in normal osteoblasts (P < 0.05), and the expression of HMGB1 in osteosarcoma cell lines was higher than that in normal osteoblasts (P < 0.05). There were binding sites between miR-129-5p and HMGB1 genes, and the luciferase activity of HMGB1-WT plasmid group was down-regulated after transfection with miR-129-5p mimic (P < 0.05). Transfection of miR-129-5p mimic significantly increased the expression of miR-129-5p in MG-63 cells (P < 0.05), inhibited the proliferation and migration of MG-63 cells (P < 0.05), and decreased the expression level of HMGB1. After transfection with miR-129-5p inhibitor, the expression of miR-129-5p in Saos-2 cells was significantly decreased (P < 0.05), the proliferation and migration abilities of Saos-2 cells were enhanced (P < 0.05), and the expression level of HMGB1 was also increased. Conclusion miR-129-5p may inhibit the proliferation and migration of osteosarcoma cells through HMGB1 gene.

Objective To investigate the promotion effect of Danhong injection (DH) on brain-derived neurotrophic factor (BDNF) expression in Schwann cells (SCs) of SD rats.Methods In experiment of SCs apoptosis induced by advanced glycation end products (AGEs),SCs were divided into control group,AGEs treatment group and DH+AGEs treatment group; 48 h after each treatment,the SCs count was compared.In experiment of DH affecting mRNA and protein BDNF expressions in SCs,real time-PCR and Western blotting were used.In the experiment of DH combined with different inhibitors (Calphostin C,LY294002,H89,U0126,FR180204 and SB203580) affecting mRNA BDNF expression in SCs,real time-PCR was used.Results The number of SCs in AGEs treatment group was significantly decreased than that in the control group,but that in DH+AGEs treatment group was statistically increased than that in AGEs group (P＜0.05).The mRNA and protein expressions of BDNF in the DH treatment group were significantly increased than those in the control group (P＜0.05).As compared with DH group,DH+Calphostin C treatment group had significantly decreased BDNF mRNA expression (P＜0.05); BDNF mRNA expression in the DH+U0126,DH+FR180204 and DH+SB203580 treatment groups was significantly decreased as compared with that in the DH treatment group (P＜0.05).Conclusions DH could effectively inhibit SCs apoptosis induced by AGEs and significantly promote BDNF expression;protein kinase C (Calphostin C) and mehtyl ethyl ketone (U0126)/extracellular regulated protein kinases (FR180204EK)/p38 (SB203580) may be the important signaling transconduction pathways for BDNF expression.

Objective:To evaluate the role of Jumonji domain-containing 3 (JMJD3) in cisplatin-induced renal fibrosis following acute kidney injury in mice.Methods:Forty-eight healthy C57BL/6 male mice, aged 8-10 weeks, weighing 20-30 g, were divided into 4 groups ( n=12 each) using a random number table method: control group (group CON), control plus JMJD3 inhibitor group (group CON-A), cisplatin group (group CIS), and cisplatin plus JMJD3 inhibitor group (group CIS-A). In group CIS and group CIS-A, cisplatin was intraperitoneally administered on 1st and 14th days, respectively, to develop a renal fibrosis model in mice with acute kidney injury, and the JMJD3 inhibitor GSKJ4 10 mg/kg and equal volume of PBS were intraperitoneally injected on 4th day, respectively, once every 3 days, 6 injections in total.The equal volume of PBS and GSKJ4 10 mg/kg were intraperitoneally injected at the corresponding time points in group CON and group CON-A, respectively.Six mice in each group were selected, and orbital blood samples were collected on 3rd day after the first injection of cisplatin to determine the concentrations of serum creatinine (Cr) and blood urea nitrogen (BUN), then the animals were sacrificed, and kidney tissues were obtained for microscopic examination of pathological changes after HE and PAS staining (with a light microscope), and the damage to kidneys was assessed and scored.Six mice were sacrificed on 28th day after the first injection of cisplatin, and kidney tissues were removed for determination of the area of renal fibrosis ( via Sirius red and Masson staining), expression of fibronectin (Fn), collagen type Ⅰ (Col Ⅰ) and α-smooth muscle actin (α-SMA) (by immunofluorescence), F4/80 + cell and CD3 + cell count (using immunohistochemical method), and expression of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), CXC chemokine ligand 16 (CXCL16), and monocyte chemoattractant protein1 (MCP-1) mRNA (by real-time polymerase chain reaction). Results:Compared with group CON, the serum BUN and Cr concentrations, renal injury scores, and area of renal fibrosis were significantly increased, the expression of Fn, Col Ⅰ and α-SMA was up-regulated, the F4/80 + cell and CD3 + cell count was increased, and the expression of IL-6, CXCL16, TNF-α and MCP-1 mRNA was up-regulated in group CIS ( P<0.05), and no significant change was found in the parameters mentioned above in group CON-A ( P>0.05). Compared with group CON-A, the serum BUN and Cr concentrations, renal injury scores, and area of renal fibrosis were significantly increased, the expression of Fn, Col Ⅰ and α-SMA was up-regulated, the F4/80 + cell and CD3 + cell count was increased, and the expression of IL-6, CXCL16, TNF-α and MCP-1 mRNA was up-regulated in group CIS-A ( P<0.05). Compared with group CIS, the serum BUN and Cr concentrations, renal injury scores, and area of renal fibrosis were significantly decreased, the expression of Fn, Col Ⅰ and α-SMA was down-regulated, the F4/80 + cell and CD3 + cell count was decreased, and the expression of IL-6, CXCL16, TNF-α and MCP-1 mRNA was down-regulated in group CIS-A ( P<0.05). Conclusions:JMJD3 is involved in the process of renal fibrosis following acute kidney injury in mice, and the mechanism may be related to promotion of inflammatory responses.

Objective:To evaluate the role of histone demethylase (JMJD3) in drug-induced acute kidney injury (AKI) in mice.Methods:Twenty-four male C57BL/6 mice, aged 8-10 weeks, weighing 20-30 g, were divided into 4 groups ( n =6 each) using a random number table method: control group (C group), AKI group, a specific JMJD3 inhibitor GSKJ4+ control group (GSKJ4 group), and GSKJ4-AKI group.Folic acid 250 mg/kg was injected intraperitoneally to develop AKI model.GSKJ4 20 mg/kg was intraperitoneally injected at 1 h before developing AKI model in GSKJ4-AKI group and at the corresponding time point in GSKJ4 group.Blood samples were collected at 72 h after development of AKI model for determination of serum BUN and Cr concentrations.The animals were then sacrificed and renal tissues were collected for microscopic examination of histopathological morphology (using HE and PAS staining) and for determination of cell apoptosis (by TUNEL) and expression of JMJD3, Bax and cleaved caspase-3 (by Western blot), the number of JMJD3, myeloperoxidase (MPO), F4/80 and CD3 positive cells, expression of cleaved caspase-3 and Bax, and expression of IL-1β, IL-6, TNF-α and monocyte chemotactic protein 1 (MCP-1) mRNA (by reverse transcription polymerase chain reaction). The damage to the renal tubules was scored. Results:Compared with C group, the serum BUN and Cr concentrations and renal tubular damage score were significantly increased, the number of JMJD3, myeloperoxidase (MPO), F4/80 and CD3 + positive cells was increased, the number of apoptotic cells was increased, and the expression of Bax, cleaved caspase-3, JMJD3 and IL-1β, TNF-α, IL-6 and MCP-1 mRNA was up-regulated in AKI group ( P<0.05), and no significant change was found in the parameters mentioned above in GSKJ4 group ( P>0.05). Compared with AKI group, the serum BUN and Cr concentrations and renal tubular damage score were significantly decreased, the number of JMJD3, myeloperoxidase (MPO), F4/80 and CD3 positive cells was decreased, the number of apoptotic cells was decreased, and the expression of Bax, cleaved caspase-3, JMJD3, and IL-1β, TNF-α, IL-6 and MCP-1 mRNA was down-regulated in GSKJ4-AKI group ( P<0.05). Conclusions:The mechanism of drug-associated AKI may be related to up-regulation of JMJD3 expression and thus induces cell apoptosis and inflammatory responses in mice.