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Contributory Cause (contributory + cause)

Distribution by Scientific Domains

Medical Sciences	60%

Selected Abstracts

Are non-poor households always less vulnerable?

DISASTERS, Issue 3 2008
The case of households exposed to protracted civil war in Southern Sudan
Civil wars in Africa are now the leading contributory cause of vulnerability of rural communities. Understanding vulnerability during civil war is critical for humanitarian response and post-conflict rehabilitation planning. The lack of understanding of vulnerability has led existing studies to make sweeping generalizations, either by equating the dynamics of vulnerability during civil wars with vulnerability in other risk events, or by projecting people in the ,war zones' as unable to cope and subsequently becoming vulnerable. This paper is an attempt to gain a more nuanced understanding of the dynamics of vulnerability during protracted civil war. It shows that during civil war the non-poor are not necessarily less vulnerable than poor households. The idea that people caught up in civil war are all vulnerable is not supported by the findings of this paper. It shows that the ,standard' pattern of vulnerability to drought is similar to that during exogenous counter-insurgency warfare, while a different pattern of vulnerability to endogenous shocks is identified. [source]

Apoptosis in oral lichen planus

EUROPEAN JOURNAL OF ORAL SCIENCES, Issue 5 2001
Evelyn Neppelberg
Apoptotic cell death may be a contributory cause of basal cell destruction in oral lichen planus (OLP). Therefore, the purpose of this study was to investigate the rate of apoptosis in OLP and the expression of two proteins (FasR and FasL) regulating this process. Biopsies from 18 patients with histologically diagnosed OLP were investigated, with comparison to normal oral mucosa of healthy persons. For visualisation of DNA fragmentation, the TUNEL method was used. In order to characterise the infiltrating cell population (CD3, CD4, CD8) and expression of FasR and FasL, we used an immunohistochemical technique. The results showed that T cells dominated in the subepithelial cell infiltrate. Within the epithelium the apoptotic cells were confined to the basal cell layer, and more apoptotic cells were seen in areas with basal cell degeneration and atrophic epithelium. There was a prominent expression of FasR/FasL in OLP, with a rather uniform distribution throughout the inflammatory cell infiltrate. In the epithelium, the FasR/FasL expression was more abundant in the basal cell area compared to the suprabasal cell layer. In conclusion, apoptosis within the epithelium is significantly increased in situ in OLP compared to normal oral mucosa, and seems to be related to the epithelial thickness. [source]

Age-related plasma reference ranges for two heparin-binding proteins , vitronectin and platelet factor 4

INTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 6 2009
F. NEWALL
Summary This study was conducted to establish age-related reference ranges for two heparin-binding proteins , vitronectin and platelet factor 4 (PF4) , and to determine if the quantitative values of these proteins may contribute to the reported age-dependent effect of unfractionated heparin (UFH). Plasma samples were obtained from healthy children aged between 1 month and 16 years and from healthy adult volunteers. Two commercial kits were used to measure plasma vitronectin and PF4 levels. Results were reported as mean and boundaries including 95% of the population. Plasma vitronectin levels for children aged 1,5 years were significantly higher compared with adults. Plasma PF4 levels for infants <1 year of age were significantly lower compared with adults. The differences between reference values for both proteins in all other age-groups were not statistically significant. This study for the first time has established age-related reference ranges for vitronectin and PF4. In establishing these ranges, the quantitative values of these proteins do not appear to be the major contributory cause for the age-dependent variation in UFH effect. Future studies are required to evaluate the possible impact of age-dependent differences in binding between heparin-binding proteins and UFH. [source]

Induction of Oxidative DNA Damage in the Peri-Infarct Region After Permanent Focal Cerebral Ischemia

JOURNAL OF NEUROCHEMISTRY, Issue 4 2000
Tetsuya Nagayama
Abstract: To address the role of oxidative DNA damage in focal cerebral ischemia lacking reperfusion, we investigated DNA base and strand damage in a rat model of permanent middle cerebral artery occlusion (MCAO). Contents of 8-hydroxyl-2,-deoxyguanosine (8-OHdG) and apurinic/apyrimidinic abasic sites (AP sites), hallmarks of oxidative DNA damage, were quantitatively measured in nuclear DNA extracts from brains obtained 4-72 h after MCAO. DNA single- and double-strand breaks were detected on coronal brain sections using in situ DNA polymerase I-mediated biotin-dATP nick-translation (PANT) and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL), respectively. Levels of 8-OHdG and AP sites were markedly elevated 16-72 h following MCAO in the frontal cortex, representing the peri-infarct region, but levels did not significantly change within the ischemic core regions of the caudateputamen and parietal cortex. PANT- and TUNEL-positive cells began to be detectable 4-8 h following MCAO in the caudate-putamen and parietal cortex and reached maximal levels at 72 h. PANT- and TUNEL-positive cells were also detected 16-72 h after MCAO in the lateral frontal cortex within the infarct border, where many cells also showed colocalization of DNA single-strand breaks and DNA fragmentation. In contrast, levels of PANT-positive cells alone were transiently increased (16 h after MCAO) in the medial frontal cortex, an area distant from the infarct zone. These data suggest that within peri-infarct brain regions, oxidative injury to nuclear DNA in the form of base and strand damage may be a significant and contributory cause of secondary expansion of brain damage following permanent focal ischemia. [source]

Pre-ovulatory Granulosa Cells of Infertile Women with Endometriosis are Less Sensitive to Luteinizing Hormone

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 2 2003
David J. Cahill
Cahill DJ, Harlow CR, Wardle PG. Pre-ovulatory granulosa cells of infertile women with endometriosis are less sensitive to luteinizing hormone. AJRI 2003; 49:66,69 © Blackwell Munksgaard, 2003 PROBLEM: Reduced fertilization rates in women with minor endometriosis may be the result of direct effects on the ovary or to primary dysfunction within the hypothalamic,pituitary,ovarian axis. This controlled study was designed to examine the steroidogenic potential of luteinized granulosa cells in women with minor endometriosis. METHOD OF STUDY: Granulosa cells were harvested at oocyte recovery and incubated for 3 hr in increasing concentrations of luteinizing hormone (LH). The dissociation constant for added concentrations of LH was computed (as Km LH) and the results were compared between women with endometriosis and controls. RESULTS: Women with minor endometriosis had a higher dissociation constant than women with tubal damage [Km 0.98 (0.58,9.24) versus 0.33 (0.28,0.72) ng/mL, P=0.019], indicating reduced sensitivity to LH. CONCLUSIONS: In women with endometriosis, granulosa cells were less sensitive to LH stimulation. This provides further evidence for primary ovarian dysfunction as a significant contributory cause of the associated subfertility. [source]