Objective To explore the effects of isoalantolactone on the proliferation of human chronic myelogenous leukemia drug-resistant cell line K562/A02. Methods K562/A02 cells were treated with 6.25, 12.5, 25, 50 and 100 μmol/L isoalantolactone for 24 and 48 h, cell viability was analyzed with MMT assay. K562/A02 cells were treated with 10, 15, 20 μmol/L isoalantolactone for 24 h. Flow cytometry was used to examine the effect of isoalantolactone on the cell-cycle and apoptosis of K562/A02 cells. The related proteins were analyzed using Western blot. One-way ANOVA was used for statistical analysis. Results Isoalantolactone effectively inhibited the proliferation of K562/A02 cells in a dose-dependent manner (P<0.05) with IC50 value of (15.00 ±1.03) μmol/L at 24 h, respectively; Flow cytometry displayed that isoalantolactone may induce K562/A02 cells apoptosis in a concentration-dependent manner (P<0.05). The apoptotic rate significantly increased from (2.71 ±0.52) % in the control group to (19.10 ±1.55) %, (27.61 ± 2.32)%and (32.01±3.01)%(F=33.901, P<0.05), respectively, after treatment with 10, 15, and 20 μmol/L of isoalantolactone for 24 h. The percentage of cells in the S phase increased from (57.80±2.11) % to (68.62± 2.89)%, (78.41±3.51)%and (80.61±2.90)%, respectively (F=51.328, P<0.05). Western blot indicated that the expression of bcl-2, p-bcr-abl, p-STAT5, CDK2 and cyclin A significantly decreased (P< 0.05), and that of cytochrome C, Bax, and p21 increased with the increasing of isoalantolactone concentration (P< 0.05). Conclusion Isoalantolactone can significantly inhibit the proliferation of K562/A02 cells through bcr-abl-STAT5 signaling pathway.

Objective: This study proposed a possible molecular mechanism underlying centrosome amplification in oral squa-mous cell carcinoma (OSCC) by analyzing the relationship of centrosome amplification with the expression of STK15 and p53 in OS-CC tissues. Methods: The expression of STK15 and p53 in formalin-fixed, paraffin-embedded tissues from 8 patients with normal oral epithelium and 43 with OSCC were quantitatively analyzed by immunohistochemistry. Centrosome status was investigated by an indi-rect-immunofluorescence double-staining method to determine the message of centrosome amplification in OSCC. The correlation of the expression of the two proteins with centrosome amplification in OSCC was statistically analyzed with SPSS13.0. Results: Normal oral epithelium showed normal centrosomes in epithelium cells, whereas 33 of the 43 OSCC cases (76.74%) showed evidence of centro-some amplification. STK15 was undetectable in normal oral epithelium. The percentage of STK15 overexpression was 67.44% in OS-CC (P=0.028). The percentage of STK15 overexpression was significantly higher in OSCC with positive p53 staining than in OSCC with negative p53 staining (P=0.01). Spearman correlation analysis indicated a correlation between STK15/p53 positive co-expression and centrosome amplification of OSCC (P=0.019). Conclusion: Centrosome amplification is a common abnormal phenomenon in OS-CC. The p53/STK15 trans-activation-independent pathway plays a role in the systemic molecular regulation of centrosome in OSCC, which leads to the occurrence of OSCC.

With the increasing incidence and prevalence of male sexual dysfunction, andrologists are more and more in need of accurate and efficient tools to assess therapeutic efficacy and patients' satisfaction and to help patients achieve satisfactory treatment results. This article summarizes some of the most commonly used questionnaires for the diagnosis and assessment of the treatment of male sexual dysfunction, including International Index of Erectile Function (IIEF), Erection Hardness Score (EHS), Quality of Erection Questionnaire (QEQ), Erectile Dysfunction Inventory of Treatment Satisfaction (EDITS), Treatment Satisfaction Scale (TSS), Self-Esteem and Relationship (SEAR), Premature Ejaculation Profile (PEP), Premature Ejaculation Diagnostic Tool (PEDT), Index of Premature Ejaculation (IPE), Arabic Index of Premature Ejaculation (AIPE), Aging Male Symptoms Scale (AMS), Androgen Deficiency in the Aging Male (ADAM), and Symptomatic Inventory for Screening Late-Onset Hypogonadism in Males (SILOH), and presents an overview on their clinical application.
Erectile Dysfunction ; Humans ; Male ; Surveys and Questionnaires

Objective To explore the inhibitory effect of polyphyllin D on the proliferation of human chronic myelogenous leukemia (CML) cell line K562 and its mechanism. Methods K562 cells were treated with various concentrations of polyphyllin D (0, 0.1, 0.2, 0.4, 0.8, 1.2, 2.4 μmol/L) at 24 h, and cell viability was assessed by CCK-8 assay. Flow cytometry was used to detect the effect of polyphyllin D on the apoptosis, and the cell cycle arrest of K562 cells. The relative proteins were analyzed by using Western blot. Results The polyphyllin D could significantly inhibit the proliferation of K562 cells, and the effective inhibitory concentration (IC50) was (0.9 ± 0.1) μmol/L at 24 h. The results of flow cytometry showed that after treatment with 0.9 μmol/L polyphyllin D at 12 h and 24 h, the apoptotic rate of the cells [(11.46 ±1.51) %, (28.87 ± 2.35) %] were significantly higher than that of the control group [(2.05±0.45) %], and the difference was statistically significant (F= 38.637, P< 0.05). The expressions of bcl-2, CDK1, CyclinB1 and bcr-abl fusion protein were down-regulated by polyphyllin D, and the expressions of Bax, cytochrome C, activated caspase-3 and p21 were up-regulated (all P<0.05). In addition, polyphyllin D could arrest cell-cycle at G2/M phase (F=42.355, P<0.05). Conclusion Polyphyllin D can significantly inhibit the proliferation of human CML cell line K562, and its mechanism could play a role by inducing apoptosis and promoting cell cycle arrest.

Brain ; diagnostic imaging ; Child, Preschool ; Electroencephalography ; Female ; Gastroenteritis ; complications ; Humans ; Infant ; Male ; Seizures ; etiology ; Tomography, X-Ray Computed

Purpose The research was conducted to evaluate the stability of N-terminal site-specific PEGylated uricase. Methods The enzyme activity is used as an index to evaluate the thermal stability (at 4-80 ℃) , the pH stability, the ability of avoiding the trypsin digestion and half-life in vivo of PEG-uricase, then it is compared with uricase. Results PEGylated uricase is thermally more stable than uricase between 4 ℃ and 60 ℃, but at 70 ℃, the enzyme activity of both PEG-uricase and uricase decreases sharply. In the test of pH stability, the curve of uricase shows an obvious decrease of enzyme activity at 5 .2-6.0 and 9.2-10.0. The behavior of PEG-uricase indicates that the destabilizing was prevented effectively by PEGylation. The test of anti-trypsin digestion suggests that PEG-uricase retains 70% of its enzyme activity,but uricase only 20% ,200 minutes after being reserved in trypsin solution. Stability in vivo indicates that the half-life of PEG-uricase is 1 530 min and uricase, only 45 min. Conclusion PEGylated uricase has improved thermal stability, the pH stability, ability of protecting from trypsin digestion and stability in vivo.

Objective To evaluate the efficacy of multislice helical CT(MSCT) in the diagnosis of coronary artery disease Methods 30 patients were studied with MSCT CT data were reconstructed to demonstrate the abnormalities of coronary artery and the results were compared with that of angiography Results In patients with heart rate less than 60 BPM, there was no difference to show the main branch of left coronary artery and left descending artery compared with more than 60 BPM( P =0 197 and 0 128,Fisher′exact);and obvious differences in showing left circumflex artery (? 2=5 88, P

Objective To demonstrate the origin of the right inferior phrenic artery(RIPA) in normal and hepatocellular carcinoma(HCC) patients and provide valuable anatomical information for angiographers before and after transcatheter arterial chemoembolization(TACE).Methods Four hundred and forty consecutive patients including 133 HCC cases who had biphase abdominal CT were assessed in this study.The routine abdominal enhanced CT scan(GE,LightSpeed16) was performed with 120 kV,200—240 mAs,10 mm collimation,1.375 pitch,and 10 mm reconstruction interval at 22—25 seconds for arterial phase triggered by timing bolus,60 seconds for portal venous phase after injection of 100 ml contrast material(300 mg I/ml) at a rate of 3.5 ml/s.Multiplanar reconstruction(MPR) and maximum intensity projection(MIP) images were generated using 1.25 mm images reconstructed with 1 mm interval in arterial phase and reviewed by two radiologists.An enhanced artery medial-posterior to the IVC,originated from aorta or its branches to the diaphragmatic dome was interpreted as the RIPA.Results The RIPA was showed in all(440 patients)(100%).Among 218(49.5%) RIPAs originated from the aorta,140 were from the right side of the aorta,22 from the left side of the aorta,56 from the anterior wall of the aorta,36 RIPAs had the same origin with the left inferior phrenic artery.Among 138(31.4%) RIPAs from the celiac artery,10 RIPAs had the same origin with the left gastric artery,and 33 RIPAs had the same origin with the left inferior phrenic artery.78(17.7%) were from the right renal artery,6(1.4%) were from the left gastric artery(the left gastric artery from aorta).The dilatation of the RIPA was demonstrated in 16 of(133 hepatocellular) carcinoma patients.Conclusion Multislice helical CT could demonstrate the origin of the RIPA in arterial phase and provide useful anatomical information for angiographer before and after TACE.

0.05) and CT values of mesenteric panniculitis on unenhanced scan were significantly higher than those of the same patients′retroperitoneal fat(-91——115 HU)(P

Objective To investigate the effects of alantolactone on cell proliferation,cell-cycle and cell cycle-related proteins in human chronic myelogenous leukemia drug-resistant cell line K562/ADR.Methods K562/ADR cells were treated with 0,1.0,2.0,4.0,6.0,8.0,and 10.0 μmol/L of alantolactone for 12,24 and 48 h,with its cell viability analyzed by MTT assay.Flow cytometry was used to examine the effect of alantolactone on the cell-cycle of K562/ADR cells.The cell cycle-related proteins were analyzed by using Western blot after treatment with alantolactone.Results The results of MTT showed that alantolactone effectively inhibited the proliferation of K562/ADR cells in dose and time-dependent way,and the IC50 value of alantolactone in K562/ADR cells was about 5 μmol/L.Flow cytometric analysis displayed that alantolactone could arrest cell cycle at G2/M phase.The percentage of accumulated cells in the G2/M phase was increased from (15.8±1.7) ％ in the control group to (21.0±2.4) ％,(26.4±2.7) ％,and (30.1±3.9) ％ in cells treated with 2.5,5.0,and 7.5 μmol/L of alantolactone for 24 h,respectively (P ＜ 0.05).Alantolactone significantly decreased the expression of CDK1 and CyclinB1 and increased the expression of cyclin-dependent kinase inhibitor p21.Meanwhile,the treatment of K562/ADR with alantolactone led to a dose-dependent decrease in bcr-abl protein levels.Conclusion Alantolactone can significantly inhibit the proliferation and cell-cycle arrest in G2/M phase of K562/ADR cells,in which mechanism may be associated with the regulation of cell cycle-related proteins and downregulation of bcr-abl protein.