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Human Mate Poaching Tactics Are Effective: Evidence From a Dyadic Prospective Study on Opposite-Sex "Friendships"

SOCIAL PSYCHOLOGICAL AND PERSONALITY SCIENCE 2016年第4期7卷 374-380页

作者： Lemay, Edward Paul, Jr. Wolf, Noah R. Univ Maryland Biol Psychol Bldg College Pk MD 20742 USA Univ Maryland Social Decis & Org Sci PhD Program College Pk MD 20742 USA

Mate poaching refers to efforts to attract people who are already involved in committed relationships. The current dyadic, 5-week prospective study examined mate poaching behaviors in the context of opposite-sex friendships. Actors' mate poaching behaviors predicted decreases in their friend's commitment to their romantic partners, increases in their friend's perceptions of actors' mate value, and increases in their friend's romantic desire for actors over time. These results are the first to suggest an interpersonal process in which mate poaching behaviors elicit psychological changes in targets that facilitate actors' mate poaching goals. Furthermore, these results are the first to demonstrate the effectiveness of mate poaching tactics in friendships.

关键词： mate poaching evolutionary psychology friendship romantic relationships commitment

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CARMA1 Regulation of Regulatory T Cell Development Involves Modulation of Interleukin-2 Receptor Signaling

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JOURNAL OF BIOLOGICAL CHEMISTRY 2010年第21期285卷 15696-15703页

作者： Lee, Andrew Joon Wu, Xuefeng Cheng, Hanyin Zhou, Xiaofei Cheng, Xuhong Sun, Shao-Cong Univ Texas MD Anderson Canc Ctr Dept Immunol Houston TX 77030 USA Univ Texas Grad Sch Biomed Sci Houston Houston TX 77030 USA Penn State Univ Coll Med MD PhD Program Hershey PA 17033 USA

T cell receptor-stimulated NF-kappa B activation requires CARMA1 and is negatively regulated by the deubiquitinase CYLD. Recent studies suggest that CARMA1 regulates regulatory T cell (Treg) development, although the role of NF-kappa B in this event is incompletely understood. We show that CYLD deficiency causes constitutive NF-kappa B activation in thymocytes, which is associated with enhanced frequency of Treg cells. The NF-kappa B activation in CYLD-deficient thymocytes is independent of CARMA1, because the NF-kappa B activation was also detected in CYLD/CARMA1 double knock-out thymocytes. Interestingly, although loss of CYLD causes NF-kappa B activation in the CARMA1-deficient thymocytes, the CYLD deficiency fails to rescue the defect of CARMA1 knock-out mice in Treg development. Furthermore, inhibition of canonical NF-kappa B by an I kappa B alpha transgene only partially inhibits Treg development. We demonstrate that CARMA1 regulates IL-2 receptor signaling and controls the IL-2-stimulated maturation of Treg precursors to mature Tregs. These results suggest that the role of CARMA1 in Treg regulation involves both NF-kappa B activation and IL-2 receptor signaling.

关键词： T cells NF-kappa B (DNA-binding protein) INTERLEUKIN-2 MICE as laboratory animals CELLS

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BEDSIDE CARDIAC ULTRASOUND: SUPRASTERNAL NOTCH VIEW-DETECTED PULMONARY ARTERY CLOT IN TRANSIT

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JOURNAL OF EMERGENCY MEDICINE 2020年第2期58卷 E93-E94页

作者： Nwanaji-Enwerem, Jamaji C. Bernier, Denie Lipsitz, Mindy C. Harvard Med Sch MD PhD Program Boston MA 02115 USA Harvard Med Sch Brigham & Womens Hosp Dept Emergency Med Boston MA 02115 USA

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Evidence for an interaction of the metalloprotease-disintegrin tumour necrosis factor α convertase (TACE) with mitotic arrest deficient 2 (MAD2), and of the metalloprotease-disintegrin mdC9 with a novel MAD2-related protein, MAD2β

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BIOCHEMICAL JOURNAL 1999年第Pt 3期343卷 673-680页

作者： Nelson, KK Schlöndorff, J Blobel, CP Mem Sloan Kettering Canc Ctr Sloane Kettering Inst Cellular Biochem & Biophys Program New York NY 10021 USA Cornell Univ Rochester Univ Mem Sloan Kettering Canc Ctr Triinst MD PhD Training Program New York NY 10021 USA

Metalloprotease-disintegrins are a family of transmembrane glycoproteins that have a role in fertilization, sperm migration, myoblast fusion, neural development and ectodomain shedding. In the present study we used the yeast two-hybrid system to search for proteins that interact with the cytoplasmic domain of two metalloproteas-disintegrins, tumour necrosis factor alpha convertase (TACE;ADAM17) and mdC9 (ADAM9;meltrin gamma). We have identified mitotic arrest deficient 2 (MAD2) as a binding partner of the TACE cytoplasmic domain, and a novel MAD2-related protein, MAD2 beta, as a binding partner of the mdC9 cytoplasmic domain. MAD2 beta has 23% sequence identity with MAD2, which is a component of the spindle assembly (or mitotic) checkpoint mechanism. Northern blot analysis of human tissues indicates that MAD2 beta mRNA is expressed ubiquitously. The interaction of the TACE and mdC9 cytoplasmic domains with their binding partners has been confirmed biochemically. The independent identification of MAD2 and MAD2 beta as potential interacting partners of distinct metalloprotease-disintegrins raises the possibility of a link between metalloprotease-disintegrins and the cell cycle, or of functions for MAD2 and MAD2 beta that are not related to cell cycle control.

关键词： ADAMs MAD2 mdC9 TACE yeast two-hybrid screen

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Accounting for future populations in health research

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BIOETHICS 2024年第5期38卷 401-409页

作者： Pierson, Leah Harvard Med Sch Harvard MIT MD PhD Program Boston MA 02115 USA Harvard TH Chan Sch Publ Hlth Dept Global Hlth & Populat Boston MA USA

The research we fund today will improve the health of people who will live tomorrow. But future people will not all benefit equally: decisions we make about what research to prioritize will predictably affect when and how much different people benefit from research. Organizations that fund health research should thus fairly account for the health needs of future populations when setting priorities. To this end, some research funders aim to allocate research resources in accordance with disease burden, prioritizing illnesses that cause more morbidity and mortality. In this article, I defend research funders' practice of aligning research funding with disease burden but argue that funders should aim to align research funding with future-rather than present-disease burden. I suggest that research funders should allocate research funding in proportion to aggregated estimates of disease burden over the period when research could plausibly start to yield benefits until indefinitely into the future.

关键词： disease burden health policy longtermism priority setting resource allocation

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IMPROVING CRYSTALLOGRAPHIC MACROMOLECULAR IMAGES - THE REAL-SPACE APPROACH

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ANNUAL REVIEW OF BIOPHYSICS AND BIOPHYSICAL CHEMISTRY 1987年第1期16卷 351-373页

作者： PODJARNY, AD BHAT, TN ZWICK, M UNIV CHICAGO DEPT BIOCHEM & MOLEC BIOLCHICAGOIL 60637 PORTLAND STATE UNIV SYST SCI PHD PROGRAMPORTLANDOR 97207 NIDDK MOLEC BIOL LABBETHESDAMD 20892

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Dysregulation of mTOR signalling is a converging mechanism in lissencephaly

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NATURE 2025年第8049期638卷 1-10页

作者： Zhang, Ce Liang, Dan Ercan-Sencicek, A. Gulhan Bulut, Aybike S. Cortes, Joelly Cheng, Iris Q. Henegariu, Octavian Nishimura, Sayoko Wang, Xinyuan Peksen, A. Buket Takeo, Yutaka Caglar, Caner Lam, TuKiet T. Koroglu, Merve Nur Narayanan, Anand Lopez-Giraldez, Francesc Miyagishima, Danielle F. Mishra-Gorur, Ketu Barak, Tanyeri Yasuno, Katsuhito Erson-Omay, E. Zeynep Yalcinkaya, Cengiz Wang, Guilin Mane, Shrikant Kaymakcalan, Hande Guzel, Aslan Caglayan, A. Okay Tuysuz, Beyhan Sestan, Nenad Gunel, Murat Louvi, Angeliki Bilguvar, Kaya Yale Univ Interdept Neurosci Program New Haven CT USA Yale Sch Med MD PhD Program New Haven CT USA Yale Sch Med Dept Neurosci New Haven CT 06520 USA Yale Sch Med Dept Neurosurg New Haven CT 06520 USA Yale Sch Med Yale Program Neurogenet New Haven CT 06510 USA Acibadem Univ Hlth Sci Inst Dept Genome Studies Istanbul Turkiye Brigham & Womens Hosp Dept Neurol Boston MA USA Harvard Med Sch Boston MA USA Yale Sch Med Keck MS & Prote Resource New Haven CT USA Yale Univ Dept Mol Biophys & Biochem New Haven CT USA Acibadem Univ Hlth Sci Inst Dept Biostat & Bioinformat Istanbul Turkiye Yale Univ Yale Ctr Genome Anal New Haven CT 06520 USA Yale Sch Med Dept Genet New Haven CT 06520 USA Yale Sch Med Dept Biomed Informat & Data Sci New Haven CT USA Istanbul Univ Cerrahpasa Cerrahpasa Med Sch Dept Neurol Istanbul Turkiye Yale Sch Med Keck Microarray Shared Resource New Haven CT USA Acibadem Univ Hlth Sci Inst Dept Translat Med Istanbul Turkiye Bahcesehir Univ Fac Med Dept Neurosurg Istanbul Turkiye Med Point Hosp Dept Neurosurg Gaziantep Turkiye Dokuz Eylul Univ Fac Med Dept Med Genet Izmir Turkiye Dokuz Eylul Univ Inst Hlth Sci Dept Mol Med Izmir Turkiye Yale Sch Med Dept Comparat Med New Haven CT USA Yale Sch Med Dept Psychiat New Haven CT USA Yale Sch Med Kavli Inst Neurosci New Haven CT USA Yale Sch Med Yale Program Brain Tumor Res New Haven CT 06510 USA Yale Sch Med Yale Canc Ctr New Haven CT 06510 USA Acibadem Univ Sch Med Dept Med Genet Istanbul Turkiye Acibadem Univ Rare Dis & Orphan Drugs Applicat & Res Ctr ACURARE Istanbul Turkiye Bexorg Inc New Haven CT USA Bezmialem Vakif Univ Beykoz Inst Life Sci & Biotechnol Dept Mol Biol Istanbul Turkiye

Cerebral cortex development in humans is a highly complex and orchestrated process that is under tight genetic regulation. Rare mutations that alter gene expression or function can disrupt the structure of the cerebral cortex, resulting in a range of neurological conditions1. Lissencephaly ('smooth brain') spectrum disorders comprise a group of rare, genetically heterogeneous congenital brain malformations commonly associated with epilepsy and intellectual disability2. However, the molecular mechanisms underlying disease pathogenesis remain unknown. Here we establish hypoactivity of the mTOR pathway as a clinically relevant molecular mechanism in lissencephaly spectrum disorders. We characterized two types of cerebral organoid derived from individuals with genetically distinct lissencephalies with a recessive mutation in p53-induced death domain protein 1 (PIDD1) or a heterozygous chromosome 17p13.3 microdeletion leading to Miller-Dieker lissencephaly syndrome (mdLS). PIDD1-mutant organoids and mdLS organoids recapitulated the thickened cortex typical of human lissencephaly and demonstrated dysregulation of protein translation, metabolism and the mTOR pathway. A brain-selective activator of mTOR complex 1 prevented and reversed cellular and molecular defects in the lissencephaly organoids. Our findings show that a converging molecular mechanism contributes to two genetically distinct lissencephaly spectrum disorders.

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Clinical and In Vitro Evidence That Subclinical Hemolysis Contributes to LVAD Thrombosis

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ANNALS OF THORACIC SURGERY 2018年第3期105卷 807-814页

作者： Bartoli, Carlo R. Zhang, David Kang, Jooeun Hennessy-Strahs, Samson Restle, David Howard, Jessica Redline, Gretchen Bermudez, Christian Atluri, Pavan Acker, Michael A. Hosp Univ Penn Div Cardiovasc Surg Hill PavilRm 410B Philadelphia PA 19104 USA Washington Univ MD PhD Program St Louis MO USA Vanderbilt Univ Sch Med MD PhD Program Nashville TN 37212 USA SUNY Stony Brook Hlth Sci Ctr Sch Med Stony Brook NY 11794 USA

Background. Recent data suggest that hemolysis contributes to left ventricular assist device (LVAD) thrombosis, but the mechanism is unknown. In a clinical study, we measured plasma free hemoglobin (pfHgb) and the incidence of LVAD thrombosis. In an in vitro study, we examined biophysical relationships between shear stress, pfHgb and von Willebrand factor (vWF) metabolism toward understanding mechanisms of LVAD thrombosis. Methods. In the clinical study, blood samples were obtained from continuous-flow LVAD patients (n = 30). Plasma free hemoglobin was measured via enzyme-linked immunosorbent assay. Plasma lactate dehydrogenase (LDH) was measured with a fluorimetric assay. In the in vitro study, to investigate mechanism, human plasma (n[10) was exposed to LVAD-like shear stress (175 dyne/cm2) with and without free hemoglobin (30 mg/dL). ADAMTS-13 (the vWF protease) activity was quantified with Forster resonance energy transfer. vWF size was quantified with immunoblotting. vWF clotting function was quantified with an enzyme-linked immunosorbent assay. Results. In the clinical study, LVAD support caused subclinical hemolysis. In all patients, LDH increased significantly from 213 +/- 9 U/L to 366 +/- 31 U/L at 10 days of support (p < 0.0001) and remained significantly elevated at 280 +/- 18 U/L at 1 month of support (p < 0.01). In 21 patients that did not develop LVAD thrombosis, pfHgb increased early but decreased over time (pre-LVAD: 5.2 +/- 0.8 mg/dL;1 week: 19.8 +/- 4.4 mg/dL, p < 0.01;3 months: 9.3 +/- 2.2 mg/dL, p = 0.07). In 9 patients that developed LVAD thrombosis, pfHgb was significantly elevated versus patients without thrombosis before (p < 0.001) and after 3 months (p < 0.05) of support (pre-LVAD: 20.2 +/- 6.3 mg/dL;1 week: 17.3 +/- 3.7 mg/dL;3 months: 21.5 +/- 7.8 mg/dL). Similarly, after 3 months, patients that did not develop LVAD thrombosis had an LDH of 271 +/- 28 U/L, whereas patients that later developed LVAD thrombosis had a significantly higher LD

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ATR blocks telomerase from converting DNA breaks into telomeres

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SCIENCE 2024年第6684期383卷 763-770页

作者： Kinzig, Charles G. Zakusilo, George Takai, Kaori K. Myler, Logan R. de Lange, Titia Rockefeller Univ Lab Cell Biol & Genet New York NY 10065 USA Weill Cornell Rockefeller Sloan Kettering Triinst MD PhD Program New York NY 10065 USA

Telomerase, the enzyme that maintains telomeres at natural chromosome ends, should be repressed at double-strand breaks (DSBs), where neotelomere formation can cause terminal truncations. We developed an assay to detect neotelomere formation at Cas9- or I-SceI-induced DSBs in human cells. Telomerase added telomeric repeats to DSBs, leading to interstitial telomeric repeat insertions or the formation of functional neotelomeres accompanied by terminal deletions. The threat that telomerase poses to genome integrity was minimized by ataxia telangiectasia and Rad3-related (ATR) kinase signaling, which inhibited telomerase at resected DSBs. In addition to acting at resected DSBs, telomerase used the extruded strand in the Cas9 enzyme-product complex as a primer for neotelomere formation. We propose that although neotelomere formation is detrimental in normal human cells, it may allow cancer cells to escape from breakage-fusion-bridge cycles.

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The Emergence of Network Activity Patterns in the Somatosensory Cortex-An Early Window to Autism Spectrum Disorders

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NEUROSCIENCE 2021年第0期466卷 298-309页

作者： Iannone, Andrew F. Garcia, Natalia V. De Marco Weill Cornell Med Ctr Neurogenet Brain & Mind Res Inst New York NY 10021 USA Sloan Kettering TriInst MD PhD Program New York NY 10021 USA

Across mammalian species, patterned activity in neural populations is a prominent feature of developing sensory cortices. Numerous studies have long appreciated the diversity of these patterns, characterizing their differences in spatial and temporal dynamics. In the murine somatosensory cortex, neuronal co-activation is thought to guide the formation of sensory maps and prepare the cortex for sensory processing after birth. While pioneering studies deftly utilized slice electrophysiology and unit recordings to characterize correlated activity, a detailed understanding of the underlying circuits remains poorly understood. More recently, advances in in vivo calcium imaging in awake mouse pups and increasing genetic tractability of neuronal types have allowed unprecedented manipulation of circuit components at select developmental timepoints. These novel approaches have proven fundamental in uncovering the identity of neurons engaged in correlated activity during development. In particular, recent studies have highlighted interneurons as key in refining the spatial extent and temporal progression of patterned activity. Here, we discuss how emergent synchronous activity across the first postnatal weeks is shaped by underlying gamma aminobutyric acid (GABA)ergic contributors in the somatosensory cortex. Further, the importance of participation in specific activity patterns per se for neuronal maturation and perdurance will be of particular highlight in this survey of recent literature. Finally, we underscore how aberrant neuronal synchrony and disrupted inhibitory interneuron activity underlie sensory perturbations in neurodevelopmental disorders, particularly Autism Spectrum Disorders (ASDs), emphasizing the importance of future investigative approaches that incorporate the spatiotemporal features of patterned activity alongside the cellular components to probe disordered circuit assembly. (c) 2021 IBRO. Published by Elsevier Ltd. All rights reserved.

关键词： development interneurons GABA network activity calcium imaging barrel cortex

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