Conceptual design of a device to measure hand swelling in a micro-gravity environment

In the design of pressurized suits for use by astronauts in space, proper fit is an important consideration. One particularly difficult aspect of the suit design is the design of the gloves. If the gloves of the suit do not fit properly, the grip strength of the astronaut can be decreased by as much as fifty percent. These gloves are designed using an iterative process and can cost over 1.5 million dollars. Glove design is further complicated by the way the body behaves in a micro-gravity environment. In a micro-gravity setting, fluid from the lower body tends to move into the upper body. Some of this fluid collects in the hands and causes the hands to swell. Therefore, a pair of gloves that fit well on earth may not fit well when they are used in space. The conceptual design process for a device which can measure the swelling that occurs in the hands in a micro-gravity environment is described. This process involves developing a specifications list and function structure for the device and generating solution variants for each of the sub functions. The solution variants are then filtered, with the variants that violate any of the specifications being discarded. After acceptable solution variants are obtained, they are combined to form design concepts. These design concepts are evaluated against a set of criteria and the design concepts are ranked in order of preference. Through this process, the two most plausible design concepts were an ultrasonic imaging technique and a laser mapping technique. Both of these methods create a three dimensional model of the hand, from which the amount of swelling can be determined. In order to determine which of the two solutions will actually work best, a further analysis will need to be performed

3D‐printed, externally‐implanted, bioresorbable airway splints for severe tracheobronchomalacia

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/150571/1/lary27863_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/150571/2/lary27863.pd

Multiple Input Electrode Gap Control During Vacuum Arc Remelting

Accurate control of the electrode gap in a vacuum arc remelting (VAR) furnace has been a goal of melters for many years. The size of the electrode gap has a direct influence on ingot solidification structure. At the high melting currents (30 to 40 kA) typically used for VAR of segregation insensitive Ti and Zr alloys, process voltage is used as an indicator of electrode gap, whereas drip-short frequency (or period) is usually used at the lower currents (5 to 8 kA) employed during VAR of superalloys. Modem controllers adjust electrode position or drive velocity to maintain a voltage or drip-short frequency (or period) set-point. Because these responses are non-linear functions of electrode gap and melting current, these controllers have a limited range for which the feedback gains are valid. Models are available that relate process voltage and drip-short frequency to electrode gap. These relationships may be used to linearize the controller feedback signal. An estimate of electrode gap may then be obtained by forming a weighted sum of the independent gap estimates obtained from the voltage and drip-short signals. By using multiple independent measures to estimate the gap, a controller that is less susceptible to process disturbances can be developed. Such a controller was designed, built and tested. The tests were carried out at Allvac Corporation during VAR of 12Cr steel at intermediate current levels

Dysfunctional BMPR2 signaling drives an abnormal endothelial requirement for glutamine in pulmonary arterial hypertension

Pulmonary arterial hypertension (PAH) is increasingly recognized as a systemic disease driven by alteration in the normal functioning of multiple metabolic pathways affecting all of the major carbon substrates, including amino acids. We found that human pulmonary hypertension patients (WHO Group I, PAH) exhibit systemic and pulmonary-specific alterations in glutamine metabolism, with the diseased pulmonary vasculature taking up significantly more glutamine than that of controls. Using cell culture models and transgenic mice expressing PAH-causing BMPR2 mutations, we found that the pulmonary endothelium in PAH shunts significantly more glutamine carbon into the tricarboxylic acid (TCA) cycle than wild-type endothelium. Increased glutamine metabolism through the TCA cycle is required by the endothelium in PAH to survive, to sustain normal energetics, and to manifest the hyperproliferative phenotype characteristic of disease. The strict requirement for glutamine is driven by loss of sirtuin-3 (SIRT3) activity through covalent modification by reactive products of lipid peroxidation. Using 2-hydroxybenzylamine, a scavenger of reactive lipid peroxidation products, we were able to preserve SIRT3 function, to normalize glutamine metabolism, and to prevent the development of PAH in BMPR2 mutant mice. In PAH, targeting glutamine metabolism and the mechanisms that underlie glutamine-driven metabolic reprogramming represent a viable novel avenue for the development of potentially disease-modifying therapeutics that could be rapidly translated to human studies

Utility of echocardiography in predicting mortality in infants with severe bronchopulmonary dysplasia

This article is made available for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.Objective: To determine the relationship between interventricular septal position (SP) and right ventricular systolic pressure (RVSP) and mortality in infants with severe BPD (sBPD). Study design: Infants with sBPD in the Children's Hospitals Neonatal Database who had echocardiograms 34-44 weeks' postmenstrual age (PMA) were included. SP and RVSP were categorized normal, abnormal (flattened/bowed SP or RVSP > 40 mmHg) or missing. Results: Of 1157 infants, 115 infants (10%) died. Abnormal SP or RVSP increased mortality (SP 19% vs. 8% normal/missing, RVSP 20% vs. 9% normal/missing, both p < 0.01) in unadjusted and multivariable models, adjusted for significant covariates (SP OR 1.9, 95% CI 1.2-3.0; RVSP OR 2.2, 95% CI 1.1-4.7). Abnormal parameters had high specificity (SP 82%; RVSP 94%), and negative predictive value (SP 94%, NPV 91%) for mortality. Conclusions: Abnormal SP or RVSP is independently associated with mortality in sBPD infants. Negative predictive values distinguish infants most likely to survive

Vitamin D levels and susceptibility to asthma, elevated immunoglobulin E levels, and atopic dermatitis: A Mendelian randomization study.

BACKGROUND: Low circulating vitamin D levels have been associated with risk of asthma, atopic dermatitis, and elevated total immunoglobulin E (IgE). These epidemiological associations, if true, would have public health importance, since vitamin D insufficiency is common and correctable. METHODS AND FINDINGS: We aimed to test whether genetically lowered vitamin D levels were associated with risk of asthma, atopic dermatitis, or elevated serum IgE levels, using Mendelian randomization (MR) methodology to control bias owing to confounding and reverse causation. The study employed data from the UK Biobank resource and from the SUNLIGHT, GABRIEL and EAGLE eczema consortia. Using four single-nucleotide polymorphisms (SNPs) strongly associated with 25-hydroxyvitamin D (25OHD) levels in 33,996 individuals, we conducted MR studies to estimate the effect of lowered 25OHD on the risk of asthma (n = 146,761), childhood onset asthma (n = 15,008), atopic dermatitis (n = 40,835), and elevated IgE level (n = 12,853) and tested MR assumptions in sensitivity analyses. None of the four 25OHD-lowering alleles were associated with asthma, atopic dermatitis, or elevated IgE levels (p ≥ 0.2). The MR odds ratio per standard deviation decrease in log-transformed 25OHD was 1.03 (95% confidence interval [CI] 0.90-1.19, p = 0.63) for asthma, 0.95 (95% CI 0.69-1.31, p = 0.76) for childhood-onset asthma, and 1.12 (95% CI 0.92-1.37, p = 0.27) for atopic dermatitis, and the effect size on log-transformed IgE levels was -0.40 (95% CI -1.65 to 0.85, p = 0.54). These results persisted in sensitivity analyses assessing population stratification and pleiotropy and vitamin D synthesis and metabolism pathways. The main limitations of this study are that the findings do not exclude an association between the studied outcomes and 1,25-dihydoxyvitamin D, the active form of vitamin D, the study was underpowered to detect effects smaller than an OR of 1.33 for childhood asthma, and the analyses were restricted to white populations of European ancestry. This research has been conducted using the UK Biobank Resource and data from the SUNLIGHT, GABRIEL and EAGLE Eczema consortia. CONCLUSIONS: In this study, we found no evidence that genetically determined reduction in 25OHD levels conferred an increased risk of asthma, atopic dermatitis, or elevated total serum IgE, suggesting that efforts to increase vitamin D are unlikely to reduce risks of atopic disease

Environmental effects of ozone depletion, UV radiation and interactions with climate change : UNEP Environmental Effects Assessment Panel, update 2017

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