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SSRN 2023年

作者： Zhang, Ziyang Melzer, Madeline E. Kiani, Karun Goyal, Yogesh Department of Cell and Developmental Biology Feinberg School of Medicine Northwestern University ChicagoIL United States Center for Synthetic Biology Northwestern University ChicagoIL United States Robert H. Lurie Comprehensive Cancer Center Northwestern University Feinberg School of Medicine ChicagoIL United States Medical Scientist Training Program Perelman School of Medicine University of Pennsylvania PhiladelphiaPA United States

Single-cell RNA sequencing datasets comprise true single cells, or singlets, in addition to cells that coalesce during the protocol, or doublets. Identifying singlets with high fidelity in single-cell RNA sequencing is necessary to avoid false negative and false positive discoveries. Although several methodologies have been proposed to infer true singlets and doublets, they typically rely on datasets being highly heterogeneous. Here we develop and apply singletCode, a computational framework that leverages datasets with synthetically introduced DNA barcodes for a hitherto unexplored application: to extract ground truth singlets. We demonstrate the feasibility of singlets extracted via singletCode to evaluate the performance and robustness of existing doublet detection methods. Our proof-of-concept analysis shows that existing doublet detection methods are not as sensitive as expected when tested on doublets simulated from experimentally realistic ground truth singlets. As DNA barcoded datasets are being increasingly reported, singletCode can identify singlets and inform rational choice of doublet detecting algorithms and their associated limitations. © 2023, The Authors. All rights reserved.

关键词： Genome

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P130: Case report: Phenotypic features among four first-degree relatives with 17q11.2 microduplication syndrome

Genetics in Medicine Open

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Genetics in Medicine Open 2023年第1期1卷 100159-100159页

作者： Catherine Bradley Haley Streff Weimin Bi Janice Smith Jill Rosenfeld Ronit Marom Department of Molecular and Human Genetics Baylor College of Medicine Baylor College of Medicine Medical Scientist Training Program Texas Children’s Hospital Baylor Genetics

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Correction to: Multistate and functional protein design using RoseTTAFold sequence space diffusion (Nature Biotechnology, (2024), 10.1038/s41587-024-02395-w)

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Nature Biotechnology 2024年

作者： Lisanza, Sidney Lyayuga Gershon, Jacob Merle Tipps, Samuel W. K. Sims, Jeremiah Nelson Arnoldt, Lucas Hendel, Samuel J. Simma, Miriam K. Liu, Ge Yase, Muna Wu, Hongwei Tharp, Claire D. Li, Xinting Kang, Alex Brackenbrough, Evans Bera, Asim K. Gerben, Stacey Wittmann, Bruce J. McShan, Andrew C. Baker, David Department of Biochemistry University of Washington SeattleWA United States Institute for Protein Design University of Washington SeattleWA United States Graduate Program in Biological Physics Structure and Design University of Washington SeattleWA United States Department of Molecular Engineering University of Washington SeattleWA United States Molecular & amp Cellular Biology Medical Scientist Training Program University of Washington SeattleWA United States Faculty of Engineering Sciences Heidelberg University Heidelberg Germany School of Chemistry and Biochemistry Georgia Institute of Technology AtlantaGA United States Office of the Chief Scientific Officer Microsoft RedmondWA United States Howard Hughes Medical Institute University of Washington SeattleWA United States

Correction to: Nature Biotechnologyhttps://***/10.1038/s41587-024-02395-w, published online 25 September 2024. In the version of the article initially published, in the key to Fig. 2f the colors were swapped and have now been amended so that "W guidance" is purple and "Unconditional" is grey. In Fig. 5a, the color of "Child B" has been corrected from pink to purple, and in Fig. 5d, "β-helix" has now been amended to "β-sheet". These corrections have been made to the HTML and PDF versions of the article. © The Author(s) 2024.

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IL17A mRNA Staining Distinguishes Palmoplantar Psoriasis from Hyperkeratotic Palmoplantar Eczema in Diagnostic Skin Biopsies

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JID Innovations 2023年第4期3卷 100189-100189页

作者： Chen, Jennifer S. Murphy, Michael J. Singh, Katelyn Wang, Alice Chow, Ryan D. Kim, Sa Rang Cohen, Jeffrey M. Ko, Christine J. Damsky, William Department of Dermatology Yale School of Medicine New Haven CT United States Medical Scientist Training Program Stony Brook University School of Medicine Stony Brook NY United States Department of Genetics Yale School of Medicine New Haven CT United States Department of Pathology Yale School of Medicine New Haven CT United States

Acral dermatoses, including hyperkeratotic palmoplantar eczema (HPE), palmoplantar psoriasis (PP), and mycosis fungoides palmaris et plantaris (MFPP), can be challenging to diagnose clinically and histopathologically. In this setting, cytokine biomarkers may be able to help provide diagnostic clarity. Therefore, we evaluated IL-17A, IFN-γ, and IL-13 expression in PP, HPE, and MFPP and compared their expression profiles with nonacral sites. We used biopsy specimens from the Yale Dermatopathology database, selecting cases of HPE (n = 12), PP (n = 8), MFPP (n = 8), normal acral skin (n = 9), nonacral eczema (n = 10), and nonacral psoriasis (n = 10) with classic clinical and histopathologic features. IL17A mRNA expression by RNA in situ hybridization differentiated PP (median score 63.1 [interquartile range 9.4–104.1]) from HPE (0.8 [0–6.0];P = 0.003), MFPP (0.6 [0–2.6];P = 0.003), and normal acral skin (0 [0–0];P < 0.001). Unexpectedly, both PP and HPE showed co-expression of IFNG and IL13 mRNA. In contrast, nonacral psoriasis and eczema showed divergent patterns of IFNG and IL13 mRNA expression. Taken together, we show that IL17A mRNA expression may be a useful biomarker of PP, and we further show that acral dermatoses exhibit distinct immunology compared to nonacral sites, with implications for clinical management. © 2023 The Authors

关键词： Cat catalog HPE hyperkeratotic palmoplantar eczema IHC immunohistochemistry MFPP mycosis fungoides palmaris et plantaris PP palmoplantar psoriasis RISH RNA in situ hybridization Th T helper

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PP01.100 KRAS / TP53 Co-Mutation is Associated with Increased Tumor Immunogenicity in Non-Small Cell Lung Cancer Patients

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Journal of Thoracic Oncology 2024年第7期19卷 e44-e44页

作者： Daniel R. Principe Mary M. Pasquinelli Ryan Nguyen Lawrence Feldman Frank Weinberg Medical Scientist Training Program University of Illinois College of Medicine Chicago IL Division of Pulmonary Critical Care Sleep and Allergy University of Illinois at Chicago Chicago Illinois Division of Hematology and Oncology University of Illinois Chicago and Translational Oncology Program University of Illinois Cancer Center

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BPS2025 - Disaggregation of biomolecular condensates by molecular chaperones is heterogeneous at the single-condensate level

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Biophysical Journal 2025年第3期124卷 415a-415a页

作者： Diangen Lin Kyle M. Lin David A. Drummond Allison H. Squires Harvard Graduate Program in Biophysics Harvard University Cambridge MA USA Graduate Program in Biophysical Sciences Medical Scientist Training Program University of Chicago Chicago IL USA Department of Biochemistry and Molecular Biology and Department of Medicine Section of Genetic Medicine University of Chicago Chicago IL USA Pritzker School of Molecular Engineering University of Chicago Chicago IL USA

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Systems genetic dissection of Alzheimer's disease brain gene expression networks

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Alzheimer's & dementia : the journal of the Alzheimer's Association 2021年第S2期17卷 e058716页

作者： Zhao, Pinghan Mangleburg, Carl Grant Al-Ramahi, Ismael Botas, Juan Shulman, Joshua M. Baylor College of Medicine TX Houston United States Jan and Dan Duncan Neurological Research Institute Texas Children's Hospital TX Houston United States Baylor College of Medicine Neuroscience Program TX Houston United States Baylor College of Medicine Medical Scientist Training Program TX Houston United States

BACKGROUND: Alzheimer's disease (AD) is the most prevalent cause of dementia. Large RNA-Sequencing data sets have provided detailed molecular profiles of AD, but they cannot differentiate causal vs. non-causal gene expression changes. METHOD: We combined bioinformatic prioritization of human data with genetic screens in Drosophila melanogaster to identify human brain transcriptional changes that exacerbate or ameliorate neurodegeneration induced by Tau or amyloid-β (Aβ), the proteins which form the hallmark pathologic aggregates that define AD. First, we used large, AD-associated coexpression networks derived from Accelerating Medicines Partnership (AMP)-AD human brain RNA-Seq data to nominate candidate AD drivers based on multiple bioinformatic criteria. We then tested nominated drivers for modification of Tau- or Aβ-induced neurodegeneration in vivo using a locomotor assay in Drosophila. For one module of our interest, PHGbrown, we analyzed its overlap with published differentially expressed gene (DEG) sets from mouse models to explore its potential functional roles in AD. Finally, we used the L1000 Connectivity Map database of perturbation-associated gene expression changes to select small molecules which either reverse or promote the implicated AD-associated gene expression signatures that are causally linked with disease progression. RESULT: Through our screen, we identified a module, PHGbrown, with 14 of its 27 prioritized genes (51.9%) significantly modifying Tau/Aβ neurotoxicity in our screen. We integrated our screen data with PHGbrown's module structure to identify a subnetwork containing genes involved in synaptic function including GRIN2A, GRIN2B, KCNJ6, GABRB2, and GABRB3. This synaptic subnetwork is downregulated in human AD and contains multiple loss-of-function suppressors of Tau/Aβ neurotoxicity. Interestingly, PHGbrown shows overlap and concordant down-regulation with published mouse models of excitotoxicity. Our results suggest that PHGbrown down-

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Tissue-Derived IL-33 Is a Critical Local Signal That Targets Th1 Cells in the Small Intestine to Sustain Graft Versus Host Disease in the Absence of IL-12

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BLOOD 2020年 136卷 1-2页

作者： Dwyer, Gaelen K. Mathews, Lisa R. Lucas, Anna Blazar, Bruce R. Shlomchik, Warren D. Turnquist, Heth Medical Scientist Training Program University of Pittsburgh Pittsburgh PA Department of Surgery University of Pittsburgh Pittsburgh PA Division of Pediatric Blood and Marrow Transplantation University of Minnesota Minneapolis MN Department of Medicine University of Pittsburgh Pittsburgh PA Division of Hematology and Oncology University of Pittsburgh Pittsburgh PA

Background: Graft vs. host disease (GVHD) remains a major complication of allogeneic stem cell transplantation (alloSCT). To create space for donor stem cells and prevent their rejection, alloSCT protocols rely on conditioning regimens involving chemotherapy, frequently combined with radiation. Interleukin (IL)-33 is a nuclear protein that is found in the secondary lymphoid organs and barrier tissues. IL-33 is augmented in recipient barrier tissues by conditioning. We have established that IL-33 is a clinically-relevant signal. While we have further elucidated that IL-33 is acting directly on donor T cells to augment GVHD, neither the critical place nor timing of IL-33 stimulation of donor T cells during the alloimmune response mediating GVHD have been defined. Methods: We used both IL-33 knockout mice as recipients and ST2 (IL33 receptor) knockout mice as T cell donors in MHC mismatch alloSCT models to define the spatial and temporal importance of IL-33 in GVHD tissue damage. More specifically, to establish the role of IL-33 in T cell effector function in the small intestine during GVHD, irradiated Il33 -/- and Il33 +/+ C57BL/6 (B6) recipients were given BALB/c bone marrow (BM) and T cells. Additionally, irradiated BALB/c mice were given St2 +/+ B6 BM and Cd4 Cre x St2 fl/fl or St2 -/- and St2 +/+ T cells. To determine the role of IL-33 on T cell persistence in GVHD, we used an MHCII-disparate model. Irradiated Il33 -/- and Il33 +/+ bm12 recipients were reconstituted with B6 BM, with or without CD90.1 + B6 T cells. Results: When donor T cell responses were characterized by flow cytometry at days 7, 14, and 28 post alloSCT, the bulk of these data suggest that IL-33 sustains CD4 + T helper Type 1 (Th1) cells in the barrier tissues at late points following GVHD initiation. Specifically, B6 Il33 -/- recipients had fewer BALB/c CD4 + Tbet + cells in the small intestine lamina propria (SI LP; WT 15.9 ± 1.31, KO 9.53 ± 1.32; p=0.03; n=3/group), but not in the spleen (WT 5

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Dexmedetomidine in the Treatment of Depression: An Up-to-date Narrative Review

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Clinical Practice and Epidemiology in Mental Health 2023年 19卷

作者： Al-Mahrouqi, Tamadhir Al Alawi, Mohammed Freire, Rafael C. Department of Behavioural Medicine Sultan Qaboos University Hospital Muscat Oman Psychiatry Residency Training Program Oman Medical Speciality Board Muscat Oman Department of Psychiatry and Centre for Neuroscience Studies Queens University Kingston Canada Laboratory of Panic and Respiration Institute of Psychiatry Federal University of Rio de Janeiro Rio de Janeiro Brazil

Depressive disorders (DD) are common, and their prevalence is expected to rise over the next decade. Depressive disorders are linked to significant morbidity and mortality. The clinical conundrum of depressive disorders lies in the heterogeneity of their phenomenology and etiology. Further, the currently available antidepressants have several limitations, including a delayed onset of action, limited efficacy, and an unfavorable side effect profile. In this review, Dexmedetomidine (DEX), a highly selective and potent α2-adrenergic receptor (α2-AR) agonist, is proposed as a potentially novel antidepressant with multiple mechanisms of action targeting various depression pathophysiological processes. These mechanisms include modulation of the noradrenergic system, regulation of neuroinflammation and oxidative stress, influence on the Brain-Derived Neurotrophic Factor (BDNF) levels, and modulation of neurotransmitter systems, such as glutamate. The review begins with an introduction before moving on to a discussion of DEX's pharmacological features. The pathophysiological and phenomenological targets of DD are also explored, along with the review of the existing preclinical and clinical evidence for DEX's putative anti-depressant effects. Finally, the review ends by presenting the pertinent conclusions and future directions. © 2023 The Author(s). Published by Bentham Science Publisher.

关键词： Adrenergic alpha-agonists Antidepressant Depression Dexmedetomidine Major depressive disorder Treatment resistant-depression

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The Application of Digital Frailty Screening to Triage Nonhealing and Complex Wounds

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Journal of Diabetes Science and Technology 2024年第2期18卷 389-396页

作者： Mishra, Ram Kinker Bara, Rasha O. Zulbaran-Rojas, Alejandro Park, Catherine Fernando, Malindu E. Ross, Jeffrey Lepow, Brian Najafi, Bijan Interdisciplinary Consortium on Advanced Motion Performance (iCAMP) Michael E. DeBakey Department of Surgery Baylor College of Medicine Houston TX United States Division of Vascular Surgery and Endovascular Therapy Michael E. DeBakey Department of Surgery Baylor College of Medicine Houston TX United States VA HSR&D Center for Innovations in Quality Effectiveness and Safety Michael E. DeBakey VA Medical Center Houston TX United States Big Data Scientist Training Enhancement Program VA Office of Research and Development Washington DC United States Ulcer and Wound Healing Consortium (UHEAL) Queensland Research Centre for Peripheral Vascular Disease College of Medicine and Dentistry James Cook University Townsville QLD Australia Faculty of Health and Medicine School of Health Sciences University of Newcastle Newcastle NSW Australia School of Health Professions Baylor College of Medicine Houston TX United States

Objective: We investigated the association between the complexity of diabetic foot ulcers (DFUs) and frailty. Research Design and Methods: Individuals (n = 38) with Grade 2 Wagner DFU were classified into 3 groups based on the Society for Vascular Surgery risk-stratification for major limb amputation as Stage 1 at very low risk (n = 19), Stage 2 at low risk (n = 9), and Stage 3 to 4 at moderate-to-high risk (n = 10) of major limb amputation. Frailty status was objectively assessed using a validated digital frailty meter (FM). The FM works by quantifying weakness, slowness, rigidity, and exhaustion over a 20-second repetitive elbow flexion-extension exercise using a wrist-worn sensor. FM generates a frailty index (FI) ranging from 0 to 1;higher values indicate progressively greater severity of frailty. Skin perfusion pressure (SPP), albumin, and tissue oxygenation level (SatO₂) were also measured. One-way analysis of variance (ANOVA) was used to identify group effect for wound complexity. Pearson’s correlation coefficient was used to assess the associations with frailty and clinical endpoints. Results: Frailty index was higher in Stage 3 and 4 as compared to Stage 1 (d = 1.4, P <.01) and Stage 2 (d = 1.2, P <.01). Among assessed frailty phenotypes, exhaustion was correlated with SPP (r = −0.63, P <.01) and albumin (r = −0.5, P <.01). Conclusion: Digital biomarkers of frailty may predict complexity of DFU and thus triage individuals who can be treated more simply in their primary clinic versus higher risk patients who require prompt referral to multidisciplinary, more complex care. © 2022 Diabetes Technology Society.

关键词： diabetes foot ulcer digital health frailty remote assessment telemedicine WIfI wound healing

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