A More Rapid Routine Control Method for the Estimation of Titanium Dioxide in Paper

A procedure is given for estimation of titanium dioxide in paper, whereby ashing the sample is omitted thru simultaneous destruction of the paper and solution of the titanium. This method is compared with the standard methods of analysis in regard to time required and precision

Analytical and experimental investigation of flow fields of annular jets with and without swirling flow

Analytical and experimental studies were performed to define the flowfield of annular jets, with and, without swirling flow. The analytical model treated configurations with variations of flow angularities, radius ratio, and swirl distributions. Swirl distributions characteristic of stator vanes and rotor blade rows, where the total pressure and swirl distributions are related were incorporated in the mathematical model. The experimental studies included tests of eleven nozzle models, both with and, without swirling exhaust flow. Flowfield surveys were obtained and used for comparison with the analytical model. This comparison of experimental and analytical studies served as the basis for evaluation of several empirical constants as required for application of the analysis to the general flow configuration. The analytical model developed during these studies is applicable to the evaluation of the flowfield and overall performance of the exhaust of statorless lift fan systems that contain various levels of exhaust swirl

Design, fabrication and acoustic tests of a 36 inch (0.914 meter) statorless turbotip fan

The LF336/E is a 36 inch (0.914 meter) diameter fan designed to operate in a rotor-alone configuration. Design features required for modification of the existing LF336/A rotor-stator fan into the LF336/E statorless fan configuration are discussed. Tests of the statorless fan identified an aerodynamic performance deficiency due to inaccurate accounting of the fan exit swirl during the aerodynamic design. This performance deficiency, related to fan exit static pressure levels, produced about a 20 percent thrust loss. A study was then conducted for further evaluation of the fan exit flow fields typical of statorless fan systems. This study showed that through proper selection of fan design variables such as pressure ratio, radius ratio, and swirl distributions, performance of a statorless fan configuration could be improved with levels of thrust approaching the conventional rotor-stator fan system. Acoustic measurements were taken for the statorless fan system at both GE and NASA, and when compared to other lift fan systems, showed noise levels comparable to the quietest lift fan configuration which included rotor-stator spacing and acoustic treatment. The statorless fan system was also used to determine effects of rotor leading edge serrations on noise generations. A cascade test program identified the serration geometry based on minimum pressure losses, wake turbulence levels and noise generations

Cystic fibrosis transmembrane regulator correction attenuates heart failure-induced lung inflammation

Heart failure (HF) affects 64 million people worldwide. Despite advancements in prevention and therapy, quality of life remains poor for many HF patients due to associated target organ damage. Pulmonary manifestations of HF are well-established. However, difficulties in the treatment of HF patients with chronic lung phenotypes remain as the underlying patho-mechanistic links are still incompletely understood. Here, we aim to investigate the cystic fibrosis transmembrane regulator (CFTR) involvement in lung inflammation during HF, a concept that may provide new mechanism-based therapies for HF patients with pulmonary complications. In a mouse model of HF, pharmacological CFTR corrector therapy (Lumacaftor (Lum)) was applied systemically or lung-specifically for 2 weeks, and the lungs were analyzed using histology, flow cytometry, western blotting, and qPCR. Experimental HF associated with an apparent lung phenotype characterized by vascular inflammation and remodeling, pronounced tissue inflammation as evidenced by infiltration of pro-inflammatory monocytes, and a reduction of pulmonary CFTR+ cells. Moreover, the elevation of a classically-activated phenotype of non-alveolar macrophages coincided with a cell-specific reduction of CFTR expression. Pharmacological correction of CFTR with Lum mitigated the HF-induced downregulation of pulmonary CFTR expression and increased the proportion of CFTR+ cells in the lung. Lum treatment diminished the HF-associated elevation of classically-activated non-alveolar macrophages, while promoting an alternatively-activated macrophage phenotype within the lungs. Collectively, our data suggest that downregulation of CFTR in the HF lung extends to non-alveolar macrophages with consequences for tissue inflammation and vascular structure. Pharmacological CFTR correction possesses the capacity to alleviate HF-associated lung inflammation

Quantitative pharmacologic MRI: Mapping the cerebral blood volume response to cocaine in dopamine transporter knockout mice

The use of pharmacologic MRI (phMRI) in mouse models of brain disorders allows noninvasive in vivo assessment of drug-modulated local cerebral blood volume changes (ΔCBV) as one correlate of neuronal and neurovascular activities. In this report, we employed CBV-weighted phMRI to compare cocaine-modulated neuronal activity in dopamine transporter (DAT) knockout (KO) and wild-typemice. Cocaine acts to block the dopamine, norepinephrine, and serotonin transporters (DAT, NET, and SERT) that clear their respective neurotransmitters from the synapses, helping to terminate cognate neurotransmission. Cocaine consistently reduced CBV, with a similar pattern of regional ΔCBV in brain structures involved inmediating reward in both DAT genotypes. The largest effects (−20% to −30% ΔCBV) were seen in the nucleus accumbens and several cortical regions. Decreasing response amplitudes to cocaine were noted in more posterior components of the cortico-mesolimbic circuit. DAT KO mice had significantly attenuated ΔCBV amplitudes, shortened times to peak response, and reduced response duration in most regions. This study demonstrates that DAT knockout does not abolish the phMRI responses to cocaine, suggesting that adaptations to loss of DAT and/or retained cocaine activity in other monoamine neurotransmitter systems underlie these responses in DAT KO mice

Ivacaftor therapy post myocardial infarction augments systemic inflammation and evokes contrasting effects with respect to tissue inflammation in brain and lung

Acquired cystic fibrosis transmembrane regulator (CFTR) dysfunctions have been associated with several conditions, including myocardial infarction (MI). Here, CFTR is downregulated in brain, heart, and lung tissue and associates with inflammation and degenerative processes. Therapeutically increasing CFTR expression attenuates these effects. Whether potentiating CFTR function yields similar beneficial effects post-MI is unknown. The CFTR potentiator ivacaftor is currently in clinical trials for treatment of acquired CFTR dysfunction associated with chronic obstructive pulmonary disease and chronic bronchitis. Thus, we tested ivacaftor as therapeutic strategy for MI-associated target tissue inflammation that is characterized by CFTR alterations. MI was induced in male C57Bl/6 mice by ligation of the left anterior descending coronary artery. Mice were treated with ivacaftor starting ten weeks post-MI for two consecutive weeks. Systemic ivacaftor treatment ameliorates hippocampal neuron dendritic atrophy and spine loss and attenuates hippocampus-dependent memory deficits occurring post-MI. Similarly, ivacaftor therapy mitigates MI-associated neuroinflammation (i.e., reduces higher proportions of activated microglia). Systemically, ivacaftor leads to higher frequencies of circulating Ly6C+ and Ly6Chi cells compared to vehicle-treated MI mice. Likewise, an ivacaftor-mediated augmentation of MI-associated pro-inflammatory macrophage phenotype characterized by higher CD80-positivity is observed in the MI lung. In vitro, ivacaftor does not alter LPS-induced CD80 and tumor necrosis factor alpha mRNA increases in BV2 microglial cells, while augmenting mRNA levels of these markers in mouse macrophages and differentiated human THP-1-derived macrophages. Our results suggest that ivacaftor promotes contrasting effects depending on target tissue post-MI, which may be largely dependent on its effects on different myeloid cell types

Therapeutic CFTR correction normalizes systemic and lung-specific S1P level alterations associated with heart failure

Heart failure (HF) is among the main causes of death worldwide. Alterations of sphingosine-1-phosphate (S1P) signaling have been linked to HF as well as to target organ damage that is often associated with HF. S1P’s availability is controlled by the cystic fibrosis transmembrane regulator (CFTR), which acts as a critical bottleneck for intracellular S1P degradation. HF induces CFTR downregulation in cells, tissues and organs, including the lung. Whether CFTR alterations during HF also affect systemic and tissue-specific S1P concentrations has not been investigated. Here, we set out to study the relationship between S1P and CFTR expression in the HF lung. Mice with HF, induced by myocardial infarction, were treated with the CFTR corrector compound C18 starting ten weeks post-myocardial infarction for two consecutive weeks. CFTR expression, S1P concentrations, and immune cell frequencies were determined in vehicle- and C18-treated HF mice and sham controls using Western blotting, flow cytometry, mass spectrometry, and qPCR. HF led to decreased pulmonary CFTR expression, which was accompanied by elevated S1P concentrations and a pro-inflammatory state in the lungs. Systemically, HF associated with higher S1P plasma levels compared to sham-operated controls and presented with higher S1P receptor 1-positive immune cells in the spleen. CFTR correction with C18 attenuated the HF-associated alterations in pulmonary CFTR expression and, hence, led to lower pulmonary S1P levels, which was accompanied by reduced lung inflammation. Collectively, these data suggest an important role for the CFTR-S1P axis in HF-mediated systemic and pulmonary inflammation

Smith-Forbes, E., Howell, Dana M., Pitts, G., Willoughby, J., & Uhl, T. (Minimal Clinical Important Difference of the Quick Disabilities of the Arm, Shoulder, and Hand (Quickdash) for Post-Surgical Finger Phalanx Fractures

Purpose: STUDY DESIGN: Retrospective, multiple-group observational design. Objective: To determine the minimal clinically important difference (MCID) for the Quick Disabilities of the Arm, Should,er, and Hand (QuickDASH) outcome measure, for post-surgical palanx fracture diagnosis, using a triangulation of distribution-and-anchor-based approaches. Backgroudn: The MCID for the QuickDASH has been established using a pool of multiple conditions, and specifically for the shoulder, and other diagnoses in the elbow and wrist, but not for post-surgical finger fracture. Understanding specific threshold change values for post-surgical finger fracture can enhance the clinical decision-making process

Efficacy of power training to improve physical function in individuals diagnosed with frailty and chronic disease: A meta-analysis

Muscle power training with emphasis on high-velocity of concentric movement improves physical functionality in healthy older adults, and, maybe superior to traditional exercise programs. Power training may also be advantageous for patients with acute and chronic illnesses, as well as frail individuals. To determine the efficacy of power training compared with traditional resistance training on physical function outcomes in individuals diagnosed with frailty, acute illness or chronic disease. PubMed (MEDLINE), CINAHL, PEDro, Web of Science, and Google Scholar. (1) at least one study group receives muscle power training of randomized controlled trial (RCT) (2) study participants diagnosed as prefrail, frail or have an ongoing acute or chronic disease, condition or illness; (3) study participants over the age of 18; (4) publication in English language; (5) included physical function as the primary or secondary outcome measures. Two independent reviewers assessed articles for inclusion and graded the methodological quality using Cochrane Risk-of- Bias tool for RCTs. Fourteen RCTs met the inclusion criteria. In seven studies, muscle power training was more effective at improving physical function compared to control activities with a mean fixed effect size (ES) of 0.41 (p = 0.006; 95% CI 0.12 to 0.71). Power training and conventional resistance training had similar effectiveness in eight studies with a mean fixed ES of 0.10 (p = 0.061; 95% CI –0.01 to 0.40). Muscle power training is just as efficacious for improving physical function in individuals diagnosed with frailty and chronic disease when compared to traditional resistance training. The advantages of power training with reduced work per session may support power training as a preferential exercise modality for clinical populations. The findings should be interpreted with caution since generalizability is questioned due to the heterogeneity of patient populations enrolled and participants were relatively mobile at baseline