Utilization of Chicken Eggshell Waste: A Potential Calcium Source for Incorporation into Vegetable Soup Mix

Calcium, an important mineral in bones, is widely available in the form of calcium carbonate (CaCO₃) in eggshells. However, tonnes of eggshells have been wasted every year all around the globe. The current work was aimed at valorizing the eggshell waste and incorporating it as an alternative Ca source for calcium deficient people. Soup mixes (named 1-5) were formulated by varying the ratio of starch (4-12 g) and vegetables (2-10 g) along with the constant quantity of mushroom and eggshell powder. The formulated soup mix was assessed for physiochemical properties and proximate analysis. The results showed that the soup mix 4 with 4 g vegetables, 10 g corn starch, 1 g onion, and garlic, 2 g salt and sugar, 2 g mushroom, and 1 g eggshell powder was found similar to the commercial soup mix along with 3069.095 mg/kg calcium content which meets individuals' RDA requirement. The results suggest that the formulated soup mix can act as a proper preload for all individuals and is used as a supplement for commercial calcium foods. Further research is required to increase the soup's acceptability, its bioavailability, and shelf stability

Quantification and Verification of Cardiorespiratory Fitness in Adults with Prehypertension

Background: Low cardiorespiratory fitness is associated with increased risk of hypertension and atherosclerosis in adults with prehypertension. The purpose of this study was to quantify cardiorespiratory fitness and to examine the utility of supramaximal constant-load verification testing for validating maximal oxygen uptake (VO2max) attainment in adults with prehypertension. Methods: Eleven adults (four women) with prehypertension (22.5 +/- 2.9 y; body mass index (BMI): 24.6 +/- 3.2 kg center dot m(2)) underwent an incremental exercise test followed 15 min later by a verification test at 105% of maximal work rate on a cycle ergometer. Results: There was no statistical difference in VO2 between the incremental (2.23 +/- 0.54 L center dot min(-1)) and verification tests (2.28 +/- 0.54 L center dot min(-1); p = 0.180). Only three out of eleven participants had a higher VO2 during the verification when compared with the incremental test. If the verification test had not been conducted, one participant would have been incorrectly classified as having low cardiorespiratory fitness based on incremental test results alone. Conclusions: Verification testing validates the attainment of VO2max and can potentially reduce the over-diagnosis of functional impairment (i.e., deconditioning) in adults with prehypertension

Frameshift Mutagenesis and Microsatellite Instability Induced by Human Alkyladenine DNA Glycosylase

Human alkyladenine DNA glycosylase (hAAG) excises alkylated purines, hypoxanthine, and etheno bases from DNA to form abasic (AP) sites. Surprisingly, elevated expression of hAAG increases spontaneous frameshift mutagenesis. By random mutagenesis of eight active site residues, we isolated hAAG-Y127I/H136L double mutant that induces even higher rates of frameshift mutation than does the wild-type hAAG; the Y127I mutation accounts for the majority of the hAAG-Y127I/H136L-induced mutator phenotype. The hAAG-Y127I/H136L and hAAG-Y127I mutants increased the rate of spontaneous frameshifts by up to 120-fold in S. cerevisiae and also induced high rates of microsatellite instability (MSI) in human cells. hAAG and its mutants bind DNA containing one and two base-pair loops with significant affinity, thus shielding them from mismatch repair; the strength of such binding correlates with their ability to induce the mutator phenotype. This study provides important insights into the mechanism of hAAG-induced genomic instability.National Institutes of Health (U.S.) (Grant CA055042)National Institutes of Health (U.S.) (Grant CA115802)National Institutes of Health (U.S.) (Grant ES02109

Aag DNA Glycosylase Promotes Alkylation-Induced Tissue Damage Mediated by Parp1

Alkylating agents comprise a major class of front-line cancer chemotherapeutic compounds, and while these agents effectively kill tumor cells, they also damage healthy tissues. Although base excision repair (BER) is essential in repairing DNA alkylation damage, under certain conditions, initiation of BER can be detrimental. Here we illustrate that the alkyladenine DNA glycosylase (AAG) mediates alkylation-induced tissue damage and whole-animal lethality following exposure to alkylating agents. Aag-dependent tissue damage, as observed in cerebellar granule cells, splenocytes, thymocytes, bone marrow cells, pancreatic β-cells, and retinal photoreceptor cells, was detected in wild-type mice, exacerbated in Aag transgenic mice, and completely suppressed in Aag−/− mice. Additional genetic experiments dissected the effects of modulating both BER and Parp1 on alkylation sensitivity in mice and determined that Aag acts upstream of Parp1 in alkylation-induced tissue damage; in fact, cytotoxicity in WT and Aag transgenic mice was abrogated in the absence of Parp1. These results provide in vivo evidence that Aag-initiated BER may play a critical role in determining the side-effects of alkylating agent chemotherapies and that Parp1 plays a crucial role in Aag-mediated tissue damage.National Institutes of Health (U.S.) (NIH grant R01-CA075576)National Institutes of Health (U.S.) (NIH grant R01-CA055042)National Institutes of Health (U.S.) (NIH grant R01-CA149261)National Institutes of Health (U.S.) (NIH grant P30-ES00002)National Institutes of Health (U.S.) (NIH grant P30-ES02109)National Center for Research Resources (U.S.) (grant number M01RR-01066)National Center for Research Resources (U.S.) (grant number UL1 RR025758, Harvard Clinical and Translational Science Center

Epicardial cells derived from human embryonic stem cells augment cardiomyocyte-driven heart regeneration.

The epicardium and its derivatives provide trophic and structural support for the developing and adult heart. Here we tested the ability of human embryonic stem cell (hESC)-derived epicardium to augment the structure and function of engineered heart tissue in vitro and to improve efficacy of hESC-cardiomyocyte grafts in infarcted athymic rat hearts. Epicardial cells markedly enhanced the contractility, myofibril structure and calcium handling of human engineered heart tissues, while reducing passive stiffness compared with mesenchymal stromal cells. Transplanted epicardial cells formed persistent fibroblast grafts in infarcted hearts. Cotransplantation of hESC-derived epicardial cells and cardiomyocytes doubled graft cardiomyocyte proliferation rates in vivo, resulting in 2.6-fold greater cardiac graft size and simultaneously augmenting graft and host vascularization. Notably, cotransplantation improved systolic function compared with hearts receiving either cardiomyocytes alone, epicardial cells alone or vehicle. The ability of epicardial cells to enhance cardiac graft size and function makes them a promising adjuvant therapeutic for cardiac repair.: This work was supported by the British Heart Foundation (BHF; Grants NH/11/1/28922, G1000847, FS/13/29/30024 and FS/18/46/33663), Oxford-Cambridge Centre for Regenerative Medicine (RM/13/3/30159), the UK Medical Research Council (MRC) and the Cambridge Hospitals National Institute for Health Research Biomedical Research Centre funding (SS), as well as National Institutes of Health Grants P01HL094374, P01GM081619, R01HL12836 and a grant from the Fondation Leducq Transatlantic Network of Excellence (CEM). J.B. was supported by a Cambridge National Institute for Health Research Biomedical Research Centre Cardiovascular Clinical Research Fellowship and subsequently, by a BHF Studentship (Grant FS/13/65/30441). DI received a University of Cambridge Commonwealth Scholarship. LG is supported by BHF Award RM/l3/3/30159 and LPO is funded by a Wellcome Trust Fellowship (203568/Z/16/Z). NF was supported by BHF grants RG/13/14/30314. NL was supported by the Biotechnology and Biological Sciences Research Council (Institute Strategic Programmes BBS/E/B/000C0419 and BBS/E/B/000C0434). SS and MB were supported by the British Heart Foundation Centre for Cardiovascular Research Excellence. Core support was provided by the Wellcome-MRC Cambridge Stem Cell Institute (203151/Z/16/Z), The authors thank Osiris for provision of the primary mesenchymal stem cells (59

The James Webb Space Telescope Mission

Twenty-six years ago a small committee report, building on earlier studies, expounded a compelling and poetic vision for the future of astronomy, calling for an infrared-optimized space telescope with an aperture of at least $4m$. With the support of their governments in the US, Europe, and Canada, 20,000 people realized that vision as the $6.5m$ James Webb Space Telescope. A generation of astronomers will celebrate their accomplishments for the life of the mission, potentially as long as 20 years, and beyond. This report and the scientific discoveries that follow are extended thank-you notes to the 20,000 team members. The telescope is working perfectly, with much better image quality than expected. In this and accompanying papers, we give a brief history, describe the observatory, outline its objectives and current observing program, and discuss the inventions and people who made it possible. We cite detailed reports on the design and the measured performance on orbit.Comment: Accepted by PASP for the special issue on The James Webb Space Telescope Overview, 29 pages, 4 figure

Quantification and Verification of Cardiorespiratory Fitness in Adults with Prehypertension

Background: Low cardiorespiratory fitness is associated with increased risk of hypertension and atherosclerosis in adults with prehypertension. The purpose of this study was to quantify cardiorespiratory fitness and to examine the utility of supramaximal constant-load verification testing for validating maximal oxygen uptake (VO2max) attainment in adults with prehypertension. Methods: Eleven adults (four women) with prehypertension (22.5 ± 2.9 y; body mass index (BMI): 24.6 ± 3.2 kg·m2) underwent an incremental exercise test followed 15 min later by a verification test at 105% of maximal work rate on a cycle ergometer. Results: There was no statistical difference in VO2 between the incremental (2.23 ± 0.54 L·min−1) and verification tests (2.28 ± 0.54 L·min−1; p = 0.180). Only three out of eleven participants had a higher VO2 during the verification when compared with the incremental test. If the verification test had not been conducted, one participant would have been incorrectly classified as having low cardiorespiratory fitness based on incremental test results alone. Conclusions: Verification testing validates the attainment of VO2max and can potentially reduce the over-diagnosis of functional impairment (i.e., deconditioning) in adults with prehypertension