tbuckley/cabot-search huggingface dataset:
Imbalance of the intestinal virome and altered viral-bacterial interactions caused by a conditional deletion of the vitamin D receptor
Authors: Jilei Zhang, Yongguo Zhang, Yinglin Xia, Jun Sun
Journal: Gut Microbes (2021)

Vitamin D receptor (VDR) deficiency is associated with cancer, infection, and chronic inflammation. Prior research has demonstrated VDR regulation of bacteria; however, little is known regarding VDR and viruses. We hypothesize that VDR deficiency impacts on the intestinal virome and viral-bacterial interactions. We specifically deleted VDR from intestinal epithelial cells (VDRΔIEC), Paneth cells (VDRΔPC), and myeloid cells (VDRΔLyz) in mice. Feces were collected for shotgun metagenomic sequencing and metabolite profiling. To test the functional changes, we evaluated pattern recognition receptors (PRRs) and analyzed microbial metabolites. Vibrio phages, Lactobacillus phages, and Escherichia coli typing phages were significantly enriched in all three conditional VDR-knockout mice. In the VDRΔLyz mice, the levels of eight more virus species (2 enriched, 6 depleted) were significantly changed. Altered virus species were primarily observed in female VDRΔLyz (2 enriched, 3 depleted) versus male VDRΔLyz (1 enriched, 1 depleted). Altered alpha and beta diversity (family to species) were found in VDRΔLyz. In VDRΔIEC mice, bovine viral diarrhea virus 1 was significantly enriched. A significant correlation between viral and bacterial alterations was found in conditional VDR knockout mice. There was a positive correlation between Vibrio phage JSF5 and Cutibacterium acnes in VDRΔPC and VDRΔLyz mice. Also, there were more altered viral species in female conditional VDR knockout mice. Notably, there were significant changes in PRRs: upregulated TLR3, TLR7, and NOD2 in VDRΔLyz mice and increased CLEC4L expression in VDRΔIEC and VDRΔPC mice. Furthermore, we identified metabolites related to virus infection: decreased glucose in VDRΔIEC mice, increased ribulose/xylulose and xylose in VDRΔLyz mice, and increased long-chain fatty acids in VDRΔIEC and VDRΔLyz female mice. Tissue-specific deletion of VDR changes the virome and functionally changes viral receptors, which leads to dysbiosis, metabolic dysfunction, and infection risk. This study helps to elucidate VDR regulating the virome in a tissue-specific and sex-specific manner.
Phenotype–genotype associations in primary ciliary dyskinesia: where do we stand?
Authors: Myrofora Goutaki, Eva S.L. Pedersen
Journal: European Respiratory Journal (2021)

<b>Defining distinct PCD clinical phenotypes and their associations to genotypes in large collaborative clinical and research networks could have important implications for clinical management and subsequently patients' quality of life</b>https://bit.ly/2ZQItzR
Autophagy inhibition by targeting PIKfyve potentiates response to immune checkpoint blockade in prostate cancer
Authors: Yuanyuan Qiao, Jae Eun Choi, Jean C. Tien, Stephanie A. Simko, Thekkelnaycke Rajendiran, Josh N. Vo, Andrew D. Delekta, Lisha Wang, Lanbo Xiao, Nathan B. Hodge, Parth Desai, Sergio Mendoza, Kristin Juckette, Alice Xu, Tanu Soni, Fengyun Su, Rui Wang, Xuhong Cao, Jiali Yu, Ilona Kryczek, Xiao-Ming Wang, Xiaoju Wang, Javed Siddiqui, Zhen Wang, Amélie Bernard, Ester Fernandez-Salas, Nora M. Navone, Stephanie J. Ellison, Ke Ding, Eeva-Liisa Eskelinen, Elisabeth I. Heath, Daniel J. Klionsky, Weiping Zou, Arul M. Chinnaiyan
Journal: Nature Cancer (2021)
Distinct roles for PARP-1 and PARP-2 in c-Myc–driven B-cell lymphoma in mice
Authors: Miguel A. Galindo-Campos, Nura Lutfi, Sarah Bonnin, Carlos Martínez, Talia Velasco-Hernandez, Violeta García-Hernández, Juan Martín-Caballero, Coral Ampurdanés, Ramón Gimeno, Lluis Colomo, Gaël Roué, Guillaume Guilbaud, Françoise Dantzer, Pilar Navarro, Matilde Murga, Oscar Fernández-Capetillo, Anna Bigas, Pablo Menéndez, Julian E. Sale, José Yélamos
Journal: Blood (2021)
Trauma exposure and mental health of prisoners and ex-prisoners: A systematic review and meta-analysis
Authors: Huinan Liu, Tsz Wai Li, Li Liang, Wai Kai Hou
Journal: Clinical Psychology Review (2021)

The present meta-analytic review examined the associations between different forms of trauma and mental disorders among prisoners and ex-prisoners. Studies published from 1998 to March 31 2021 were identified by searching PsycINFO, PubMed, Medline and Web of Science. Data were meta-analyzed using a random-effect model. Moderator and mediator analyses were conducted. The protocol was registered in PROSPERO (CRD42020181587). We identified 62 studies (50 non-duplicated samples) with 15,115 (97.86%) prisoners and 330 (2.14%) ex-prisoners in 16 countries. A multi-level meta-analysis found that overall trauma was positively associated with more diagnoses or symptoms of mental disorders (Zr = 0.198, 95% CI = [0.167, 0.229], p < 0.001). Stronger effect sizes were found between childhood trauma (Zr = 0.357, 95% CI = [0.147, 0.568], p < 0.01) and sexual trauma (Zr = 0.326, 95% CI = [0.216, 0.435], p < 0.001) and stress-related disorders. Multilevel moderator analysis showed that effect size was stronger in imprisonment trauma (β = 0.247, 95% CI = [0.177, 0.316], p < 0.01), mixed trauma (β = 0.234, 95% CI = [0.196, 0.272], p < 0.001), and stress-related disorders (β = 0.261, 95% CI = [0.214, 0.307], p < 0.01). Associations between trauma and mental disorders were mediated by social support but not coping. Our findings provide an evidence base for future research on the impact of trauma and inform assessments and interventions in correctional settings.
CAR T cells targeting CD99 as an approach to eradicate T-cell acute lymphoblastic leukemia without normal blood cells toxicity
Authors: Jiangzhou Shi, Zijian Zhang, Hong Cen, Han Wu, Shangkun Zhang, Jiaxing Liu, Yingqi Leng, Anqi Ren, Xiyu Liu, Zhijie Zhang, Xiqin Tong, Jinjue Liang, Zhe Li, Fuling Zhou, Liang Huang, You Qin, Kunyu Yang, Tongcun Zhang, Haichuan Zhu
Journal: Journal of Hematology & Oncology (2021)

Abstract CAR T cell therapy has shown dramatic clinical success in relapsed or refractory B-ALL and other hematological malignancies. However, the loss of specific antigens, cell fratricide, T cell aplasia, and normal T cell separation are challenges in treating T cell leukemia/lymphoma with CAR T therapy. CD99 is a promising antigen to target T-ALL and AML as it is strongly expressed on the majority of T-ALL and AML. Here, we isolated a low-affinity CD99 (12E7) antibody, which specifically recognizes leukemia cells over normal blood cells. Moreover, T cells transduced with an anti-CD99-specific CAR that contained the 12E7 scFv expanded with minor fratricide and without normal blood cells toxicity. We observed that our anti-CD99 CAR T cells showed robust cytotoxicity specifically against CD99+ T-ALL cell lines and primary tumor cells in vitro and significantly prolonged cell line-derived xenografts (CDXs) or patient-derived xenografts (PDXs) models survival in vivo. Together, our results demonstrate that anti-CD99 CAR T cells could specifically recognize and efficiently eliminate CD99+ leukemia cells.
Mature tertiary lymphoid structures predict immune checkpoint inhibitor efficacy in solid tumors independently of PD-L1 expression
Authors: Lucile Vanhersecke, Maxime Brunet, Jean-Philippe Guégan, Christophe Rey, Antoine Bougouin, Sophie Cousin, Sylvestre Le Moulec, Benjamin Besse, Yohann Loriot, Mathieu Larroquette, Isabelle Soubeyran, Maud Toulmonde, Guilhem Roubaud, Simon Pernot, Mathilde Cabart, François Chomy, Corentin Lefevre, Kevin Bourcier, Michèle Kind, Ilenia Giglioli, Catherine Sautès-Fridman, Valérie Velasco, Félicie Courgeon, Ezoglin Oflazoglu, Ariel Savina, Aurélien Marabelle, Jean-Charles Soria, Carine Bellera, Casimir Sofeu, Alban Bessede, Wolf H. Fridman, François Le Loarer, Antoine Italiano
Journal: Nature Cancer (2021)
SPOP-mediated ubiquitination and degradation of PDK1 suppresses AKT kinase activity and oncogenic functions
Authors: Qiwei Jiang, Nana Zheng, Lang Bu, Xiaomei Zhang, Xiaoling Zhang, Yuanzhong Wu, Yaqing Su, Lei Wang, Xiaomin Zhang, Shancheng Ren, Xiangpeng Dai, Depei Wu, Wei Xie, Wenyi Wei, Yasheng Zhu, Jianping Guo
Journal: Molecular Cancer (2021)

Abstract Background 3-phosphoinositide-dependent protein kinase-1 (PDK1) acts as a master kinase of protein kinase A, G, and C family (AGC) kinase to predominantly govern cell survival, proliferation, and metabolic homeostasis. Although the regulations to PDK1 downstream substrates such as protein kinase B (AKT) and ribosomal protein S6 kinase beta (S6K) have been well established, the upstream regulators of PDK1, especially its degrader, has not been defined yet. Method A clustered regularly interspaced short palindromic repeats (CRISPR)-based E3 ligase screening approach was employed to identify the E3 ubiquitin ligase for degrading PDK1. Western blotting, immunoprecipitation assays and immunofluorescence (IF) staining were performed to detect the interaction or location of PDK1 with speckle-type POZ protein (SPOP). Immunohistochemistry (IHC) staining was used to study the expression of PDK1 and SPOP in prostate cancer tissues. In vivo and in vitro ubiquitination assays were performed to measure the ubiquitination conjugation of PDK1 by SPOP. In vitro kinase assays and mass spectrometry approach were carried out to identify casein kinase 1 (CK1) and glycogen synthase kinase 3 (GSK3)-mediated PDK1 phosphorylation. The biological effects of PDK1 mutations and correlation with SPOP mutations were performed with colony formation, soft agar assays and in vivo xenograft mouse models. Results We identified that PDK1 underwent SPOP-mediated ubiquitination and subsequent proteasome-dependent degradation. Specifically, SPOP directly bound PDK1 by the consensus degron in a CK1/GSK3β-mediated phosphorylation dependent manner. Pathologically, prostate cancer patients associated mutations of SPOP impaired PDK1 degradation and thus activated the AKT kinase, resulting in tumor malignancies. Meanwhile, mutations that occurred around or within the PDK1 degron, by either blocking SPOP to bind the degron or inhibiting CK1 or GSK3β-mediated PDK1 phosphorylation, could markedly evade SPOP-mediated PDK1 degradation, and played potently oncogenic roles via activating the AKT kinase. Conclusions Our results not only reveal a physiological regulation of PDK1 by E3 ligase SPOP, but also highlight the oncogenic roles of loss-of-function mutations of SPOP or gain-of-function mutations of PDK1 in tumorigenesis through activating the AKT kinase.
<i>N6</i>-methyladenosine–Mediated Upregulation of WTAPP1 Promotes WTAP Translation and Wnt Signaling to Facilitate Pancreatic Cancer Progression
Authors: Junge Deng, Jialiang Zhang, Ying Ye, Kaijing Liu, Lingxing Zeng, Jingyi Huang, Ling Pan, Mei Li, Ruihong Bai, Lisha Zhuang, Xudong Huang, Guandi Wu, Lusheng Wei, Yanfen Zheng, Jiachun Su, Shaoping Zhang, Rufu Chen, Dongxin Lin, Jian Zheng
Journal: Cancer Research (2021)

Pseudogenes may play important roles in cancer. Here, we explore the mechanism and function of a pseudogene WTAPP1 in the progress of pancreatic ductal adenocarcinoma (PDAC). WTAPP1 RNA was significantly elevated in PDAC and was associated with poor prognosis in patients. Overexpression of WTAPP1 RNA promoted PDAC proliferation and invasiveness in vitro and in vivo. Mechanistically, N6-methyladenosine (m6A) modification stabilized WTAPP1 RNA via CCHC-type zinc finger nucleic-acid binding protein (CNBP), resulting in increased levels of WTAPP1 RNA in PDAC cells. Excessive WTAPP1 RNA bound its protein-coding counterpart WT1-associated protein (WTAP) mRNA and recruited more EIF3 translation initiation complex to promote WTAP translation. Increased WTAP protein enhanced the activation of Wnt signaling and provoked the malignant phenotypes of PDAC. Decreasing WTAPP1 RNA significantly suppressed the in vivo growth and metastasis of PDAC cell lines and patient-derived xenografts. These results indicate that m6A-mediated increases in WTAPP1 expression promote PDAC progression and thus may serve as a therapeutic target. SIGNIFICANCE: This study reveals how aberrant m6A modification of the WTAPP1 pseudogene results in increased translation of its protein-coding counterpart to promote Wnt signaling, which contributes to pancreatic cancer progression.
完全房室ブロックを認めたProgressive Cardiac Conduction Disturbancesの一症例
Authors: 奥田啓二, 西尾まゆ, 大谷朋仁, 清水政彦, 谷池正行, 朝野仁裕, 高島成二, 朝日通雄, 南野哲男
Journal: Circulation (2004)
Neonatal Intensive Care for Very Preterm Infants in China
Authors: Matthew A. Rysavy, Edward F. Bell
Journal: JAMA Network Open (2021)

China is home to 1 in 5 people in the world. Every year, the number of infants born in China (&gt;16 million) exceeds the entire population of Sweden.1 Of these 16 million infants, more than 200 000 are estimated to be born very preterm (&lt;32 weeks’ gestation).2
Association between 9p21 Chromosome Polymorphisms rs1333040 and rs7865618 and Chronic Myeloid Leukemia
Authors: Federica Sora, Patrizia Chiusolo, Igor Giarretta, Elisabetta Abruzzese, Sara Marietti, Francesco Autore, Ilaria Gatto, Andrea Bacigalupo, Roberto Pola, Simona Sica
Journal: Blood (2017)
Glycemic Changes and Weight Loss Precede Pancreatic Ductal Adenocarcinoma by up to 3 Years in a Diverse Population
Authors: Marlon J. Brewer, John T. Doucette, Ariel Bar-Mashiah, Jacob W. Glickman, Elizabeth Kessel, Anne Aronson, Aimee L. Lucas
Journal: Clinical Gastroenterology and Hepatology (2021)
Insulin and IGF-1 receptors regulate complex I–dependent mitochondrial bioenergetics and supercomplexes via FoxOs in muscle
Authors: Gourav Bhardwaj, Christie M. Penniman, Jayashree Jena, Pablo A. Suarez Beltran, Collin Foster, Kennedy Poro, Taylor L. Junck, Antentor O. Hinton, Rhonda Souvenir, Jordan D. Fuqua, Pablo E. Morales, Roberto Bravo-Sagua, William I. Sivitz, Vitor A. Lira, E. Dale Abel, Brian T. O’Neill
Journal: Journal of Clinical Investigation (2021)

Decreased skeletal muscle strength and mitochondrial dysfunction are characteristic of diabetes. The actions of insulin and IGF-1 through the insulin receptor (IR) and IGF-1 receptor (IGF1R) maintain muscle mass via suppression of forkhead box O (FoxO) transcription factors, but whether FoxO activation coordinates atrophy in concert with mitochondrial dysfunction is unknown. We show that mitochondrial respiration and complex I activity were decreased in streptozotocin (STZ) diabetic muscle, but these defects were reversed in muscle-specific FoxO1, -3, and -4 triple-KO (M-FoxO TKO) mice rendered diabetic with STZ. In the absence of systemic glucose or lipid abnormalities, muscle-specific IR KO (M-IR–/–) or combined IR/IGF1R KO (MIGIRKO) impaired mitochondrial respiration, decreased ATP production, and increased ROS. These mitochondrial abnormalities were not present in muscle-specific IR, IGF1R, and FoxO1, -3, and -4 quintuple-KO mice (M-QKO). Acute tamoxifen-inducible deletion of IR and IGF1R also decreased muscle pyruvate respiration, complex I activity, and supercomplex assembly. Although autophagy was increased when IR and IGF1R were deleted in muscle, mitophagy was not increased. Mechanistically, RNA-Seq revealed that complex I core subunits were decreased in STZ-diabetic and MIGIRKO muscle, and these changes were not present with FoxO KO in STZ-FoxO TKO and M-QKO mice. Thus, insulin-deficient diabetes or loss of insulin/IGF-1 action in muscle decreases complex I–driven mitochondrial respiration and supercomplex assembly in part by FoxO-mediated repression of complex I subunit expression.
A critical role of nuclear m6A reader YTHDC1 in leukemogenesis by regulating MCM complex–mediated DNA replication
Authors: Yue Sheng, Jiangbo Wei, Fang Yu, Huanzhou Xu, Chunjie Yu, Qiong Wu, Yin Liu, Lei Li, Xiao-long Cui, Xueying Gu, Bin Shen, Wei Li, Yong Huang, Sumita Bhaduri-McIntosh, Chuan He, Zhijian Qian
Journal: Blood (2021)
Defining paediatric metabolic (dysfunction)-associated fatty liver disease: an international expert consensus statement
Authors: Mohammed Eslam, Naim Alkhouri, Pietro Vajro, Ulrich Baumann, Ram Weiss, Piotr Socha, Claude Marcus, Way Seah Lee, Deirdre Kelly, Gilda Porta, Mohamed A El-Guindi, Anna Alisi, Jake P Mann, Nezha Mouane, Louise A Baur, Anil Dhawan, Jacob George
Journal: The Lancet. Gastroenterology & hepatology (2021)
... or elsewhere
Authors: L. Bayliss, S. Connolly, R. Flint, E. Garthwaite
Journal: BMJ (1996)

EDITOR,-The report of the Interdepartmental Working Group on sensible drinking' has aroused critical comment.2The core recommendation is an increase in the safe limits for drinking from 21 units a week to 3-4 units a day for men and from 14 units a week to 2-3 units a day for women.The apparent aims are to discourage binge drinking and to promote health through moderate daily consumption.3We investigated how drinkers had interpreted the new guidelines and what effect the guidelines would have on their drinking.Over the Christmas
Recurrence of Colorectal Neoplastic Polyps After Incomplete Resection
Authors: Heiko Pohl, Joseph C. Anderson, Andres Aguilera-Fish, Audrey H. Calderwood, Todd A. Mackenzie, Douglas J. Robertson
Journal: Annals of Internal Medicine (2021)

Incomplete resection of neoplastic polyps is considered an important reason for the development of colorectal cancer. However, there are no data on the natural history of polyps that were incompletely removed.
Pulmonary sarcoidosis
Authors: H. Nunes, P. Soler, D. Valeyre
Journal: Allergy (2005)

Sarcoidosis is a multisystemic disease of unknown aetiology characterized by the formation of immune granulomas in involved organs. It is a worldwide disease that mainly affects 25–40 years old people with a lifetime incidence rate of 0.85–2.4%. Multiple clinical phenotypes are observed according to presentation, involved organs, disease duration and severity. Sarcoidosis primarily affects the lungs and the lymphatic system. The prevailing pathogenic hypothesis is that various antigens could promote sarcoidosis in genetically susceptible hosts, both these factors modulating the incidence and the clinical phenotype of sarcoidosis. So far, environmental agents have been suspected, including possible mycobacteria and propionibacteria. Interferon‐ γ , tumour necrosis factor (TNF)‐ α , interleukin (IL)‐12 and IL‐18 play a critical role in driving the Th1 commitment in the course of granulomatous process. Evolution of sarcoidosis is often marked by spontaneous resolution within 12–36 months, but can be severe because of chronic cases with pulmonary fibrosis or involving other organs, including heart, central nervous system and eyes. Mortality, ranging between 0.5 and 5%, is most often related to pulmonary fibrosis. Corticosteroids can reverse the granulomatous process, but are only suspensive, and their long‐term benefit remains under question. Corticosteroids are recommended when sarcoidosis shows unfavourable clinical tolerance and evolution. Alternative and corticosteroid‐sparing therapies are of increased interest in difficult cases, while targeted new drugs such as anti‐TNF‐ α are still under investigation.
Intracorporeal Versus Extracorporeal Robot-assisted Kidney Autotransplantation: Experience of the ERUS RAKT Working Group
Authors: Alberto Breda, Pietro Diana, Angelo Territo, Andrea Gallioli, Alberto Piana, Josep Maria Gaya, Pavel Gavrilov, Liesbeth Desender, Benjamin Van Parys, Charles Van Praet, Edward Lambert, Zine-Eddine Khene, Van Thi Dang, Nicolas Doumerc, Karel Decaestecker
Journal: European Urology (2021)
Dual Ultrasound and Photoacoustic Tracking of Magnetically Driven Micromotors: From In Vitro to In Vivo
Authors: Azaam Aziz, Joost Holthof, Sandra Meyer, Oliver G. Schmidt, Mariana Medina‐Sánchez
Journal: Advanced Healthcare Materials (2021)

Abstract The fast evolution of medical micro‐ and nanorobots in the endeavor to perform non‐invasive medical operations in living organisms has boosted the use of diverse medical imaging techniques in the last years. Among those techniques, photoacoustic imaging (PAI), considered a functional technique, has shown to be promising for the visualization of micromotors in deep tissue with high spatiotemporal resolution as it possesses the molecular specificity of optical methods and the penetration depth of ultrasound. However, the precise maneuvering and function's control of medical micromotors, in particular in living organisms, require both anatomical and functional imaging feedback. Therefore, herein, the use of high‐frequency ultrasound and PAI is reported to obtain anatomical and molecular information, respectively, of magnetically‐driven micromotors in vitro and under ex vivo tissues. Furthermore, the steerability of the micromotors is demonstrated by the action of an external magnetic field into the uterus and bladder of living mice in real‐time, being able to discriminate the micromotors’ signal from one of the endogenous chromophores by multispectral analysis. Finally, the successful loading and release of a model cargo by the micromotors toward non‐invasive in vivo medical interventions is demonstrated.
Leveraging Large Clinical Data Sets for Artificial Intelligence in Medicine
Authors: David Ouyang, Christine M. Albert
Journal: JAMA Cardiology (2021)

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Genome‐wide association of individual vulnerability with alcohol‐associated liver disease: A Korean genome and epidemiology study
Authors: Kwang Yoon Kim, Jung Oh Kim, Young‐Sang Kim, Ja‐Eun Choi, Jae‐Min Park, Kunhee Han, Da‐Hyun Park, Yon Chul Park, Bom Taeck Kim, Kyung‐Won Hong
Journal: Hepatology (2021)

The quantity of alcohol leading to alcohol-associated liver disease (ALD) varies individually. Genetic backgrounds contributing to the divergence in individual susceptibility to alcohol-induced liver damage have not been elucidated in detail.Based on the Korean Genome and Epidemiology Study Health Examination (KoGES_HEXA) cohort data, 21,919 participants (40-79 years old) were included and divided into cases and controls based on the ALD diagnostic criteria proposed by the American College of Gastroenterology. Data generated by a genome wide-association study were analyzed using logistic regression to assess the risk of ALD development in nondrinkers, light drinkers, and heavy drinkers. We detected three loci, gamma-glutamyltransferase 1 (GGT1), zinc protein finger 827 (ZNF827) and HNF1 homeobox A (HNF1A), which were significantly associated with ALD risk. The GGT1 rs2006227 minor allele was strongly associated with all groups. Among the minor alleles of single nucleotide polymorphisms (SNPs) in HNF1A, rs1183910 had the strongest association with a protective effect from ALD in light drinkers. However, this association was not observed in heavy drinkers. Five SNPs on chromosome 11 showed suggestive significance in protective effects against ALD.SNPs, including HNF1A rs1183910 minor allele, are the most promising genetic candidates for protection against ALD. The expression of genes contributing to ALD development may be altered by the amount of alcohol consumed.