The Effects of Zinc Sulphate, Manganese Sulphate, and Iron Sulphate on the Lead Storage Cell.

The lead storage battery as it is used today is made up of the pasted type plates of lead dioxide, the anode, and sponge lead, the cathode, and wooden or hard rubber separators, which serve to insulate these from one another. In manufacturing these, it is desirable to keep them free from impurities

Comprehensive comparative outcomes in children with congenital heart disease: The rationale for the Congenital Catheterization Research Collaborative

Clinical research in the treatment of patients with congenital heart disease (CHD) is limited by the wide variety of CHD manifestations and therapeutic options as well as the generally low incidence of CHD. The availability of comprehensive, contemporary outcomes studies is therefore limited. This inadequacy may result in a lack of data‐driven medical decision making. In 2013, clinician scientists at two centers began a research collaboration, the Congenital Catheterization Research Collaborative (CCRC). Over time, the CCRC has grown to include nine cardiac centers from across the United States, with a common data coordinating center. The CCRC seeks to generate high‐quality, contemporary, statistically robust, and generalizable outcomes research which can help address important clinical questions in the treatment of CHD. To date, the CCRC has reported on multicenter outcomes in: neonates with congenital aortic stenosis, infants undergoing right ventricular decompression for pulmonary atresia and intact ventricular septum, and infants with ductal‐dependent pulmonary blood flow. The CCRC has been successful at leveraging large multicenter cohorts of patients in a contemporary period to perform comparative studies. In the future, the CCRC plans to continue to perform hypothesis‐driven retrospective and prospective observational studies of CHD populations where controversy exists or where novel interventions or therapies have emerged. Quality improvement efforts including lesion‐specific registry development may be an additional potential future target.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/149494/1/chd12737.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/149494/2/chd12737_am.pd

Characterization of the Moraxella catarrhalis uspA1 and uspA2 Genes and Their Encoded Products

The uspA1 and uspA2 genes of M. catarrhalis O35E encode two different surface-exposed proteins which were previously shown to share a 140-amino-acid region with 93% identity (C. Aebi, I. Maciver, J. L. Latimer, L. D. Cope, M. K. Stevens, S. E. Thomas, G. H. McCracken, Jr., and E. J. Hansen, Infect. Immun. 65:4367–4377, 1997). The N-terminal amino acid sequences of the mature forms of both UspA1 and UspA2 from strain O35E were determined after enzymatic treatment to remove the N-terminal pyroglutamyl residue that had blocked Edman degradation. Mass spectrometric analysis indicated that the molecular mass of UspA1 from M. catarrhalis O35E was 83,500 ± 116 Da. Nucleotide sequence analysis of the uspA1 and uspA2 genes from three other M. catarrhalis strains (TTA24, ATCC 25238, and V1171) revealed that the encoded protein products were very similar to those from strain O35E. Western blot analysis was used to confirm that each of these three strains of M. catarrhalis expressed both UspA1 and UspA2 proteins. Several different and repetitive amino acid motifs were present in both UspA1 and UspA2 from these four strains, and some of these were predicted to form coiled coils. Linear DNA templates were used in an in vitro transcription-translation system to determine the sizes of the monomeric forms of the UspA1 and UspA2 proteins from strains O35E and TTA24

New constraints on the evolution of the stellar-to-dark matter connection : a combined analysis of galaxy-galaxy lensing, clustering, and stellar mass functions from z = 0.2 to z = 1

Using data from the COSMOS survey, we perform the first joint analysis of galaxy-galaxy weak lensing, galaxy spatial clustering, and galaxy number densities. Carefully accounting for sample variance and for scatter between stellar and halo mass, we model all three observables simultaneously using a novel and self-consistent theoretical framework. Our results provide strong constraints on the shape and redshift evolution of the stellar-to-halo mass relation (SHMR) from z = 0.2 to z = 1. At low stellar mass, we find that halo mass scales as Mh vpropM 0.46 * and that this scaling does not evolve significantly with redshift from z = 0.2 to z = 1. The slope of the SHMR rises sharply at M * > 5 × 1010 M ☉ and as a consequence, the stellar mass of a central galaxy becomes a poor tracer of its parent halo mass. We show that the dark-to-stellar ratio, Mh /M *, varies from low to high masses, reaching a minimum of Mh /M * ~ 27 at M * = 4.5 × 1010 M ☉ and Mh = 1.2 × 1012 M ☉. This minimum is important for models of galaxy formation because it marks the mass at which the accumulated stellar growth of the central galaxy has been the most efficient. We describe the SHMR at this minimum in terms of the "pivot stellar mass," M piv *, the "pivot halo mass," M piv h , and the "pivot ratio," (Mh /M *)piv. Thanks to a homogeneous analysis of a single data set spanning a large redshift range, we report the first detection of mass downsizing trends for both M piv h and M piv *. The pivot stellar mass decreases from M piv * = 5.75 ± 0.13 × 1010 M ☉ at z = 0.88 to M piv * = 3.55 ± 0.17 × 1010 M ☉ at z = 0.37. Intriguingly, however, the corresponding evolution of M piv h leaves the pivot ratio constant with redshift at (Mh /M *)piv ~ 27. We use simple arguments to show how this result raises the possibility that star formation quenching may ultimately depend on Mh /M * and not simply on Mh , as is commonly assumed. We show that simple models with such a dependence naturally lead to downsizing in the sites of star formation. Finally, we discuss the implications of our results in the context of popular quenching models, including disk instabilities and active galactic nucleus feedback

Satellite content and quenching of star formation in galaxy groups at z ~ 1.8

We study the properties of satellites in the environment of massive star-forming galaxies at z ~ 1.8 in the COSMOS field, using a sample of 215 galaxies on the main sequence of star formation with an average mass of ~1011M⊙. At z> 1.5, these galaxies typically trace halos of mass ≳1013M⊙. We use optical-near-infrared photometry to estimate stellar masses and star formation rates (SFR) of centrals and satellites down to ~ 6 × 109M⊙. We stack data around 215 central galaxies to statistically detect their satellite halos, finding an average of ~3 galaxies in excess of the background density. We fit the radial profiles of satellites with simple β-models, and compare their integrated properties to model predictions. We find that the total stellar mass of satellites amounts to ~68% of the central galaxy, while spectral energy distribution modeling and far-infrared photometry consistently show their total SFR to be 25-35% of the central's rate. We also see significant variation in the specific SFR of satellites within the halo with, in particular, a sharp decrease at <100 kpc. After considering different potential explanations, we conclude that this is likely an environmental signature of the hot inner halo. This effect can be explained in the first order by a simple free-fall scenario, suggesting that these low-mass environments can shut down star formation in satellites on relatively short timescales of ~0.3 Gyr

Chronic non-specific low back pain - sub-groups or a single mechanism?

Copyright 2008 Wand and O'Connell; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Background: Low back pain is a substantial health problem and has subsequently attracted a considerable amount of research. Clinical trials evaluating the efficacy of a variety of interventions for chronic non-specific low back pain indicate limited effectiveness for most commonly applied interventions and approaches. Discussion: Many clinicians challenge the results of clinical trials as they feel that this lack of effectiveness is at odds with their clinical experience of managing patients with back pain. A common explanation for this discrepancy is the perceived heterogeneity of patients with chronic non-specific low back pain. It is felt that the effects of treatment may be diluted by the application of a single intervention to a complex, heterogeneous group with diverse treatment needs. This argument presupposes that current treatment is effective when applied to the correct patient. An alternative perspective is that the clinical trials are correct and current treatments have limited efficacy. Preoccupation with sub-grouping may stifle engagement with this view and it is important that the sub-grouping paradigm is closely examined. This paper argues that there are numerous problems with the sub-grouping approach and that it may not be an important reason for the disappointing results of clinical trials. We propose instead that current treatment may be ineffective because it has been misdirected. Recent evidence that demonstrates changes within the brain in chronic low back pain sufferers raises the possibility that persistent back pain may be a problem of cortical reorganisation and degeneration. This perspective offers interesting insights into the chronic low back pain experience and suggests alternative models of intervention. Summary: The disappointing results of clinical research are commonly explained by the failure of researchers to adequately attend to sub-grouping of the chronic non-specific low back pain population. Alternatively, current approaches may be ineffective and clinicians and researchers may need to radically rethink the nature of the problem and how it should best be managed

Redressing Inequity in Parent Care Among Siblings

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72515/1/j.1741-3737.2003.00201.x.pd

Specific ion channels contribute to key elements of pathology during secondary degeneration following neurotrauma

Background: Following partial injury to the central nervous system, cells beyond the initial injury site undergo secondary degeneration, exacerbating loss of neurons, compact myelin and function. Changes in Ca 2+ flux are associated with metabolic and structural changes, but it is not yet clear how flux through specific ion channels contributes to the various pathologies. Here, partial optic nerve transection in adult female rats was used to model secondary degeneration. Treatment with combinations of three ion channel inhibitors was used as a tool to investigate which elements of oxidative and structural damage related to long term functional outcomes. The inhibitors employed were the voltage gated Ca 2+ channel inhibitor Lomerizine (Lom), the Ca 2+ permeable AMPA receptor inhibitor YM872 and the P2X 7 receptor inhibitor oxATP. Results: Following partial optic nerve transection, hyper-phosphorylation of Tau and acetylated tubulin immunoreactivity were increased, and Nogo-A immunoreactivity was decreased, indicating that axonal changes occurred acutely. All combinations of ion channel inhibitors reduced hyper-phosphorylation of Tau and increased Nogo-A immunoreactivity at day 3 after injury. However, only Lom/oxATP or all three inhibitors in combination significantly reduced acetylated tubulin immunoreactivity. Most combinations of ion channel inhibitors were effective in restoring the lengths of the paranode and the paranodal gap, indicative of the length of the node of Ranvier, following injury. However, only all three inhibitors in combination restored to normal Ankyrin G length at the node of Ranvier. Similarly, HNE immunoreactivity and loss of oligodendrocyte precursor cells were only limited by treatment with all three ion channel inhibitors in combination. Conclusions: Data indicate that inhibiting any of a range of ion channels preserves certain elements of axon and node structure and limits some oxidative damage following injury, whereas ionic flux through all three channels must be inhibited to prevent lipid peroxidation and preserve Ankyrin G distribution and OPCs