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导读:2006年4月29日。97岁的哈佛大学经济系教授约翰·肯尼思·加尔布雷思辞世。这位高龄老人一生经历了20世纪几乎所有重大历史,并置身于那个时代许多重要的经济和政治分歧的中心。他著述颇丰,但其思想的巨大影响与引起的广泛争议在经济学界也首屈一指。这位被称作"美国的世纪经济学家"的学者一生致力于将经济学运用到美国人民的实际生活当中去,而非建立抽象深奥的理论模型。他那流畅的文笔、冷嘲式的幽默亦使经济学著作具有了妙趣横生的特点。

关键词：加尔布雷思经济学家哈佛大学肯尼思

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新冠红利真实存在吗

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商业周刊（中文版） 2021年第22期 7-8页

作者： stephanie flanders 王忠(译) 不详

衰退会对经济造成永久性损害:这是历史经验。不过,看到政府和企业面对新冠疫情冲击的反应如此迅速,一些人很想知道的是--这一次是否会有所不同。

关键词：永久性损害政府和企业真实存在

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How small could a pup sound？ The physical bases of signaling body size in harbor seals

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Current Zoology 2017年第4期63卷 457-465页

作者： Andrea RAVIGNANI stephanie GROSS Maxime GARCIA Ana RUBIO-GARCIA Bart DE BOER Veterinary & Research Department Sealcentre Pieterburen Hoofdstraat 94a Pieterburen AG 9968 The Netherlands Artificial Intelligence Laboratory Vrije Universiteit Brussel Pleinlaan 2 Brussels 1050 Belgium Language and Cognition Department Max Planck Institute for Psycholinguistics Wundtlaan 1 Nijmegen XD 6525 The Netherlands Institute for Terrestrial and Aquatic Wildlife Research University of Veterinary Medicine Hannover Foundation Werftstrasse 6 Buesum 25761 Germany ENES Lab/Neuro-PSI CNRS UMR9197 University of Lyon/Saint Etienne 23 rue Paul Michelon 42023 Saint-Etienne cedex 2 France

Vocal communication is a crucial aspect of animal behavior. The mechanism which most mammals use to vocalize relies on three anatomical components. First, air overpressure is generated inside the lower vocal tract. Second, as the airstream goes through the glottis, sound is produced via vocal fold vibration. Third, this sound is further filtered by the geometry and length of the upper vocal tract. Evidence from mammalian anatomy and bioacoustics suggests that some of these three components may covary with an animal's body size. The framework provided by acoustic allometry suggests that, because vocal tract length (VTL) is more strongly constrained by the growth of the body than vocal fold length (VFL), VTL generates more reliable acoustic cues to an animal's size. This hypothesis is often tested acoustically but rarely anatomically, especially in pinnipeds. Here, we test the anatomical bases of the acoustic allometry hypothesis in harbor seal pups . We dissected and measured vocal tract, vocal folds, and other anatomical features of 15 harbor seals post-mortem. We found that, while VTL correlates with body size, VFL does not. This suggests that, while body growth puts anatomical constraints on how vocalizations are filtered by harbor seals' vocal tract, no such constraints appear to exist on vocal folds, at least during puppyhood. It is particularly interesting to find anatomical constraints on harbor seals' vocal tracts, the same anatomical region partially enabling pups to produce individually distinctive vocalizations.

关键词：物理基础海豹声音信号传导港口解剖部位解剖学特征动物行为

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Disrupted Ca^(2+) h homeostasis and immunodeficiency in patients with functional IP_(3) receptor subtype 3 defects

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Cellular & Molecular Immunology 2023年第1期20卷 11-25页

作者： 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 VIB Center for Brain and Disease Research LeuvenBelgium Department of Microbiology and Immunology KU LeuvenLeuvenBelgium UZ Leuven LeuvenBelgium Department of Pharmacology and Physiology University of RochesterRochesterNY14526USA Laboratory of Molecular and Cellular Signaling Department of Cellular and Molecular MedicineLeuven KankerinstituutKU LeuvenLeuvenBelgium Laboratory of Immunobiology Department Microbiology and ImmunologyRega InstituteKU LeuvenLeuvenBelgium Department of Biochemistry and Molecular Biology Structural Biology Imaging CenterMcGovern Medical School at The University of Texas Health Science Center at HoustonHoustonTX77030USA Pediatric Department Academic Children Hospital Queen FabiolaUniversitéLibre de BruxellesBrusselsBelgium Department of Pediatric Neurology University Hospitals LeuvenLeuvenBelgium Department of Pulmonology University Hospitals LeuvenLeuvenBelgium Laboratory for Inborn Errors of Immunity Department of Immunology and MicrobiologyKU LeuvenLeuvenBelgium Laboratory for Allergy and Clinical Immunology and Immunogenetics Research Group Department of MicrobiologyImmunology and TransplantationKU LeuvenLeuvenBelgium Immunology Programme The Babraham InstituteBabraham Research CampusCambridgeCB223ATUK

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.

关键词： Primary immunodeficiency Calcium signalling Whole exome sequencing

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