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Journal articles on the topic "06a061"
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Xu, L., B. T. Keenan, A. S. Wiemken, A. I. Pack, and R. J. Schwab. "0569 Soft Palate Fat Between Lean Adults with Obstructive Sleep Apnea and Healthy Control." Sleep 43, Supplement_1 (April 2020): A218. http://dx.doi.org/10.1093/sleep/zsaa056.566.
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Abstract Introduction Previous studies have shown that obese patients with obstructive sleep apnea (OSA) have a significantly greater percentage of fat tissue in soft palate than normal subjects. However, the influence of soft palate fat is not clear in non-obese adults with OSA. This study compared the volume of fat in the soft palate between lean adults with OSA and lean controls. Methods We examined soft palate fat in 21 lean OSA cases and 16 lean controls with body mass index (BMI) <25 kg/m2. All subjects underwent a magnetic resonance imaging (MRI) with three-point Dixon scan. We used volumetric reconstruction algorithms to quantify the amount of soft palate fat, which was compared between apnecis and controls. Analysis reproducibility was quantified using intraclass correlation coefficients (ICC) from repeated analyses of 20 randomly-chosen MRIs. Results Analysis of soft palate fat was highly reproducible, with an ICC (95% confidence interval) of 0.968 (0.923, 0.987). Lean apneics were younger than lean controls (45.3±13.0 vs. 62.1±10.4 years; p<0.0001). No significant differences between apneics and controls were observed in the average BMI (23.4±2.2 vs. 23.5 ± 2.6 kg/m2; p=0.824), the fat pads volume (4198±1728 vs. 3880±1544 mm3; p=0.646), and the proportion of males (61.9% vs. 68.8%; p=0.666). In unadjusted analyses, the lean OSA group showed significantly higher soft palate fat volume than lean controls (7605±2109 vs. 5327±1783 mm3; p=0.003). When adjusting for age, gender and BMI, no differences was observed between groups in soft palate fat volume (p=0.122) and fat pads volume (p=0.702). Conclusion Analysis of soft palate fat volume from Dixon MRI is highly reproducible. Our results indicate no significant difference in deposition of fat at soft palate between lean patients with OSA and lean controls when accounting for age, gender and BMI. Support This study is supported by National Institutes of Health Grant: 2P01HL094307-06A1. LX is supported by Young Elite Scientists Sponsorship Program of China Association for Science and Technology.
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Kundel, V., P. Darko, P. Taweesedt, A. Parekh, I. Ayappa, A. Lee, J. Darby, S. Kaali, and K. Asante. "0966 Sleep-Wake Patterns in Mothers and Children in a Rural Community With Limited Access to Electricity: Results from the Ghana Randomized Air Pollution and Health Study." Sleep 43, Supplement_1 (April 2020): A367. http://dx.doi.org/10.1093/sleep/zsaa056.962.
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Abstract Introduction Studies measuring objective sleep duration in rural/indigenous populations are limited, showing sleep duration similar to that of industrialized countries. Little is known about sleep duration in women of reproductive age, and children within these populations. Our study is the first to objectively characterize sleep in mothers and children in an agrarian community with limited access to electricity, utilizing data from the Ghana Randomized Air Pollution and Heath Study (GRAPHS). Methods The GRAPHS cohort, a cluster-randomized trial, evaluated the efficacy of clean fuels on birthweight and infant pneumonia incidence in central Ghana. The study initially recruited pregnant women and newborns in 2013. This study is now utilizing wrist-actigraphy to analyze sleep-wake patterns among mothers and children of GRAPHS. We have thus far analyzed actigraphy in 39 mothers and 49 children (including 25 mother-child pairs), using the Motionlogger-MicroWatch with the Cole-Kripke algorithm to assess total sleep time (TST). We report baseline characteristics and sleep-wake patterns of our sample. Results Mean age of mothers was 33.5 years, (range 22-48), and mean age of children was 3.9 years (3-4). Average nights recorded were 4 (standard deviation [SD] 2.1). For mothers, average median time-in-bed was 7.9 (SD 1.2) hours, TST was 6.4 (SD .9) hours, and sleep efficiency was 82% (SD 7.9). Median bedtime was 9:33pm (SD 1.5 hours), and median wake-time was 5:56am (SD 1.4 hours). For children, average median time-in-bed was 9.9 (SD 1.0) hours, TST was 8.2 (SD 0.9) hours, and sleep efficiency was 83% (SD 6). Median bedtime was 8:03pm (SD 0.8 hours), and median wake-time was 6:06am (SD 0.6 hours). There was no correlation between sleep measures in mother-child pairs. Conclusion In an agrarian Ghanaian community with limited access to electricity, objective sleep measures in women were similar to prior studies conducted in indigenous/rural populations of developing African countries (Ndiaye et.al.2007, Samson et.al.2016), though data in children is lacking for comparison. When compared with post-industrialized countries, objective sleep measures for this age group of non-gravid women are sparse. In toddlers however, TST was lower in our cohort when compared with objective sleep amongst toddlers in industrialized nations. Support 2K24HL109156-06A1
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Afangbedji, Nowah Kokou Apeadoufia, James G. Taylor, Sergei Nekhai, and Marina Jerebtsova. "Elevated Plasma Soluble Urokinase-Type Plasminogen Activator Receptor (suPAR) in Sickle Cell Disease - a Marker of Chronic Kidney Disease." Blood 138, Supplement 1 (November 5, 2021): 968. http://dx.doi.org/10.1182/blood-2021-153938.
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Abstract Background: Sickle cell nephropathy (SCN) is one of the most common complications of SCD, leading in most cases to chronic kidney disease (CKD) and end-stage renal disease (ESRD). Despite the high prevalence of CKD in sickle cell disease (SCD) patients, there remains a poor understanding of the pathophysiological mechanism of SCN and a lack of biomarkers for early detection of SCD-associated CKD. Soluble urokinase-type plasminogen activator receptor (suPAR) is an emerging biomarker of CKD. suPAR is a member of the fibrinolytic system, which is dysregulated in SCD patients. Objective: To evaluate suPAR as a biomarker of SCD-associated nephropathy and identify plasma proteases responsible for its increase in SCD. Methods: The study was approved by Howard University review board (IRB) and all subjects provided written inform consent prior to the sample collection. Whole blood and urine samples were collected from 77 SCD patients and 10 healthy individuals, and plasma was isolated. Levels of creatinine and cystatin C in plasma and albumin and creatinine in urine were measured by ELISA. eGFR was calculated using CKD-EPI creatinine-cystatin equation, and CKD stages were assigned. Plasma suPAR was measured by ELISA and was correlated with CKD stages. The activities of candidates uPAR proteases: Neutrophile elastase (NE), urokinase-type plasminogen activator (uPA) and plasmin in plasma samples from SCD patients were measured and compared to healthy participants. Results: The average age of SCD patients was 42.5 years (range 18-67 years). Most patients had HbSS genotype (67.5%),19.5% of patients were HbSC (hemoglobin C sickle cell compound heterozygous), and 13% had HbS β-thalassemia. More than half (53.2 %) were females. We observed an increased level of plasma suPAR (>3ng/ml) in more than 60% of SCA patients without renal disease, representing a risk factor for CKD progression. Plasma suPAR levels further increased in the patients with CKD and positively correlated with stages of CKD (r=0.419, R2=0.1696). Analysis of plasma proteases that cleaved uPAR producing soluble peptides (suPAR) demonstrated increased urokinase-type plasminogen activator (uPA) activity without significant changes in neutrophile elastase. Conclusion: This study validated plasma suPAR as a potential marker of CKD in SCD patients and identified plasma uPA as a uPAR protease that may increase circulating suPAR in SCD. Future longitudinal analysis of suPAR levels in patients with SCA is needed. Acknowledgments: We thank Drs. Namita Kumari and Xiaomei Niu for their help in samples identification. This work was supported by NIH Research Grants 1R01HL125005-06A1, 5U54MD007597, 1P30AI117970-06,1UM1AI26617, and 1SC1HL150685. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.
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HEIANZA, YORIKO, XUAN WANG, QIAOCHU XUE, LAWRENCE J. APPEL, FRANK SACKS, and LU QI. "114-OR: Genetic Variants in GIPR and Effects of Dietary Carbohydrate Quantity and Quality on Glycemic Responses to an Oral Glucose Load—The OmniCarb Trial." Diabetes 72, Supplement_1 (June 20, 2023). http://dx.doi.org/10.2337/db23-114-or.
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The gut incretin hormone, glucose-dependent insulinotropic polypeptide (GIP), may play a pivotal role in mediating adverse effects of high glycemic index (GI) foods on metabolic diseases. GIP exerts its effects by binding to a receptor, GIPR; genome-wide association studies have identified variants in the GIPR region related to type 2 diabetes (T2D) and glycemic/GIP responses to glucose tolerance tests. We examined whether GIPR variants were related to impaired glycemic responses during oral glucose tolerance tests (OGTTs) after consuming 4 diets (each for 5 weeks) with different carbohydrate (Carb) content and GI levels in the OmniCarb randomized crossover feeding trial. A genetic risk score (GRS) was calculated by counting T2D-risk alleles of SNPs rs1800437, rs11671664, and rs2238689 at GIPR (n=146). We found that GRS was related to greater glycemic responses after consuming a high GI/high Carb diet, regardless of baseline glycemic status (Fig). When testing diet replacement effects, combined effects of high GI and high Carb (vs. low GI/low Carb) on glycemic responses were significantly modified by GRS (Pinteraction<0.05). In conclusion, T2D-risk-related GIPR variants modified the effects of dietary carbohydrates on glucose tolerance. GIPR variants may be related to deteriorating glucose tolerance after eating a high GI, high Carb diet. Disclosure Y.Heianza: None. X.Wang: None. Q.Xue: None. L.J.Appel: None. F.Sacks: None. L.Qi: None. Funding National Institutes of Health (2P20GM109036-06A1-7233, DK091718, DK100383, DK115679)
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BACHOR, TOMAS P., KUSH ATTAL, EIRINI VAGENA, FRANCOIS MIFSUD, VIANA PHAM, MARTIN VALDEARCOS-CONTRERAS, CHRISTIAN VAISSE, and ALLISON XU. "1522-P: Identification of AgRP Cells in the Murine Hindbrain That Drive Feeding." Diabetes 72, Supplement_1 (June 20, 2023). http://dx.doi.org/10.2337/db23-1522-p.
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The central melanocortin system is essential for the regulation of food intake and body weight in humans and rodents. Agouti-related protein (AgRP) is the sole orexigenic component of the central melanocortin system and is conserved across mammalian species. AgRP is currently known to express exclusively in the mediobasal hypothalamus, and hypothalamic AgRP-expressing neurons are essential for feeding regulation. Here we describe a previously unknown population of AgRP cells in the area postrema (AP) and the adjacent commissural nucleus of the solitary tract (cNTS) of the causal brainstem. AgRP was expressed in the embryonic AP, and hindbrain AgRP expression in adult mice was low under ad libitum fed condition but increased with food deprivation. AgRP cells in the AP and cNTS consisted of locally projecting neurons as well as tanycyte-like cells. In mice that lack hypothalamic AgRP neurons, diphtheria-toxin mediated ablation of AgRP cells led to anorexia and weight loss, whereas chemogenetic activation of AgRP neurons resulted in hyperphagia and weight gain. Moreover, focal transcranial photo-stimulation of AgRP cells in the AP and cNTS with a step-function opsin with ultra-high light sensitivity (SOUL) stimulated feeding in mice with or without hypothalamic AgRP neurons, suggesting that the hyperphagic effects of hindbrain AgRP neurons are independent of hypothalamic AgRP neurons. Collectively, our study indicates that the hindbrain has a balanced melanocortin system, complete with both orexigenic and anorexigenic components, and that AgRP neurons in the hindbrain drive feeding in adult animals. Disclosure T.P.Bachor: None. K.Attal: None. E.Vagena: None. F.Mifsud: None. V.Pham: None. M.Valdearcos-contreras: None. C.Vaisse: None. A.Xu: Advisory Panel; Pennington Biomedical Research Center, Research Support; Eli Lilly and Company. Funding National Institute of Diabetes and Digestive and Kidney Diseases (1P30DK098722-01A1, P30DK63720-06A1)
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Doyle, Brendan M., Sara M. F. Turner, Bobbi Johnson, Kristi A. Streeter, Darin J. Falk, Ronald J. Mandel, Barry J. Byrne, and David D. Fuller. "Comparison of Hypoglossal Motoneuron Transgene Expression following Single vs Dual Tongue Injection of AAV9‐CBA‐GFP." FASEB Journal 30, S1 (April 2016). http://dx.doi.org/10.1096/fasebj.30.1_supplement.lb739.
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Retrograde transport of viral vectors following intramuscular injection allows for targeted gene delivery to motoneuron pools. Gene delivery to the hypoglossal (XII) motoneurons is of potential interest in disorders involving impaired tongue muscle control such as dysphagia, dysarthria, and possibly obstructive sleep apnea. Using a murine model of Pompe disease, our group has shown that a single intramuscular injection of 1.00e11 vector genomes (vg) of recombinant adeno‐associated virus serotype 9 (AAV9) into the base of the tongue produces sustained transgene expression in a subset of XII motoneurons. Here we investigated whether distributing the virus over a broader portion of the tongue via two near‐simultaneous injections would increase XII motoneuron transduction as compared to a single injection. Four week old 129SVE mice were anesthetized and administered either a unilateral, single 20μL injection (n=2) or bilateral, 10μL injections (n=2) to the anterior base of the tongue targeting the insertion point for the genioglossus muscle. In both cases, a total of 1.00e11 vg of AAV9 encoding green fluorescent protein (GFP) with expression driven by the chicken β‐actin promotor (AAV9‐CBA‐GFP) was given. The medulla was histologically evaluated 6 weeks after tongue injection; GFP was detected using immunohistochemistry. Robust XII motoneuron GFP expression was observed in the caudal XII nucleus after either single or dual AAV9 injection; initial observations suggest no differences in XII motoneuron transduction between the two delivery methods. With both approaches, GFP expression was primarily restricted to XII motoneurons, but was also sporadically present in neurons throughout the medulla. The data confirm that tongue injection of AAV9 drives robust transgene expression in the XII motoneuron pool, and suggest that expression is similar whether using the single or dual injection approach.Support or Funding Information2R01HD052682‐06A1
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HEIANZA, YORIKO, QIAOCHU XUE, JENNIFER ROOD, GEORGE BRAY, FRANK SACKS, and LU QI. "48-LB: Changes in Plasma Levels of Nonnutritive Sweetener Erythritol Are Related to Two-Year Changes of Insulin Sensitivity in Response to Weight-Loss Diets—The POUNDS Lost trial." Diabetes 72, Supplement_1 (June 20, 2023). http://dx.doi.org/10.2337/db23-48-lb.
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Evidence on the benefits of non-nutritive sweeteners for weight management and improving insulin sensitivity and glucose metabolism is inconsistent. Recently, high levels of circulating erythritol, a sugar alcohol used as one of the non-nutritive sweeteners, have been linked to increased risks of type 2 diabetes and its vascular complications. Whether changes in circulating erythritol levels are related to insulin sensitivity and glucose metabolism remains unknown. Here, we investigated whether changes in plasma erythritol induced by weight-loss diet interventions were related to improved insulin sensitivity and glucose metabolism. This study included overweight or obese participants without diabetes or unstable cardiovascular disease from the POUNDS Lost trial with available data on circulating erythritol at baseline (n=805) and its changes from baseline to 6 months (n=670) and 2 years (n=533) during weight-loss diet interventions. At baseline, higher plasma levels of erythritol were related to hyperinsulinemia and greater degrees of insulin resistance assessed by HOMA-IR, even after adjusting for covariates, including BMI (P <0.05 for all). In response to weight-loss dietary interventions, a greater decrease in plasma erythritol was significantly associated with larger reductions of fasting insulin (p= 0.0001) and HOMA-IR (p=0.039) at 6 months, regardless of the initial levels of BMI, erythritol, and the respective outcome. Similarly, we found a significant association between long-term changes in erythritol and a 2-year reduction of fasting insulin (p=0.0027). In conclusion, circulating plasma erythritol, a marker of non-nutritive sweetener consumption, was significantly associated with hyperinsulinemia and insulin sensitivity among adults with overweight or obesity. Weight-loss diet-induced decreases in plasma erythritol were related to improved insulin sensitivity. Disclosure Y. Heianza: None. Q. Xue: None. J. Rood: None. G. Bray: Advisory Panel; Medifast, Inc., Herbalife International of America, Inc. F. Sacks: None. L. Qi: None. Funding National Institutes of Health (DK091718, DK100383, DK115679, 2P20GM109036-06A1-7233)
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PALANISAMY, SRIKANTH, UGUR PARLATAN, MEHMET OZEN, ASMA H. KARIM, DEMIR AKIN, UTKAN DEMIRCI, and LATHA PALANIAPPAN. "1712-P: Serum miRNA-1 Levels as a Potential Marker for Myocardial Steatosis in Normal Weight and Obese/Overweight Diabetic Individuals—A Pilot Study." Diabetes 72, Supplement_1 (June 20, 2023). http://dx.doi.org/10.2337/db23-1712-p.
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Of the 37 million Americans with type II diabetes, a substantial proportion have a normal body mass index (BMI). These populations suffer a disproportionately high burden of mortality; the development of diabetic cardiomyopathy (DCM) is likely a contributor. Myocardial steatosis, a known consequence of diabetes, is a significant part of DCM's pathogenesis; unfortunately, there is no feasible way to screen patients for steatosis. Exosomal microRNAs (miRNAs) are a promising biomarker for this purpose. However, no study has evaluated miRNA signatures in normal-weight patients with diabetes. Serum samples of obese/overweight and normal-weight diabetic subjects were obtained via IMPACT and STRONG-D clinical trial protocols respectively. Exosomes were extracted using the ExoTIC (exosome total isolation chip) platform. MiRNA-1 levels from extracellular vesicles were quantified using RT-qPCR and compared via unpaired student's two-tailed t-test. A total of 8 samples (4 normal-weight and 4 overweight/obese) were analyzed. Overall, the obese cohort had a mean age of 63.7 vs. 57.2 for the normal-weight cohort. The obese cohort had a mean BMI of 29.7 vs. 23.1 for the normal weight cohort. Both cohorts were composed of 75% men and 25% women. The obese cohort had a mean hemoglobin A1c of 7.2% vs. 8.0% in the normal-weight cohort. Serum miRNA-1 levels were significantly higher in normal-weight diabetic subjects (p = 0.0004). In this pilot study, patients with diabetes of a normal weight had significantly higher levels of serum miRNA-1, implying that they may have more myocardial steatosis and possibly, more cardiac dysfunction. This pathophysiologic difference could help explain the significant morbidity and mortality that diabetic patients of a normal weight suffer. Further directions for our study include the complete quantification of both miRNA-1 and miRNA-133a among our entire cohort, as well as assessment of echocardiographic parameters. Disclosure S.Palanisamy: None. U.Parlatan: None. M.Ozen: None. A.H.Karim: None. D.Akin: None. U.Demirci: None. L.Palaniappan: None. Funding National Institutes of Health (1R18DK096394-01A1, 2R01DK081371-06A1)
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Turner, Sara, Aaron Hoyt, Darin Falk, Barry Byrne, and David Fuller. "Genome‐wide Assessment of the Pompe (Gaa−/−) Mouse Cervical Spinal Cord Confirms Widespread Neuropathology." FASEB Journal 30, S1 (April 2016). http://dx.doi.org/10.1096/fasebj.30.1_supplement.1285.2.
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Pompe disease, caused by deficiency of acid alpha‐glucosidase (GAA), leads to glycogen accumulation, disruption of cellular architecture and neuromuscular impairments. Respiratory and lingual motor systems often decline first, and respiratory motoneurons typically show profound histopathology and glycogen accumulation at an early age. Although neuropathology is now firmly established in Pompe tissues from both humans and animal models, the associated mechanisms have not been evaluated. Therefore, we studied the cervical spinal cord of adult Pompe (Gaa−/−) and wild‐type (129SVE) mice using histological methods and mRNA analyses with the Affymetrix Mouse Gene Array 2.0ST. Pathway analyses of the mRNA data were done using the Broad Institute's Molecular Signature Database. In separate animals, cervical tissues were stained for terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), and ionized calcium binding adaptor molecule 1 (IBA‐1) to assess DNA fragmentation and microglial morphology, respectively. From these analyses, several themes emerged (FDR q values <0.01). First, neuronal loss is an important feature of Pompe disease, and occurs in motoneurons before the onset of overt respiratory symptoms. Putative phrenic motoneurons were TUNEL‐positive, and pathway analyses showed significant upregulation of apoptotic processes in the Gaa−/− cervical spinal cord. Second, pro‐inflammatory mRNA signaling is significantly upregulated in the Gaa−/− cervical cord, and this is associated with greater neuronal co‐localization of microglia. Third, multiple signal transduction pathways are altered in the Gaa−/− cervical spinal cord. Glutamatergic signaling pathways were downregulated, as were well‐known “synaptic plasticity pathways” including genes related to long‐term potentiation. Finally, there was a robust change in cellular metabolism pathways in the Gaa−/− spinal cord that included upregulation of macromolecule, lipid, carbohydrate, and protein metabolic pathways. These data confirm that absence of functional GAA protein triggers a complex neurodegenerative process, and suggest that alterations in synaptic transmission and neuroplasticity processes may contribute to motor phenotypes in Pompe disease. Most importantly, the results underscore the importance of therapeutically targeting neuropathology in Pompe disease.Support or Funding InformationCTSA U54‐TR001012; Craig H. Neilsen Foundation 313369 (SMFT); 2R01HD052682‐06A1 (DDF, BJB)
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Bertaux‐Skeirik, Nina, Mark Wunderlich, Emma Teal, Maxime Mahe, Nambirajan Sundaram, Joel Gabre, Jennifer Hawkins, et al. "CD44v9 Emerges in Response to Injury and Contributes to the Regeneration of the Gastric Epithelium." FASEB Journal 31, S1 (April 2017). http://dx.doi.org/10.1096/fasebj.31.1_supplement.893.1.
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Cluster‐of‐differentiation gene 44, in particular CD44 variant isoforms (CD44v), emerges during regeneration of the gastric epithelium in response to injury. In particular, CD44v9 is expressed within Spasmolytic Polypeptide/TFF2‐Expressing Metaplasia (SPEM) glands during gastric repair, but the function is unknown. Here we tested the hypothesis that CD44v9 marks a regenerative cell lineage that plays a functional role in gastric repair. Acetic acid injury was induced in CD44‐deficient (CD44KO) and C57BL/6 (BL6) mice. Mouse‐derived gastric organoids expressing CD44v9 were transplanted at the ulcer site of CD44KO mice. Ulcers, expression of CD44v9, proliferation and histology were measured at days 1, 3, 5 and 7 post‐injury. Human‐derived gastric organoids from elderly patients (>55 years) or young patients (14–20 years) were generated and transplanted into the stomachs of NOD scid gamma (NSG) mice post‐injury. Ulcers were induced in NRGS mice expressing human‐derived immune cells (huNRGS) and the immune phenotype analyzed by CyTOF. CD44v9 expression emerged at the ulcer margin during gastric ulcer repair. Compared to BL6 mice that healed within 7 days post‐injury, CD44KO mice exhibited loss of ulcer repair and gastric epithelial regeneration. Transplantation of CD44v9‐expressing gastric organoids into the stomachs of CD44KO mice promoted ulcer repair. Compared to NSG mice exhibiting loss of CD44v9 expression and gastric repair in response to injury, transplantation of human‐derived gastric organoids from young stomachs promoted repair. Transplantation of organoids derived from aged stomachs did not promote repair. Compared to NRGS mice, huNRGS animals exhibited smaller ulcer sizes and an infiltration of human CD163+ macrophages that correlated with an emergence of CD44v9 expression. Thus, CD44v9 marks a regenerative cell lineage. Macrophages infiltrating the injured gastric mucosa may induce the emergence of CD44v9 during regeneration of the epithelium.Support or Funding InformationThis work was supported by NIH 2 R01 DK083402‐06A1 grant, College of Medicine Bridge Funding Program (Zavros), and the University of Cincinnati Graduate School Dean's Fellowship, Albert J. Ryan Fellowship and 2T32GM105526‐04 (Bertaux‐Skeirik).
Dissertations / Theses on the topic "06a061"
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Amer, Rawya M. Tawfik. "State-society relations and regional role : comparing Egypt and South Africa." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:c00e6d89-06a1-40b5-b760-33965d32bcef.
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The study explains the regional roles of Egypt and South Africa in the last two decades by reference to the state’s relationship with society, a variable that has long been underplayed in international relations and foreign policy literature. It suggests that the different character of this relationship in each country has shaped the opportunities and constraints affecting the foreign policy choices of both the state and societal institutions in the two countries. The study adopts a cross-disciplinary approach using debates on state capacity and its relationship with regime type in comparative politics and political economy to understand and evaluate the two countries' foreign policies in their respective regions. After analysing the impact of state-society relationships on the regional role conceptions of the state and societal actors, the study compares the performance of these actors in two case studies; the Palestinian-Israeli conflict in the case of Egypt and the Zimbabwean crisis in the case of South Africa. It concludes that although the role of each state in resolving its respective regional conflict has been less than effective, the post-apartheid democratic dispensation has provided opportunities for South African social forces to play roles that complemented, checked and balanced the role of the state, compared to their Egyptian counterparts. On the other hand, the soft authoritarian Egyptian state used its role in the Palestinian-Israeli conflict to maintain the international alliances that helped to sustain its domestic control. This constrained the state's foreign policy options. It made marketing peace as 'a strategic choice' and containing resistance movements the priorities of Egypt's intervention in the Palestinian issue. The co-optation of the Egyptian business community and the exclusion of Islamist forces by the state weakened their roles in conflict resolution, depriving the state of tools of effectiveness. In the case of South Africa, racial politics, the ANC's liberation movement psyche, and the domination of the presidency over foreign policy making have hindered the promotion of NEPAD's principles of democracy and respect for human rights in the case of Zimbabwe. However, South African civil society played a crucial role in supporting its Zimbabwean counterpart, holding the South African state accountable to its foreign policy principles and its democratic institutions, and intervening where the state's role was missing or insufficient.
Books on the topic "06a061"
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Philosophy of Free Will: Essential Readings from the Contemporary Debates. Oxford University Press, Incorporated, 2013.
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Hitchcock's America. Oxford University Press, 1999.
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Sturmfels, Bernd, and Mateusz Michaek. Invitation to Nonlinear Algebra. American Mathematical Society, 2021.
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