A subjective evaluation of current contact lens wetting solutions

There have been many studies made as to the importance of the use of wetting solutions in the wearing of contact lenses. It is generally concluded that proper wettability of lenses is a significantly important factor in the improvement of wearing comfort. Wettability basically refers to a physio-chemical mechanism by means of which tears spread evenly over the lenses to form a coherent film. The compositions of the individual wetting solutions contribute in varying degrees to the wettability and wearing comfort. It is the purpose of this study to subjectively evaluate the variability in degrees of comfort and desirability of a number of wetting solutions currently available

Body composition estimated by bioelectrical impedance analyses is diminished by prenatal stress in neonatal lambs and by heat stress in feedlot wethers

Body composition correlates to carcass value in livestock, which makes the ability to accurately estimate body composition in the live animal beneficial (Berg and Marchello, 1994). Bioelectrical impedance analysis (BIA) is a clinical tool used to assess body composition in humans (Lukaski et al., 1985), but its use in livestock has been minimal. Lean and fat content contribute to profitability for livestock producers, and poor body composition can be caused by stress that occurs either during in utero development (De Blasio et al., 2007) or during postnatal growth (Boyd et al., 2015). Maternal hyperthermia-induced placental insufficiency (Brown et al., 2015) and sustained maternal inflammation (Cadaret et al., 2018) are two established causes of intrauterine growth restriction (IUGR). IUGR-born animals are characterized by asymmetrical growth restriction that alters lifelong body composition due to impaired muscle growth capacity (Yates et al., 2018). In addition, acute heat stress during periods of peak postnatal growth can alter body composition in livestock (Boyd et al., 2015). We postulate that BIA can detect these changes in the live animal. Thus, the objective of this study was to determine whether BIA measurements can predict changes to body composition in live neonatal lambs exposed to intrauterine stress and in heat-stressed feedlot lambs

Spectrophotometry of HII Regions, Diffuse Ionized Gas and Supernova Remnants in M31: The Transition from Photo- to Shock-Ionization

We present results of KPNO 4-m optical spectroscopy of discrete emission-line nebulae and regions of diffuse ionized gas (DIG) in M31. Long-slit spectra of 16 positions in the NE half of M31 were obtained over a 5-15 kpc range in radial distance from the center of the galaxy. The spectra have been used to confirm 16 supernova remnant candidates from the Braun & Walterbos (1993) catalog. The slits also covered 46 HII regions which show significant differences among the various morphological types (center-brightened, diffuse, rings). Radial gradients in emission-line ratios such as [OIII]/H$\beta$ and [OII]/[OIII] are observed most prominently in the center-brightened HII regions. These line ratio trends are either much weaker or completely absent in the diffuse and ring nebulae. The line ratio gradients previously seen in M31 SNRs (Blair, Kirshner, & Chevalier 1981; 1982) are well reproduced by our new data. The spectra of center-brightened HII regions and SNRs confirm previous determinations of the radial abundance gradient in M31. We use diagnostic diagrams which separate photoionized gas from shock-ionized gas to compare the spectral properties of HII regions, SNRs and DIG. This analysis strengthens earlier claims (Greenawalt, Walterbos, & Braun 1997) that the DIG in the disk of M31 is photoionized by a dilute radiation field.Comment: 45 pages, 9 figures, 7 tables, to appear in the Astronomical Journal (December 1999

ASAS-SSR Triennnial Reproduction Symposium: Looking Back and Moving Forward—How Reproductive Physiology has Evolved: Fetal origins of impaired muscle growth and metabolic dysfunction: Lessons from the heat-stressed pregnant ewe

Intrauterine growth restriction (IUGR) is the second leading cause of perinatal mortality and predisposes offspring to metabolic disorders at all stages of life. Muscle-centric fetal adaptations reduce growth and yield metabolic parsimony, beneficial for IUGR fetal survival but detrimental to metabolic health after birth. Epidemiological studies have reported that IUGRborn children experience greater prevalence of insulin resistance and obesity, which progresses to diabetes, hypertension, and other metabolic disorders in adulthood that reduce quality of life. Similar adaptive programming in livestock results in decreased birth weights, reduced and inefficient growth, decreased carcass merit, and substantially greater mortality rates prior to maturation. High rates of glucose consumption and metabolic plasticity make skeletal muscle a primary target for nutrient-sparing adaptations in the IUGR fetus, but at the cost of its contribution to proper glucose homeostasis after birth. Identifying the mechanisms underlying IUGR pathophysiology is a fundamental step in developing treatments and interventions to improve outcomes in IUGR-born humans and livestock. In this review, we outline the current knowledge regarding the adaptive restriction of muscle growth and alteration of glucose metabolism that develops in response to progressively exacerbating intrauterine conditions. In addition, we discuss the evidence implicating developmental changes in β adrenergic and inflammatory systems as key mechanisms for dysregulation of these processes. Lastly, we highlight the utility and importance of sheep models in developing this knowledge

Neuronal cell cycle re-entry mediates Alzheimer disease-type changes

AbstractEvidence showing the ectopic re-expression of cell cycle-related proteins in specific vulnerable neuronal populations in Alzheimer disease led us to formulate the hypothesis that neurodegeneration, like cancer, is a disease of inappropriate cell cycle control. To test this notion, we used adenoviral-mediated expression of c-myc and ras oncogenes to drive postmitotic primary cortical neurons into the cell cycle. Cell cycle re-entry in neurons was associated with increased DNA content, as determined using BrdU and DAPI, and the re-expression of cyclin B1, a marker for the G2/M phase of the cell cycle. Importantly, we also found that cell cycle re-entry in primary neurons leads to tau phosphorylation and conformational changes similar to that seen in Alzheimer disease. This study establishes that the cell cycle can be instigated in normally quiescent neuronal cells and results in a phenotype that shares features of degenerative neurons in Alzheimer disease. As such, our neuronal cell model may be extremely valuable for the development of novel therapeutic strategies

An Integrated Approach to Weather Radar Calibration and Monitoring Using Ground Clutter and Satellite Comparisons

The stability and accuracy of weather radar reflectivity calibration are imperative for quantitative applications, such as rainfall estimation, severe weather monitoring and nowcasting, and assimilation in numerical weather prediction models. Various radar calibration and monitoring techniques have been developed, but only recently have integrated approaches been proposed, that is, using different calibration techniques in combination. In this paper the following three techniques are used: 1) ground clutter monitoring, 2) comparisons with spaceborne radars, and 3) the self-consistency of polarimetric variables. These techniques are applied to a C-band polarimetric radar (CPOL) located in the Australian tropics since 1998. The ground clutter monitoring technique is applied to each radar volumetric scan and provides a means to reliably detect changes in calibration, relative to a baseline. It is remarkably stable to within a standard deviation of 0.1 dB (decibels). To obtain an absolute calibration value, CPOL observations are compared to spaceborne radars on board TRMM (Tropical Rainfall Measuring Mission) and GPM (Global Precipitation Measurement) using a volume-matching technique. Using an iterative procedure and stable calibration periods identified by the ground echoes technique, we improve the accuracy of this technique to about 1 dB. Finally, we review the self-consistency technique and constrain its assumptions using results from the hybrid TRMM-GPM and ground echo technique. Small changes in the self-consistency parameterization can lead to 5 dB of variation in the reflectivity calibration. We find that the drop-shape model of Brandes et al. with a standard deviation of the canting angle of 12 degrees best matches our dataset

Primary myoblasts from intrauterine growth-restricted fetal sheep exhibit intrinsic dysfunction of proliferation and differentiation that coincides with enrichment of inflammatory cytokine signaling pathways

Intrauterine growth restriction (IUGR) is linked to lifelong reductions in muscle mass due to intrinsic functional deficits in myoblasts, but the mechanisms underlying these deficits are not known. Our objective was to determine if the deficits were associated with changes in inflammatory and adrenergic regulation of IUGR myoblasts, as was previously observed in IUGR muscle. Primary myoblasts were isolated from IUGR fetal sheep produced by hyperthermia-induced placental insufficiency (PI-IUGR; n = 9) and their controls (n = 9) and from IUGR fetal sheep produced by maternofetal inflammation (MI-IUGR; n = 6) and their controls (n = 7). Proliferation rates were less (P \u3c 0.05) for PI-IUGR myoblasts than their controls and were not affected by incubation with IL-6, TNF-α, norepinephrine, or insulin. IκB kinase inhibition reduced (P \u3c 0.05) proliferation of control myoblasts modestly in basal media but substantially in TNF-α-added media and reduced (P \u3c 0.05) PI-IUGR myoblast proliferation substantially in basal and TNF-α-added media. Proliferation was greater (P \u3c 0.05) for MI-IUGR myoblasts than their controls and was not affected by incubation with TNF-α. Insulin increased (P \u3c 0.05) proliferation in both MI-IUGR and control myoblasts. After 72-h differentiation, fewer (P \u3c 0.05) PI-IUGR myoblasts were myogenin+ than controls in basal and IL-6 added media but not TNF-α-added media. Fewer (P \u3c 0.05) PI-IUGR myoblasts were desmin+ than controls in basal media only. Incubation with norepinephrine did not affect myogenin+ or desmin+ percentages, but insulin increased (P \u3c 0.05) both markers in control and PI-IUGR myoblasts. After 96-h differentiation, fewer (P \u3c 0.05) MI-IUGR myoblasts were myogenin+ and desmin+ than controls regardless of media, although TNF-α reduced (P \u3c 0.05) desmin+ myoblasts for both groups. Differentiated PI-IUGR myoblasts had greater (P \u3c 0.05) TNFR1, ULK2, and TNF-α-stimulated TLR4 gene expression, and PI-IUGR semitendinosus muscle had greater (P \u3c 0.05) TNFR1 and IL6 gene expression, greater (P \u3c 0.05) c-Fos protein, and less (P \u3c 0.05) IκBα protein. Differentiated MI-IUGR myoblasts had greater (P \u3c 0.05) TNFR1 and IL6R gene expression, tended to have greater (P = 0.07) ULK2 gene expression, and had greater (P \u3c 0.05) β-catenin protein and TNF-α-stimulated phosphorylation of NFκB. We conclude that these enriched components of TNF-α/TNFR1/NFκB and other inflammatory pathways in IUGR myoblasts contribute to their dysfunction and help explain impaired muscle growth in the IUGR fetus. Lay Summary-- Myoblasts are stems cells whose functional capacity can limit muscle growth. However, stressful intrauterine conditions cause these cells to be intrinsically dysfunctional. This restricts muscle growth capacity, leading to intrauterine growth restriction (IUGR) of the fetus, low birth weight, and less muscle mass after birth. Consequently, meat yield is reduced in IUGR-born food animals and glucose homeostasis is impaired in IUGR-born humans, which contributes to metabolic dysfunction. Intrinsic dysfunction of IUGR myoblasts has been previously observed, but the fetal programming changes (i.e., permanent changes in the development of cellular mechanisms that explains different functional outcomes) have not been identified. This study shows that one mechanism is the enhancement of signaling pathways for TNF-α and other inflammatory cytokines. These cytokines have roles in stress responses and regulation of muscle growth. Programmed enhancement of these pathways means that IUGR myoblasts are more responsive to even normal amounts of circulating cytokines. Unfortunately, the primary response of myoblasts to cytokines is slower differentiation (i.e., cellular transformation necessary for muscle growth). Programmed enhancement of this response directly impedes myoblast-dependent muscle growth, and the deficit is lifelong. However, identifying this mechanism is a fundamental step for developing strategies to improve muscle growth in low birth weight offspring