Incorporating glass transition concepts to explain rice milling-quality reductions during the drying process

Previous research has indicated that while drying rough rice using air temperatures above the glass transition temperature (Tg), head rice yield (HRY) reductions are incurred if a state transition occurs when severe intra-kernel moisture content (MC) gradients are present. State transitions can occur by extended drying using high-temperature air or by cooling kernels below Tg before sufficient tempering has occurred. The objectives of this experiment were to determine the maximum MC removal per initial drying pass and the associated tempering durations required to prevent HRY reduction. Two long-grain cultivars, ‘Francis’ and ‘Wells’, at two harvest moisture contents (HMC) were used. Samples were dried with air conditions of either 60°C/17% RH or 50°C/28% RH for various durations to create a range of intra-kernel MC gradients and were subsequently tempered in sealed bags for durations ranging from 0 to 160 min. After tempering, samples were cooled to cause a state transition, and then slowly dried to 12.2% MC. Samples were then milled to determine HRY. Control samples were dried at 21°C/60% RH. Results showed that the amount of moisture that could be removed in the initial drying pass was directly related to the HMC and the drying air condition. The tempering duration required to prevent HRY reductions increased with the amount of MC removed from the kernel in a drying pass. The HRY reduction patterns concur with a hypothesis that explains fissure formation during the drying process based on the Tg of rice kernels

Gender differences : the effects of economic distress on subjective well-being

With the emphasis on consumption in contemporary society, there is increasing concern about the consequences of consumers’ heavy dependence on credit over the past decade, and about indications of a slowing economy. These concerns in consumerism and use of credit encourage examination of the relationship between financial problems and individuals\u27 sense of well-being. A review of research into the financial stress and subjective well-being relationship raises questions about the role of gender and the role of satisfaction with financial situation. While previous researchers suggest satisfaction with financial situation to be a significant determinant of subjective well-being, the results are mixed for the impact of gender. The goal of this study is to address the four following questions: (a) What effects if any do objective measures of financial stress, such as being evicted from one\u27s home or repossession of belongings, have on subjective well-being? (b) How do these objective measures of financial stress affect satisfaction with financial situation? (c) What effects if any does satisfaction with financial situation have on subjective wellbeing? and (d) Are there gender differences in these relationships? Employing data from a sub sample (N = 784) of the 1991 General Social Survey, this study examines overall life happiness, as well as three domain specific types of happiness, i.e. happiness with family, happiness with health, and happiness with friendships. Questions about financial stress include three domains: (a) inability to purchase necessities, such as food, healthcare, or health insurance, (b) experiences of pressure from others to pay bills, such as when one reports pawning valuables to make ends meet or reports pressure from creditors and bill collectors, and (c) experiences of loss such as when one is evicted from their home, or has belongings repossessed. Four models (one for each of the types of subjective well-being) are examined. Structural equation modeling is employed to examine the relationships among the measures of financial stress, financial satisfaction, and the subjective well-being indicators, as well as to examine the role of gender in these relationships. As expected, the results indicate a significant negative relationship between objective measures of financial stress and satisfaction with financial situation, as well as between financial stress and subjective well-being. Yet, the results also indicate that while objective measures of financial stress have negative effects on various types of subjective well-being, satisfaction with financial situation is a more significant determinant of subjective well-being. For all four models, gender did not demonstrate any significant effect on these relationships

Patient satisfaction reported by in-visit and after-visit surveys

Patient experience measurement has become a basic requirement for every healthcare provider organization. Yet, when the timing and mode of survey administration are considered, there is skepticism about the usefulness of ‘after- visit’ patient experience surveys to measure satisfaction and identify opportunities to improve service or health care quality. The aim of this observational study was to compare patient satisfaction among those who rated the patient experience at the conclusion of their outpatient appointment while still in the office, to that among those who rated the patient experience up to one month after their outpatient appointment via a mailed survey. Two sampling strategies were used to collect patient experience data from patients of the University of Maryland Family and Community Medicine practice: a postal survey to collect data from patients approximately 30 days after their visit (the After-Visit survey), and a within-visit survey to collect data from patients during their visit (the In-Visit survey). Nineteen survey questions measured comparable constructs between the After-Visit and In-Visit. This study did not find any significant differences between the data sources for any of these questions. The study showed that patient satisfaction could be assessed within a visit or by mail 30 days later without a statistically significant effect on mean responses

Combined mutation screening of NKX2-5, GATA4, and TBX5 in congenital heart disease: multiple heterozygosity and novel mutations

Background: Variants of several genes encoding transcription modulators, signal transduction, and structural proteins are known to cause Mendelian congenital heart disease (CHD). NKX2-5 and GATA4 were the first CHD-causing genes identified by linkage analysis in large affected families. Mutations of TBX5 cause Holt–Oram syndrome, which includes CHD as a clinical feature. All three genes have a well-established role in cardiac development. Design: In order to investigate the possible role of multiple mutations in CHD, a combined mutation screening was performed in NKX2-5, GATA4, and TBX5 in the same patient cohort. Samples from a cohort of 331 CHD patients were analyzed by polymerase chain reaction, double high-performance liquid chromatography and sequencing in order to identify changes in the NKX2-5, GATA4, and TBX5 genes. Results: Two cases of multiple heterozygosity of putative disease-causing mutations were identified. One patient was found with a novel L122P NKX2-5 mutation in combination with the private A1443D mutation of MYH6. A patient heterozygote for a D425N GATA4 mutation carries also a private mutation of the MYH6 gene (V700M). Conclusions: In addition to reporting two novel mutations of NKX2-5 in CHD, we describe families where multiple individual mutations seem to have an additive effect over the pathogenesis of CHD. Our findings highlight the usefulness of multiple gene mutational analysis of large CHD cohorts

Congenital Heart Disease–Causing Gata4 Mutation Displays Functional Deficits In Vivo

Defects of atrial and ventricular septation are the most frequent form of congenital heart disease, accounting for almost 50% of all cases. We previously reported that a heterozygous G296S missense mutation of GATA4 caused atrial and ventricular septal defects and pulmonary valve stenosis in humans. GATA4 encodes a cardiac transcription factor, and when deleted in mice it results in cardiac bifida and lethality by embryonic day (E)9.5. In vitro, the mutant GATA4 protein has a reduced DNA binding affinity and transcriptional activity and abolishes a physical interaction with TBX5, a transcription factor critical for normal heart formation. To characterize the mutation in vivo, we generated mice harboring the same mutation, Gata4 G295S. Mice homozygous for the Gata4 G295S mutant allele have normal ventral body patterning and heart looping, but have a thin ventricular myocardium, single ventricular chamber, and lethality by E11.5. While heterozygous Gata4 G295S mutant mice are viable, a subset of these mice have semilunar valve stenosis and small defects of the atrial septum. Gene expression studies of homozygous mutant mice suggest the G295S protein can sufficiently activate downstream targets of Gata4 in the endoderm but not in the developing heart. Cardiomyocyte proliferation deficits and decreased cardiac expression of CCND2, a member of the cyclin family and a direct target of Gata4, were found in embryos both homozygous and heterozygous for the Gata4 G295S allele. To further define functions of the Gata4 G295S mutation in vivo, compound mutant mice were generated in which specific cell lineages harbored both the Gata4 G295S mutant and Gata4 null alleles. Examination of these mice demonstrated that the Gata4 G295S protein has functional deficits in early myocardial development. In summary, the Gata4 G295S mutation functions as a hypomorph in vivo and leads to defects in cardiomyocyte proliferation during embryogenesis, which may contribute to the development of congenital heart defects in humans

ALDH1A2 (RALDH2) genetic variation in human congenital heart disease

Abstract\ud \ud \ud \ud Background\ud \ud Signaling by the vitamin A-derived morphogen retinoic acid (RA) is required at multiple steps of cardiac development. Since conversion of retinaldehyde to RA by retinaldehyde dehydrogenase type II (ALDH1A2, a.k.a RALDH2) is critical for cardiac development, we screened patients with congenital heart disease (CHDs) for genetic variation at the ALDH1A2 locus.\ud \ud \ud \ud Methods\ud \ud One-hundred and thirty-three CHD patients were screened for genetic variation at the ALDH1A2 locus through bi-directional sequencing. In addition, six SNPs (rs2704188, rs1441815, rs3784259, rs1530293, rs1899430) at the same locus were studied using a TDT-based association approach in 101 CHD trios. Observed mutations were modeled through molecular mechanics (MM) simulations using the AMBER 9 package, Sander and Pmemd programs. Sequence conservation of observed mutations was evaluated through phylogenetic tree construction from ungapped alignments containing ALDH8 s, ALDH1Ls, ALDH1 s and ALDH2 s. Trees were generated by the Neighbor Joining method. Variations potentially affecting splicing mechanisms were cloned and functional assays were designed to test splicing alterations using the pSPL3 splicing assay.\ud \ud \ud \ud Results\ud \ud We describe in Tetralogy of Fallot (TOF) the mutations Ala151Ser and Ile157Thr that change non-polar to polar residues at exon 4. Exon 4 encodes part of the highly-conserved tetramerization domain, a structural motif required for ALDH oligomerization. Molecular mechanics simulation studies of the two mutations indicate that they hinder tetramerization. We determined that the SNP rs16939660, previously associated with spina bifida and observed in patients with TOF, does not affect splicing. Moreover, association studies performed with classical models and with the transmission disequilibrium test (TDT) design using single marker genotype, or haplotype information do not show differences between cases and controls.\ud \ud \ud \ud Conclusion\ud \ud In summary, our screen indicates that ALDH1A2 genetic variation is present in TOF patients, suggesting a possible causal role for this gene in rare cases of human CHD, but does not support the hypothesis that variation at the ALDH1A2 locus is a significant modifier of the risk for CHD in humans.Work supported by grants from Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) 01/000090; 00/030722; 01/142381; 02/113402; 03/099982; 04/116068; 04/157044 and Conselho Nacional de Desenvolvimento Científico e Tecnológico 481872/20078. We would like to thank the careful work and thoughtful suggestions of the two reviewers responsible for the reviewing editorial process.Work supported by grants from Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) 01/00009-0; 00/03072-2; 01/14238-1; 02/11340-2; 03/09998-2; 04/11606-8; 04/15704-4 and Conselho Nacional de Desenvolvimento Científico e Tecnológico 481872/2007-8. We would like to thank the careful work and thoughtful suggestions of the two reviewers responsible for the reviewing editorial process

Fibulin-5, an integrin-binding matricellular protein: its function in development and disease

Interactions between the extracellular matrix (ECM) and cells are critical in embryonic development, tissue homeostasis, physiological remodeling, and tumorigenesis. Matricellular proteins, a group of ECM components, mediate cell-ECM interactions. One such molecule, Fibulin-5 is a 66-kDa glycoprotein secreted by various cell types, including vascular smooth muscle cells (SMCs), fibroblasts, and endothelial cells. Fibulin-5 contributes to the formation of elastic fibers by binding to structural components including tropoelastin and fibrillin-1, and to cross-linking enzymes, aiding elastic fiber assembly. Mice deficient in the fibulin-5 gene (Fbln5) exhibit systemic elastic fiber defects with manifestations of loose skin, tortuous aorta, emphysematous lung and genital prolapse. Although Fbln5 expression is down-regulated after birth, following the completion of elastic fiber formation, expression is reactivated upon tissue injury, affecting diverse cellular functions independent of its elastogenic function. Fibulin-5 contains an evolutionally conserved arginine-glycine-aspartic acid (RGD) motif in the N-terminal region, which mediates binding to a subset of integrins, including α5β1, αvβ3, and αvβ5. Fibulin-5 enhances substrate attachment of endothelial cells, while inhibiting migration and proliferation in a cell type- and context-dependent manner. The antagonistic function of fibulin-5 in angiogenesis has been demonstrated in vitro and in vivo; fibulin-5 may block angiogenesis by inducing the anti-angiogenic molecule thrompospondin-1, by antagonizing VEGF165-mediated signaling, and/or by antagonizing fibronectin-mediated signaling through directly binding and blocking the α5β1 fibronectin receptor. The overall effect of fibulin-5 on tumor growth depends on the balance between the inhibitory property of fibulin-5 on angiogenesis and the direct effect of fibulin-5 on proliferation and migration of tumor cells. However, the effect of tumor-derived versus host microenvironment-derived fibulin-5 remains to be evaluated

Investigation of Association between PFO Complicated by Cryptogenic Stroke and a Common Variant of the Cardiac Transcription Factor GATA4

Patent foramen ovale (PFO) is associated with clinical conditions including cryptogenic stroke, migraine and varicose veins. Data from studies in humans and mouse suggest that PFO and the secundum form of atrial septal defect (ASDII) exist in an anatomical continuum of septal dysmorphogenesis with a common genetic basis. Mutations in multiple members of the evolutionarily conserved cardiac transcription factor network, including GATA4, cause or predispose to ASDII and PFO. Here, we assessed whether the most prevalent variant of the GATA4 gene, S377G, was significantly associated with PFO or ASD. Our analysis of world indigenous populations showed that GATA4 S377G was largely Caucasian-specific, and so subjects were restricted to those of Caucasian descent. To select for patients with larger PFO, we limited our analysis to those with cryptogenic stroke in which PFO was a subsequent finding. In an initial study of Australian subjects, we observed a weak association between GATA4 S377G and PFO/Stroke relative to Caucasian controls in whom ASD and PFO had been excluded (OR = 2.16; p = 0.02). However, in a follow up study of German Caucasians no association was found with either PFO or ASD. Analysis of combined Australian and German data confirmed the lack of a significant association. Thus, the common GATA4 variant S377G is likely to be relatively benign in terms of its participation in CHD and PFO/Stroke

The Social Ecology of Parenting: Systematically Modeling The Antecedents of Supportive and Intrusive Parenting

One of the significant contributions of this study is its inclusion of the role of social contextual factors in determining parenting. I built on the ecological model proposed by Belsky (1984). As such, the parenting model tested in this dissertation included individual level determinants of parenting: 1) parent characteristics (e.g., developmental history), and 2) child characteristics (e.g., behavior problems). Yet, rather than include a social context domain as described by Belsky, I distinguished between within family context (e.g., interparental hostility) and external to family context (e.g., work-family conflict, neighborhood disorganization) as social contextual sources of stress and support to the parent-child relationship. A second significant contribution of this study is attention to parent gender. I included assessments of both mother and father parenting and specifically test for hypothesized differences in how the predictive model might operate differently depending on the parent’s gender. It is important to note further that the accomplishment of this examination of parent gender involved the use of a methodology that is itself an important contribution to the existing work. Specifically, my methodology involves simultaneous testing of mother and father data, something that has not typically been done in past studies. Critically, this methodology controls for any overlap or similarity between mother and father parenting and thereby allows for a better test of the uniqueness of mother and father parenting and of patterns of predicting mother and father parenting. This study employed parent reported data from the NIMH-funded Ogden Youth and Family Project, a longitudinal, sequential-cohort study of families with adolescent children (N = 933). Using structural equation modeling, we found that the model adequately fit the data while direct and indirect effects on parenting were found. The individual level parenting determinants of child behavior problems and parental depression were significantly directly associated with parenting, particularly for fathers. The within family contextual variable of covert marital conflict was directly associated with father parenting, and directly and indirectly associated with mother intrusive parenting through maternal depression. As risk factors external to the family, workfamily conflict was not significantly related to parenting, and neighborhood disorganization was indirectly related to intrusive mothering (but not her supportive parenting or to father’s parenting), through elevated levels of marital conflict and depression