Regulation of sulfate uptake and assimilation in barley (<i>Hordeum vulgare</i>) as affected by rhizospheric and atmospheric sulfur nutrition

To study the regulation of sulfate metabolism in barley (Hordeum vulgare), seedlings were exposed to atmospheric hydrogen sulfide (H2S) in the presence and absence of a sulfate supply. Sulfate deprivation reduced shoot and root biomass production by 60% and 70%, respectively, and it affected the plant’s mineral nutrient composition. It resulted in a 5.7- and 2.9-fold increased shoot and root molybdenum content, respectively, and a decreased content of several other mineral nutrients. Particularly, it decreased shoot and root total sulfur contents by 60% and 70%, respectively. These decreases could be ascribed to decreased sulfate contents. Sulfate deficiency was additionally characterized by significantly lowered cysteine, glutathione and soluble protein levels, enhanced dry matter, nitrate and free amino acid contents, an increased APS reductase (APR) activity and an increased expression and activity of the root sulfate uptake transporters. When sulfate-deprived barley was exposed to 0.6 µl l−1 atmospheric H2S, the decrease in biomass production and the development of other sulfur deficiency symptoms were alleviated. Clearly, barley could use H2S, absorbed by the foliage, as a sulfur source for growth. H2S fumigation of both sulfate-deprived and sulfate-sufficient plants downregulated APR activity as well as the expression and activity of the sulfate uptake transporters. Evidently, barley switched from rhizospheric sulfate to atmospheric H2S as sulfur source. Though this indicates that sulfate utilization in barley is controlled by signals originating in the shoot, the signal transduction pathway involved in the shoot-to-root regulation must be further elucidated

Floral displays suffer from sulphur deprivation

Nutrient deficiency is known to constrain plant growth in numerous ways, but how it impacts floral displays and pollination success remains unclear. Here we investigate how insufficient availability of sulphur – a vital plant nutrient that is a limiting factor in natural and agricultural regions throughout the world – influences the production of floral displays in Brassica rapa, Physalis philadelphica and three Petunia species with differently coloured flowers. Sulphur deficiency led to a drastic reduction in the number of open flowers, an aberrant flower morphology and smaller pollen with an altered mineral nutrient content. Intriguingly, sulphur deprivation also led to a clear reduction in pigmentation of yellow flowers, but not in flowers with white, purple and red colours. The pale yellow flower colour was due to decreased amounts of violaxanthin, lutein and other carotenoids, suggesting that the carotenoid synthesis pathway is particularly susceptible to sulphur deficiency. Additional experiments with nitrogen and phosphorus depletion confirmed that observed colour and morphological changes were not a general nutrient limitation response, but could be ascribed to sulphur depletion specifically. Taken together, our results showed that (mild) sulphur deficiency deteriorates a suite of floral traits, and that the effects may cascade to pollinators and so have the potential to undermine (agro-)ecosystem functioning.<br/

Molybdate toxicity in Chinese cabbage is not the direct consequence of changes in sulphur metabolism

In polluted areas, plants may be exposed to supra-optimal levels of the micronutrient molybdenum. The physiological basis of molybdenum phytotoxicity is poorly understood. Plants take up molybdenum as molybdate, which is a structural analogue of sulphate. Therefore, it is presumed that elevated molybdate concentrations may hamper the uptake and subsequent metabolism of sulphate, which may induce sulphur deficiency. In the current research, Chinese cabbage (Brassica pekinensis) seedlings were exposed to 50, 100, 150 and 200 lM Na2MoO4 for 9 days. Leaf chlorosis and a decreased plant growth occurred at concentrations ≥100 lM. Root growth was more affected than shoot growth. At ≥100 lM Na2MoO4, the sulphate uptake rate and capacity were increased, although only when expressed on a root fresh weight basis. When expressed on a whole plant fresh weight basis, which corrects for the impact of molybdate on the shoot-to-root ratio, the sulphate uptake rate and capacity remained unaffected. Molybdate concentrations ≥100 lM altered the mineral nutrient composition of plant tissues, although the levels of sulphur metabolites (sulphate, water-soluble non-protein thiols and total sulphur) were not altered. Moreover, the levels of nitrogen metabolites (nitrate, amino acids, proteins and total nitrogen), which are generally strongly affected by sulphate deprivation, were not affected. The root water-soluble non-protein thiol content was increased, and the tissue nitrate levels decreased, only at 200 lM Na2MoO4. Evidently, molybdenum toxicity in Chinese cabbage was not due to the direct interference of molybdate with the uptake and subsequent metabolism of sulphate

Effect of the Implantable Atrial Defibrillator on the Natural History of Atrial Fibrillation

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/75480/1/j.1540-8167.1999.tb00296.x.pd

Twenty-five years in the making: flecainide is safe and effective for the management of atrial fibrillation

Atrial fibrillation (AF) is the most common arrhythmia in clinical practise and its prevalence is increasing. Over the last 25 years, flecainide has been used extensively worldwide, and its capacity to reduce AF symptoms and provide long-term restoration of sinus rhythm (SR) has been well documented. The increased mortality seen in patients treated with flecainide in the Cardiac Arrhythmia Suppression Trial (CAST) study, published in 1991, still deters many clinicians from using flecainide, denying many new AF patients a valuable treatment option. There is now a body of evidence that clearly demonstrates that flecainide has a favourable safety profile in AF patients without significant left ventricular disease or coronary heart disease. As a result of this evidence, flecainide is now recommended as one of the first-line treatment options for restoring and maintaining SR in patients with AF under current treatment guidelines. The objective of this article is to review the literature pertaining to the pharmacological characteristics, safety and efficacy of flecainide, and to place this drug in the context of current therapeutic management strategies for AF

Rationale and current perspective for early rhythm control therapy in atrial fibrillation

Atrial fibrillation (AF) is the most common sustained arrhythmia and an important source for mortality and morbidity on a population level. Despite the clear association between AF and death, stroke, and other cardiovascular events, there is no evidence that rhythm control treatment improves outcome in AF patients. The poor outcome of rhythm control relates to the severity of the atrial substrate for AF not only due to the underlying atrial remodelling process but also due to the poor efficacy and adverse events of the currently available ion-channel antiarrhythmic drugs and ablation techniques. Data suggest, however, an association between sinus rhythm maintenance and improved survival. Hypothetically, sinus rhythm may also lead to a lower risk of stroke and heart failure. The presence of AF, thus, seems one of the modifiable factors associated with death and cardiovascular morbidity in AF patients. Patients with a short history of AF and the underlying heart disease have not been studied before. It is fair to assume that abolishment of AF in these patients is more successful and possibly also safer, which could translate into a prognostic benefit of early rhythm control therapy. Several trials are now investigating whether aggressive early rhythm control therapy can reduce cardiovascular morbidity and mortality and increase maintenance of sinus rhythm. In the present paper we describe the background of these studies and provide some information on their design

Applying Harmonic Optical Microscopy for Spatial Alignment of Atrial Collagen Fibers

BACKGROUND: Atrial fibrosis creates a vulnerable tissue for atrial fibrillation (AF), but the spatial disarray of collagen fibers underlying atrial fibrosis is not fully elucidated. OBJECTIVE: This study hypothesizes that harmonics optical microscopy can illuminate the spatial mal-alignment of collagen fibers in AF via a layer-by-layer approach. PATIENTS AND METHODS: Atrial tissues taken from patients who underwent open-heart surgery were examined by harmonics optical microscopy. Using the two-dimensional Fourier transformation method, a spectral-energy description of image texture was constituted and its entropy was used to quantify the mal-alignment of collagen fibers. The amount of collagen fiber was derived from its area ratio to total atrial tissue in each image. Serum C-terminal pro-collagen pro-peptide (CICP), pro-matrix metalloproteinase-1 (pro-MMP-1), and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) were also evaluated. RESULTS: 46 patients were evaluated, including 20 with normal sinus rhythm and 26 with AF. The entropy of spectral-energy distribution of collagen alignment was significantly higher in AF than that in sinus rhythm (3.97 ± 0.33 vs. 2.80 ± 0.18, p<0.005). This difference was more significant in the permanent AF group. The amount of collagen was also significantly higher in AF patients (0.39 ± 0.13 vs. 0.18 ± 0.06, p<0.005) but serum markers of cardiac fibrosis were not significantly different between the two groups. CONCLUSIONS: Harmonics optical microscopy can quantify the spatial mal-alignment of collagen fibers in AF. The entropy of spectral-energy distribution of collagen alignment is a potential tool for research in atrial remodeling

Dedifferentiation and Proliferation of Mammalian Cardiomyocytes

It has long been thought that mammalian cardiomyocytes are terminally-differentiated and unable to proliferate. However, myocytes in more primitive animals such as zebrafish are able to dedifferentiate and proliferate to regenerate amputated cardiac muscle.Here we test the hypothesis that mature mammalian cardiomyocytes retain substantial cellular plasticity, including the ability to dedifferentiate, proliferate, and acquire progenitor cell phenotypes. Two complementary methods were used: 1) cardiomyocyte purification from rat hearts, and 2) genetic fate mapping in cardiac explants from bi-transgenic mice. Cardiomyocytes isolated from rodent hearts were purified by multiple centrifugation and Percoll gradient separation steps, and the purity verified by immunostaining and RT-PCR. Within days in culture, purified cardiomyocytes lost their characteristic electrophysiological properties and striations, flattened and began to divide, as confirmed by proliferation markers and BrdU incorporation. Many dedifferentiated cardiomyocytes went on to express the stem cell antigen c-kit, and the early cardiac transcription factors GATA4 and Nkx2.5. Underlying these changes, inhibitory cell cycle molecules were suppressed in myocyte-derived cells (MDCs), while microRNAs known to orchestrate proliferation and pluripotency increased dramatically. Some, but not all, MDCs self-organized into spheres and re-differentiated into myocytes and endothelial cells in vitro. Cell fate tracking of cardiomyocytes from 4-OH-Tamoxifen-treated double-transgenic MerCreMer/ZEG mouse hearts revealed that green fluorescent protein (GFP) continues to be expressed in dedifferentiated cardiomyocytes, two-thirds of which were also c-kit(+).Contradicting the prevailing view that they are terminally-differentiated, postnatal mammalian cardiomyocytes are instead capable of substantial plasticity. Dedifferentiation of myocytes facilitates proliferation and confers a degree of stemness, including the expression of c-kit and the capacity for multipotency