Oleg, the Sorcerer, and the Two Alexanders (The Political Subtext of Pushkin’s Ballad “The Song of the Wise Oleg”)

Alexander Pushkin wrote his ballad “The Song of the Wise Oleg” (1822) in Kishinev during his forced administrative presence in the South (1820–1824). The poem retells, with meaningful differences, a legend in Nikolay Karamzin’s History of the Russian State that describes the miraculous death of the Kievan Prince Oleg, who is bitten by a snake hiding in the skull of the hero’s dead horse. The poem was inspired by Pushkin’s visit to Kamenka and Kiev in 1821 and his acquaintance there with the assembled members of the future Decembrist uprising, as well as his visit to the supposed site of Oleg’s grave. An examination of the work in the context of Pushkin’s Southern Text reveals that the poem is an allegory of the poet’s relationship with Alexander I and reflects his fears about the coming political upheaval in Russia and the potential death of the Tsar. The ballad contains the first instance of a motif that becomes familiar in his subsequent work, namely the miracle (chudo) as a sudden, unexpected, and life-changing event. The poetics of the poem represents an important step towards Pushkin’s masterpiece The Comedy of Tsar Boris and Grishka Otrepyev (1825; published in 1831 with the title Boris Godunov).Баллада Александра Пушкина Песнь о вещем Олеге (1822) была написана в Кишиневе во время ссылки поэта под видом служебной поездки на юг России (1820–1824). Баллада пересказывает, но со значительными изменениями, легенду из Истории государства Российского Николая Карамзина о смерти киевского князя Олега от укуса змеи, которая выползла из черепа его любимого коня. На создание стихотворения поэта вдохновило посещение Каменки и Киева в 1821 г. Здесь он познакомился с будущими декабристами, членами так называемого «Союза благоденствия», и увидел предполагаемое место могилы Олега. Анализ баллады как части Южного текста показывает, что произведение является аллегорией, в которой поэт выражает свои опасения по поводу возможности политического переворота в России и скорого ухода из жизни Александра I. В Песни… встречается мотив (прием), ставший важным элементом в последующих произведениях поэта, а именно чудо как внезапное, неожиданное событие, меняющее ход жизни. В целом Песнь… – важный шаг в развитии творчества поэта, который привел его к созданию Комедии о царе Борисе и Гришке Отрепьеве (1825), опубликованной в 1831 г. под заглавием Борис Годунов

Summary of CPWF research in the Nile river basin

Three major river basins flow out of Ethiopia into Sudan, constituting the Eastern Nile basin (the White Nile flows from the south). These are the Tekeze-Atbara flowing out of northern Ethiopia, the Baro-Akoba- Sobat flowing from southern Ethiopia, and the Blue Nile (Abay) sandwiched between the other two. The Blue Nile Basin, called the Abay in Ethiopia, is the largest branch of the Nile draining the Ethiopian highlands. It covers an estimated area of 311,437 square kilometers and is shared by Ethiopia and Sudan. It joins the White Nile in Khartoum, Sudan. The Ethiopian highlands portion of the Blue Nile river basin was the focus of the Nile Basin Development Challenge under the Challenge Program on Water and Food

Targeting mitochondrial fitness as a strategy for healthy vascular aging.

Cardiovascular diseases (CVD) are the leading cause of death worldwide and aging is the primary risk factor for CVD. The development of vascular dysfunction, including endothelial dysfunction and stiffening of the large elastic arteries (i.e., the aorta and carotid arteries), contribute importantly to the age-related increase in CVD risk. Vascular aging is driven in large part by oxidative stress, which reduces bioavailability of nitric oxide and promotes alterations in the extracellular matrix. A key upstream driver of vascular oxidative stress is age-associated mitochondrial dysfunction. This review will focus on vascular mitochondria, mitochondrial dysregulation and mitochondrial reactive oxygen species (ROS) production and discuss current evidence for prevention and treatment of vascular aging via lifestyle and pharmacological strategies that improve mitochondrial health. We will also identify promising areas and important considerations ('research gaps') for future investigation.REVIEW ARTICLE| JUNE 25 2020 Targeting mitochondrial fitness as a strategy for healthy vascular aging Matthew J. Rossman ; Rachel A. Gioscia-Ryan ; Zachary S. Clayton ; Michael P. Murphy ; Douglas R. Seals Crossmark: Check for Updates Clin Sci (Lond) (2020) 134 (12): 1491–1519. https://doi.org/10.1042/CS20190559 Article history Split-Screen Views Icon Views PDF Link PDF Share Icon Share Cite Icon Cite Get Permissions Abstract Cardiovascular diseases (CVD) are the leading cause of death worldwide and aging is the primary risk factor for CVD. The development of vascular dysfunction, including endothelial dysfunction and stiffening of the large elastic arteries (i.e., the aorta and carotid arteries), contribute importantly to the age-related increase in CVD risk. Vascular aging is driven in large part by oxidative stress, which reduces bioavailability of nitric oxide and promotes alterations in the extracellular matrix. A key upstream driver of vascular oxidative stress is age-associated mitochondrial dysfunction. This review will focus on vascular mitochondria, mitochondrial dysregulation and mitochondrial reactive oxygen species (ROS) production and discuss current evidence for prevention and treatment of vascular aging via lifestyle and pharmacological strategies that improve mitochondrial health. We will also identify promising areas and important considerations (‘research gaps’) for future investigation. Keywords:arterial stiffness, endothelial function, mitophagy, oxidative stress, reactive oxygen species Subjects:Aging, Cardiovascular System & Vascular Biology, Translational Science Cardiovascular diseases (CVD) remain the largest contributor to morbidity and mortality in both developed and many developing nations [1,2]. Aging is by far the strongest risk factor for CVD, with >90% of all deaths occurring in adults 50 years of age and older [1,2]. Importantly, the changing demographics of aging characterized by a shift toward older populations [3] predicts a progressive, marked increase in prevalence of CVD in the absence of effective intervention [4]. A key mechanism by which aging increases CVD risk is the development of vascular dysfunction [5,6]. A number of adverse changes to the vasculature occur with aging, but two major clinically relevant expressions are endothelial dysfunction, as assessed by reduced arterial dilation in response to endothelium-derived nitric oxide (NO), and stiffening of the large elastic arteries (i.e., the aorta and carotid arteries) [5,6]. In combination, endothelial dysfunction and arterial stiffening contribute to a ‘vascular aging’ phenotype that drives much of the adverse effects of age on CVD. Vascular endothelial dysfunction The vascular endothelium is a single-cell layer lining the lumen of blood vessels. Endothelial cells play a critical role regulating vasomotor tone, metabolism, immune function, thrombosis and many other processes via synthesis and release of a variety of vasoactive molecules [7]. A major vasodilatory and largely vasoprotective molecule released by endothelial cells is NO, which is produced in response to mechanical (i.e., blood flow) and chemical (e.g., acetylcholine [ACh]) stimuli by the enzyme nitric oxide synthase (eNOS); eNOS catalyzes the generation of NO from L-arginine and oxygen, with NO subsequently diffusing to vascular smooth muscle cells where it induces vascular smooth muscle relaxation and vasodilation [7]. Endothelial dysfunction occurs with aging and is characterized by a decline in endothelium-dependent dilation (EDD), largely as a consequence of reductions in NO, although changes in concentrations of vasoactive factors such as prostaglandins, endothelin-1, norepinephrine and angiotensin II also contribute [7]. NO-mediated EDD can be determined in pre-clinical models by assessing changes in artery diameter in response to flow in vivo [8,9] or changes in diameter of isolated artery segments ex vivo in response to mechanical or pharmacological stimuli, such as ACh [10]. In humans, the gold-standard non-invasive assessment of NO-mediated EDD is brachial artery flow-mediated dilation (FMD), in which the change in brachial artery diameter in response to increases in blood flow is determined [10,11]. Brachial artery FMD primarily assesses macrovascular (conduit artery) function. Microvascular (resistance vessel) function can be determined by measuring changes in blood flow in response to intra-arterial infusions of ACh and is primarily assessed in the forearm [10,11]. These experimental approaches all demonstrate reduced endothelial function with aging in pre-clinical models and humans [12–17]. Endothelial dysfunction is the major antecedent of atherosclerosis [5,18] and both reduced brachial artery FMD and lower forearm blood flow responses to ACh are independent predictors of CV events and CVD in middle-aged and older adults free from clinical disease in large, community-based cohort studies [19–21]. Large elastic artery stiffening The aorta and carotid arteries expand and recoil as blood is ejected into the arterial system by the left ventricle during systole [22]. This action limits arterial pulsatile pressures by providing a dampening function and protects the downstream microvasculature from potentially damaging fluctuations in blood pressure and flow [23]. Moreover, the elastic recoil of the aorta aids in the propulsion of blood to the periphery and maintains perfusion of the heart during diastole [22]. With aging, aortic stiffening results in blood being ejected into a stiffer aorta, which augments central systolic blood pressure because the ejected pressure wave travels at a higher velocity in stiffer arteries and is reflected by points of impedance such that the returning pressure wave reaches the heart at mid-to-late systole [22,24]. In addition, the greater forward moving pressure wave amplitude (from systolic ejection, prior to the return of wave reflections) is a major contributor to the age-related increase in central systolic blood pressure after age 60, particularly in women, as a consequence of a plateau or decrease in reflected wave amplitude [25,26]. The augmented systolic blood pressure, in turn, contributes to isolated systolic hypertension and results in a loss of diastolic pressure augmentation, such that aortic pulse pressure is widened [22,24]. Aortic stiffening therefore increases left ventricular afterload during systole, promoting left ventricular hypertrophy and dysfunction, and compromises coronary perfusion during diastole because of the reduced augmentation of diastolic pressure [24,27]. The loss of pulsatility-dampening effects of the aorta and the carotid artery also allows for transmission of high pulsatile pressures to the delicate small vessels in the microcirculation, which is particularly harmful for high-flow, low-resistance organs such as the brain and kidney, and a potential causative factor in target organ damage [23]. Structural changes to arteries, functional influences (i.e., factors influencing vascular smooth muscle tone) and the stiffness of vascular smooth muscle cells contribute to large elastic artery stiffening with aging [28,29]. The primary structural changes mediating arterial stiffening occur in the extracellular matrix and include degradation/fragmentation of elastin (e.g., by matrix metalloproteinases), an increase in the deposition of collagen and formation of advanced glycation end products (AGEs), which cross-link collagen fibers, increasing their stiffness [5,30,31]. Increased vascular smooth muscle tone is a consequence of changes such as reductions in NO and increased sympathetic nervous system, endothelin-1 and renin–angiotensin aldosterone system activity [32–34]. These factors also influence the intrinsic stiffness of the vascular smooth muscle cells, which adds to the stiffness of the arterial wall [29]. The mechanical stiffness of the large elastic arteries can be determined ex vivo in pre-clinical models by directly measuring properties such as compliance by creating stress-strain curves [35,36]. In vivo, arterial stiffness can be assessed in pre-clinical settings and humans with pulse wave velocity (PWV), which is a measure of the (regional) speed of the pulse wave generated by the heart when blood is ejected into the arterial system [22]. Aortic PWV is the predominant measure in rodents and carotid-femoral PWV is the reference standard measure of aortic stiffness in humans [10,22]. Carotid-femoral PWV increases with aging and is a strong, independent predictor of CVD risk in older adults [37,38]. Moreover, consistent with aortic stiffness-associated end organ damage, growing evidence supports an association between elevated carotid-femoral PWV and other age-related clinical disorders such as cognitive decline, dementia, including Alzheimer’s disease, and decreases in renal function/chronic kidney disease [39–43]. The local distensibility of the carotid artery can also be determined in humans by measuring carotid artery compliance (the change in artery diameter for a given change in arterial pressure) and determining the carotid distensibility coefficient (i.e., changes in artery diameter normalized to diastolic lumen diameter) and/or carotid beta-stiffness index, which is largely independent of blood pressure [10,22]. Carotid artery compliance is associated with incident stroke, independent of aortic stiffness [44]. Mechanisms of vascular dysfunction with aging The primary molecular mechanisms of vascular aging are oxidative stress and chronic, low grade inflammation [45,46] (Figure 1). Excessive production of reactive oxygen species (ROS) in combination with unchanged or decreased abundance/activity of antioxidant enzymes (e.g., superoxide dismutase, SOD) results in the development of oxidative stress in arteries with aging [24,45]. Excess superoxide rapidly reacts with NO to form the secondary reactive species peroxynitrite (ONOO−), decreasing the bioavailability of NO [24,45], causing endothelial dysfunction. Peroxynitrite is also the primary molecule that reacts with and oxidizes tetrahydrobiopterin (BH4), an essential co-factor for NO production by eNOS [47]. Loss of BH4 leads to eNOS uncoupling, whereby eNOS produces more superoxide and less NO, exacerbating oxidative stress and decreasing bioavailable NO and endothelial cell function [47]. Excess ROS also can activate pro-inflammatory networks such as those regulated by the transcription factor nuclear factor kappa B (NF-kB), which up-regulates the production of pro-inflammatory cytokines that can impair vascular function and activate other ROS producing systems and enzymes, creating an adverse feed-forward (vicious) cycle of inflammation and oxidative stress [24,45]. Figure 1 Aging is associated with mitochondrial dysfunction-induced increases in reactive oxygen species (ROS) and oxidative stress and increases in pro-inflammatory cytokine signaling and chronic low-grade inflammation. Together, these processes induce vascular dysfunction, featuring: (lower left) large elastic artery stiffening mediated by degradation of elastin fibers (blue), increased deposition of collagen (brown), and greater cross-linking of structural proteins by advanced glycation end-products (dashed connecting lines); and (right) vascular endothelial dysfunction characterized by reduced nitric oxide (NO) bioavailability and endothelium-dependent dilation. These and other changes to arteries, in turn, increase the risk of developing cardiovascular diseases, chronic kidney disease, and Alzheimer’s disease and related dementias. VIEW LARGEDOWNLOAD SLIDE Mechanisms of age-associated vascular dysfunction and related clinical disorders Aging is associated with mitochondrial dysfunction-induced increases in reactive oxygen species (ROS) and oxidative stress and increases in pro-inflammatory cytokine signaling and chronic low-grade inflammation. Together, these processes induce vascular dysfunction, featuring: (lower left) large elastic artery stiffening mediated by degradation of elastin fibers (blue), increased deposition of collagen (brown), and greater cross-linking of structural proteins by advanced glycation end-products (dashed connecting lines); and (right) vascular endothelial dysfunction characterized by reduced nitric oxide (NO) bioavailability and endothelium-dependent dilation. These and other changes to arteries, in turn, increase the risk of developing cardiovascular diseases, chronic kidney disease, and Alzheimer’s disease and related dementias. This overall state of oxidative stress and inflammation also contributes to arterial stiffening with aging by altering the structural properties of the arterial wall. Production of collagen by fibroblasts is stimulated by superoxide-related oxidative stress [30,48,49]. Matrix metalloproteinases are up-regulated and elastin content is lower in aorta of SOD-deficient mice, consistent with the concept that elastin degradation is induced by oxidative stress [50]. Vascular oxidative stress also promotes transforming growth factor β signaling and this, in turn, stimulates inflammation, which further reinforces arterial stiffness via activation of the pro-oxidant enzyme, NADPH oxidase [48]. AGEs interact with the receptor for AGEs to activate NFkB-regulated pro-inflammatory pathways and oxidative stress, which ultimately perpetuates arterial stiffening and further increases production of AGEs [51]. Mitochondrial dysfunction is emerging as a key source of vascular oxidative stress and contributor to age-related vascular dysfunction. The remaining sections of this article will focus on mitochondrial dysfunction as a driver of vascular aging and review current evidence for prevention/treatment of age-associated vascular dysfunction via lifestyle and pharmacological strategies that improve mitochondrial health. We will also discuss current ‘research gaps’ and future directions for the field. Vascular mitochondria, mitochondrial dysregulation and ROS Mitochondria are cytoplasmic organelles that are present in the majority of cell types in the human body, including vascular endothelial and smooth muscle cells. Mitochondria are often referred to as the ‘powerhouse’ of the cell for their role in ATP production by oxidative phosphorylation, which occurs via a series of electron transfers through the respiratory chain in the mitochondrial inner membrane that is coupled to ATP synthesis by the FoF1-ATP synthase by the protonmotive force across the inner membrane. However, mitochondria are also vital for a number of additional cellular processes, including regulation of metabolism, calcium homeostasis, immune function, cell growth and stem cell function, and cell death pathways. Although mitochondrial density in vascular tissues is considerably lower than other tissues such as skeletal muscle, liver and heart [52,53], increasing evidence indicates that these organelles are critical for maintenance of cellular and tissue homeostasis in the vasculature. This topic has been reviewed in detail elsewhere [54–61], but below we briefly summarize some of the key roles of mitochondria in the vasculature. A first important distinction is to consider the vascular cell type in question, as the density and subcellular distribution of mitochondria vary between endothelial and vascular smooth muscle cells, and indeed even among the same cell types in different vascular beds [54,60]. In general, unlike in highly metabolically active tissues with greater ATP demand, the principal role of mitochondria in the vasculature appears to be cellular signaling rather than energy provision [54]. Cellular energy demand is quite low in endothelial cells, and ATP demand is met primarily via glycolysis. However, endothelial mitochondria are critical in the regulation of calcium homeostasis, apoptosis/necrosis, cellular response to stress, and immune and inflammatory pathways. An essential feature of these roles is the regulated production of signaling molecules including redox-active molecules (reactive oxygen, nitrogen and other species; mtROS), mitochondrial DNA, mitochondria-derived peptides and damage-associated molecular pattern molecules (DAMPs), which exert effects intra- and extra-cellularly [62]. Importantly, there is cross-talk between mitochondrial and nuclear signaling pathways, whereby mitochondria-derived signaling is both influenced by and can influence nuclear events including gene expression [63]. Similarly, in vascular smooth muscle cells, mitochondria have an important role in cellular signaling. Mitochondria are involved in signaling pathways for regulation of vascular smooth muscle cell growth and proliferation (e.g., TGF-β activity) [64], as well as maintenance of the dynamic balance among synthesis and breakdown of extracellular structural proteins, including collagen and elastin (e.g., matrix metalloproteinase enzyme activities) [65]. There is also emerging evidence demonstrating interplay between mtROS signaling and inflammatory pathways known to be important for regulating vascular smooth muscle cell function, including those involving NFkB and the NLRP3-inflammasome [66–69], further highlighting the crucial role of mtROS in vascular homeostasis. Mitochondrial ROS The signaling functions of vascular mitochondria are thought to be mediated in large part by the production of ROS at low, physiological levels. However, the dysregulation of this mtROS production also has the potential to lead to pathophysiological sequelae that disrupt other mitochondrial functions, cellular homeostasis, and ultimately vascular function. The production of ROS by mitochondria can occur at several sites (Figure 2), including but not limited to the electron transport proteins, and this topic has been reviewed in detail elsewhere [54,60,70]. The most important sites for ROS production within mitochondria appear to be complexes I and III. These ROS are thought to be critical transducers of signaling mediated by mitochondria, leading to post-transcriptional modification of proteins and interactions with immune and inflammatory cellular pathways, although the mechanistic details are still uncertain. In the vasculature, the proximal mtROS species is superoxide, which is generated primarily at the electron transport chain in the mitochondrial inner membrane via interaction between oxygen and unpaired electrons, influenced by the proton motive force and the redox state of the coenzyme Q pool and integrity of intrinsic electron transport chain proteins [54,58,60,70]. Superoxide is released into the matrix (complex I) or into both the matrix and intermembrane space (complex III); it can also undergo dismutation to hydrogen peroxide by the antioxidant enzyme manganese superoxide dismutase (MnSOD) [59,60,62,70]. Hydrogen peroxide is also generated de novo on the surface of the mitochondrial outer membrane or in the intermembrane space mitochondria by p66SHC, a growth factor adapter protein referred to as a sensor/marker and ‘master regulator’ of mitochondrial redox signaling whose activity is indicative of the rate of mtROS production [71]. In addition, NADPH oxidase 4 (NOX4) is viewed as a primarily mitochondrial isoform of the NOX monoamine oxidase family of enzymes that contributes to mitochondrial hydrogen peroxide generation [72], although more research is needed to confirm the mitochondrial specificity of NOX4. Figure 2 Aging is associated with dysregulated mitochondrial quality control featuring reduced mitochondrial biogenesis (upper left) and reduced mitophagy (upper right), increased mitochondrial fission (upper middle right), reduced mitochondrial fusion (lower middle right), reduced mitochondrial stress resistance (lower right), increased mitochondrial DNA damage (middle left of mitochondria image) and increased bioactivity of mitochondrial reactive oxygen species (e.g., superoxide and other reactive oxygen species [ROS], middle of mitochondria image) relative to antioxidant defenses (e.g., manganese superoxide dismutase [SOD], lower right of mitochondria). VIEW LARGEDOWNLOAD SLIDE Mechanisms of age-associated mitochondrial dysfunction Aging is associated with dysregulated mitochondrial quality control featuring reduced mitochondrial biogenesis (upper left) and reduced mitophagy (upper right), increased mitochondrial fission (upper middle right), reduced mitochondrial fusion (lower middle right), reduced mitochondrial stress resistance (lower right), increased mitochondrial DNA damage (middle left of mitochondria image) and increased bioactivity of mitochondrial reactive oxygen species (e.g., superoxide and other reactive oxygen species [ROS], middle of mitochondria image) relative to antioxidant defenses (e.g., manganese superoxide dismuta

Shearmeter floats in the area of the WHOI Brazil Basin Tracer Release Experiment : technical and oceanographic data

Six drifting floats designed to measure shear were deployed in the vicinity of the Brazil Basin Tracer Release Experiment. The one-year long time series of oceanographic conditions obtained by the floats are for direct comparison with long-term tracer dispersion. The purpose of the tracer dispersion experiment was to study mixing of Antarctic Bottom Water at approximately 4000 m depth with less dense water above. Two of the floats returned shear records, one from about 1660 m depth and one from about 2800 m depth. Mean shear at 1660 m was 2.2 x 10 -3 s-1 with N = 1.1 cph, about 1.9 times the Garrett-Munk model amount. Mean shear at 2800 m was 1.1 x 10-3 with N = 0.5 cph, about 2.2 times Garrett-Munk. There was no apparent depth structure to the shear recorded by the near-bottom float moving over the mountainous seafloor. The two shear time series and the local tidal velocities were not strongly correlated, but the tide and shear series did have some similarities. Some variability in the 1660-m shear may be due to atmospheric forcing. Three floats deeper than 2800 m returned one-year long trajectories. Two trajectories were persistently eastward.Funding was provided by the National Science Foundation under Grant Nos. OCE-9416014 and OCE-9906685

New Caledonian crows learn the functional properties of novel tool types.

New Caledonian crows were presented with Bird and Emery's (2009a) Aesop's fable paradigm, which requires stones to be dropped into a water-filled tube to bring floating food within reach. The crows did not spontaneously use stones as tools, but quickly learned to do so, and to choose objects and materials with functional properties. Some crows discarded both inefficient and non-functional objects before observing their effects on the water level. Interestingly, the crows did not learn to discriminate between functional and non-functional objects and materials when there was an arbitrary, rather than causal, link between object and reward. This finding suggests that the crows' performances were not based on associative learning alone. That is, learning was not guided solely by the covariation rate between stimuli and outcomes or the conditioned reinforcement properties acquired by functional objects. Our results, therefore, show that New Caledonian crows can process causal information not only when it is linked to sticks and stick-like tools but also when it concerns the functional properties of novel types of tool

FUSE Measurements of Far Ultraviolet Extinction. I. Galactic Sight Lines

We present extinction curves that include data down to far ultraviolet wavelengths (FUV; 1050 - 1200 A) for nine Galactic sight lines. The FUV extinction was measured using data from the Far Ultraviolet Spectroscopic Explorer. The sight lines were chosen for their unusual extinction properties in the infrared through the ultraviolet; that they probe a wide range of dust environments is evidenced by the large spread in their measured ratios of total-to-selective extinction, R_V = 2.43 - 3.81. We find that extrapolation of the Fitzpatrick & Massa relationship from the ultraviolet appears to be a good predictor of the FUV extinction behavior. We find that predictions of the FUV extinction based upon the Cardelli, Clayton & Mathis (CCM) dependence on R_V give mixed results. For the seven extinction curves well represented by CCM in the infrared through ultraviolet, the FUV extinction is well predicted in three sight lines, over-predicted in two sight lines, and under-predicted in 2 sight lines. A Maximum Entropy Method analysis using a simple three component grain model shows that seven of the nine sight lines in the study require a larger fraction of grain materials to be in dust when FUV extinction is included in the models. Most of the added grain material is in the form of small (radii < 200 A) grains.Comment: Accepted for publication in the Astrophysical Journal. 31 pages with 7 figure

Late-time Light Curves of Type II Supernovae: Physical Properties of SNe and Their Environment

We present BVRIJHK band photometry of 6 core-collapse supernovae, SNe 1999bw, 2002hh, 2003gd, 2004et, 2005cs, and 2006bc measured at late epochs (>2 yrs) based on Hubble Space Telescope (HST), Gemini north, and WIYN telescopes. We also show the JHK lightcurves of a supernova impostor SN 2008S up to day 575. Of our 43 HST observations in total, 36 observations are successful in detecting the light from the SNe alone and measuring magnitudes of all the targets. HST observations show a resolved scattered light echo around SN 2003gd at day 1520 and around SN 2002hh at day 1717. Our Gemini and WIYN observations detected SNe 2002hh and 2004et, as well. Combining our data with previously published data, we show VRIJHK-band lightcurves and estimate decline magnitude rates at each band in 4 different phases. Our prior work on these lightcurves and other data indicate that dust is forming in our targets from day ~300-400, supporting SN dust formation theory. In this paper we focus on other physical properties derived from the late time light curves. We estimate 56Ni masses for our targets (0.5-14 x 10^{-2} Msun) from the bolometric lightcurve of each for days ~150-300 using SN 1987A as a standard (7.5 x 10^{-2} Msun). The flattening or sometimes increasing fluxes in the late time light curves of SNe 2002hh, 2003gd, 2004et and 2006bc indicate the presence of light echos. We estimate the circumstellar hydrogen density of the material causing the light echo and find that SN 2002hh is surrounded by relatively dense materials (n(H) >400 cm^{-3}) and SNe 2003gd and 2004et have densities more typical of the interstellar medium (~1 cm^{-3}). The 56Ni mass appears well correlated with progenitor mass with a slope of 0.31 x 10^{-2}, supporting the previous work by Maeda et al. (2010), who focus on more massive Type II SNe. The dust mass does not appear to be correlated with progenitor mass.Comment: We corrected the 56Ni mass of SN2005cs and Figures 8 (a) and 8 (c

Dynamics of particles floating on liquid flowing in a semicircular open channel

The dynamic characteristics of surface-floating particles in liquids flowing in a two-dimensional, semicircular open channel is studied experimentally. For high visibility in the experiments, relatively large particles are employed whose particle-liquid density ratio is either equal to or less than unity. Particles of different size and geometry are tested in a water-glycerin mixture. A video camera traces the pathline of each particle from which the velocity and direction of particle motion are evaluated. Liquid velocity distribution is determined by hot-film anemometry. A modified dynamics (Basset-Boussinesq-Oseen) equation is derived and numerically solved by means of a finite-difference technique to determine fluid velocity. A new dimensionless parameter is disclosed which is pertinent to both particle geometry and fluid flow conditions. It correlates particle trajectory and velocity, trajectory dispersion and fluid-particle velocity ratio.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47062/1/348_2004_Article_BF00226574.pd

An Exploration into Fern Genome Space

Ferns are one of the few remaining major clades of land plants for which a complete genome sequence is lacking. Knowledge of genome space in ferns will enable broad-­‐scale comparative analyses of land plant genes and genomes, provide insights into genome evolution across green plants, and shed light on genetic and genomic features that characterize ferns, such as their high chromosome numbers and large genome sizes. As part of an initial exploration into fern genome space, we used a whole genome shotgun sequencing approach to obtain low-­‐density coverage (~0.4X to 2X) for six fern species from the Polypodiales (Ceratopteris, Pteridium, Polypodium, Cystopteris), Cyatheales (Plagiogyria), and Gleicheniales (Dipteris). We explore these data to characterize the proportion of the nuclear genome represented by repetitive sequences (including DNA transposons, retrotransposons, rDNA, and simple repeats) and protein-­‐coding genes, and to extract chloroplast and mitochondrial genome sequences. Such initial sweeps of fern genomes can provide information useful for selecting a promising candidate fern species for whole genome sequencing. We also describe variation of genomic traits across our sample and highlight some differences and similarities in repeat structure between ferns and seed plants