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Search Results: 1 - 10 of 878 matches for " Olivia Belbin "
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Multiple Insulin Degrading Enzyme Variants Alter In Vitro Reporter Gene Expression
Olivia Belbin, Michael Crump, Gina D. Bisceglio, Minerva M. Carrasquillo, Kevin Morgan, Steven G. Younkin
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0021429
Abstract: The insulin degrading enzyme (IDE) variant, v311 (rs6583817), is associated with increased post-mortem cerebellar IDE mRNA, decreased plasma β-amyloid (Aβ), decreased risk for Alzheimer's disease (AD) and increased reporter gene expression, suggesting that it is a functional variant driving increased IDE expression. To identify other functional IDE variants, we have tested v685, rs11187061 (associated with decreased cerebellar IDE mRNA) and variants on H6, the haplotype tagged by v311 (v10; rs4646958, v315; rs7895832, v687; rs17107734 and v154; rs4646957), for altered in vitro reporter gene expression. The reporter gene expression levels associated with the second most common haplotype (H2) successfully replicated the post-mortem findings in hepatocytoma (0.89 fold-change, p = 0.04) but not neuroblastoma cells. Successful in vitro replication was achieved for H6 in neuroblastoma cells when the sequence was cloned 5′ to the promoter (1.18 fold-change, p = 0.006) and 3′ to the reporter gene (1.29 fold change, p = 0.003), an effect contributed to by four variants (v10, v315, v154 and v311). Since IDE mediates Aβ degradation, variants that regulate IDE expression could represent good therapeutic targets for AD.
The Impact of Political Reforms in Improving Quality Health Services: The Case Study of Shamva District  [PDF]
Olivia Gumbo
Open Journal of Political Science (OJPS) , 2019, DOI: 10.4236/ojps.2019.92023
Abstract: Zimbabweans continue to experience challenges in combating communicable diseases such as tuberculosis, diarrheal diseases, and HIV/AIDS. The country’s health sector decentralisation implementation is moving at a snail’s speed, triggering complaints of unsatisfactory service delivery at rural health centres. The study examined the impact of political reforms in improving quality health services in Shamva District. The identified political reforms were decentralisation and the second republic that emerged in November 2018 that embraced the 100-day plans approach, civil service reform agenda, development of transitional stabilisation plan and vision 2030 agenda. The study was guided by interpretive and critical post-modernist paradigms. Qualitative methodology was utilised; key informant interviews, focus group discussion and desk reviews were data generation tools that were utilised. The data generated were analysed using grounded theory. The key findings are that decentralisation enabled district health officials to interact with communities through social accountability strategies such as community scorecard, results-based financing and village health worker model that is implemented in Shamva District by Civil Society Organisations. The second republic political reforms enforced the user fee policy in the health sector and focused on improving primary health care. The political reforms led to improved health rights knowledge of communities and quality health services in Shamva District. The study concluded that lack of continuous funding and sustainable plans led to the reversal of positive results that were brought in by the political reforms. The major recommendation is that government should understand that service delivery is not poor by accident; rather it is a symptom of the
Replication by the Epistasis Project of the interaction between the genes for IL-6 and IL-10 in the risk of Alzheimer's disease
Onofre Combarros, Cornelia M van Duijn, Naomi Hammond, Olivia Belbin, Alejandro Arias-Vásquez, Mario Cortina-Borja, Michael G Lehmann, Yurii S Aulchenko, Maaike Schuur, Heike K?lsch, Reinhard Heun, Gordon K Wilcock, Kristelle Brown, Patrick G Kehoe, Rachel Harrison, Eliecer Coto, Victoria Alvarez, Panos Deloukas, Ignacio Mateo, Rhian Gwilliam, Kevin Morgan, Donald R Warden, A David Smith, Donald J Lehmann
Journal of Neuroinflammation , 2009, DOI: 10.1186/1742-2094-6-22
Abstract: We examined this interaction in the Epistasis Project, a collaboration of 7 AD research groups, contributing DNA samples from 1,757 cases of AD and 6,295 controls.We replicated the interaction. For IL6 rs2069837 AA × IL10 rs1800871 CC, the synergy factor (SF) was 1.63 (95% confidence interval: 1.10–2.41, p = 0.01), controlling for centre, age, gender and apolipoprotein E ε4 (APOEε4) genotype. Our results are consistent between North Europe (SF = 1.7, p = 0.03) and North Spain (SF = 2.0, p = 0.09). Further replication may require a meta-analysis. However, association due to linkage disequilibrium with other polymorphisms in the regulatory regions of these genes cannot be excluded.We suggest that dysregulation of both IL-6 and IL-10 in some elderly people, due in part to genetic variations in the two genes, contributes to the development of AD. Thus, inflammation facilitates the onset of sporadic AD.Alzheimer's disease (AD) is accompanied by a chronic inflammatory process, including activation of microglia and astrocytes that express pro-inflammatory cytokines [1,2]. It is unclear to what extent this inflammation is a reaction to the pathology of AD, and to what extent it contributes to the onset or progression of the disease.Two multi-functional cytokines, interleukin-6 (IL-6) and interleukin-10 (IL-10), may be relevant to this question. IL-6 is a potent pro-inflammatory cytokine [3], while IL-10 acts to limit inflammation in the brain [4]. Both are produced by activated microglia and astrocytes [3,4]. Two single nucleotide polymorphisms (SNPs), rs1800795 (-174G/C) and rs1800896 (-1082G/A), in the regulatory regions of the genes, IL6 and IL10, respectively, have been widely studied. However, the ongoing AlzGene meta-analyses of the two SNPs [5]http://www.alzforum.org/res/com/gen/alzgene/ webcite are both currently negative (4 July 2009): pooled odds ratios for Caucasians in single-locus analyses of IL6-174C versus G alleles = 0.93 (95% confidence interval: 0.79–1.08,
Replication of EPHA1 and CD33 associations with late-onset Alzheimer's disease: a multi-centre case-control study
Minerva M Carrasquillo, Olivia Belbin, Talisha A Hunter, Li Ma, Gina D Bisceglio, Fanggeng Zou, Julia E Crook, V Pankratz, Sigrid B Sando, Jan O Aasly, Maria Barcikowska, Zbigniew K Wszolek, Dennis W Dickson, Neill R Graff-Radford, Ronald C Petersen, Peter Passmore, Kevin Morgan, for the Alzheimer's Research UK (ARUK) consortium, Steven G Younkin
Molecular Neurodegeneration , 2011, DOI: 10.1186/1750-1326-6-54
Abstract: We found no significant evidence of series heterogeneity. Associations with LOAD were successfully replicated for EPHA1 (rs11767557; OR = 0.87, p = 5 × 10-4) and CD33 (rs3865444; OR = 0.92, p = 0.049), with odds ratios comparable to those previously reported. Although the two ARID5B variants (rs2588969 and rs494288) showed significant association with LOAD in meta-analysis of our dataset (p = 0.046 and 0.008, respectively), the associations did not survive adjustment for covariates (p = 0.30 and 0.11, respectively). We had insufficient evidence in our data to support the association of the CD2AP variant (rs9349407, p = 0.56).Our data overwhelmingly support the association of EPHA1 and CD33 variants with LOAD risk: addition of our data to the results previously reported (total n > 42,000) increased the strength of evidence for these variants, providing impressive p-values of 2.1 × 10-15 (EPHA1) and 1.8 × 10-13 (CD33).Following the identification of the APOE ε4 allele as a risk factor for late-onset Alzheimer's disease (LOAD) in 1993 [1], consistent replication of subsequently identified candidates was not achieved until 2009, when two genome-wide association studies (GWAS) [2,3] identified associations of variants in or near CLU, PICALM , and CR1 with LOAD, which were consistently replicated in multiple large, independent case-control studies [4-17]. Subsequently, a variant near BIN1 was reported [4] to achieve genome-wide significant association in a later GWAS published in 2010 that also replicated well in follow-up studies [14-19]. These results demonstrate the utility of the hypothesis-free GWAS approach for identifying loci that associate with LOAD and the necessity of pooling samples and data from multiple centers to obtain resources with sufficient statistical power (GWAS typically > 14,000, follow-up typically total > 28,000) to detect the modest ORs (e.g. 0.8/1.2) associated with these variants in GWAS and follow-up studies.Two recently published companion s
Linking Protective GAB2 Variants, Increased Cortical GAB2 Expression and Decreased Alzheimer’s Disease Pathology
Fanggeng Zou, Olivia Belbin, Minerva M. Carrasquillo, Oliver J. Culley, Talisha A. Hunter, Li Ma, Gina D. Bisceglio, Mariet Allen, Dennis W. Dickson, Neill R. Graff-Radford, Ronald C. Petersen, the Genetic and Environmental Risk for Alzheimer’s disease (GERAD1) Consortium , Kevin Morgan, Steven G. Younkin
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0064802
Abstract: GRB-associated binding protein 2 (GAB2) represents a compelling genome-wide association signal for late-onset Alzheimer’s disease (LOAD) with reported odds ratios (ORs) ranging from 0.75–0.85. We tested eight GAB2 variants in four North American Caucasian case-control series (2,316 LOAD, 2,538 controls) for association with LOAD. Meta-analyses revealed ORs ranging from (0.61–1.20) with no significant association (all p>0.32). Four variants were hetergeneous across the populations (all p<0.02) due to a potentially inflated effect size (OR = 0.61–0.66) only observed in the smallest series (702 LOAD, 209 controls). Despite the lack of association in our series, the previously reported protective association for GAB2 remained after meta-analyses of our data with all available previously published series (11,952-22,253 samples; OR = 0.82–0.88; all p<0.04). Using a freely available database of lymphoblastoid cell lines we found that protective GAB2 variants were associated with increased GAB2 expression (p = 9.5×10?7?9.3×10?6). We next measured GAB2 mRNA levels in 249 brains and found that decreased neurofibrillary tangle (r = ?0.34, p = 0.0006) and senile plaque counts (r = ?0.32, p = 0.001) were both good predictors of increased GAB2 mRNA levels albeit that sex (r = ?0.28, p = 0.005) may have been a contributing factor. In summary, we hypothesise that GAB2 variants that are protective against LOAD in some populations may act functionally to increase GAB2 mRNA levels (in lymphoblastoid cells) and that increased GAB2 mRNA levels are associated with significantly decreased LOAD pathology. These findings support the hypothesis that Gab2 may protect neurons against LOAD but due to significant population heterogeneity, it is still unclear whether this protection is detectable at the genetic level.
Antimicrobial Resistance and β-Lactamase Production among Hospital Dumpsite Isolates  [PDF]
Olivia Sochi Egbule
Journal of Environmental Protection (JEP) , 2016, DOI: 10.4236/jep.2016.77094
Abstract:

Metallo-β-Lactamases (MBLs) and Extended Spectrum β-Lactamses (ESBLs) have emerged world-wide as a significant source of β-lactam resistance. The emergence of MBLs and ESBLs encoded on plasmids among Gram-negative pathogens in hospital dumpsites was investigated. Soils of different government and private hospitals were collected and processed following standard bacteriological techniques. Antimicrobial susceptibility testing was carried out by the disk-diffusion technique using Ceftazidime (30 μg), Cefuroxime (30 μg), Cefotaxime (30 μg), Cefixime (5 μg), Trimethprim-sulfamethoxazole (25 μg), Gentamycin (100 μg) Amoxicillin-Clavunalate (30 μg), Ciprofloxacin (5 μg), Ofloxacin (5 μg), Nitrofurantoin (300 μg) and Imipenem (10 μg). The role of plasmids in resistance was evaluated by subjecting isolates to curing using Sodium Dodecyl Sulfate (SDS). ESBLs production by Double-Disk Synergy Test (DDST) was carried out. Isolates resistant to Imipenem were subjected to a confirmatory test using Modified Hodge’s test and to MBLs production by DDST. Eighty-two Gram-negative isolates comprising of 32 (39.02%) Escherichia coli, 20 (24.39%) Serratia marcescens, 14 (17.07%) Klebsiella pneumonia, 10 (12.28%) Proteus mirabilis and 6 (7.32%) Enterobacter aerogenes were obtained. Susceptibility results revealed a 100% resistance of all isolates to Ceftazidime, Cefuroxime, Cefixime, Amoxycillin-clavulanate and Cefotaxime. A total of 66 (80.48%) isolates harboured plasmids out of which 26 (31.71%) isolates were ESBL producers. MBLs production was observed in 8 (25.00%) E. coli, 2 (2.41%) Klebsiella pneumonia and 2 (2.41%) Proteus mirabilis isolates. All MBLs producing isolates were ESBLs producers. The finding of highly resistant isolates producing ESBLs and MBLs in a hospital environment is quite disturbing and should be addressed urgently.

Detection and Transfer of Extended Spectrum Beta Lactamase Enzymes from Untreated Hospital Waste Water  [PDF]
Olivia Sochi Egbule
Advances in Microbiology (AiM) , 2016, DOI: 10.4236/aim.2016.67051
Abstract: Untreated Hospital wastewater piped into septic tanks contributes to the spread of antibiotic resistance in developing countries. This study was conducted to determine the resistant profile, and Extended Spectrum Beta-Lactamases (ESBLs) production in isolates from hospital waste water, of 2 hospitals in Delta State, Nigeria. A total of 147 organisms were isolated from 32 waste water samples. One hundred and twenty three isolates were Gram negative and 24 were Gram positive. Escherichia coli was the most prevalent in the two locations. Antimicrobial susceptibility by standard disk diffusion method was performed. All isolates were resistant to 4 or more antimicrobial agents. Out of the 123 Gram negative Bacteria, 33 were pan drug resistant and were selected for plasmid curing, DNA extraction and phenotypic detection of ESBL. Transfer of resistant by broth mating technique was performed. Plasmid curing and extraction result indicated that isolates carried resistance on the plasmid and harboured similar multiple high molecular weight plasmids of 23.13 kb and 9.4 kb. ESBL production was detected in 15.15%. Transfer of resistant genes between ESBL producing and non-ESBL producing isolates was observed. Incidence of ESBL in untreated hospital waste water has public health implications. Therefore establishment of treatment plants in our hospital is paramount in achieving sustainable health.
The dopamine β-hydroxylase -1021C/T polymorphism is associated with the risk of Alzheimer's disease in the Epistasis Project
Onofre Combarros, Donald R Warden, Naomi Hammond, Mario Cortina-Borja, Olivia Belbin, Michael G Lehmann, Gordon K Wilcock, Kristelle Brown, Patrick G Kehoe, Rachel Barber, Eliecer Coto, Victoria Alvarez, Panos Deloukas, Rhian Gwilliam, Reinhard Heun, Heike K?lsch, Ignacio Mateo, Abderrahim Oulhaj, Alejandro Arias-Vásquez, Maaike Schuur, Yurii S Aulchenko, M Arfan Ikram, Monique M Breteler, Cornelia M van Duijn, Kevin Morgan, A David Smith, Donald J Lehmann
BMC Medical Genetics , 2010, DOI: 10.1186/1471-2350-11-162
Abstract: We genotyped eight single nucleotide polymorphisms (SNPs) in the three genes, DBH, IL1A and IL6. We used logistic regression models and synergy factor analysis to examine potential interactions and associations with AD.We found that the presence of the -1021T allele was associated with AD: odds ratio = 1.2 (95% confidence interval: 1.06-1.4, p = 0.005). This association was nearly restricted to men < 75 years old: odds ratio = 2.2 (1.4-3.3, 0.0004). We also found an interaction between the presence of DBH -1021T and the -889TT genotype (rs1800587) of IL1A: synergy factor = 1.9 (1.2-3.1, 0.005). All these results were consistent between North Europe and North Spain.Extensive, previous evidence (reviewed here) indicates an important role for noradrenaline in the control of inflammation in the brain. Thus, the -1021T allele with presumed low activity may be associated with misregulation of inflammation, which could contribute to the onset of AD. We suggest that such misregulation is the predominant mechanism of the association we report here.The loss of noradrenergic neurones of the locus coeruleus is a striking feature of sporadic Alzheimer's disease (AD). A gradual, moderate loss is found with ageing in healthy people [1-3], but a more dramatic loss is seen in AD. A meta-analysis [4] showed similarly high losses of noradrenergic neurones (24 studies) as of cholinergic neurones (33 studies), with losses four times greater than those of dopaminergic cells in AD. Noradrenergic neurones project from the brainstem to innervate wide areas of the forebrain [5]. Levels of noradrenaline (NA, norepinephrine) in target regions have also sometimes been reported lowered in ageing [6,7], e.g. in the hippocampus and hypothalamus. They have generally been found to be further reduced in AD [8-13], e.g. in the hippocampus, hypothalamus, caudate nucleus, putamen and neocortex, although not in one small study [14]. Both the loss of noradrenergic neurones [15] and that of NA in target re
"TROCABAN EL TRABAJO EN FIESTA Y REGOCIJO": ACERCA DEL VALOR DEL TRABAJO EN LOS ANDES HISTóRICOS Y CONTEMPORáNEOS
Harris,Olivia;
Chungará (Arica) , 2010, DOI: 10.4067/S0717-73562010000100031
Abstract: sixteenth century sources associate the notion of labour in the andes with that of enjoyment, while most colonial spaniards and modern anthropologists see it as obligatory, ignoring its ritual dimensions. generally speaking, western theorists of labour, whether marxist or not, link labour and production with alienation. drawing on her fieldwork experience, the author notes that there is no aymara word for labour in general. more important is the purpose and beneficiary of labour. andeans not only value labour aimed at strengthening their own social networks, but more specifically labour that benefits the community to which they belong. the andean ethic of labour therefore leads it to be considered as a blessing, in opposition to judaeo-christian ways of considering it as a curse.
Pensadoras de peso: o pensamento de Judith Butler e Adriana Cavarero
Guaraldo, Olivia;
Revista Estudos Feministas , 2007, DOI: 10.1590/S0104-026X2007000300010
Abstract: the work presents the standpoint of two important contemporary feminist philosophers, adriana cavarero and judith butler, on subjectivity and relationality, showing how both moved away from the specific feminism motif in order to deepen and broaden their reflection on politics and ethics. calling tradition into question, cavarero agrees neither with the metaphysical binary, nor with the post-modern impersonality, combining a feminist and the arendtian perspectives of the subjectivity based on relationality. contrary to cavarero's thought, though, under butler's deconstructionist standpoint language shapes body and identity. subjectivity is "trapped" into social norms and values. both butler and cavarero rethink subjectivity based on relationality, that is, displacing politics from the immune individual and reallocating it on the vulnerable individual in relation with the other and with the social rules and values imposed on them.
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