11 results on '"Pacora, Percy N."'
Search Results
2. Risk of placental abruption in relation to migraines and headaches
- Author
-
Ananth Cande V, Pacora Percy N, Williams Michelle A, Sanchez Sixto E, Qiu Chungfang, Aurora Sheena K, and Sorensen Tanya K
- Subjects
Gynecology and obstetrics ,RG1-991 ,Public aspects of medicine ,RA1-1270 - Abstract
Abstract Background Migraine, a common chronic-intermittent disorder of idiopathic origin characterized by severe debilitating headaches and autonomic nervous system dysfunction, and placental abruption, the premature separation of the placenta, share many common pathophysiological characteristics. Moreover, endothelial dysfunction, platelet activation, hypercoagulation, and inflammation are common to both disorders. We assessed risk of placental abruption in relation to maternal history of migraine before and during pregnancy in Peruvian women. Methods Cases were 375 women with pregnancies complicated by placental abruption, and controls were 368 women without an abruption. During in-person interviews conducted following delivery, women were asked if they had physician-diagnosed migraine, and they were asked questions that allowed headaches and migraine to be classified according to criteria established by the International Headache Society. Logistic regression procedures were used to calculate odds ratios (aOR) and 95% confidence intervals (CI) adjusted for confounders. Results Overall, a lifetime history of any headaches or migraine was associated with an increased odds of placental abruption (aOR = 1.60; 95% CI 1.16-2.20). A lifetime history of migraine was associated with a 2.14-fold increased odds of placental abruption (aOR = 2.14; 95% CI 1.22-3.75). The odds of placental abruption was 2.11 (95% CI 1.00-4.45) for migraineurs without aura; and 1.59 (95% 0.70-3.62) for migraineurs with aura. A lifetime history of tension-type headache was also increased with placental abruption (aOR = 1.61; 95% CI 1.01-2.57). Conclusions This study adds placental abruption to a growing list of pregnancy complications associated with maternal headache/migraine disorders. Nevertheless, prospective cohort studies are needed to more rigorously evaluate the extent to which migraines and/or its treatments are associated with the occurrence of placental abruption.
- Published
- 2010
- Full Text
- View/download PDF
3. Placental genetic variations in circadian clock-related genes increase the risk of placental abruption
- Author
-
Chunfang, Qiu, Gelaye, Bizu, Denis, Marie, Tadesse, Mahlet G., Enquobahrie, Daniel A., Ananth, Cande V., Pacora, Percy N., Salazar, Manuel, Sanchez, Sixto E., Williams, Michelle A., and Chun-fang.Qiu@Swedish.org
- Subjects
Pregnancy ,Circadian gene ,Placental abruption ,L53 - Physiologie animale - Reproduction ,L10 - Génétique et amélioration des animaux ,Placentae ,SNPs - Abstract
The genetic architecture of placental abruption (PA) remains poorly understood. We examined variations in SNPs of circadian clock-related genes in placenta with PA risk. We also explored placental and maternal genomic contributions to PA risk. Placental genomic DNA samples were isolated from 280 PA cases and 244 controls. Genotyping was performed using the Illumina Cardio-MetaboChip. We examined 116 SNPs in 13 genes known to moderate circadian rhythms. Logistic regression models were fit to estimate odds ratios (ORs). The combined effect of multiple SNPs on PA risk was estimated using a weighted genetic risk score. We examined independent and joint associations of wGRS derived from placental and maternal genomes with PA. Seven SNPs in five genes (ARNTL2, CRY2, DEC1, PER3 and RORA), in the placental genome, were associated with PA risk. Each copy of the minor allele (G) of a SNP in the RORA gene (rs2899663) was associated with a 30% reduced odds of PA (95% CI 0.52-0.95). The odds of PA increased with increasing placental-wGRS (Ptrend
- Published
- 2016
- Full Text
- View/download PDF
4. Placental genetic variations in circadian clock-related genes increase the risk of placental abruption
- Author
-
Qiu, Chunfang, Gelaye, Bizu, Denis, Marie, Tadesse, Mahlet G., Enquobahrie, Daniel A., Ananth, Cande V., Pacora, Percy N., Salazar, Manuel, Sanchez, Sixto E., Williams, Michelle A., Qiu, Chunfang, Gelaye, Bizu, Denis, Marie, Tadesse, Mahlet G., Enquobahrie, Daniel A., Ananth, Cande V., Pacora, Percy N., Salazar, Manuel, Sanchez, Sixto E., and Williams, Michelle A.
- Abstract
The genetic architecture of placental abruption (PA) remains poorly understood. We examined variations in SNPs of circadian clock-related genes in placenta with PA risk. We also explored placental and maternal genomic contributions to PA risk. Placental genomic DNA samples were isolated from 280 PA cases and 244 controls. Genotyping was performed using the Illumina Cardio-MetaboChip. We examined 116 SNPs in 13 genes known to moderate circadian rhythms. Logistic regression models were fit to estimate odds ratios (ORs). The combined effect of multiple SNPs on PA risk was estimated using a weighted genetic risk score. We examined independent and joint associations of wGRS derived from placental and maternal genomes with PA. Seven SNPs in five genes (ARNTL2, CRY2, DEC1, PER3 and RORA), in the placental genome, were associated with PA risk. Each copy of the minor allele (G) of a SNP in the RORA gene (rs2899663) was associated with a 30% reduced odds of PA (95% CI 0.52-0.95). The odds of PA increased with increasing placental-wGRS (Ptrend<0.001). The ORs were 1.00, 2.16, 3.24 and 4.48 across quartiles. Associations persisted after the maternal-wGRS was included in the model. There was evidence of an additive contribution of placental and maternal genetic contributions to PA risk. Participants with placental- and maternal-wGRS in the highest quartile, compared with those in the lowest quartile, had a 15.57-fold (95% CI 3.34-72.60) increased odds of PA. Placental variants in circadian clock-related genes are associated with PA risk; and the association persists after control of genetic variants in the maternal genome.
- Published
- 2016
5. A genome-wide association study of variations in maternal cardiometabolic genes and risk of placental abruption
- Author
-
Moore, Amy, Enquobahrie, Daniel A., Sanchez, Sixto E., Ananth, Cande V., Pacora, Percy N., and Williams, Michelle A.
- Subjects
Desprendimiento prematuro de la placenta ,Polimorfismo de nucleótido simple ,Estudio de asociación del genoma completo ,Complicaciones del embarazo - Abstract
Accumulating evidence suggests that placental abruption has a complex multifactorial pathogenesis that involves cardiovascular risk and metabolic dysfunction. However, comprehensive assessment of variations in genes involved in cardiometabolic traits associated with the risk of placental abruption is lacking. We conducted a case-control study investigating associations of variations in maternal cardiometabolic genes (characterized using 217,697 SNPs on the Illumina Cardio-Metabo Chip) with risk of placental abruption. A total of 253 abruption cases and 258 controls were selected from among participants enrolled in the Peruvian Abruptio Placentae Epidemiology Study in Lima, Peru. In the genome-wide association analyses, top hits did not surpass genome-wide significance. However, we observed suggestive associations of placental abruption with several SNPs, including SNPs in SMAD2 (P-value=1.88e-6), MIR17HG (P-value=7.8e-6], and DGKB (P-value=8.35e-6] loci. In candidate gene analyses, we observed associations of variations in a priori selected genes involved in coagulation, rennin-angiotensin, angiogenesis, inflammation, and B-vitamin metabolism with the risk of abruption. Our study suggests that variations in maternal cardiovascular and metabolic genes may be associated with risk of placental abruption. Future studies with large sample sizes are warranted. National Institute of Health, the Eunice Kennedy Shriver National Institute of Child Health and Human Development (5 R01-HD059827; T32HD052462) and the National Heart Lung and Blood Institute (K01HL10374).
- Published
- 2012
6. Risk of placental abruption in relation to maternal depressive, anxiety and stress symptoms
- Author
-
de Paz, Nicole C., Sanchez, Sixto E., Huaman, Luis E., Diez Chang, Guillermo, Pacora, Percy N., Garcia, Pedro J., Ananth, Cande V., Qiu, Chungfang, and Williams, Michelle A.
- Subjects
Ansiedad ,Desprendimiento prematuro de la placenta ,Embarazo ,Depresión ,Epidemiología ,Factores de riesgo - Abstract
Background Little is known about the influence of psychiatric factors on the etiology of placental abruption (PA), an obstetrical condition that complicates 1–2% of pregnancies. We examined the risk of PA in relation to maternal psychiatric symptoms during pregnancy. Methods This case–control study included 373 PA cases and 368 controls delivered at five medical centers in Lima, Peru. Depressive, anxiety and stress symptoms were assessed using the Patient Health Questionnaire (PHQ-9) and the Depression Anxiety Stress Scales (DASS-21). Multivariable logistic regression models were fit to calculate odds ratios (aOR) and 95% confidence intervals (CI) adjusted for confounders. Results Depressive symptoms of increasing severity (using the DASS depression subscale) was associated with PA (p for trend = 0.02). Compared with women with no depressive symptoms, the aOR (95%CI) for PA associated with each level of severity of depression symptoms based on the DASS assessment were as follows: mild 1.84 (0.91–3.74); moderate 1.25 (0.67–2.33); and severe 4.68 (0.98–22.4). The corresponding ORs for mild, moderate, and moderately severe depressive symptoms based on the PHQ assessment were 1.10 (0.79–1.54), 3.31 (1.45–7.57), and 5.01 (1.06–23.6), respectively. A positive gradient was observed for the odds of PA with severity of anxiety (p for trend = 0.002) and stress symptoms (p for trend = 0.002). Limitations These cross-sectionally collected data may be subject to recall bias. Conclusions Maternal psychiatric disorders may be associated with an increased occurrence of AP. Larger studies that allow for more precise evaluations of maternal psychiatric health in relation to PA risk are warranted.
- Published
- 2011
7. Risk of placental abruption in relation to maternal depressive, anxiety and stress symptoms
- Author
-
de Paz, Nicole C., primary, Sanchez, Sixto E., additional, Huaman, Luis E., additional, Chang, Guillermo Diez, additional, Pacora, Percy N., additional, Garcia, Pedro J., additional, Ananth, Cande V., additional, Qiu, Chungfang, additional, and Williams, Michelle A., additional
- Published
- 2011
- Full Text
- View/download PDF
8. Risk of placental abruption in relation to migraines and headaches
- Author
-
Sanchez, Sixto E, primary, Williams, Michelle A, additional, Pacora, Percy N, additional, Ananth, Cande V, additional, Qiu, Chungfang, additional, Aurora, Sheena K, additional, and Sorensen, Tanya K, additional
- Published
- 2010
- Full Text
- View/download PDF
9. Placental genetic variations in circadian clock-related genes increase the risk of placental abruption.
- Author
-
Qiu C, Gelaye B, Denis M, Tadesse MG, Enquobahrie DA, Ananth CV, Pacora PN, Salazar M, Sanchez SE, and Williams MA
- Abstract
The genetic architecture of placental abruption (PA) remains poorly understood. We examined variations in SNPs of circadian clock-related genes in placenta with PA risk. We also explored placental and maternal genomic contributions to PA risk. Placental genomic DNA samples were isolated from 280 PA cases and 244 controls. Genotyping was performed using the Illumina Cardio-MetaboChip. We examined 116 SNPs in 13 genes known to moderate circadian rhythms. Logistic regression models were fit to estimate odds ratios (ORs). The combined effect of multiple SNPs on PA risk was estimated using a weighted genetic risk score. We examined independent and joint associations of wGRS derived from placental and maternal genomes with PA. Seven SNPs in five genes (ARNTL2, CRY2, DEC1, PER3 and RORA), in the placental genome, were associated with PA risk. Each copy of the minor allele (G) of a SNP in the RORA gene (rs2899663) was associated with a 30% reduced odds of PA (95% CI 0.52-0.95). The odds of PA increased with increasing placental-wGRS (Ptrend<0.001). The ORs were 1.00, 2.16, 3.24 and 4.48 across quartiles. Associations persisted after the maternal-wGRS was included in the model. There was evidence of an additive contribution of placental and maternal genetic contributions to PA risk. Participants with placental- and maternal-wGRS in the highest quartile, compared with those in the lowest quartile, had a 15.57-fold (95% CI 3.34-72.60) increased odds of PA. Placental variants in circadian clock-related genes are associated with PA risk; and the association persists after control of genetic variants in the maternal genome.
- Published
- 2016
10. Genome-wide and candidate gene association studies of placental abruption.
- Author
-
Workalemahu T, Enquobahrie DA, Moore A, Sanchez SE, Ananth CV, Pacora PN, Liang L, Salazar M, and Williams MA
- Abstract
Placental abruption (PA), a pregnancy-related vascular disorder, is a leading cause of maternal and perinatal morbidity and mortality. The success of identifying genetic susceptibility loci for PA, a multi-factorial heritable disorder, has been limited. We conducted a genome-wide association study (GWAS) and candidate gene association study using 470 PA cases and 473 controls from Lima, Peru. Genotyping for common genetic variations (single nucleotide polymorphisms, SNPs) was conducted using the Illumina Cardio-Metabo Chip platform. Common variations in 35 genes that participate in mitochondrial biogenesis (MB) and oxidative phosphorylation (OS) were selected for the candidate gene study. Regression models were fit to examine associations of each SNP with risk of PA. In pathway analyses, we examined functions and functional relationships of genes represented by the top GWAS hits. Genetic risk scores (GRS), based on top hits of the GWAS and candidate gene analyses, respectively, were computed using the risk allele counting method. The top hit in the GWAS analyses was rs1238566 (empirical P-value=1.04e-4 and FDR-adjusted P-value=5.65E-04) in FLI-1 gene, a megakaryocyte-specific transcription factor. Networks of genes involved in lipid metabolism and cell signaling were significantly enriched by the 51 genes whose SNPs were among the top 200 GWAS hits (P-value <2.1e-3). SNPs known to regulate MB (e.g. CAMK2B, NR1H3, PPARG, PRKCA, and THRB) and OP (e.g., COX5A, and NDUF family of genes) were associated with PA risk (P-value <0.05). GRS was significantly associated with PA risk (trend P-value <0.001 and 0.01 for GWAS and candidate gene based GRS, respectively). Our study suggests that integrating multiple analytical strategies in genetic association studies can provide opportunities for identifying genetic risk factors and novel molecular mechanisms that underlie PA.
- Published
- 2013
11. A genome-wide association study of variations in maternal cardiometabolic genes and risk of placental abruption.
- Author
-
Moore A, Enquobahrie DA, Sanchez SE, Ananth CV, Pacora PN, and Williams MA
- Abstract
Accumulating evidence suggests that placental abruption has a complex multifactorial pathogenesis that involves cardiovascular risk and metabolic dysfunction. However, comprehensive assessment of variations in genes involved in cardiometabolic traits associated with the risk of placental abruption is lacking. We conducted a case-control study investigating associations of variations in maternal cardiometabolic genes (characterized using 217,697 SNPs on the Illumina Cardio-Metabo Chip) with risk of placental abruption. A total of 253 abruption cases and 258 controls were selected from among participants enrolled in the Peruvian Abruptio Placentae Epidemiology Study in Lima, Peru. In the genome-wide association analyses, top hits did not surpass genome-wide significance. However, we observed suggestive associations of placental abruption with several SNPs, including SNPs in SMAD2 (P-value=1.88e-6), MIR17HG (P-value=7.8e-6], and DGKB (P-value=8.35e-6] loci. In candidate gene analyses, we observed associations of variations in a priori selected genes involved in coagulation, rennin-angiotensin, angiogenesis, inflammation, and B-vitamin metabolism with the risk of abruption. Our study suggests that variations in maternal cardiovascular and metabolic genes may be associated with risk of placental abruption. Future studies with large sample sizes are warranted.
- Published
- 2012
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.