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

Nanofluids Research: Key Issues

Nanofluids are a new class of fluids engineered by dispersing nanometer-size structures (particles, fibers, tubes, droplets) in base fluids. The very essence of nanofluids research and development is to enhance fluid macroscopic and megascale properties such as thermal conductivity through manipulating microscopic physics (structures, properties and activities). Therefore, the success of nanofluid technology depends very much on how well we can address issues like effective means of microscale manipulation, interplays among physics at different scales and optimization of microscale physics for the optimal megascale properties. In this work, we take heat-conduction nanofluids as examples to review methodologies available to effectively tackle these key but difficult problems and identify the future research needs as well. The reviewed techniques include nanofluids synthesis through liquid-phase chemical reactions in continuous-flow microfluidic microreactors, scaling-up by the volume averaging and constructal design with the constructal theory. The identified areas of future research contain microfluidic nanofluids, thermal waves and constructal nanofluids

Randomised controlled trial of a family-led mutual support programme for people with dementia

2011-2012 > Academic research: refereed > Publication in refereed journalAuthor’s OriginalPublishe

Lithium-conductive LiNbO₃ coated high-voltage LiNi₀₅Co₀₂Mn₀₃O₂ cathode with enhanced rate and cyclability

LiNi_{0.5}Co_{0.2}Mn_{0.3}O_{2} (NCM523) cathode materials can operate at extremely high voltages and have exceptional energy density. However, their use is limited by inherent structure instability during charge/discharge and exceptionally oxidizing Ni^{4+} at the surface. Herein, we have developed a citrate-assisted deposition concept to achieve a uniform lithium-conductive LiNbO_{3} coating layer on the NCM523 surface that avoids self-nucleation of Nb-contained compounds in solution reaction. The electrode–electrolyte interface is therefore stabilized by physically blocking the detrimental parasitic reactions and Ni^{4+} dissolution whilst still maintaining high Li+ conductivity. Consequently, the modified NCM523 exhibits an encouraging Li-storage specific capacity of 207.4 mAh g^{−1} at 0.2C and 128.9 mAh g^{−1} at 10C over the range 3.0–4.5 V. Additionally, a 92% capacity retention was obtained after 100 cycles at 1C, much higher than that of the pristine NCM523 (73%). This surface engineering strategy can be extended to modify other Ni-rich cathode materials with durable electrochemical performances

An experimental study on the effectiveness of a mutual support group for family caregivers of a relative with dementia in mainland China

2011-2012 > Academic research: refereed > Publication in refereed journalAccepted ManuscriptPublishe

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

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

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