OBJECTIVETo design and improve signal processing algorithms of ophthalmic ultrasonography based on FPGA.

METHODSAchieved three signal processing modules: full parallel distributed dynamic filter, digital quadrature demodulation, logarithmic compression, using Verilog HDL hardware language in Quartus II.

RESULTSCompared to the original system, the hardware cost is reduced, the whole image shows clearer and more information of the deep eyeball contained in the image, the depth of detection increases from 5 cm to 6 cm.

CONCLUSIONThe new algorithms meet the design requirements and achieve the system's optimization that they can effectively improve the image quality of existing equipment.

Algorithms ; Data Compression ; Diagnostic Imaging ; Ophthalmology ; Signal Processing, Computer-Assisted ; Ultrasonography

Objective Currently,pediatric 18F-FDG dose and acquisition durations are generally based on coarse extrapolation from adult guidelines.This study sought to determine whether shorter acquisition durations or a lower 18F-FDG injected activity could be used during pediatric 18F-FDG PET/CT examinations while maintaining diagnostic utility.Methods Thirty-six whole-body 18F-FDG PET/CT examinations were performed on 36 patients (weight,13-89 kg,(46.51±5.63) kg; age range,3-14 years old,(9.22±3.16) years old) with a weight-based injected activity (5.3 MBq/kg (0.144 mCi/kg)),fixed acquisition durations 180 S/FOV,VIP record acquisition mode using Discovery STE.For each examination,the Vip-mode data was truncated to form multiple datasets with shorter acquisition durations down to a minimum of 60 s/FOV (i.e.,60,80,100,120,140,160 s/FOV data were formed from single 180 s/FOV acquisition).168 image volumes were generated,randomized,and reviewed in a masked manner with corresponding CT image volumes by 6 radiologists.Overall,subjective adequacy and objective lesion detection accuracy by body region were evaluated.Results All examinations with maximum acquisition duration were graded as adequate and were used as the reference standard for detection accuracy.For patients more than 30 kg,when acquisition duration was more than 120 s/FOV,all PET/CT examinations were graded as adequate for clinical tasks,whereas,when acquisition duration was reduced to less than 120 s/FOV,lesion detection became less accurate.For patients less than 30 kg,lesion detection accuracy was perfect for acquisition times between 140 s/FOV and 180 s/FOV for all regions of the body.However,lesion detection became less accurate when imaging acquisition time was reduced less than 140 s/FOV.Conclusions When GE Discovery STE PET/CT was applied during pediatric PET/CT examination,using decreased acquisition times as a surrogate for 18F-FDG dose,18F-FDG dose can be reduced by approximately 33.33％ when patients weigh over 30 kg were scanned for 180 s/FOV.For patients less than 30 kg,18F-FDG dose can be reduced by approximately 22.22％ without losing diagnostic quality.Reduction of overall scan time potentially reduces motion artifacts,improves patient comfort,and decreases length of sedation.Alternatively,decreased 18F-FDG dose minimizes radiation risk.

Burn patients often suffer from different degrees of dysfunction, such as residual burn wounds, formation of hyperplastic scar, scar itching, cardiopulmonary dysfunction, limitation of motion, and psychological disorders, which exert severe impact on their daily life. This article reviews various rehabilitation treatments for dysfunction after burn injury to promote rehabilitation of burn patients.
Burns ; physiopathology ; rehabilitation ; China ; Humans ; Rehabilitation ; methods

Background Diabetic complication is associated with lipid peroxidation.Aldehyde dehydrogenases (ALDH) catalyze the irreversible oxidation of a variety of biological aldehydes,including lipid-derived aldehydes (LDAs),and thus protect organs and tissues from toxic LDAs.Understanding the activity of ALDH in different ocular tissues in diabetic subjects is very important for prevention and treatment of diabetic ocular complications.Objective This research aimed to investigate the activity and expression of ALDH in different ocular tissues in diabetic rats and to explore the mechanism of ALDH in diabetes-induced eye disease.Methods Twenty-eight healthy SPF male Sprague-Dawley(SD) rats weighted 170-180 g were randomly divided into the normal control group and diabetic group.The diabetic animal model was established by intraperitonial injection of 4％ streptozotocin at 65 mg/kg.Isometric citric acid buffer was injected in the rats of the normal control group.The rats were sacrificed in each group 2 and 4 months after the establishment of the diabetic models,and eyeballs were obtained for the preparation of corneal,lens and retinal homogenates.ALDH activity was detected using a multifunctional microplate reader SpectraMax M5,and ALDH content was measured by ELISA at the wavelength of 450 nm with the SpectraMax M5 ELISA reader.Results The blood glucose level in diabetic rats was significantly elevated at various time points compared with the normal control group(P=0.000),and body weights were evidently lower in the diabetic group than in the normal group (P =0.000).The activities of ALDH (A340) in corneal,lens and retinal tissues in the diabetic group were increased in comparison with the normal control group (F =396.601,P=0.000),and showed an enhancement with the lapsing of time (F =53.139,P =0.000).In addition,the highest level of ALDH was found in the cornea and the lowest level in the lens(F =6973.000,P=0.000).The expression level of ALDH in the corneal,lens and retinal homogenates was significantly higher in the diabetic group compared with the normal control group (F=312.985,P =0.000) and showed a considerable increase over the course (F =19.203,P=0.000).The highest expression level was seen in the cornea and the lowest was in the lens,with a significant difference among these three kinds of tissues (F =3243.000,P =0.000).Conclusions ALDH can protect ocular tissue from the damage of lipid peroxidation.Thess results suggest that ALDH plays a role in preventing diabetes-related ocular complications.

Background Retinal neovascular diseases affect visual function.Although many drugs have been used to manage the visual diseases,their effectiveness is less than satisfactory.Studies showed that ursolic acid has multiple biological effects including anti-vascularization.However,the effect of ursolic acid on retinal neovascular diseases is unclear now.Objective This study was to observe the inhibitory effect of ursolic acid on the high oxygen-induced mouse retinal neovascularization after intravitreal injection.Methods Sixty clean 7-day-old C57BL/6J mice were divided into the blank control group,PBS control group,positive control group (triamcinolone) and low,moderate and high dose (1.5,3.0 and 6.0 μg) ursolic acid groups randomly.The blank control group mice were raised in normal environment,and the mice from other groups were fed in the environment with O2 concentration at (75±2)％ for 5 days together with the maternal mice.The mice then were back to the normal air environment to induce retinal neovascularization.Then,the drugs were intravitreally immediately injected in the mice of the different groups.The mice were sacrificed at the 17-day old for the preparation of retinal sections.Retinal new blood vessel was examined by haematoxylin and eosin stain under the light microscope,and the number of vascular endothelial cell nucleus breaking the inner limiting membrane was counted.The gene expressions of vascular endothelial growth factor (VEGF),cyclooxygenase-2 (COX-2) and matrix metalloproteinase-2 (MMP-2) in the mouse retinas were quantitatively assayed using reverse transcription PCR.Results The number of endothelial nuclei newly-generated vessel breaking internal limiting membrane in the mice of PBS control group was (18.65±3.24)/field,which was more than (0.78±0.11)/field of the blank control group obviously (t =2.24,P＜0.05).The number of endothelial nuclei newly-generated breaking internal limiting membrane in the moderate-or high-dose ursolic acid group was less than that of moderate group obviously,it was statistically significant(P＜0.05).The number of vascular endothelial cell nuclei breaking internal limiting membrane in high high-dose group was (13.32 ± 1.87)/field and (8.93 ± 1.09) /field,showing significant decreases in comparison with the PBS control group and low-dose ursolic acid group (18.65±3.24)/field (15.44±2.02)/field (all at P＜0.05).However,no significant difference were seen in the number of new vascular endothelial cell nucleus between the high-dose ursolic acid group and the positive control group(9.14±1.13)/field (t=1.17,P＞0.05).The relative expressions of COX-2 mRNA,VEGF mRNA and MMP-2 mRNA in the mouse retinas were higher in the PBS control group than those in the blank control group (t =13.45,12.49,14.32,all at P＜0.05),and those in the moderate-dose or high-dose ursolic acid group were lowed in comparison with the PBS control group and the low-dose ursolic acid group (all at P＜0.05),but there were no significant differences between the high-dose ursolic acid group and the positive control group (all at P＞0.05).Conclusions Ursolic acid can suppress retinal neovascularization by down-regulating the expressions of VEGF,COX-2 and MMP-2 in oxygen-induced retinopathy of mouse in dose-dependent manner.

Objective:Cancer stem cells (CSCs) are resistant to chemotherapy. Our study aimed to investigate the stem cell-like proper-ties of doxorubicin-resistant osteosarcoma cell line 143B and its correlation with Notch signaling. Methods:We generated doxorubicin-resistant osteosarcoma cells by treating them with 2μm doxorubicin. Stem cell-like properties such as morphology change, Stro-1/CD117 double positive ratio, stem cell-related gene expression, sphere formation efficiency, and EMT character were assessed on day 5 after doxorubicin withdrawal. Notch receptor and its target genes were examined using qPCR and Western blot analysis. The stem cell-like properties of doxorubicin-resistant osteosarcoma cells were assessed when pretreated with Notch inhibitor or vehicle. The an-ti-tumor effect of Notch inhibitor was tested using a xenograft model. Results:Doxorubicin-resistant osteosarcoma cells were enriched in Stro-1+/CD117+cells, which showed obvious increased expression of stem cell-related genes, and exhibited enhanced spheroid for-mation and evident mesenchymal characteristics unlike doxorubicin-sensitive cells. qPCR and Western blot assays showed that Notch intracellular domain 1 (NICD1) and target genes Hes1 and Hey1 were upregulated in doxorubicin-resistant osteosarcoma stem cells compared with those in vehicle cells. Furthermore, pretreatment with a γ-secretase inhibitor (GSI) to prevent Notch signaling en-hanced chemo-sensitivity and inhibited doxorubicin-enriched osteosarcoma stem cell activity in vitro. Finally, the Notch inhibitor pre-vented tumor growth in mice xenograft models. Conclusion: Doxorubicin induced the enrichment of osteosarcoma stem-like cells through Notch signaling, and inactivation of Notch could be useful for overcoming drug resistance and eliminating osteosarcoma.

Carcinoma, Hepatocellular ; genetics ; Cloning, Molecular ; DNA, Complementary ; isolation & purification ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Humans ; Liver Neoplasms ; genetics ; Male ; Middle Aged ; Nucleic Acid Hybridization ; methods ; Sequence Analysis, DNA

OBJECTIVETo study the roles of platelet (PLT) and its regulating factors, megakaryocyte, thrombopoietin (TPO) and transforming growth factor beta1 (TGF-beta1), in immune vasculitis in young rabbits.

METHODSAn experimental model of Kawasaki disease (KD) of weanling rabbits was reproduced by bovine serum. PLT count, total number and differentiating count of megakaryocyte, and serum TPO and TGF-beta1 levels were measured 0, 4, 8, 12, 16, 20, 24 and 28 days after KD induction. Pathological analysis of coronary artery, liver, spleen, kidney and brain was performed 17 and 28 days after KD induction.

RESULTSIn the KD group, PLT count, the total number of megakaryocyte, and the middle board megakaryocyte percentage increased 12, 16, 20, 24 and 28 days; serum TPO level increased 8, 12, 16, 20, 24 and 28 days; serum TGF-beta1 level increased 16, 20, 24 and 28 days after KD induction compared with those in the normal control group (p<0.05). The pathological examinations of coronary artery, liver, spleen, kidney and brain showed severe inflammatory injuries of tiny arteries and small/medium-sized arteries 17 and 28 days after KD induction, respectively in the KD group. The aortas were showed as mild inflammatory injuries.

CONCLUSIONSPLT, megakaryocyte, TPO and TGF-beta1 participate in the pathogenesis of KD, and they may play an important role in the injuries of immune vasculitis. This suggests that they may serve as markers for the assessment of severity in KD.

Animals ; Blood Platelets ; physiology ; Disease Models, Animal ; Humans ; Megakaryocytes ; physiology ; Mucocutaneous Lymph Node Syndrome ; etiology ; Rabbits ; Thrombopoietin ; physiology ; Transforming Growth Factor beta1 ; physiology ; Vasculitis ; etiology ; immunology ; pathology

Biomarkers, Tumor ; genetics ; Carcinoma, Hepatocellular ; genetics ; Cell Line ; Hepatocytes ; cytology ; Humans ; Liver Neoplasms ; genetics ; Transfection

The aim of this study is to explore the tissue distribution of PEGylated puerarin in acute myocardial ischemia model rats. Healthy male SD rats were randomly divided into two groups (30 each). Both were given PEGylated puerarin at a dose of 488 mg x kg(-1). After 5 min of medication, one group was normal rats, another group with acute myocardial ischemia was established by peritoneal injection of 50 mg x kg(-1) isoprenaline. After administration, the animals were executed at 30, 60, 90, 120, 150 and 180 min, then heart, liver, spleen, lung, kidney were extracted. The content of puerarin in organ tissue was determined by HPLC. The results showed that the AUC of tissue distribution of PEGylated puerarin in normal rats was liver > kidney > heart ≈ spleen > lung > brain. While the AUC of tissue distribution of PEGylated puerarin in acute myocardial ischemia model rats was liver ≈ heart > kidney > lung ≈ spleen > brain. AUC(heart) of PEGylated puerarin in acute myocardial ischemia model rats was 1.7 times than that of the normal rats, and there was significant difference (P < 0.05). Thus, PEGylated puerarin had a good heart-targeting property in early myocardial infarction area, drugs could accumulate in the ischemic myocardium. It provided important information for further study and clinic use of PEGylated puerarin.
Animals ; Brain ; metabolism ; Isoflavones ; pharmacokinetics ; Kidney ; metabolism ; Liver ; metabolism ; Lung ; metabolism ; Male ; Myocardial Ischemia ; metabolism ; Myocardium ; metabolism ; Rats ; Rats, Sprague-Dawley ; Spleen ; metabolism ; Tissue Distribution