A Chinese version of the psychotic symptom rating scales : psychometric properties in recent-onset and chronic psychosis

2016-2017 > Academic research: refereed > Publication in refereed journal201804_a bcmaVersion of RecordPublishe

Collateral Formation After Repeated Transient Dearterialization of the Rat Liver

Hepatic artery ligation is used for the palliation of patients with malignant liver tumours. Collaterals are developed rapidly and could to some extent explain why the growth is affected for only a short period. With intermittent dearterialization, collaterals seem to be avoided and possibly a more extended effect should be expected. The most efficient period of dearterialization to avoid collaterals was studied in this experiment. Five groups of rats were treated with daily repeated transient dearterializations for 0 (n = 3), 60 (n = 6), 120 (n = 6), 180 (n = 6) and 240 minutes (n = 6) respectively for 5 days and compared to another group (n = 3) that was permanently dearterialized. After treatment, celiac angiograms were obtained. All hepatic arteries were reliably occluded and patent after 5 days of daily blockades in all but two rats. There were no collaterals demonstrable on the angiograms in the first four groups after 5 days of intermittent obstruction of the arterial blood flow to the liver. After 240 minutes of dearterialization as well as after collaterals developed and were clearly demonstrated on the angiograms after six days. Liver enzymes were normal even after 4 hours of dearterialization. Repeated occlusions of the hepatic artery was reliably achieved with the implantable minioccluder. Repeated, transient dearterializations for 1, 2 or 3 hours could be performed without development of collaterals and without damage to the liver

The influence of portal deviation on the effect of repeat dearterializations of a transplantable adenocarcinoma to the rat liver

As liver tumours receive some of their blood supply from the portal vein, we wanted to illustrate the influence of portal blood flow in combination with dearterialization in the treatment of liver tumours. Forty male, inbred Wistar/Furth rats with an adenocarcinoma transplanted to the liver were treated with various inflow occlusions repeated daily for 5 days. Deviation of the portal blood flow alone with an end-side porto-caval shunt did not alter the tumour growth (p = 0.089). Thirty min of repeat dearterializations was potentiated by portal deviation so that tumour growth was delayed (p = 0.004). However, repeat dearterializations for 60 min in portal deviated rats induced irreversible liver damage and all rats died in a few days. Repeated dearterializations for 60 minutes alone retarded the tumour growth as efficiently (p = 0.007). Simultaneous occlusion of the hepatic artery and the portal vein for 30 minutes with a side-side porto-caval shunted (total devascularization) did not affect tumour growth (p = 0.154). Liver aminotransferases (ASAT and ALAT) were substantially increased following dearterialization for 30 min in rats with either an end-side or a side-side porto-caval shunt. Dearterialization for 60 min in rats with end-side porto-caval shunts gave a further release of ASAT and ALAT. In conclusion, portal deviation did not augment the therapeutic benefit of repeat dearterializations for the treatment of this experimental liver tumour. Repeat dearterializations alone seemed to be a feasible and efficient therapy for liver tumours

Epigenetic inactivation of miR-9 family microRNAs in chronic lymphocytic leukemia--implications on constitutive activation of NFκB pathway

published_or_final_versio

Epigenetic inactivation of mir-34b/c in addition to mir-34a and DAPK1 in chronic lymphocytic leukemia

BACKGROUND: TP53 mutation/deletion is uncommon in chronic lymphocytic leukemia (CLL). We postulated that components of TP53-centered tumor suppressor network, miR-34b/c, in addition to DAPK1 and miR-34a might be inactivated by DNA hypermethylation. Moreover, we tested if miR-34b/c methylation might correlate with miR-203 or miR-124-1 methylation in CLL. METHODS: miR-34b/c, miR-34a and DAPK1 methylation was studied in 11 normal controls, 7 CLL cell lines, and 78 diagnostic CLL samples by methylation-specific polymerase chain reaction. MEC-1 cells were treated with 5-Aza-2'-deoxycytidine for reversal of methylation-associated miRNA silencing. Tumor suppressor properties of miR-34b were demonstrated by over-expression of precursor miR-34b in MEC-1 cells. RESULTS: miR-34b/c promoter was unmethylated in normal controls, but completely methylated in 4 CLL cell lines. miR-34b/c expression was inversely correlated with miR-34b/c methylation. Different MSP statuses of miR-34b/c, including complete methylation and complete unmethylation, were verified by quantitative bisulfite pyrosequencing. 5-Aza-2'-deoxycytidine treatment resulted in promoter demethylation and miR-34b re-expression in MEC1 cells. Moreover, over-expression of miR-34b resulted in inhibition of cellular proliferation and increased cell death. In primary CLL samples, miR-34a, miR-34b/c and DAPK1 methylation was detected in 2.6%, 17.9% and 34.6% of patients at diagnosis respectively. Furthermore, 39.7%, 3.8% and 2.6% patients had methylation of one, two or all three genes respectively. Overall, 46.2% patients had methylation of at least one of these three genes. Besides, miR-34b/c methylation was associated with methylation of miR-34a (P = 0.03) and miR-203 (P = 0.012) in CLL. CONCLUSIONS: Taken together, miR-34b/c is a tumor suppressor miRNA frequently methylated, and hence silenced in CLL. Together with DAPK1 methylation, miR-34b/c methylation is implicated in the disruption of the TP53-centered tumor suppressor network. Moreover, the association of miRNA methylation warrants further study.published_or_final_versio

Biomimetic intrafibrillar mineralization of type I collagen with intermediate precursors-loaded mesoporous carriers

published_or_final_versio

Variations of Particle Size Distribution, Black Carbon, and Brown Carbon during a Severe Winter Pollution Event over Xi'an, China

Real-time particulate matter (PM) size distributions, 4-hour time resolution, PM2.5, carbonaceous materials, and their optical properties were measured during a severe pollution event in Xi'an, China High PM2.5 /PM10 ratios were observed on both pollution (0.83) and non-pollution (0.73) days, emphasizing the abundance of fine particles during sampling days. The particle number (PN) first peaked with a wide size range (30-100 nm) before morning rush hours (approximately 01:00-05:00) on pollution and non-pollution days, demonstrating that PN was governed by the accumulation of freshly emitted diesel particles and characterized by distinct aerosol condensation growth. By contrast, the second peak time and size range differed between pollution and non-pollution days because of different formation mechanisms The light-absorbing coefficients of both black carbon (BC, b(abs-880nm,BC)) and brown carbon (BrC, b(abs-370nm, BrC)) were high on pollution days and decreased to approximately half of those values on non-pollution days, indicating that the degree of light absorption is reduced by rain. The diurnal variation in b(abs-880nm, BC) pollution peaked with traffic on January 1 and 2. By contrast, it remained in relatively stable and high ranges (120-160 Mm(-1)) in the second period (January 3-5) without traffic peaks, illustrating that the dominant sources changed even during the same pollution period. High values of both b(abs-370nm, BrC) and b(abs-880nm,) (BC )coincided in the afternoon and evening due to emissions from primary sources, and abundant aqueous secondary organic carbon, respectively. A highly variable mass absorption coefficient of BrC also indicated the variety of fuel combustion sources of primary BrC in Xi'an

An epidemiologic study of early biologic effects of benzene in Chinese workers.

Benzene is a recognized hematotoxin and leukemogen, but its mechanisms of action in humans are still uncertain. To provide insight into these processes, we carried out a cross-sectional study of 44 healthy workers currently exposed to benzene (median 8-hr time-weighted average; 31 ppm), and unexposed controls in Shanghai, China. Here we provide an overview of the study results on peripheral blood cells levels and somatic cell mutation frequency measured by the glycophorin A (GPA) gene loss assay and report on peripheral cytokine levels. All peripheral blood cells levels (i.e., total white blood cells, absolute lymphocyte count, platelets, red blood cells, and hemoglobin) were decreased among exposed workers compared to controls, with the exception of the red blood cell mean corpuscular volume, which was higher among exposed subjects. In contrast, peripheral cytokine levels (interleukin-3, interleukin-6, erythropoietin, granulocyte colony-stimulating factor, tissue necrosis factor-alpha) in a subset of the most highly exposed workers (n = 11) were similar to values in controls (n = 11), suggesting that benzene does not affect these growth factor levels in peripheral blood. The GPA assay measures stem cell or precursor erythroid cell mutations expressed in peripheral red blood cells of MN heterozygous subjects, identifying NN variants, which result from loss of the GPA M allele and duplication of the N allele, and N phi variants, which arise from gene inactivation. The NN (but not N phi) GPA variant cell frequency was elevated in the exposed workers compared with controls (mean +/- SD, 13.9 +/- 8.4 mutants per million cells versus 7.4 +/- 5.2 per million cells, (respectively; p = 0.0002), suggesting that benzene produces gene-duplicating but not gene-inactivating mutations at the GPA locus in bone marrow cells of exposed humans. These findings, combined with ongoing analyses of benzene macromolecular adducts and chromosomal aberrations, will provide an opportunity to comprehensively evaluate a wide range of early biologic effects associated with benzene exposure in humans

A pivotal role for starch in the reconfiguration of 14C-partitioning and allocation in Arabidopsis thaliana under short-term abiotic stress.

Plant carbon status is optimized for normal growth but is affected by abiotic stress. Here, we used 14C-labeling to provide the first holistic picture of carbon use changes during short-term osmotic, salinity, and cold stress in Arabidopsis thaliana. This could inform on the early mechanisms plants use to survive adverse environment, which is important for efficient agricultural production. We found that carbon allocation from source to sinks, and partitioning into major metabolite pools in the source leaf, sink leaves and roots showed both conserved and divergent responses to the stresses examined. Carbohydrates changed under all abiotic stresses applied; plants re-partitioned 14C to maintain sugar levels under stress, primarily by reducing 14C into the storage compounds in the source leaf, and decreasing 14C into the pools used for growth processes in the roots. Salinity and cold increased 14C-flux into protein, but as the stress progressed, protein degradation increased to produce amino acids, presumably for osmoprotection. Our work also emphasized that stress regulated the carbon channeled into starch, and its metabolic turnover. These stress-induced changes in starch metabolism and sugar export in the source were partly accompanied by transcriptional alteration in the T6P/SnRK1 regulatory pathway that are normally activated by carbon starvation