tbuckley/cabot-search huggingface dataset:
Modified hyaluronic acid hydrogels with chemical groups that facilitate adhesion to host tissues enhance cartilage regeneration
Authors: Jiaqing Chen, Jiabei Yang, Li Wang, Xuewei Zhang, Boon Chin Heng, Dong-An Wang, Zigang Ge
Journal: Bioactive Materials (2020)

Stable integration of hydrogel implants with host tissues is of critical importance to cartilage tissue engineering. Designing and fabricating hydrogels with high adhesive strength, stability and regeneration potential are major challenges to be overcome. This study fabricated injectable adhesive hyaluronic acid (HA) hydrogel modified by aldehyde groups and methacrylate (AHAMA) on the polysaccharide backbone with multiple anchoring mechanisms (amide bond through the dynamic Schiff base reaction, hydrogen bond and physical interpenetration). AHAMA hydrogel exhibited significantly improved durability and stability within a humid environment (at least 7 days), together with higher adhesive strength (43 KPa to skin and 52 KPa to glass), as compared to commercial fibrin glue (nearly 10 KPa) and HAMA hydrogel (nearly 20 KPa). The results showed that AHAMA hydrogel was biocompatible and could be easily and rapidly prepared in situ. In vitro cell culture experiments showed that AHAMA hydrogel could enhance proliferation (1.2-folds after 3 days) and migration (1.5-folds after 12 h) of bone marrow stem cells (BMSCs), as compared to cells cultured in a culture dish. Furthermore, in a rat osteochondral defect model, implanted AHAMA hydrogel significantly promoted integration between neo-cartilage and host tissues, and significantly improved cartilage regeneration (modified O'Driscoll histological scores of 16.0 ± 4.1 and 18.3 ± 4.6 after 4 and 12-weeks of post-implantation in AHAMA groups respectively, 12.0 ± 2.7 and 12.2 ± 2.8 respectively in HAMA groups, 9.8 ± 2.4 and 11.5 ± 2.1 respectively in untreated groups). Hence, AHAMA hydrogel is a promising adhesive biomaterial for clinical cartilage regeneration and other biomedical applications.
Computed Tomography of the Coronary Arteries: More Than Meets the (Angiographic) Eye**Editorials published in the Journal of the American College of Cardiologyreflect the views of the authors and do not necessarily represent the views of JACCor the American College of Cardiology.
Authors: Stephan Achenbach, Werner G. Daniel
Journal: Journal of the American College of Cardiology (2005)
Nebulette Mutations in Cardiac Remodeling: Big Effects From a Small Mechanosensor⁎⁎Editorials published in the Journal of the American College of Cardiologyreflect the views of the authors and do not necessarily represent the views of JACCor the American College of Cardiology.
Authors: Rashmi Ram, Burns C. Blaxall
Journal: Journal of the American College of Cardiology (2010)
Screening for Barrett’s oesophagus: are we looking for the right thing?
Authors: Stuart J Spechler
Journal: Gut (2020)

Over the past several decades, while the incidence of oesophageal adenocarcinoma (OAC) in Western countries has risen dramatically, our primary strategy for preventing OAC deaths has been an endoscopic screening of individuals with gastro-oesophageal reflux disease (GORD) symptoms for Barrett’s oesophagus (BO) and regular endoscopic surveillance for those found to have BO. However, there is no definitive study establishing that endoscopic surveillance prevents OAC deaths, and observational studies on this issue have reached contradictory conclusions.

While there is no proof that surveillance for BO is effective, there is indisputable evidence that current screening practices are not. Only ~12% of patients diagnosed with OAC have a prior diagnosis of BO.1 Thus, our endoscopic screening policy has failed to identify the large majority of patients who develop this malignancy. The reasons for this failure are not clear, but one of several proposed explanation is that OACs might develop from a precursor other than the BO sought during endoscopic screening.2 An interesting study by Curtius et al in Gut suggests otherwise.3

Curtius et al used a sophisticated, multiscale computational model of OAC to determine whether all expected cases of BO in the US adult population could account for the incidence of OAC reported in the Surveillance, Epidemiology, and End Results Program (SEER) cancer registry.3 The model used published estimates of GORD prevalence and SEER-provided OAC incidence curves to calibrate the prevalence of BO and its rate of neoplastic progression. For the year 2010, the model predicted that 2.2 million adults in the USA had …
Stool-based Xpert MTB/RIF Ultra assay as a tool for detecting pulmonary tuberculosis in children with abnormal chest imaging: A prospective cohort study
Authors: Xu-hui Liu, Lu Xia, Bin Song, Heng Wang, Xue-qin Qian, Jian-hao Wei, Tao Li, Xiu-hong Xi, Yuan-lin Song, Shan-qun Li, Douglas B. Lowrie, Xiao-yong Fan, Shui-hua Lu
Journal: Journal of Infection (2020)
Abstract 11224: Prevalence of Statin Non-adherence Determined by Therapeutic Drug Monitoring (TDM) in Patients With Uncontrolled Hypertension
Authors: Bryan Wu, Shishir Sharma, Hamza Lodhi, Kevin Schesing, Sandeep R Das, Nancy Brown, Elizabeth Moss, Ethan A Halm, Wanpen Vongpatanasin
Journal: Circulation (2019)

Non-adherence to statin therapy is known to be associated with increased cardiovascular mortality. Previous studies have reported prevalence of non-adherence to statin to be between 20-80%, dependi...
Task-sharing interventions for improving control of diabetes in low-income and middle-income countries: a systematic review and meta-analysis
Authors: Joseph Linju Maria, T N Anand, Boban Dona, Jose Prinu, Dorairaj Prabhakaran, Panniyammakal Jeemon
Journal: The Lancet Global Health (2020)

Task-sharing interventions using non-physician health-care workers might be a potential diabetes management strategy in health systems that are constrained by physician shortages, such as those in low-income and middle-income countries (LMICs).We did a systematic review and meta-analysis of task-sharing intervention strategies for managing type 2 diabetes in LMICs. We searched PubMed, Embase, and CINAHL from database inception to Sept 25, 2019, for studies that were randomised control trials or cluster randomised trials with task-shifted or task-shared interventions delivered to adults (≥18 years) by non-physician health workers versus usual care, done in LMICs with glycated haemoglobin (HbA1c) or fasting blood sugar (FBS) as outcome measures. The methodological quality of included studies was assessed using the Cochrane risk of bias tool. Random-effects model meta-analysis was used to estimate the population average pooled mean difference for HbA1c and FBS with 95% CIs. Our study protocol was registered in the PROSPERO database (CRD42018081015).We found 4213 studies from the literature search, of which 46 (1·1%) were eligible for the narrative synthesis, including a total of 16 973 participants. 16 of these studies were excluded from the meta-analysis due to high risk of bias. 24 studies with a total of 5345 participants were included in the meta-analysis of HbA1c and 18 studies with a total of 3287 participants for FBS. Interventions led to an average reduction in HbA1c when tasks were delivered by nurses (averaged pooled mean difference -0·54% [95% CI -0·89 to -0·18]; I2=80%) and pharmacists (-0·91% [-1·15 to -0·68]; I2=58%), but not when they were delivered by dietitians (-0·50% [-1·10 to 0·09]; I2=54%) or community health workers (0·05% [0·03 to 0·07]; I2=0%). A reduction in average FBS was also observed when interventions were delivered by pharmacists (average pooled mean difference -36·26 mg/dL [-52·60 to -19·92]; I2=78%) but not nurses (-7·46 mg/dL [-18·44 to 3·52]; I2=79%) or community health workers (-5·41 [-12·74 to 1·92]; I2=71%). Only one study reported on FBS when tasks were delivered by dietitians, with a mean difference of -35·00 mg/dL (-65·96 to -4·04).Task sharing interventions with non-physician healthcare workers show moderate effectiveness in diabetes management in LMIC settings. Although relatively high heterogeneity limits the interpretation of the overall findings, interventions led by pharmacists and nurses in LMICs with relatively high physician density are effective strategies in the management of diabetes.Wellcome Trust-Department of Biotechnology India Alliance.
China Kidney Disease Network (CK-NET) 2016 Annual Data Report
Authors: Luxia Zhang, Ming-Hui Zhao, Li Zuo, Yue Wang, Feng Yu, Hong Zhang, Haibo Wang, Rui Chen, Hong Chu, Xinwei Deng, Lanxia Gan, Bixia Gao, Yifang Jiang, Lili Liu, Jianyan Long, Ying Shi, Zaiming Su, Xiaoyu Sun, Wen Tang, Fang Wang, Huai-Yu Wang, Jinwei Wang, Song Wang, Chao Yang, Dongliang Zhang, Xinju Zhao, Liren Zheng, Zhiye Zhou
Journal: Kidney International Supplements (2020)
DNA Demethylase transforms normal cells into highly invasive and metastatic cancer cells: Identification and characterization of novel metastatic cancer targets, therapeutic intervention for these targets, and signaling pathways leading to DNA demethylation
Authors: Stephen Andrews, Jerome Torrisani, Bushra Ateq, Alexander Unterberger, Patrick Salame, Sebastian Alvarado, Jing-Ni Ou, Catalina D'Allessio, Nadine Provencal, Sachin Tendulakar, Marilyne Blain, Joanne Wyglinski, Shaffat Rabbani, Moshe Szyf
Journal: Cancer Research (2008)

13  Introduction: Cancer cells are hallmarked by global DNA hypomethylation. MBD2 is the only protein that has been implicated in removal of methyl groups from CG di-nucleotides. Inhibition of MBD2 attenuates tumorigenesis, metastasis, and reverses the hypomethylation of metastatic genes. Additionally, germ line deletion of the mbd2 gene protects mice from intestinal tumors; therefore, we tested the hypothesis that oncogenic signals induce MBD2 resulting in metastatic transformation of cells through the triggering of global DNA hypomethylation resulting in metastatic gene activation.  Results: Ectopic MBD2 expression but not mutant MBD2 causes global genomic demethylation in normal (NIH 3T3, MCF10A, Primary Human Fibroblasts, and Primary Hepatocytes) and transformed (MCF7, HA-RAS-NIH3T3, and T24) cell lines. MBD2 knockdown in these cell lines results in increased DNA methylation supporting the hypothesis that MBD2 is involved in global hypomethylation. Furthermore, cell lines with increased MBD2 have greater in-vitro demethylase activity. Ectopic MBD2 causes normal cells to become highly transformed and invasive and increases the invasiveness of transformed cell lines. MBD2 overexpressing cells are tumorgenic in NUDE mice and invade and degrade the bone of SCID mice. We show that MBD2 causes this by binding to and demethylating the gene promoters of cell type specific gene sets. We have identified several metastatic promoting genes like MerTK as well as novel metastatic genes that are regulated by MBD2 promoted demethylation. We have proven that these genes are required for metastasis using siRNA strategies in transformed cell lines and developed a therapeutic intervention strategy against a novel metastatic target. Finally, we show that MBD2 is induced by activated HA-RAS, regulates demethylation and metastatic gene activation in these cells, and is regulated by HA-RAS associated transcription factors.  Summary: Our results have unraveled a critical transformation pathway leading from RAS through MBD2 to global hypomethylation and activation of metastatic genes as well. These data support a new therapeutic approach to metastasis, which would involve targeting MBD2 and DNA demethylation.  Supported by a grant from the National Cancer Institute of Canada to MS.
Abstract IA15: Metabolic coordination of cancer cell fate
Authors: Lydia Finley
Journal: Cancer Research (2020)

Abstract Increasing evidence demonstrates that intracellular metabolic pathways can be critical drivers of tumor progression. Metabolites provide the biomass required for cancer cell proliferation and contribute to antioxidant defenses that promote survival and metastatic dissemination. Moreover, oncogenic mutations in several metabolic enzymes lead to accumulation of pathological levels of metabolites that interfere with histone and DNA demethylation and impose a block to differentiation. However, absent these mutations, whether the metabolic profile of cancer cells contributes to the establishment or maintenance of malignant cell identity remains poorly understood. Combining in vitro culture of cancer cells with mouse models of tumor progression, we aim to define the metabolic changes driven by common oncogenes and tumor suppressors and elucidate how these metabolic alterations affect cancer-associated phenotypes. In particular, we focus on how metabolic alterations influence regulation of the chromatin landscape and differentiation programs that antagonize tumor progression. These studies will provide insight into the mechanisms through which tumor cells evade differentiation and sustain malignancy. Citation Format: Lydia Finley. Metabolic coordination of cancer cell fate [abstract]. In: Abstracts: AACR Special Virtual Conference on Epigenetics and Metabolism; October 15-16, 2020; 2020 Oct 15-16. Philadelphia (PA): AACR; Cancer Res 2020;80(23 Suppl):Abstract nr IA15.
Obesity, kidney dysfunction, and inflammation: interactions in hypertension
Authors: John E Hall, Alan J Mouton, Alexandre A da Silva, Ana C M Omoto, Zhen Wang, Xuan Li, Jussara M do Carmo
Journal: Cardiovascular Research (2020)

Abstract Obesity contributes 65–75% of the risk for human primary (essential) hypertension (HT) which is a major driver of cardiovascular and kidney diseases. Kidney dysfunction, associated with increased renal sodium reabsorption and compensatory glomerular hyperfiltration, plays a key role in initiating obesity-HT and target organ injury. Mediators of kidney dysfunction and increased blood pressure include (i) elevated renal sympathetic nerve activity (RSNA); (ii) increased antinatriuretic hormones such as angiotensin II and aldosterone; (iii) relative deficiency of natriuretic hormones; (iv) renal compression by fat in and around the kidneys; and (v) activation of innate and adaptive immune cells that invade tissues throughout the body, producing inflammatory cytokines/chemokines that contribute to vascular and target organ injury, and exacerbate HT. These neurohormonal, renal, and inflammatory mechanisms of obesity-HT are interdependent. For example, excess adiposity increases the adipocyte-derived cytokine leptin which increases RSNA by stimulating the central nervous system proopiomelanocortin-melanocortin 4 receptor pathway. Excess visceral, perirenal and renal sinus fat compress the kidneys which, along with increased RSNA, contribute to renin–angiotensin–aldosterone system activation, although obesity may also activate mineralocorticoid receptors independent of aldosterone. Prolonged obesity, HT, metabolic abnormalities, and inflammation cause progressive renal injury, making HT more resistant to therapy and often requiring multiple antihypertensive drugs and concurrent treatment of dyslipidaemia, insulin resistance, diabetes, and inflammation. More effective anti-obesity drugs are needed to prevent the cascade of cardiorenal, metabolic, and immune disorders that threaten to overwhelm health care systems as obesity prevalence continues to increase.
There is still a place for optimised thiopurine therapy in IBD
Authors: Femke Crouwel, Hans J C Buiter, Nanne K H de Boer
Journal: Gut (2020)

With great interest, we have read the letter by Verstockt et al 1 considering the response rate and outcome of thiopurine monotherapy in patients with Crohn’s disease (CD). The title, however, stating that thiopurine monotherapy has a limited place in treatment of patients with mild-to-moderate CD raised some questions. Almost all patients in this retrospective cohort were treated with azathioprine (AZA) and nowhere is mentioned if patients who experience intolerance were switched to another thiopurine or received a rechallenge. A retrospective study among 1327 patients exposed both to AZA or mercaptopurine (MP) demonstrated, however, that almost half of patients intolerant to the first thiopurine were able to tolerate the second.2 In addition, another study demonstrated that almost 65% had clinical improvement during thioguanine (TG) treatment after AZA or MP failure, so switching could potentially lead to a higher response rate.3 Moreover, the discussed lack of therapeutic drug …
Abstract 14731: Impact of Gender on Coronary Flow Reserve and Microvascular Function as Assessed by Cardiac Magnetic Resonance (CMR) Imaging
Authors: Raksha Indorkar, Brent White, Jennifer Jue, Simone Romano, Mohammed Al-Yafi, Afshin Farzaneh-Far
Journal: Circulation (2017)

Introduction: Coronary microvascular dysfunction has been proposed as a possible explanation for angina in the absence of obstructive coronary artery disease (CAD) in women. However, the impact of ...
Determinants of Long-Term Survival Following Allogeneic Stem Cell Transplantation for Multiple Myeloma: A Multi-Centre Analysis Across the United Kingdom and Australia
Authors: Salvatore Fiorenza, David J M Routledge, Jenny Collins, Michael J Shipton, Simon J. Harrison, James Cavet, Eleni Tholouli, David Ritchie
Journal: Blood (2017)
Intercellular Mitochondria Transfer to Macrophages Regulates White Adipose Tissue Homeostasis and Is Impaired in Obesity
Authors: Jonathan R. Brestoff, Craig B. Wilen, John R. Moley, Yongjia Li, Wei Zou, Nicole P. Malvin, Marina N. Rowen, Brian T. Saunders, Hongming Ma, Madison R. Mack, Barry L. Hykes, Dale R. Balce, Anthony Orvedahl, Jesse W. Williams, Nidhi Rohatgi, Xiaoyan Wang, Michael R. McAllaster, Scott A. Handley, Brian S. Kim, John G. Doench, Bernd H. Zinselmeyer, Michael S. Diamond, Herbert W. Virgin, Andrew E. Gelman, Steven L. Teitelbaum
Journal: Cell Metabolism (2020)
Characteristics and Reporting of Number Needed to Treat, Number Needed to Harm, and Absolute Risk Reduction in Controlled Clinical Trials, 2001-2019
Authors: Marissa H. Elliott, Joshua J. Skydel, Sanket S. Dhruva, Joseph S. Ross, Joshua D. Wallach
Journal: JAMA Internal Medicine (2020)

life. 7 Although there are important limitations on current data regarding outcomes of IHCA for patients with COVID-19, we have enough data to conclude that it is important to implement programs to promote conversations about values and goals in the community and early goals-of-care discussions for patients hospitalized with COVID-19.
<i>Bifidobacterium animalis</i>: the missing link for the cancer-preventive effect of <i>Gynostemma pentaphyllum</i>
Authors: Weilin Liao, Imran Khan, Guoxin Huang, Shengshuang Chen, Liang Liu, Wai Kit Leong, Xiao Ang Li, Jianlin Wu, W. L. Wendy Hsiao
Journal: Gut Microbes (2020)

Colorectal cancer (CRC) ranks the third most common cancer type in both men and women. Besides the known genetic and epigenetic changes in the gut epithelial cells, we now know that disturbed gut microbes could also contribute to the onset and progression of CRC. Hence, keeping a balanced gut microbiota (GM) has become a novel pursue in the medical field, particularly in the area of gastrointestinal disorders. Gynostemma pentaphyllum (Gp) is a dietary herbal medicine. In our previous study, Gp saponins (GpS) displayed prebiotic and cancer-preventive properties through the modulation of GM in ApcMin/+ mice. However, the specific group(s) of GM links to the health effects of GpS remains unknown. To track down the missing link, we first investigated and found that inoculation with fecal materials from GpS-treated ApcMin/+ mice effectively reduces polyps in ApcMin/+ mice. From the same source of the fecal sample, we successfully isolated 16 bacterial species. Out of the 16 bacteria, Bifidobacterium animalis stands out as the responder to the GpS-growth stimulus. Biochemical and RNAseq analysis demonstrated that GpS enhanced expressions of a wide range of genes encoding biogenesis and metabolic pathways in B. animalis culture. Moreover, we found that colonization of B. animalis markedly reduces the polyp burden in ApcMin/+ mice. These findings reveal a mutualistic interaction between the prebiotic and a probiotic to achieve anticancer and cancer-preventive activities. Our result, for the first time, unveils the anticancer function of B. animalis and extend the probiotic horizon of B. animalis.
Liquid biopsy for esophageal cancer: Is detection of circulating cell‐free DNA as a biomarker feasible?
Authors: Zuyang Yuan, Xinfeng Wang, Xiao Geng, Yin Li, Juwei Mu, Fengwei Tan, Qi Xue, Shugeng Gao, Jie He
Journal: Cancer Communications (2020)

Abstract Esophageal cancer (EC) is a common cancer and is histopathologically classified into esophageal squamous cell carcinoma and esophageal adenocarcinoma. EC is a worldwide public health issue because of late diagnosis and lack of effective therapy. In contrast to standard tumor biopsies, liquid biopsies are emerging as a tool which is minimally invasive that can complement or even substitute more classical approaches. Specifically, cell‐free DNA (cfDNA) has shown promise in cancer‐related clinical applications. Indeed, cfDNA has been shown to be an effective circulating biomarker for non‐invasive cancer diagnosis and monitoring of cancer patients. Although the clinical application of cfDNA has been reported on other cancers, few studies have evaluated its use in EC. Here, we review this relevant literature and discuss limitations and advantages of its application in the diagnosis and monitoring of EC.