Establishing the cut-off point for the Oppositional Defiant Behavior Inventory

The definitive version is available at www.blackwell-synergy.com.ArticlePSYCHIATRY AND CLINICAL NEUROSCIENCES. 62(1): 120-122 (2008)journal articl

Reply to Letter to the Editor : Is HPV-18 present in human breast cancer cell lines

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Downregulation of ETS Rescues Diabetes-Induced Reduction of Endothelial Progenitor Cells

Transplantation of vasculogenic progenitor cells (VPC) improves neovascularization after ischemia. However, patients with type 2 diabetes mellitus show a reduced VPC number and impaired functional activity. Previously, we demonstrated that p38 kinase inhibition prevents the negative effects of glucose on VPC number by increasing proliferation and differentiation towards the endothelial lineage in vitro. Moreover, the functional capacity of progenitor cells is reduced in a mouse model of metabolic syndrome including type 2 diabetes (Lepr(db)) in vivo.The aim of this study was to elucidate the underlying signalling mechanisms in vitro and in vivo. Therefore, we performed DNA-protein binding arrays in the bone marrow of mice with metabolic syndrome, in blood-derived progenitor cells of diabetic patients as well as in VPC ex vivo treated with high levels of glucose. The transcriptional activation of ETS transcription factors was increased in all samples analyzed. Downregulation of ETS1 expression by siRNA abrogated the reduction of VPC number induced by high-glucose treatment. In addition, we observed a concomitant suppression of the non-endothelial ETS-target genes matrix metalloproteinase 9 (MMP9) and CD115 upon short term lentiviral delivery of ETS-specific shRNAs. Long term inhibition of ETS expression by lentiviral infection increased the number of cells with the endothelial markers CD144 and CD105.These data demonstrate that diabetes leads to dysregulated activation of ETS, which blocks the functional activity of progenitor cells and their commitment towards the endothelial cell lineage

Comparisons of trace constituents from ground stations and the DC‐8 aircraft during PEM‐West B

Chemical data from ground stations in Asia and the North Pacific are compared with data from the DC‐8 aircraft collected during the Pacific Exploratory Measurements in the Western Pacific Ocean (PEM‐West B) mission. Ground station sampling took place on Hong Kong, Taiwan, Okinawa, and Cheju; and at three Pacific islands, Shemya, Midway, and Oahu. Aircraft samples were collected during 19 flights, most over the western North Pacific. Aluminum was used as an indicator of mineral aerosol, and even though the aircraft did sample Asian dust, strong dust storms were not encountered. The frequency distribution for non‐sea‐salt sulfate (nss SO4=) in the aircraft samples was bimodal: the higher concentration mode (∼1 μg m−3) evidently originated from pollution or, less likely, from volcanic sources, while the lower mode, with a peak at 0.040 μg m−3, probably was a product of biogenic emissions. In addition, the concentrations of aerosol sulfate varied strongly in the vertical: arithmetic mean SO4= concentrations above 5000 m ( = 0.21±0.69 μg m−3) were substantially lower than those below ( = 1.07±0.87 μg m−3), suggesting the predominance of the surface sources. Several samples collected in the stratosphere exhibited elevated SO4=, however, probably as a result of emissions from Mount Pinatubo. During some boundary layer legs on the DC‐8, the concentrations of CO and O3 were comparable to those of clean marine air, but during other legs, several chemically distinct air masses were sampled, including polluted air in which O3 was photochemically produced. In general, the continental outflow sampled from the aircraft was substantially diluted with respect to what was observed at the ground stations. Higher concentrations of aerosol species, O3, and CO at the Hong Kong ground station relative to the aircraft suggest that much of the continental outflow from southeastern Asia occurs in the lower troposphere, and extensive long‐range transport out of this part of Asia is not expected. In comparison, materials emitted farther to the north apparently are more susceptible to long‐range transport

Overexpression of the p53-inducible brain-specific angiogenesis inhibitor 1 suppresses efficiently tumour angiogenesis

The brain-specific angiogenesis inhibitor 1 gene has been isolated in an attempt to find fragments with p53 “functional” binding sites. As reported herein and by others, brain-specific angiogenesis inhibitor 1 expression is present in some normal tissues, but is reduced or lost in tumour tissues. Such data and its particular structure prompted the hypothesis that brain-specific angiogenesis inhibitor 1 may act as a mediator in the local angiogenesis balance. We herein demonstrate that brain-specific angiogenesis inhibitor 1 over-expression suppresses tumour angiogenesis, delaying significantly the human tumour growth in immunodeficient mice. The inhibitory effect of brain-specific angiogenesis inhibitor 1 was documented using our intravital microscopy system, strongly implicating brain-specific angiogenesis inhibitor 1 as a mediator in the control of tumour angiogenesis. In contrast, in vitro tumour cell proliferation was not inhibited by brain-specific angiogenesis inhibitor 1 transfection, whereas some level of cytotoxicity was assessed for endothelial cells. Immunohistochemical analysis of tumour samples confirmed a reduction in the microvessel density index in brain-specific angiogenesis inhibitor 1-overexpressing tumours. At messenger level, moderate changes could be detected, involving the down-regulation of vascular endothelial growth factor and collagenase-1 expression. Furthermore, brain-specific angiogenesis inhibitor 1 expression that was lost in a selection of human cancer cell lines could be restored by wild-type p53 adenoviral transfection. Brain-specific angiogenesis inhibitor 1 should be considered for gene therapy and development of efficient drugs based on endogenous antiangiogenic molecules

Genetic alterations on chromosome 17p associated with response to radiotherapy in bulky cervical cancer

Chromosome 17 alterations are found in more cancers than those of any other chromosome, and frequently involve the p53 gene on 17p13. The aim of this study was to identify the correlations between the presence of loss of heterozygosity (LOH) and microsatellite instability (MI) on chromosome 17p13 in patients with cervical cancer and the patients’ response to radiotherapy. A total of 50 patients were treated with definitive radiotherapy. We performed biopsies and took specimens from the tumour and venous blood of all patients. Tumour and normal DNAs were analysed by polymerase chain reaction for genetic losses and instability at three polymorphic microsatellite loci mapped to 17p13. Nineteen of the 50 tumours (38%) displayed a genetic alteration (GA) on 17p13, 16 (32%) were found to have LOH, and three (6%) showed MI. The sizes of the tumours of the GA-positive patients were significantly greater than those of the GA-negative patients (P = 0.009). The mean tumour diameter of all patients was 6 ± 2.4 cm. We divided the patients into those with tumours smaller than 6 cm in diameter (n = 26) and those with tumours equal to or greater than 6 cm in diameter (n = 24). The former group survived significantly longer compared to the latter group (P = 0.0002). Among the patients with < 6 cm tumours, all six GA-positive patients are alive with no evidence of disease (NED), whereas of the 20 GA-negative patients, 18 have NED and two are alive with disease (AWD) or suffered cancer-caused death (CD). Thus, there was no correlation between GA and radiotherapy response in the tumours smaller than 6 cm. However, among the patients with ≥ 6 cm tumours, two of the GA-positive patients have NED and 11 are AWD/CD, whereas seven of the GA-negative patients have NED and four are AWD/CD. Among the patients with ≥ 6 cm tumours, the response to radiotherapy of the GA-positive patients were significantly poorer than those of the GA-negative patients (P = 0.02). In addition, the GA-negative patients survived significantly longer compared to the GA-positive patients (P = 0.026). The results of this study suggest that GA increases with tumour growth. Improved success in the management of bulky cervical cancer requires a better understanding of its biological behaviour. © 1999 Cancer Research Campaig