Objective To evaluate the electrocardiographic(ECG)-gated 4-dimensional computed tomographic angiography (4D-CTA) in the determination of pulsation of unruptured cerebral aneurysms (URCAs).Methods This study included 48 patients with 62 URCAs.Examinations of ECG gated 4D-CTA of dual-source CT were performed.Twenty sets of image data with the time intervals of 5％ in a cardiac cycle were obtained after postprocessing on the workstation.The convex was defined as the point of pulsation if small bubble or small pointed convex could be found in continuous three or more images at the same location.The 62 URCAs were divided into two groups based on whether having a point of pulsation.All the URCAs were scanned at the follow-up by 3D-CTA or ECG gated 4D-CTA more than 120 days later.The diameters of aneurysms and aspect ratio between the two groups were compared with independent t test,while neck of aneurysms and follow-up time were compared with two-independent samples Mann-Whitney U test.The other variables including history of hypertension,type 2 diabetes,smoking et al between the two groups were analyzed by x2 test.The sensitivity and specificity of aspect ratio for diagnosis of pulsation were analyzed by receiver operating characteristic (ROC) curve.Results Pulsation was observed in 28 of the 62 URCAs.Aspect ratios in whose pulsation was or was not detected were 1.5±0.3 and 1.1±0.3,respectivelyThe difference between the two groups was statistically significant (t=-2.274,P＜0.001).The sensitivity and specificity of the aspect ratio were 75.0％ and 70.6％.After follow-up more than 3 months,of the 28 URCAs in which pulsation was observed,11 showed a change in shape,while in 34 URCAs without visible pulsation,5 showed a change in shape.The aneurysms with detectable pulsation were more likely to show a change in shape (x2=4.891,P=0.027),with an odds ratio of 3.753.Conclusions URCAs with a large aspect ratio are easily to show the pulsation by ECG gated 4D-CTA.Besides,the aneurysms with visible pulsation are more likely to show a change in shape after follow-up,which suggests a higher risk of rupture.

Huntington disease (HD) is a neurodegenerative disorder caused by an expansion of the polyglutamine tract in the N-terminal huntingtin (Htt). Htt is a substrate of caspases and calpains, the proteases involved in initiation and execution of neuronal apoptosis. Caspase- and calpain-mediated cleavage of mutant Htt results in the production of toxic Nterminal Htt fragments. Recent studies suggest that Htt cleavage may be a crucial step in the pathogenesis of HD and may be a potential molecular target for HD therapy.

To compare the differences on current ethical issues in the areas of epidemiological practice between China and America,to identify the major ethical problems existing in the epidemiological studies in China.Through searching and reviewing papers published on Chinese Journal of Epidemiology and American Journal of Epidemiology from Jan.2006 to Dec.2010,we made a comparison on ethical issues involved in the original studies that focusing on human beings.In total,749 Chinese articles and 1221 American articles were recruited,with the following findings: (1)The proportion with announcements of “Informed consent by the subjects” was 29.24％ in Chinese literature and 38.08％ in the Americans (x2=16.02,P＜0.001 ).The proportion with “having had approvals from the ethic committees” was 29.24％ in Chinese,while 38.08％ in American ( x2=604.40,P＜ 0.0001 ).(2) Both in China and America,there had been an increase of ethical issues in the last 5 years.(3)Articles derived from trial studies had better involvement on ethics than those from observational studies.(4) The level on ethical issues in the American Research Institutes exceeded those in China (5)American studies also had showed better ideas on Ethic issues on biological specimens collection and privacy protection,than those in Chinese studies.Among the studies on Chinese Journal of Epidemiology,the proportion of ‘informed consent' was higher than in ethical review,but both ethical review and awareness on ‘informed consent' had left far behind than the American Journal of Epidemiology.This could be seen at the institution level of the writers,during specimen collection and privacy protection,as well as at the overall level.The results reminded us that the Departments of Technology Management should spend more efforts on the improvement of public education regarding ethics for researchers and to update the process of edition for Journals as well as to reinforce the rules of ethics in epidemiological research.

OBJECTIVEWilms' Tumor Trial (WT-99) of Shanghai Children's Medical Center was designed and conducted by applying therapeutic regimens stratified by stage and histology in accordance with National Wilms' Tumor Study (NWTS) criteria of U.S.A. The main aim of WT-99 was to reduce treatment of low-stage, favorable-histology (FH) tumors without impairing survival and to improve prognosis of stage III and IV (FH) and unfavorable-histology (UFH) tremors with more intensive chemotherapy.

METHODSDiagnosis and treatment was decided by the multi-disciplinary team including oncologists, surgeons, pathologists, radiologists and diagnostic radiologists. Twenty consecutively diagnosed patients were recruited between October 1998 and October 2002. The regimen for patients at favorable-histology (FH) stage I and II and anaplastic stage I was vincristine (Vcr) and dactinomycin (Act-D) only, while for those at focal anaplastic stage II to IV and FH stage III and IV the regimen was Vcr, Act-D and adriamycin (Adr). Patients at diffuse anaplastic stage II to IV and clear cell stage I to IV received four-drug regimen including Vcr, etoposide (VP16), Adr and cytoxan (CTX). For those at rhabdoid stage I to IV the regimen was carboplatin, VP-16 and CTX. Un-resectable patients received 2 courses of Ifosfamide, Vcr and VP-16 as pre-surgery therapy. No radiation therapy was used for patients at stage I and FH stage II.

RESULTSTwenty patients, from 7 months to 12 years old, were enrolled. Pathologic analysis showed fourteen cases were at their FH, three at unfavorable-histology (UFH), two at clear cell and one at rhabdoid stage. Five patients were at stage I, five at stage II, six at stage III, three at stage IV and one at stage V. Eighteen reached complete response (90%), and two failed. One relapsed after 24 months of CCR and reached the second CR after intensive chemotherapy. No therapy-related death happened. Survival rate (SR) was 90% (18/20) and event-free survival (EFS) was 85% (17/20) at 11-45 months, average 27 months.

CONCLUSIONMulti-disciplinary team work model and protocol WT-99 are safe and effective for Wilms' tumor.

Academic Medical Centers ; Bone Transplantation ; Child ; Child, Preschool ; China ; Combined Modality Therapy ; Female ; Humans ; Infant ; Kidney Neoplasms ; classification ; therapy ; Male ; Neoplasm Staging ; Transplantation, Autologous ; Treatment Outcome ; Wilms Tumor ; classification ; therapy

BACKGROUNDUrsolic acid (UA) is a ubiquitous molecule in the plant kingdom with specific anticancer effects that have been shown in vitro and in vivo. Although UA can inhibit the proliferation of liver cancer cells and induce apoptosis of many types of tumor cells, the molecular mechanism of its anti-hepatoma activity is still not well defined. The objective of this study was to investigate the inhibitory effect and mechanisms of UA on the human hepatoma cell line SMMC-7721.

METHODSAfter treatment with UA, the growth inhibition of SMMC-7721 cells was assessed by MTT assay. Cells were also evaluated by flow cytometric analysis, Wright-Giemasa staining, Hoechst 33258 staining and transmission electron microscope after they were induced by UA. DNA microarray technology was used to investigate the gene expression pattern of SMMC-7721 cells exposed to UA 40 micromol/L. The molecular mechanism of cells death was analyzed by real-time RT-PCR and Western blotting.

RESULTSThe proliferation of SMMC-7721 cells was significantly inhibited in a dose- and time-dependent manner after UA treatment. UA induced cell cycle arrest and apoptosis. The DNA microarray analysis indicated that 64 genes were found to be markedly up- or down-expressed, including GDF15, SOD2, ATF3, and fos. The result of Western blotting showed the apoptotic proteins p53 and Bax were up-regulated while the anti-apoptotic protein Bcl-2 was down-regulated. Real-time RT-PCR confirmed UA could up-regulate the mRNA expressions of GDF15, SOD2, ATF3 and down-regulate the mRAN expression of fos. Meanwhile these effects were partly blocked by pretreatment with the p53 inhibitor Pft-alpha.

CONCLUSIONActivation of the p53 pathway is involved in UA inhibition of SMMC-7721 human hepatocellular carcinoma cell growth and induction of apoptosis.

Apoptosis ; drug effects ; Blotting, Western ; Carcinoma, Hepatocellular ; drug therapy ; metabolism ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Flow Cytometry ; Humans ; Liver Neoplasms ; drug therapy ; metabolism ; Microscopy, Electron, Transmission ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; drug effects ; Triterpenes ; therapeutic use ; Tumor Suppressor Protein p53 ; metabolism

OBJECTIVETo optimize the process of tomato genetic transformation, screening and seed selection using multiepitope antigenic gene (MAG) and truncated major surface antigen 1 (tSAG1) of Toxoplasma gondii as the target insert genes.

METHODSTomato high-frequency regeneration system was optimized with different choices of media and explants. The genetic transformation procedure was optimized using different tomato cultivars, explants, culture temperatures, media and acetosyringone (AS) supplements. Three concentrations of kanamycin were utilized for resistant selection of the transgenic candidate roots. The selected lines were trained, transplanted to soil and grown in a greenhouse till maturity. Sterile seeding using kanamycin-incorporated medium was conducted for screening transgenic tomato generations.

RESULTS AND CONCLUSIONCotyledons were better than hypocotyls as the regeneration explants. The regeneration rate of cotyledons reached 98% (59/60) using the optimized regeneration medium ZB3. The culture medium and temperature were the key factors for tomato transgenic shoot induction. The number of transgenic buds increased significantly at the appropriate temperature condition (23-/+1 degrees celsius;), and AS of 100 micromol/L in the medium before inoculation also significantly raised transformation rate. The budding rate of Zhongshu No.5 cotyledons was 35% (28/81) using the medium ZB2 under (23-/+1) degrees celsius;. Kanamycin at 80 mg/L was optimal for transgenic plantlet rooting selection with the rooting rate of 48% (31/65). 117 transgenic lines were obtained. Non-transgenic tomato plant growth, especially the root and elongation, was inhibited obviously with kanamycin at 100 mg/L or above, and the roots became purple and lacked lateral roots. The transgenic tomato seeds could be selected effectively with kanamycin at 150 mg/L.

Animals ; Antigens, Protozoan ; genetics ; Drug Resistance ; Kanamycin ; pharmacology ; Lycopersicon esculentum ; drug effects ; genetics ; Plants, Genetically Modified ; drug effects ; genetics ; Protozoan Proteins ; genetics ; Seeds ; drug effects ; genetics ; Toxoplasma ; genetics ; Transformation, Genetic

To achieve fast and accurate analysis of weak current signal of nanopore-based single molecule detection, we designed a real-time adaptive threshold data processing algorithm with data buffering technique and finite impulse response filtering. The system, which is designed based on the data processing algorithm, could realize real-time recognition and analysis of nanopore events during the data recording process. In order to verify the performance of the system, the ideal signals with different noise level (20-100 pA) and recording bandwidth (3 - 100 kHz) was generated. The results showed that the system was stable to analyze the generated signals even at high noise. In addition, the system was also suitable for the data recording conditions of low bandwidth and high sampling rate (250 kHz). The proposed nanopore data processing system was further applied in the Aerolysin nanopore experiment for the detection of poly(dA) 4 molecules. The results showed that the data processing system could be applied in real nanopore recording system with high accuracy and speed.

Objective:Preliminary study on rats with delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) model intervention agent tBHQ before and after the nuclear factor E2-related factor 2(Nrf2) and its downstream target genes of heme oxygenase 1(HO-1) change in hippocampus associated,in order to further study the pathogenesis of DEACMP,at the same time for the targeted therapy of provide a certain experimental basis.Methods: One hundred and twenty rats were randomly divided into carbon monoxide poisoning group(CO group),air control group(AC group),carbon monoxide+3% ethanol group(EC group),carbon monoxide+tBHQ group(group TC),then the rats in exposure after 1 d,3 d,7 d,14 d,21 d,28 d,with the machine was divided into 6 sub groups,followed by the Morris water maze test to observe the behavior of rats,immunohistochemistry and protein Western blot method of chemical(Western blot) detecting expression of Nrf2 and HO-1 mploying intervention agent tBHQ before and after,and then TUNEL staining was detected cell apoptosis.Results: CO group,EC group,TC group Nrf2 in hippocampus of rats and the expression of HO-1 were increased in the first day and reach a peak at the third day,then gradually decreased,and at each time point in AC group were statistically significant,TC group and CO group Nrf2 and HO-1 were increased in each sub group and the deffirences were statistically meaning.Comparison apoptotic cells in CO group,EC group,TC group with AC group rats increased significantly over time,and showed higher peak(7-14 d)-decreased.TC group compared with CO group,the apoptotic cells(7-14 d) decreased,the difference was statistically significant.Conclusion: The Nrf2/ARE/HO-1 pathway plays an important role in the development of DEACMP,and the tBHQ specific activation of the Nrf2 pathway achieves early protection and is expected to reduce or mitigate DEACMP.

Methylation, a methyl group-consuming reaction, plays a key role in the degradation (i.e., inactivation) of monoamine neurotransmitters, including catecholamines, serotonin and histamine. Without labile methyl groups, the methylation-mediated degradation cannot take place. Although high niacin (nicotinic acid and nicotinamide) intake, which is very common nowadays, is known to deplete the body's methyl-group pool, its effect on monoamine-neurotransmitter degradation is not well understood. The aim of this article was to investigate the effect of excess nicotinamide on the levels of plasma serotonin and histamine in healthy subjects. Urine and venous blood samples were collected from nine healthy male volunteers before and after oral loading with 100 mg nicotinamide. Plasma N(1)-methylnicotinamide, urinary N(1)-methyl-2-pyridone-5-carboxamide (2-Py), and plasma betaine levels were measured by using high-performance liquid chromatography (HPLC). Plasma concentrations of choline, serotonin and histamine were measured using commercial kits. The results showed that the plasma N(1)-methylnicotinamide level and the urinary excretion of 2-Py significantly increased after oral loading with 100 mg nicotinamide, which was accompanied with a decrease in the methyl-group donor betaine. Compared with those before nicotinamide load, five-hour postload plasma serotonin and histamine levels significantly increased. These results suggest that excess nicotinamide can disturb monoamine-neurotransmitter metabolism. These findings may be of significance in understanding the etiology of monoamine-related mental diseases, such as schizophrenia and autism (a neurodevelopmental disorder).
Betaine ; blood ; Choline ; blood ; Chromatography, High Pressure Liquid ; Histamine ; blood ; Humans ; Male ; Niacinamide ; administration & dosage ; analogs & derivatives ; blood ; Pyridones ; urine ; Serotonin ; blood

Huntington disease (HD) is a chronic autosomal-dominant neurodegenerative disease. The gene coding Huntingtin has been identified, but the pathogenic mechanisms of the disease are still not fully understood. This paper reviews the involvement of mitochondrial dysfunction in pathogenesis of HD.