Physiological and anatomical studies in seed coat regulation of water uptake in soybeans (Glycine max L. Merril)

This study examined i) the imbibition behaviour of a wide range of genotypes with different seed coat characteristics; ii) the use of a polymer to regulate the rate of water uptake and iii) the mechanism of regulation of water uptake by the seed coat in soybeans (Glycine max L. Merril.). Seed coat structure was studied by using light, fluorescence and scanning electron microscopy. The effects of different methanol and chloroform pre-treatments on seed coat permeability to water were also assessed. In this study, imbibition damage due to rapid water uptake was well documented in a wide range of soybean genotypes. In addition a line (VLS-1) was identified that possessed a delayed-permeability seed coat characteristic that offered protection against imbibition damage. This characteristic was likely to be due to a lack of pits in the abaxial region of the seed. In contrast, genotypes with a high proportion of deep and wide open pits in the abaxial region of the seed offered minimal protection against imbibition damage.Coating seeds (24 mg per seed) with a polymer containing vinyl acetate, vinyl chloride, ethylene and acrylate regulated the rate of water uptake, and offered protection against imbibition damage. Seedling emergence from polymer coated seeds was also improved.Deposits and pits occurred in the surface of the seed coat in most genotypes. Deposits were shown to be composed of hydrophilic polysaccharide material, since staining with calcofluor was observed. Water permeability mapping indicated that pits were the sites o f the initial water penetration. However, in hard seeds, pits appeared to function in a different way to soft seeds and this is fully discussed within the thesis. Prolonged methanol pre-treatments were highly effective in increasing the water uptake when seeds were imbibed immediately after the pre-treatments. However, drying of seeds after the organic solvent pre-treatments restored permeability to water to untreated control levels. Results from the absorption spectrum of the methanol and chloroform supernatants, indicated that the effect of the pre-treatments were not due to the extraction of UV-absorbed material from the seed coat. In hard seeds, the location of the water impermeability barrier was near the outermost part of the palisade cell layer. The nature of the barrier was not identified by comparative anatomical and histochemical studies between hard and soft seeds. A mechanism for the water uptake regulation by the soybean seed coat was proposed. The proposed mechanism involved: i) a diminished role of the cuticle and its components (epicuticular and intracuticular waxes), ii) a key role for pits as initial sites of water penetration, and iii) swelling or collapse of the cellulosic and/or pectic material in the subcuticular and palisade cell layer that could regulate water penetration through the seed coat. The common behaviour of a wide range of genotypes tested indicated that the above mechanism of regulation of water uptake by the seed coat is likely to be universal in soybeans

Severe transplantâ associated thrombotic microangiopathy in patients with hemoglobinopathies

Incidence and severity of transplantâ associated thrombotic microangiopathy (TAâ TMA) in patients with hemoglobinopathies receiving hematopoietic cell transplant is unknown. We report the outcomes for two patients with TAâ TMA who received eculizumab. A 2.5â yearâ old male with sickle cell disease developed TAâ TMAâ associated pericardial tamponade, severe hypertension, and acute kidney injury 2 months after transplant. A 7â yearâ old female with βâ thalassemia major developed TAâ TMAâ related acute kidney injury, severe hypertension, and seizures at 6 months after transplant. Both patients progressed to chronic kidney disease (CKD). In patients with hemoglobinopathies, preexisting endothelial dysfunction may place them at a greater risk for TAâ TMA and subsequent CKD.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/137747/1/pbc26503.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/137747/2/pbc26503_am.pd

Vascular Endothelial Dysfunction in β-Thalassemia Occurs Despite Increased eNOS Expression and Preserved Vascular Smooth Muscle Cell Reactivity to NO

The hereditary β-thalassemia major condition requires regular lifelong blood transfusions. Transfusion-related iron overloading has been associated with the onset of cardiovascular complications, including cardiac dysfunction and vascular anomalies. By using an untransfused murine model of β-thalassemia major, we tested the hypothesis that vascular endothelial dysfunction, alterations of arterial structure and of its mechanical properties would occur despite the absence of treatments.Vascular function and structure were evaluated ex vivo. Compared to the controls, endothelium-dependent vasodilation with acetylcholine was blunted in mesenteric resistance arteries of β-thalassemic mice while the endothelium-independent vasodilator (sodium nitroprusside) produced comparable vessel dilation, indicating endothelial cell impairment with preserved smooth muscle cell reactivity to nitric oxide (NO). While these findings suggest a decrease in NO bioavailability, Western blotting showed heightened expression of aortic endothelial NO synthase (eNOS) in β-thalassemia. Vascular remodeling of the common carotid arteries revealed increased medial elastin content. Under isobaric conditions, the carotid arteries of β-thalassemic mice exhibited decreased wall stress and softening due to structural changes of the vessel wall.A complex vasculopathy was identified in untransfused β-thalassemic mice characterized by altered carotid artery structure and endothelial dysfunction of resistance arterioles, likely attributable to reduced NO bioavailability despite enhanced vascular eNOS expression

The heart in transfusion dependent homozygous thalassaemia today – prediction, prevention and management

Cardiac disease remains the major cause of death in thalassaemia major. This review deals with the mechanisms involved in heart failure development, the peculiar clinical presentation of congestive heart failure and provides guidelines for diagnosis and management of the acute phase of cardiac failure. It emphasizes the need for intensive medical – cardiac care and aggressive iron chelating management as, with such approaches, today, the patients outcomes can be favourable in the long term. It covers advances in the assessment of cardiac iron overload with the use of magnetic resonance imaging and makes recommendations for preventing the onset of cardiac problems by tailoring iron chelation therapy appropriate to the degree of cardiac iron loading found

Quantitative analysis of left atrial function in asymptomatic patients with b-thalassemia major using real-time three-dimensional echocardiography

<p>Abstract</p> <p>Background</p> <p>There is strong evidence that left atrial (LA) size is a prognostic marker in a variety of heart diseases. Recently, real-time three-dimensional echocardiography (RT3DE) has been reported as a useful tool for studying the phasic changes of the left atrial volumes. The aim of this study was to investigate the performance of the left atrium in beta-thalassemic patients with preserved left ventricular ejection fraction (EF) and no iron overload, using RT3DE.</p> <p>Methods</p> <p>Twenty-eight asymptomatic b-thalassemic patients (32.2 ± 4.3 years old, 17 men) who were on iron chelating therapy, as well as 20 age- and sex-matched healthy controls underwent transthoracic RT3DE. The patient group had normal echocardiographic systolic and diastolic indices, while there was no myocardial iron disposition according to MRI. Apical full volume data sets were obtained and LA volumes were measured at 3 time points of the cardiac cycle: (1) maximum volume (LAmax) at end-systole, just before mitral valve opening; (2) minimum volume (LAmin) at end-diastole, just before mitral valve closure; and (3) volume before atrial active contraction (LApreA) obtained from the last frame before mitral valve reopening or at time of the P wave on the surface electrocardiogram. From the derived values, left atrial active and passive emptying volumes, as well as the respective emptying fractions were calculated.</p> <p>Results</p> <p>Left ventricular EF (59.2 ± 2.5% patients vs. 60.1 ± 2.1% controls), E/A, E/E' were similar between the two groups. Differences in the LAmax, LAmin and LApreA between b-thalassemic patients and controls were non-significant, LAmax:(35.5 ± 13.4 vs 31.8 ± 9.8)cm³, LAmin:(16.0 ± 6.0 vs. 13.5 ±4.2)cm³, and LApreA:(25.4 ± 9.8 vs. 24.3 ± 7.2)cm³. However, left atrial active emptying fraction was reduced in the patient group as compared to the healthy population (34.3 ± 16.4% vs. 43.2 ± 11.4%, p < 0.05).</p> <p>Conclusion</p> <p>RT3DE may be a novel technique for the evaluation of LA function in asymptomatic patients with b-Thalassemia Major. Among three-dimensional volumes and indices, left atrial active emptying fraction may be an early index of LA dysfunction in the specific patient population.</p

Circulating CD133+VEGFR2+ and CD34+VEGFR2+ cells and arterial function in patients with beta-thalassaemia major

Arterial dysfunction has been documented in patients with beta-thalassaemia major. This study aimed to determine the quantity and proliferative capacity of circulating CD133+VEGFR2+ and CD34+VEGFR2+ cells in patients with beta-thalassaemia major and those after haematopoietic stem cell transplantation (HSCT), and their relationships with arterial function. Brachial arterial flow-mediated dilation (FMD), carotid arterial stiffness, the quantity of these circulating cells and their number of colony-forming units (CFUs) were determined in 17 transfusion-dependent thalassaemia patients, 14 patients after HSCT and 11 controls. Compared with controls, both patient groups had significantly lower FMD and greater arterial stiffness. Despite having increased CD133+VEGFR2+ and CD34+VEGFR2+ cells, transfusion-dependent patients had significantly reduced CFUs compared with controls (p = 0.002). There was a trend of increasing CFUs across the three groups with decreasing iron load (p = 0.011). The CFUs correlated with brachial FMD (p = 0.029) and arterial stiffness (p = 0.02), but not with serum ferritin level. Multiple linear regression showed that CFU was a significant determinant of FMD (p = 0.043) and arterial stiffness (p = 0.02) after adjustment of age, sex, body mass index, blood pressure and serum ferritin level. In conclusion, arterial dysfunction found in patients with beta-thalassaemia major before and after HSCT may be related to impaired proliferation of CD133+VEGFR2+ and CD34+VEGFR2+ cells

Comparative effectiveness and safety of non-vitamin K antagonists for atrial fibrillation in clinical practice: GLORIA-AF Registry

Background and purpose: Prospectively collected data comparing the safety and effectiveness of individual non-vitamin K antagonists (NOACs) are lacking. Our objective was to directly compare the effectiveness and safety of NOACs in patients with newly diagnosed atrial fibrillation (AF). Methods: In GLORIA-AF, a large, prospective, global registry program, consecutive patients with newly diagnosed AF were followed for 3&nbsp;years. The comparative analyses for (1) dabigatran vs rivaroxaban or apixaban and (2) rivaroxaban vs apixaban were performed on propensity score (PS)-matched patient sets. Proportional hazards regression was used to estimate hazard ratios (HRs) for outcomes of interest. Results: The GLORIA-AF Phase III registry enrolled 21,300 patients between January 2014 and December 2016. Of these, 3839 were prescribed dabigatran, 4015 rivaroxaban and 4505 apixaban, with median ages of 71.0, 71.0, and 73.0&nbsp;years, respectively. In the PS-matched set, the adjusted HRs and 95% confidence intervals (CIs) for dabigatran vs rivaroxaban were, for stroke: 1.27 (0.79–2.03), major bleeding 0.59 (0.40–0.88), myocardial infarction 0.68 (0.40–1.16), and all-cause death 0.86 (0.67–1.10). For the comparison of dabigatran vs apixaban, in the PS-matched set, the adjusted HRs were, for stroke 1.16 (0.76–1.78), myocardial infarction 0.84 (0.48–1.46), major bleeding 0.98 (0.63–1.52) and all-cause death 1.01 (0.79–1.29). For the comparison of rivaroxaban vs apixaban, in the PS-matched set, the adjusted HRs were, for stroke 0.78 (0.52–1.19), myocardial infarction 0.96 (0.63–1.45), major bleeding 1.54 (1.14–2.08), and all-cause death 0.97 (0.80–1.19). Conclusions: Patients treated with dabigatran had a 41% lower risk of major bleeding compared with rivaroxaban, but similar risks of stroke, MI, and death. Relative to apixaban, patients treated with dabigatran had similar risks of stroke, major bleeding, MI, and death. Rivaroxaban relative to apixaban had increased risk for major bleeding, but similar risks for stroke, MI, and death. Registration: URL: https://www.clinicaltrials.gov. Unique identifiers: NCT01468701, NCT01671007. Date of registration: September 2013