tbuckley/cabot-search huggingface dataset:
非工業化環境における幼児の真菌と細菌性赤痢と小児アトピー性喘鳴との関連性【JST・京大機械翻訳】
Authors: Arrieta Marie-Claire, Arevalo Andrea, Stiemsma Leah, Dimitriu Pedro, E Chico Martha, Loor Sofia, Vaca Maritza, C T Boutin Rozlyn, Morien Evan, Jin Mingliang, E Turvey Stuart, Walter Jens, Parfrey Laura Wegener, J Cooper Philip, Finlay Brett
Journal: Journal of Allergy and Clinical Immunology (2018)
Evidence-Based Practices in the Cardiac Catheterization Laboratory: A Scientific Statement From the American Heart Association
Authors: Sripal Bangalore, Gregory W. Barsness, George D. Dangas, Morton J. Kern, Sunil V. Rao, Linda Shore-Lesserson, Jacqueline E. Tamis-Holland
Journal: Circulation (2021)

Cardiac catheterization procedures have rapidly evolved and expanded in scope and techniques over the past few decades. However, although some practices have emerged based on evidence, many traditions have persisted based on beliefs and theoretical concerns. The aim of this review is to highlight common preprocedure, intraprocedure, and postprocedure catheterization laboratory practices where evidence has accumulated over the past few decades to support or discount traditionally held practices.
Lymphatic Malformations: Genetics, Mechanisms and Therapeutic Strategies
Authors: Taija Mäkinen, Laurence M. Boon, Miikka Vikkula, Kari Alitalo
Journal: Circulation Research (2021)

Lymphatic vessels maintain tissue fluid homeostasis by returning to blood circulation interstitial fluid that has extravasated from the blood capillaries. They provide a trafficking route for cells of the immune system, thus critically contributing to immune surveillance. Developmental or functional defects in the lymphatic vessels, their obstruction or damage, lead to accumulation of fluid in tissues, resulting in lymphedema. Here we discuss developmental lymphatic anomalies called lymphatic malformations and complex lymphatic anomalies that manifest as localized or multifocal lesions of the lymphatic vasculature, respectively. They are rare diseases that are caused mostly by somatic mutations and can present with variable symptoms based upon the size and location of the lesions composed of fluid-filled cisterns or channels. Substantial progress has been made recently in understanding the molecular basis of their pathogenesis through the identification of their genetic causes, combined with the elucidation of the underlying mechanisms in animal disease models and patient-derived lymphatic endothelial cells. Most of the solitary somatic mutations that cause lymphatic malformations and complex lymphatic anomalies occur in genes that encode components of oncogenic growth factor signal transduction pathways. This has led to successful repurposing of some targeted cancer therapeutics to the treatment of lymphatic malformations and complex lymphatic anomalies. Apart from the mutations that act as lymphatic endothelial cell-autonomous drivers of these anomalies, current evidence points to superimposed paracrine mechanisms that critically contribute to disease pathogenesis and thus provide additional targets for therapeutic intervention. Here, we review these advances and discuss new treatment strategies that are based on the recently identified molecular pathways.
Association of Pediatric Obstructive Sleep Apnea With Elevated Blood Pressure and Orthostatic Hypertension in Adolescence
Authors: Julio Fernandez-Mendoza, Fan He, Susan L. Calhoun, Alexandros N. Vgontzas, Duanping Liao, Edward O. Bixler
Journal: JAMA Cardiology (2021)

Although pediatric guidelines have delineated updated thresholds for elevated blood pressure (eBP) in youth and adult guidelines have recognized obstructive sleep apnea (OSA) as an established risk factor for eBP, the relative association of pediatric OSA with adolescent eBP remains unexplored.
Perivalvular Abscess Causing Coronary-Artery Compression
Authors: Daniel L. Varela, Tara L. Jones
Journal: New England Journal of Medicine (2021)

A 67-year-old woman presented with fatigue and anorexia. Streptococcus mutans was grown on blood culture, and an abscess was detected in the perivalvular aortic root that was compressing the left main coronary artery, as shown in videos.
Inference of ventricular activation properties from non-invasive electrocardiography
Authors: Julia Camps, Brodie Lawson, Christopher Drovandi, Ana Minchole, Zhinuo Jenny Wang, Vicente Grau, Kevin Burrage, Blanca Rodriguez
Journal: Medical Image Analysis (2021)

The realisation of precision cardiology requires novel techniques for the non-invasive characterisation of individual patients' cardiac function to inform therapeutic and diagnostic decision-making. The electrocardiogram (ECG) is the most widely used clinical tool for cardiac diagnosis. Its interpretation is, however, confounded by functional and anatomical variability in heart and torso. In this study, we develop new computational techniques to estimate key ventricular activation properties for individual subjects by exploiting the synergy between non-invasive electrocardiography and image-based torso-biventricular modelling and simulation. More precisely, we present an efficient sequential Monte Carlo approximate Bayesian computation-based inference method, integrated with Eikonal simulations and torso-biventricular models constructed based on clinical cardiac magnetic resonance (CMR) imaging. The method also includes a novel strategy to treat combined continuous (conduction speeds) and discrete (earliest activation sites) parameter spaces, and an efficient dynamic time warping-based ECG comparison algorithm. We demonstrate results from our inference method on a cohort of twenty virtual subjects with cardiac volumes ranging from 74 cm3 to 171 cm3 and considering low versus high resolution for the endocardial discretisation (which determines possible locations of the earliest activation sites). Results show that our method can successfully infer the ventricular activation properties from non-invasive data, with higher accuracy for earliest activation sites, endocardial speed, and sheet (transmural) speed in sinus rhythm, rather than the fibre or sheet-normal speeds.
Selective Modulation of the Pulmonary Innate Immune Response Does Not Change Lung Microbiota in Healthy Mice
Authors: Jezreel Pantaleón García, Kevin J. Hinkle, Nicole R. Falkowski, Scott E. Evans, Robert P. Dickson
Journal: American Journal of Respiratory and Critical Care Medicine (2021)

"Selective Modulation of the Pulmonary Innate Immune Response Does Not Change Lung Microbiota in Healthy Mice." American Journal of Respiratory and Critical Care Medicine, 204(6), pp. 734–736
Predictors of seven-year change in homocysteine concentrations in the Coronary Artery Risk Development in Young Adults (CARDIA) Study
Authors: Catherine M Loria, Jeffrey M Roseman, Joan E Hilner, Phillip E Cornwell, Pamela J Schreiner, David S Siscovick
Journal: Circulation (2001)

P87 While blood level of total homocysteine (tHcy) is inversely related to folate intake in cross-sectional studies, few prospective studies have examined changes in tHcy, folate intake, and cardiovascular disease (CVD) risk factors. Serum tHcy was measured on 755 18-30 year old participants in the Coronary Artery Risk Development in Young Adults (CARDIA) Study using stored samples from 1985-86 (baseline) and 1992-93 (Year 7), collected prior to food fortification with folic acid. Geometric mean tHcy did not differ by race at baseline (p&gt;0.05). However by Year 7, mean tHcy was higher in blacks than whites (14.3, 13.3, 11.9, 10.9 μmol/L in black men, white men, black women, white women, respectively; p=0.001). Arithmetic mean change in tHcy differed from zero among blacks (1.3-1.4 μmol/L; p&lt;0.001) but not among whites ( -0.3-0.2 μmol/L). Mean folate intake (from diet and supplements) at baseline was higher among whites than blacks within each sex (384, 439, 291, 349 μg, respectively; p=0.001). Although mean folate intake increased in all groups by Year 7, intake was higher among black than white men but the reverse was found among women (517, 496, 339, 421 μg; p for interaction=0.002). In multivariate models, change in tHcy was associated inversely with change in total folate intake in all race-sex groups; changes in smoking status among black men, in serum cholesterol level among whites, and in body mass index among white men were also independent predictors. Thus, tHcy increased over 7 years in blacks by 1.3-1.4 μmol/L (about 1 s.d.) on average, despite increases in folate intake. Changes in CVD risk factor status may help explain this contradictory finding.
Clinical Investigation of Mitochondrial Biogenesis in Multiple Myeloma
Authors: Xin Zhan, Reinaldo Franqui-Machin, Kalyan Nadiminti, Huojun Cao, Brad A. Amendt, Yogesh Jethava, Ivana Frech, Fenghuang Zhan, Guido J. Tricot
Journal: Blood (2017)
Deceleration time of diastoric coronary blood flow velocity in patients with acute anterior myocardial infarction can predict regional left ventricular wall motion recovery: Assessment by transthoracic Doppler echocardiography
Authors: Morioka S, Yamabe K, Tamita K, Yamamuro A, Takagi T, Hozumi T, Akasaka T, Ueda Y
Journal: Journal of the American College of Cardiology (2000)
How far is Lignin from being a biomedical material?
Authors: Sigit Sugiarto, Yihao Leow, Chong Li Tan, Guan Wang, Dan Kai
Journal: Bioactive Materials (2021)

Lignin is a versatile biomass that possesses many different desirable properties such as antioxidant, antibacterial, anti-UV, and good biocompatibility. Natural lignin can be processed through several chemical processes. The processed lignin can be modified into functionalized lignin through chemical modifications to develop and enhance biomaterials. Thus, lignin is one of the prime candidate for various biomaterial applications such as drug and gene delivery, biosensors, bioimaging, 3D printing, tissue engineering, and dietary supplement additive. This review presents the potential of developing and utilizing lignin in the outlook of new and sustainable biomaterials. Thereafter, we also discuss on the challenges and outlook of utilizing lignin as a biomaterial.
Intra‐heterogeneity in transcription and chemoresistant property of leukemia‐initiating cells in murine <i>Setd2<sup>−/−</sup></i> acute myeloid leukemia
Authors: Jiachun Song, Longting Du, Ping Liu, Fuhui Wang, Bo Zhang, Yinyin Xie, Jing Lu, Yi Jin, Yan Zhou, Gang Lv, Jianmin Zhang, Saijuan Chen, Zhu Chen, Xiaojian Sun, Yuanliang Zhang, Qiuhua Huang
Journal: Cancer Communications (2021)

Abstract Background Heterogeneity of leukemia‐initiating cells (LICs) is a major obstacle in acute myeloid leukemia (AML) therapy. Accumulated evidence indicates that the coexistence of multiple types of LICs with different pathogenicity in the same individual is a common feature in AML. However, the functional heterogeneity including the drug response of coexistent LICs remains unclear. Therefore, this study aimed to clarify the intra‐heterogeneity in LICs that can help predict leukemia behavior and develop more effective treatments. Methods Spleen cells from the primary Setd2 −/− ‐AML mouse were transplanted into C57BL/6 recipient mice to generate a transplantable model. Flow cytometry was used to analyze the immunophenotype of the leukemic mice. Whole‐genome sequencing was conducted to detect secondary hits responsible for leukemia transformation. A serial transplantation assay was used to determine the self‐renewal potential of Setd2 −/− ‐AML cells. A limiting‐dilution assay was performed to identify the LIC frequency in different subsets of leukemia cells. Bulk and single‐cell RNA sequencing were performed to analyze the transcriptional heterogeneity of LICs. Small molecular inhibitor screening and in vivo drug treatment were employed to clarify the difference in drug response between the different subsets of LICs. Results In this study, we observed an aged Setd2 −/− mouse developing AML with co‐mutation of Nras G12S and Braf K520E . Further investigation identified two types of LICs residing in the c‐Kit + B220 + Mac‐1 − and c‐Kit + B220 + Mac‐1 + subsets, respectively. In vivo transplantation assay disclosed the heterogeneity in differentiation between the coexistent LICs. Besides, an intrinsic doxorubicin‐resistant transcriptional signature was uncovered in c‐Kit + B220 + Mac‐1 + cells. Indeed, doxorubicin plus cytarabine (DA), the standard chemotherapeutic regimen used in AML treatment, could specifically kill c‐Kit + B220 + Mac‐1 − cells, but it hardly affected c‐Kit + B220 + Mac‐1 + cells. Transcriptome analysis unveiled a higher activation of RAS downstream signaling pathways in c‐Kit + B220 + Mac‐1 + cells than in c‐Kit + B220 + Mac‐1 − cells. Combined treatment with DA and RAS pathway inhibitors killed both c‐Kit + B220 + Mac‐1 − and c‐Kit + B220 + Mac‐1 + cells and attenuated disease progression. Conclusions This study identified two cell subsets enriched for LICs in murine Setd2 −/− ‐AML and disclosed the transcriptional and functional heterogeneity of LICs, revealing that the coexistence of different types of LICs in this model brings about diverse drug response.
Incorporation of bacterial immunoevasins to protect cell therapies from host antibody-mediated immune rejection
Authors: Leila Peraro, Christopher M. Bourne, Megan M. Dacek, Enver Akalin, Jae H. Park, Eric L. Smith, David A. Scheinberg
Journal: Molecular Therapy (2021)

Cellular therapies are engineered using foreign and synthetic protein sequences, such as chimeric antigen receptors (CARs). The frequently observed humoral responses to CAR T cells result in rapid clearance, especially after re-infusions. There is an unmet need to protect engineered cells from host-versus-graft rejection, particularly for the advancement of allogeneic cell therapies. Here, utilizing the immunoglobulin G (IgG) protease "IdeS," we programmed CAR T cells to defeat humoral immune attacks. IdeS cleavage of host IgG averted Fc-dependent phagocytosis and lysis, and the residual F(ab')2 fragments remained on the surface, providing cells with an inert shield from additional IgG deposition. "Shield" CAR T cells efficiently cleaved cytotoxic IgG, including anti-CAR antibodies, detected in patient samples and provided effective anti-tumor activity in the presence of anti-cell IgG in vivo. This technology may be useful for repeated human infusions of engineered cells, more complex engineered cells, and expanding widespread use of "off-the-shelf" allogeneic cellular therapies.
DNMT1-mediated methylation of BEX1 regulates stemness and tumorigenicity in liver cancer
Authors: Qian Wang, Ning Liang, Tao Yang, Yuedan Li, Jing Li, Qian Huang, Chen Wu, Ligang Sun, Xile Zhou, Xiaobin Cheng, Long Zhao, Gang Wang, Zhangqian Chen, Xianli He, Chaoxu Liu
Journal: Journal of Hepatology (2021)
Association of smoking status with severe COVID-19
Authors: D. A. Puebla Neira, A. Watts, J. Seashore, E. Hsu, Y. Kuo, G. Sharma
Journal: American Journal of Respiratory and Critical Care Medicine (2021)

Rationale. The association between smoking status and severe Coronavirus Disease-2019 (COVID-19) remains controversial. To assess the risk of 14-day hospitalization, as a marker of severe COVID-19, in patients who are ever-smokers and tested positive for the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) compared to those who are never smokers and tested positive for the virus in a single academic health system in the United States. Methods. We conducted a retrospective cohort study of patients who tested positive for SARS-CoV-2 in the University of Texas Medical Branch Health System between March 1st and October 30th 2020 to identify the risk of 14-day hospitalization in ever-smokers compared to non-smokers. Results. In our study period, we identified 5,738 patients who met the inclusion criteria and had documentation of smoking habits. Out of this group, 636 (11%) were consider to be ever-smokers. One hundred and ninety one patients were current smokers and 445 were former smokers. Of the 5,738 patients, 35.1% were male, average age was 43.8 (SD± 17.6), 37.4% were Caucasian, 51.5% were obese (BMI≥30), 3.19 % had vaping history, and 76.5% had at least one comorbidity. We identified 624 (10.8%) patients who were admitted in 14 days and 49(0.8%) who died in 14 days during hospitalization. The percentage of ever smokers admitted in 14 days was greater than that of never smokers (17.9% vs 10%, p<0.0001). In addition, the percentage of smokers who died in 14 days was greater than that of never smokers (2.8% vs 0.6%, p<0.0001). However, after adjusting for other covariates the odds for 14-day hospitalization among ever smokers with COVID-19 was not significant (OR 0.96, 95% CI 0.7-1.2). Conclusions. In our single center study, smoking status was not associated with severe COVID-19 infection.
Complete cure of established murine hepatocellular carcinoma achieved by repeated infusions of retroviruses carrying the herpes simplex virus thymidine kinase gene followed by ganciclovir treatment.
Authors: Tsujii T, Fukui H, Takaya A, Yoshiji H, Yamazaki M, Tominaga K, Akahane T, Tsujinoue H, Nakatani T, Kuriyama S
Journal: Hepatology (1999)
Immunoglobulin light chain amyloidosis: 2012 update on diagnosis, prognosis, and treatment
Authors: Morie A. Gertz
Journal: American Journal of Hematology (2012)

Abstract Disease Overview: Immunoglobulin (Ig) light chain amyloidosis is a clonal but nonproliferative plasma cell disorder in which fragments of an Ig light chain are deposited in tissues. The clinical features depend on the organs involved but can include restrictive cardiomyopathy, nephrotic syndrome, hepatic failure, and peripheral/autonomic neuropathy. Diagnosis: Tissue biopsy stained with Congo red demonstrating amyloid deposits with apple‐green birefringence is required for diagnosis. Invasive organ biopsy is not required because amyloid deposits can be found in bone marrow biopsy or subcutaneous fat aspirate in 85% of patients. Prognosis: N‐terminal pro–brain natriuretic peptide and serum troponin T values are used to classify patients into three groups of approximately equal size; median survivals are 26.4, 10.5, and 3.5 months, respectively. Therapy: All patients with a visceral amyloid syndrome require therapy to prevent deposition of amyloid in other viscera and to prevent progressive organ failure of involved sites. Stem cell transplant (SCT) is a preferred technique, but only 20% of patients are eligible. Requirements for safe SCT include mild or no cardiac involvement, troponin T value &lt;0.06 ng/mL, age &lt;70 years, &lt;3 organs involved, and serum creatinine value ≤1.7 mg/dL. Nontransplant candidates can be offered melphalan–dexamethasone. Pomalidomide appears to have activity, as do other combinations of chemotherapy with agents such as cyclophosphamide–thalidomide–dexamethasone, bortezomib–dexamethasone, and melphalan–prednisone–lenalidomide. Future Challenges: Late diagnosis remains a major obstacle to initiating effective therapy when organ dysfunction is still recoverable. Recognizing the presenting syndromes is necessary for improvement in survival. Am. J. Hematol., 2011. © 2011 Wiley Periodicals, Inc.
Abstract 94: Menopausal Female Mice are Hypersensitive to Cardiovascular Disease
Authors: Christiane A Danilo, Eleni Constantopoulos, Jessica N Sanchez, Dennis P Pollow, Heddwen L Brooks, Yulia Lipovka, John P Konhilas
Journal: Circulation Research (2016)

Prior to menopause, women are protected against cardiovascular disease (CVD) compared to age-matched men; this protection is gradually lost after menopause. The mechanisms responsible for loss of protection and rise in CVD onset are unknown. A novel model of menopause utilizing 4-vinylcyclohexene diepoxide (VCD) induces gradual ovarian failure, preserving the “perimenopause” transitional period and androgen secreting capacity of residual ovarian tissue. Our central hypothesis states that menopausal females are hypersensitive to CVD-induced pathological cardiac remodeling. To address this hypothesis, we instigated menopause in 2 month-old females by daily (i.p.) injections of VCD (160mg/kg, 20 consecutive days); control mice received sesame oil as vehicle. Vaginal cytology was used to monitor estrous cycles and determine when cycling ceased. Mice were considered menopausal after 15 consecutive days in persistent diestrus, non-cycling. Female mice from cycling, perimenopausal and menopausal groups were subjected to 30 minutes of ischemia followed by 2 days of reperfusion (I/R). Following reperfusion, hearts were rapidly excised, sectioned and double-stained with Evans Blue and triphenyltetrazolium chloride to define the area at risk (AAR) and infarct size as area of necrosis (AON). On average, menopausal females displayed a significant (p&lt;0.01) increase in AON relative to the AAR when compared to perimenopausal and cycling mice. Next, female mice (cycling, perimenopausal and menopausal) received the hypertensive agent angiotensin II (Ang II, 800 ng/kg/min via alzet s.q. mini-pump, 14 days). Ang II infusion induced a significant exacerbation of hypertension (measured via tail cuff) in menopausal females. In addition, menopausal females demonstrated worsened pathological cardiac remodeling measured by functional (echocardiography), cellular (myocardial fibrosis) and molecular (fetal gene program) assessments. Using a novel model of menopause (VCD) combined with CVD by I/R or infusion of the hypertensive agent Ang II, we demonstrated that menopausal mice are more susceptible, or hypersensitive to pathological cardiac remodeling compared to cycling and perimenopausal mice.
Abstract 428: Cause of Death Among Patients Resuscitated From Out-Of-Hospital Cardiac Arrest at a Single Urban Academic Hospital
Authors: Shu Li, Christos Lazaridis, Fernando D Goldenberg, Atman Shah, David Beiser, Willard W Sharp
Journal: Circulation (2019)

Background: Approximately 30% of patients resuscitated following Out of Hospital Cardiac Arrest (OHCA) survive to hospital admission, but only 10% of these patients survive to hospital discharge. Reasons for in hospital death of these patients is not well known or categorized. Understanding the principle reason for death among successfully resuscitated OHCA patients could guide the development of therapeutic and management strategies Methods: Using a retrospective OHCA cohort database at a single urban academic hospital, death of admitted adult OHCA patients from January 1, 2016 until June 30, 2019 was classified as primarily due to withdrawal of life-sustaining treatments (WOLST), in-hospital cardiac arrest, or formal declaration of death by neurologic criteria (brain death). Family/caregiver decisions to WOLST were categorized as occurring primarily in the setting of isolated severe neurological injury, multi-organ failure, in hospital cardiac arrest, severe hemodynamic shock, pre-existing comorbidities/terminal health condition, or prior unknown DNR status. Traumatic arrests were excluded. Results: During the study period there were 578 cardiac arrests brought to the emergency department; 291 (50%) patients survived to hospital admission. Of admitted patients, 95 patients (33%) survived to hospital discharge and 194 patients (67%) died. In non-surviving patients, death was attributable to WOLST (77%), brain death 25 (13%), in-hospital cardiac arrest (9%), and failure to achieve return of spontaneous circulation on ECMO 1 (1%). Decisions to WOLST by family members were complex and multi-factorial but were determined in the context of poor neurologic prognosis 93 (62%), multi-organ failure 27 (18%), in hospital cardiac arrest 11 (7%), severe shock 11 (7%), unknown prior DNR status 7 (5%), and pre-existing terminal illness 2 (1%). Conclusion: In this single center study, the majority of OHCA patients who survived to hospital admission from the emergency department subsequently died in the hospital due to the severity of their neurological injury in the context of WOLST. Death in the setting of multiorgan failure, re-arrest, or severe hemodynamic shock was less common.