Objective To observe the clinical efficacy of pricking Sifeng (EX-UE10) plus Chinese medication in treating anorexia in kids, and to provide clinical evidence for the treatment of kid’s anorexia with traditional Chinese medicine. Method Seventy-six eligible anorexia patients were randomized into an observation group and a control group. The control group was intervened by orally taking Chinese medication, while the observation group was by pricking Sifeng plus Chinese medication, and the clinical efficacies were compared 1 month later. Result After treatment, the scores of poor appetite and decreased food intake in the observation group were significantly lower than that in the control group (P<0.05); the recovery rate was 34.2% in the observation group versus 13.2% in the control group, and the recovery rate in the observation group was significantly higher than that in the control group (P<0.05). Conclusion Pricking Sifeng plus Chinese medication can produce a significant clinical efficacy in treating anorexia in kids.

Aim To study the effect of ginsenoside Rg1(Rg1)on cardio myocyte hypertrophy induced by prostaglandin F2?(PGF2?),and to probe primarily into its mechanism.Methods The cultured neonatal rat cardiomyocyte hypertrophic response and the antihypertrophic effects of Rg1 were observed by measuring the cell diameter,protein content and the expression of atrial natriuretic factor(ANF) mRNA,which was assayed by real-time PCR.For mechanism studies,the intracellular free calcium concentration(i) in cultured cardiomyocytes was measured by using Fura-2/AM as a fluorescent indicator,nitric oxide(NO) metabolite level in the culture medium was tested by using Nitric Oxide Synthase Detection Kit.Results PGF2? 0.1 ?mol?L-1 caused the increases in the cardiomyocyte cell diameter,protein content and the expression of ANF mRNA.It could increase the i in cultured cardiomyocytes.Rg1 15.6、31.2、62.4 ?mol?L-1 could concentration-dependently inhibit the cardiomyocyte hypertrophy induced by PGF2?,and the cell diameter of cardiomyocyte treated by PGF2? was decreased by 18.4%、32.7%、43.8%(P

OBJECTIVE:To optimize Azelastine hydrochloride (AH) thermosensitive in-situ gel nasal drops formulation. METHODS:Using poloxamer 407(P407)and poloxamer 188(P188)as excipients,AH thermosensitive in-situ gel was prepared by cold solution method. The formulation was optimized by central composite design-response surface methodology using the amount of P407 and P188(g/100 ml)as factors and phase-transition temperature as index. Binomial expression was fitted,and pre-dicted and measured values were compared. RESULTS:The correlation coefficient R2 fitted by binomial expression was equal to 0.986 5. The optimal formulation was as follows as P407 for 20.414 4%,P188 for 5.035 4%,measured value of(30.81±0.02)℃, predicted values of 31 ℃,deviation of 0.61%. CONCLUSIONS:AH thermosensitive in-situ gel nasal drops formulation is opti-mized by central composite design-response surface methodology.

Objective:To study the effects of cells ’ and bacteria ’s adhesion and proliferation on different fiber diameters of polypyrrole coating with electricity.Methods:Titanium coated with polypyr-role was divided into no electrical stimulation and stimulation groups,each group had 30-60 nm,70-1 00 nm,1 30-1 70 nm diameters of the fiber.MC3 T3 cells and Staphylococcus aureus (S.aureus)were inoculated on different fiber diameters of polypyrrole coating with and without electric stimulation .We gave the electrical stimulation group 1 00 mV for 1 h and every 24 hours gave it 1 h stimulation,and no e-lectrical stimulation group was not managed.We used scanning electron microscope (SEM)to observe the cells’and bacteria’s morphology.The cells were given 20 mL CCK-8 solutions after 1 ,3,7 days’ cultivation,then incubated for 2 h,the solution was transferred to 96-well plate,we measured the cells’ CCK-8 of the 30-60 nm,70-1 00 nm,and 1 30-1 70 nm groups by Elisa.The cells on different fiber diameters were also stained by live-dead cell staining kit,TritonX-1 00 and DAPI.We used PBS to wash and glycerin to seal them.The live-dead situation and morphology were tested by co focal microscope. The bacterial were stained by Live/dead baclight bacterial viability kits,we detect the suspension’s D of the 30-60 nm,70-1 00 nm,and 1 30-1 70 nm groups,and also observed the bacteria’s survival situa-tion by co focal microscope.Results:The CCK-8 of the cells with direct current stimulation was higher than that of the unpowered group (F=1 2.248,P=0.006).The smaller the fiber diameter,the better was the cell’s adhesion and proliferation (F=9.261 ,P=0.005).The bacterial suspension’s D of the electric group was lower than that of the unpowered group,and the fiber diameter had no significant effect on the bacteria’s growth(F=9.641 ,P=0.036).Conclusion:Polypyrrole coating with electricity can promote the cell’s proliferation and inhibit the bacteria’s proliferation,and the cell growth on small fiber diameter coating is better.There is no difference in the bacterial growth of different fiber diameter coatings.

Objective To investigate the phenotype, genotype and molecular mechanisms in four Chinese pedigrees with venous thrombosis caused by hereditary PC deficiency. Methods The plasma activity of PC: A, TPS: A and FPS: A of the probands and their family members were detected with chromogenic and coagulation assay. The antigen of PC and FPS were identified with ELISA. Thrombin generation tests were applied to indicate the coagulation status. All of the nine exons and intron-exon boundaries of PC gene and PS gene were amplified by PCR and directly sequenced for mutaiton investigation. Results Compound heterozygous mutations of L-34P, K150del and A209V with 36% of PC: A and 57% of PC: Ag were identified in proband 1. PC: A was 46% , PC: Ag was 64. 4% while TPS: A, FPS: A and FPS: Ag were 36% , 19.5% and 20.9% respectively in proband 2. Two independent heterozygous mutations of R147W in PC gene inherited from his mother and T519stop in PS gene inherited from his father were identified. The anticoagulant activity of Proband 2 and his parents were declined in thrombin generation assay. In proband with PS defeciency and his father, the inhibition of thrombin generation capacity was decreased with exogenous APC, while his mother did not have significant difference. In Proband 3, PC: A was 32% while PC: Ag was 48.42% . Two independent mutations of R147W and R178W in Exon 7 were detected. Compound heterozygous mutations of R178W and D255H,with 21% of PC : A and 18. 36% of PC: Ag were identified in the Proband 4. Conclusions Hereditary PC deficiency or combined PC and PS deficiency result in venous thrombosis in four Chinese families. Mutants of L-34P, A209V, R178W, R147W and D255H might be the molecular mechanisms of PC deficiency.

Objective To investigate the clinical phenotype and genotype in three probands with antithmmbin(AT)deficiency and their families,and to identify the molecular mechanism of AT deficiency.Methods Chromogenic substrate method and immunoturbidimetry assay was used to detect the plasma levels of AT:A and AT:Ag,respectively.Genomic DNA was extracted from the peripheral blood.All 7 exons and the flanking sequences were amplified by PCR.and the abnormal mutant genes were analyzed by direct sequencing.Western blot was used to detect the AT levels and thrombin generation tests were used to detect coagulation status.Results The plasma levels of AT:A and AT:Ag of the three probands declined by 50%.G7386C(Trp225Cys)mutation in exon 4,C2591G(Ser36stop)in exon 2 and C9819T(Arg359stop)in exon 5 were characterized in the three prebands and they could result in W(Trp)225C(Cys)missense mutation,S(Set)36X(stop)nonsense mutation and R(Arg)359X(stop)nonsense mutation respectively,The testing results of phenotype and genotype from some of their family members showed consistent with results from the probands.Western blot results indicated that the Icyels of PC:Ag were lower compared with the normal pooled plasma.The hypercoagulative status was present in the probands using thrombin generation tests.Conclusions Type Ⅰ hereditary AT deficiency was found in these three families.The 3 heterozygous mutations.W225C,S36X and R359X are genetic defects of hereditary AT deficiency.W225C and S36X have not been described before.

Objective To describe the clinical features and imaging characteristics of nodular splenic sarcoidosis. Methods We describe a patient with splenic sarcoidosis and review the related medical literature, the etiology, symptomatology, pathology, diagnosis, differential diagnosis, management and prognosis of splenic sarcoidosis. Results The etiology of this rare disease remains unknown. Symptoms are scanty and usually mild; computed tomography usually reveals splenomegaly or the presence of multiple nodules, confusing with metastatic tumor in spleen. On histopathologic examination, sarcoid produces noncaseating granulomas. Sarcoid is typically treated only when symptomatic. Oral corticosteroids is the most important method of treatment in patients with progressive loss of organ functions. Prognosis has closed relationship with early clinical manifestation. Conclusion Splenic sarcoidosis is rare and often misdiagnosis as other diseases.

10.3969/j.issn.1000-3606.2013.06.019

With the improvement of system frame and reconstruction methods in fluorescent molecules tomography (FMT), the FMT technology has been widely used as an important experimental tool in biomedical research. It is necessary to get the 3D-surface profile of the experimental object as the boundary constraints of FMT reconstruction algorithms. We proposed a new 3D-surface reconstruction method based on Fourier transform profilometry (FTP) method under the blue-purple light condition. The slice images were reconstructed using proper image processing methods, frequency spectrum analysis and filtering. The results of experiment showed that the method properly reconstructed the 3D-surface of objects and has the mm-level accuracy. Compared to other methods, this one is simple and fast. Besides its well-reconstructed, the proposed method could help monitor the behavior of the object during the experiment to ensure the correspondence of the imaging process. Furthermore, the method chooses blue-purple light section as its light source to avoid the interference towards fluorescence imaging.
Algorithms ; Biophysical Phenomena ; Fluorescence ; Fourier Analysis ; Image Processing, Computer-Assisted ; Imaging, Three-Dimensional ; methods ; Surface Properties ; Tomography ; methods

Objective To investigate the protective effects of selenium on nitric oxide(NO)-mediated myocardial apoptosis.Methods The AC16 cardiomyocyte cultured in vitro were divided into control group,selenium treatmentgroup,sodium nitroprusside(SNP) treatment group and selenium + SNP treatment group,SNP was the exogenous NO donor.There was no intervention in the control group,and an equal volume of the culture solution was added to the treatment groups.The selenium treatment group added a dose of 100 μg/L of selenium,the SNP treatment group added a dose of 1.0 mmol/L of SNP,and the selenium + SNP treatment group was pretreated by 100 μg/L selenium for 4 h followed by 1.0 mmol/L SNP;the cells or supernatants were collected after 24 h of culture.The content of NO was detected by Griess method in supernatants.The level of cell reactive oxygen species was detected by flow cytometry.The changes of cell mitochondrial membrane potential and apoptosis were observed under fluorescence microscope.The real-time quantitative PCR and Western blotting were used to detect the mRNA and protein expression levels of apoptosis-related genes B-cell lymphoma-2 (Bcl-2) associated X protein (Bax) and Bcl-2,respectively.Results The NO content in the control group,selenium treatment group,SNP treatment group and selenium + SNP treatment group were (10.3 ± 1.8),(9.2 ± 2.1),(15.2 ± 3.5),(14.3 ± 2.6) μmmol/L,respectively;SNP had a main effect on NO content (F =23.33,P ＜ 0.05).The cell reactive oxygen species were 31.63 ± 1.40,29.52 ± 2.86,60.62 ± 4.83,50.08 ± 2.41,respectively;selenium and SNP had main effects on reactive oxygen species (F =12.19,187.20,P ＜ 0.05),selenium combined with SNP had an interactive effect on reactive oxygen species (F =5.42,P ＜ 0.05).The cell mitochondrial membrane potential levels were 0.42 ± 0.11,0.37 ± 0.07,7.25 ± 1.91,and 5.21 ± 1.59,respectively;selenium and SNP had main effects on cell mitochondrial membrane potential levels (F =14.21,440.01,P ＜ 0.05),selenium combined with SNP had an interactive effect on cell mitochondrial membrane potential levels (F =12.89,P ＜ 0.05).Selenium had main effects on nuclear pyknosis ratio,Bcl-2 mRNA and Bax protein expressions (F =9.52,10.84,22.17,P ＜ 0.05);SNP had main effects on nuclear pyknosis ratio,Bax and Bcl-2 mRNA expressions,and Bcl-2 protein expression (F =192.86,21.90,16.09,18.39,P ＜ 0.05);selenium combined with SNP had an interactive effect on Bax,Bcl-2 mRNA and protein expressions (F =20.51,7.59,15.38,11.97,P ＜ 0.05).Conclusion The SNP can induce apoptosis of AC16 cardiomyocyte;selenium combined with SNP has an interactive effect on AC16 cardiomyocyte,indicating that selenium has protective effect on NO modiated myocardial apoptosis.