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您的检索式：作者名="Taylor Neumann"
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| 1 | Flexible thermoelectric generator with liquid metal interconnects and low thermal conductivity silicone filler显示文摘Harvesting body heat using thermoelectricity provides a promising path to realizing self-powered,wearable electronics that can achieve continuous,long-term,uninterrupted health monitoring.This paper reports a flexible thermoelectric generator(TEG)that provides efficient conversion of body heat to electrical energy.The device relies on a low thermal conductivity aerogel–silicone composite that secures and thermally isolates the individual semiconductor elements that are connected in series using stretchable eutectic gallium-indium(EGaIn)liquid metal interconnects.The composite consists of aerogel particulates mixed into polydimethylsiloxane(PDMS)providing as much as 50%reduction in the thermal conductivity of the silicone elastomer.Worn on the wrist,the flexible TEGs present output power density figures approaching 35μWcm^(−2)at an air velocity of 1.2 ms^(−1),equivalent to walking speed.The results suggest that these flexible TEGs can serve as the main energy source for low-power wearable electronics. | Viswanath Padmanabhan Ramesh Yasaman Sargolzaeiaval Taylor Neumann Veena Misra Daryoosh Vashaee Michael D.Dickey Mehmet C.Ozturk | 2021 | npj Flexible Electronics2021，5，1： | 3 |
| 2 | Disrupted Ca^(2+) h homeostasis and immunodeficiency in patients with functional IP_(3) receptor subtype 3 defects显示文摘Calcium signaling is essential for lymphocyte activation, with genetic disruptions of store-operated calcium (Ca^(2+)) entry resulting in severe immunodeficiency. The inositol 1,4,5-trisphosphate receptor (IP_(3)R), a homo- or heterotetramer of the IP_(3)R1-3 isoforms, amplifies lymphocyte signaling by releasing Ca^(2+) from endoplasmic reticulum stores following antigen stimulation. Although knockout of all IP_(3)R isoforms in mice causes immunodeficiency, the seeming redundancy of the isoforms is thought to explain the absence of variants in human immunodeficiency. In this study, we identified compound heterozygous variants of ITPR3 (a gene encoding IP_(3)R subtype 3) in two unrelated Caucasian patients presenting with immunodeficiency. To determine whether ITPR3 variants act in a nonredundant manner and disrupt human immune responses, we characterized the Ca^(2+) signaling capacity, the lymphocyte response, and the clinical phenotype of these patients. We observed disrupted Ca^(2+) signaling in patient-derived fibroblasts and immune cells, with abnormal proliferation and activation responses following T-cell receptor stimulation. Reconstitution of IP_(3)R3 in IP_(3)R knockout cell lines led to the identification of variants as functional hypomorphs that showed reduced ability to discriminate between homeostatic and induced states, validating a genotype–phenotype link. These results demonstrate a functional link between defective endoplasmic reticulum Ca^(2+) channels and immunodeficiency and identify IP_(3)Rs as diagnostic targets for patients with specific inborn errors of immunity. These results also extend the known cause of Ca^(2+)-associated immunodeficiency from store-operated entry to impaired Ca^(2+) mobilization from the endoplasmic reticulum, revealing a broad sensitivity of lymphocytes to genetic defects in Ca^(2+) signaling. | Julika Neumann Erika Van Nieuwenhove Lara E.Terry Frederik Staels Taylor R.Knebel Kirsten Welkenhuyzen Kourosh Ahmadzadeh Mariah R.Baker Margaux Gerbaux Mathijs Willemsen John S.Barber Irina I.Serysheva Liesbeth De Waele François Vermeulen Susan Schlenner Isabelle Meyts David IYule Geert Bultynck Rik Schrijvers Stephanie Humblet-Baron Adrian Liston | 2023 | Cellular & Molecular Immunology2023，20，1： | 0 |
| 3 | Author Correction: Disrupted Ca2+ homeostasis and immunodeficiency in patients with functional IP3 receptor subtype 3 defects显示文摘In this article the statement in the Acknowledgements section was incorrectly given as “MRB and IIS are supported by the NIH R01GM080139 grant (to IIS), the Welch Foundation Research Grant AU-2014-20190331 (to IIS), and the American Heart Association grant 18CDA34110086 (to MRB)” and should have been, “MRB and IIS are supported by the NIH R01GM072804 grant (to IIS), the Welch Foundation Research Grant AU-2014-20190331 (to IIS), and the American Heart Association grant 18CDA34110086 (to MRB).” | Julika Neumann Erika Van Nieuwenhove Lara E.Terry Frederik Staels Taylor R.Knebel Kirsten Welkenhuyzen Kourosh Ahmadzadeh Mariah R.Baker Margaux Gerbaux Mathijs Willemsen John S.Barber Irina I.Serysheva Liesbeth De Waele François Vermeulen Susan Schlenner Isabelle Meyts David I.Yule Geert Bultynck Rik Schrijvers Stephanie Humblet-Baron Adrian Liston | 2023 | Cellular & Molecular Immunology2023，20，1： | 0 |
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