tbuckley/cabot-search huggingface dataset:
Metagenomic analysis of faecal microbiome as a tool towards targeted non-invasive biomarkers for colorectal cancer
Authors: Jun Yu, Qiang Feng, Sunny Hei Wong, Dongya Zhang, Qiao yi Liang, Youwen Qin, Longqing Tang, Hui Zhao, Jan Stenvang, Yanli Li, Xiaokai Wang, Xiaoqiang Xu, Ning Chen, William Ka Kei Wu, Jumana Al-Aama, Hans Jørgen Nielsen, Pia Kiilerich, Benjamin Anderschou Holbech Jensen, Tung On Yau, Zhou Lan, Huijue Jia, Junhua Li, Liang Xiao, Thomas Yuen Tung Lam, Siew Chien Ng, Alfred Sze-Lok Cheng, Vincent Wai-Sun Wong, Francis Ka Leung Chan, Xun Xu, Huanming Yang, Lise Madsen, Christian Datz, Herbert Tilg, Jian Wang, Nils Brünner, Karsten Kristiansen, Manimozhiyan Arumugam, Joseph Jao-Yiu Sung, Jun Wang
Journal: Gut (2015)

To evaluate the potential for diagnosing colorectal cancer (CRC) from faecal metagenomes.We performed metagenome-wide association studies on faecal samples from 74 patients with CRC and 54 controls from China, and validated the results in 16 patients and 24 controls from Denmark. We further validated the biomarkers in two published cohorts from France and Austria. Finally, we employed targeted quantitative PCR (qPCR) assays to evaluate diagnostic potential of selected biomarkers in an independent Chinese cohort of 47 patients and 109 controls.Besides confirming known associations of Fusobacterium nucleatum and Peptostreptococcus stomatis with CRC, we found significant associations with several species, including Parvimonas micra and Solobacterium moorei. We identified 20 microbial gene markers that differentiated CRC and control microbiomes, and validated 4 markers in the Danish cohort. In the French and Austrian cohorts, these four genes distinguished CRC metagenomes from controls with areas under the receiver-operating curve (AUC) of 0.72 and 0.77, respectively. qPCR measurements of two of these genes accurately classified patients with CRC in the independent Chinese cohort with AUC=0.84 and OR of 23. These genes were enriched in early-stage (I-II) patient microbiomes, highlighting the potential for using faecal metagenomic biomarkers for early diagnosis of CRC.We present the first metagenomic profiling study of CRC faecal microbiomes to discover and validate microbial biomarkers in ethnically different cohorts, and to independently validate selected biomarkers using an affordable clinically relevant technology. Our study thus takes a step further towards affordable non-invasive early diagnostic biomarkers for CRC from faecal samples.
Gene Polymorphisms and Variability of Human Apolipoproteins
Authors: E A Fisher, P M Coates, J A Cortner
Journal: Annual Review of Nutrition (1989)

INTRODUCTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 40 Transport of Exogenous (Dietary) Li pids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 40 Transport of Endogenous Lipids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 4 1 HDL and Reverse Cholesterol Transport . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 4 1 APOLIPOPROTEIN GENES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 42 Chromosomal Localization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 42 Evolutionary Considerations .. . . . . . . . . ... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 42 APOLIPOPROTEIN GENE VARIATION . . . . . . . . .. . . .. . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . 1 45 Meth ods to Study Varia bility of Apolipoprotein Genes... . . . .   . . . . . . . . 1 45 ApoA-/IC-III1A-/V Gene Cluster. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 46 ApoA-1I Gene . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 48 ApoB Gene . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 49 ApoC-lI Gene . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 52 ApoE Gene . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 53 Apo(a ) Gene . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 155 ApoD Gene. . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 155 CONCLUDING REMARKS . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 55
New Type 2 Diabetes Portal Open to Researchers and Public
Authors: Julie A. Jacob
Journal: JAMA (2015)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
European Consensus Statement on congenital hypogonadotropic hypogonadism—pathogenesis, diagnosis and treatment
Authors: Ulrich Boehm, Pierre-Marc Bouloux, Mehul T. Dattani, Nicolas de Roux, Catherine Dodé, Leo Dunkel, Andrew A. Dwyer, Paolo Giacobini, Jean-Pierre Hardelin, Anders Juul, Mohamad Maghnie, Nelly Pitteloud, Vincent Prevot, Taneli Raivio, Manuel Tena-Sempere, Richard Quinton, Jacques Young
Journal: Nature Reviews Endocrinology (2015)

Congenital hypogonadotropic hypogonadism (CHH)—a rare disorder caused by deficient production, secretion or action of gonadotropin-releasing hormone—results in an absence of puberty and infertility. Here, Ulrich Boehm and colleagues summarize approaches for the diagnosis and treatment of CHH in light of recent discoveries. This Consensus Statement differs from existing guidelines for the treatment of hypogonadism as it focuses exclusively on CHH. Congenital hypogonadotropic hypogonadism (CHH) is a rare disorder caused by the deficient production, secretion or action of gonadotropin-releasing hormone (GnRH), which is the master hormone regulating the reproductive axis. CHH is clinically and genetically heterogeneous, with >25 different causal genes identified to date. Clinically, the disorder is characterized by an absence of puberty and infertility. The association of CHH with a defective sense of smell (anosmia or hyposmia), which is found in ∼50% of patients with CHH is termed Kallmann syndrome and results from incomplete embryonic migration of GnRH-synthesizing neurons. CHH can be challenging to diagnose, particularly when attempting to differentiate it from constitutional delay of puberty. A timely diagnosis and treatment to induce puberty can be beneficial for sexual, bone and metabolic health, and might help minimize some of the psychological effects of CHH. In most cases, fertility can be induced using specialized treatment regimens and several predictors of outcome have been identified. Patients typically require lifelong treatment, yet ∼10–20% of patients exhibit a spontaneous recovery of reproductive function. This Consensus Statement summarizes approaches for the diagnosis and treatment of CHH and discusses important unanswered questions in the field.
Hyperdiploidy and chromosomal rearrangements define the anaplastic variant of Wilms' tumor.
Authors: E C Douglass, A T Look, B Webber, D Parham, J A Wilimas, A A Green, P K Roberson
Journal: Journal of Clinical Oncology (1986)

Flow cytometric measurement of the DNA content of Wilms' tumor cells revealed a striking correspondence with the histologic subtype and treatment outcome. In the 48 cases studied, a hyperdiploid DNA content ranging from 1.7 to 3.2 times the result for normal diploid cells distinguished all but one of the ten anaplastic tumors. Lower values, from 1.0 to 1.4 times the diploid DNA content, characterized the nonanaplastic specimens. By Kaplan-Meier analysis, the probability of achieving 3 years of relapse-free survival was significantly lower in the group with higher DNA content (0.42 v 0.87, P less than .01). Analysis of banded chromosomes for a subset of 22 patients contributed important information beyond the flow cytometric study. Cases of anaplasia associated with poorer responses to therapy showed numerous complex translocations, whereas all others lacked such changes. By combining flow cytometric techniques and conventional methods of chromosome analysis, it should be possible to identify those patients with Wilms' tumor who are most likely to fail therapy. The biologic implication of these findings is that the development of clinical drug resistance in Wilms' tumor is a result of the genetic instability of the malignant clone.
B cell acute lymphocytic leukemia in adults. Clinical, morphologic, and immunologic findings.
Authors: P S Gill, P R Meyer, Z Pavlova, A M Levine
Journal: Journal of Clinical Oncology (1986)

Acute lymphocytic leukemia (ALL) is a heterogeneous group of disorders, clinically, immunologically, and pathologically. ALL of a B cell phenotype (B-ALL) is the least common. We have studied ten adult patients with B-ALL, none of whom had a tumor mass. The median age was 56 years (range, 30 to 90). A history of an altered immune state was noted in four cases: a distant history of Hashimoto's thyroiditis in one, pregnancy in one, and acquired immunodeficiency syndrome in two. Two patients presented with CNS involvement, and in two additional patients CNS leukemia developed during the course of disease. By the French-American-British (FAB) classification system, L3 leukemic morphology was present in nine, whereas L2 was present in one. Circulating leukemic blasts varied from less than 500/dL to greater than 15,000/dL. Eight patients were thrombocytopenic, and eight were anemic at presentation. Immunologic marker studies on leukemic blasts revealed monoclonal kappa light chain marking in nine and monoclonal lambda in one. Following chemotherapy, complete remission was achieved in three patients, two of whom experienced relapse within 9 months. The median survival for the group was 3 months, and only one patient experienced long-term, disease-free survival. We conclude that B-ALL in the adult presents with the classic L3 morphologic picture in the majority and is associated with extremely short survival.
A phase II study of tivozanib in patients with metastatic and nonresectable soft-tissue sarcomas.
Authors: Lauren Elizabeth Nye, Ariel Polish, Susan E. Abbinanti, Claudia Roxana Vintilescu, Alfred Rademaker, Catherine Humphreys, Rasima Cehic, Thomas McFarland, Mohammed M. Milhem, Keith M. Skubitz, Brian Andrew Van Tine, Scott H. Okuno, Mark Agulnik
Journal: Journal of Clinical Oncology (2014)

TPS10604 Background: Despite the multi-modality approach, many patients with early stage soft tissue sarcomas will develop recurrent or metastatic disease. Complete responses to chemotherapy for metastatic sarcomas are rare and do not translate to improved overall survival (OS). Given the lack of efficacy with current chemotherapy, investigational studies are needed to identify new antitumor agents. Angiogenesis plays an important role in cancer progression. Most tumors overexpress vascular endothelial growth factor receptors (VEGFRs), which allow the tumor to grow and metastasize. VEGFR1, VEGFR2 and VEGFR3 are high affinity receptor tyrosine kinases localized in the endothelium of tumor vasculature and are involved in tumor angiogenesis. VEGFR tyrosine kinase inhibitors (TKI) block phosphorylation of the VEGFR and inhibit activation of angiogenesis and, indirectly, tumor growth. Previous phase II data with a VEGFR TKI demonstrated improved progression-free survival (PFS) in patients with relapsed or refractory soft tissue sarcoma. Tivozanib is a potent and highly selective VEGFR TKI with activity against all three VEGFRs and thus a potential novel agent in the treatment of metastatic sarcoma. Methods: A total of 54 patients with metastatic sarcoma who have failed one previous therapy will be enrolled. Key inclusion criteria include diagnosis of metastatic and/or locally advanced or recurrent disease and measurable disease. Patients with alveolar soft-part sarcoma, chondrosarcoma, dermatofibrosarcoma, Ewing sarcoma, GIST, Kaposi sarcoma, mixed mesodermal tumor/carcinosarcoma, osteosarcoma, low grade sarcomas, rhabdomyosarcoma, interdigitating dendritic sarcoma and giant cell tumor of bone are ineligible. Eligible patients will receive tivozanib 1.5mg oral daily for 21 days in a 28 day cycle. The primary endpoint is PFS. Secondary objectives include overall response rate, clinical benefit rate, OS, toxicity and correlation of clinical outcome with antibodies for VEGFR1 and VEGFR2. Enrollment began in 03/2013. As of 01/2014, 22 of 54 patients have been enrolled. Clinical trial information: NCT01782313.
Defects in the Fanconi Anemia Pathway in Head and Neck Cancer Cells Stimulate Tumor Cell Invasion through DNA-PK and Rac1 Signaling
Authors: Lindsey E. Romick-Rosendale, Elizabeth E. Hoskins, Lisa M. Privette Vinnedge, Grant D. Foglesong, Marion G. Brusadelli, S. Steven Potter, Kakajan Komurov, Samantha A. Brugmann, Paul F. Lambert, Randall J. Kimple, Elizabeth L. Virts, Helmut Hanenberg, Maura L. Gillison, Susanne I. Wells
Journal: Clinical Cancer Research (2015)

Head and neck squamous cell carcinoma (HNSCC) remains a devastating disease, and Fanconi anemia (FA) gene mutations and transcriptional repression are common. Invasive tumor behavior is associated with poor outcome, but relevant pathways triggering invasion are poorly understood. There is a significant need to improve our understanding of genetic pathways and molecular mechanisms driving advanced tumor phenotypes, to develop tailored therapies. Here we sought to investigate the phenotypic and molecular consequences of FA pathway loss in HNSCC cells.Using sporadic HNSCC cell lines with and without FA gene knockdown, we sought to characterize the phenotypic and molecular consequences of FA deficiency. FA pathway inactivation was confirmed by the detection of classic hallmarks of FA following exposure to DNA cross-linkers. Cells were subjected to RNA sequencing with qRT-PCR validation, followed by cellular adhesion and invasion assays in the presence and absence of DNA-dependent protein kinase (DNA-PK) and Rac1 inhibitors.We demonstrate that FA loss in HNSCC cells leads to cytoskeletal reorganization and invasive tumor cell behavior in the absence of proliferative gains. We further demonstrate that cellular invasion following FA loss is mediated, at least in part, through NHEJ-associated DNA-PK and downstream Rac1 GTPase activity.These findings demonstrate that FA loss stimulates HNSCC cell motility and invasion, and implicate a targetable DNA-PK/Rac1 signaling axis in advanced tumor phenotypes.
Active specific immunotherapy of metastatic melanoma with an antiidiotype vaccine: a phase I/II trial of I-Mel-2 plus SAF-m.
Authors: W D Quan, G E Dean, L Spears, C P Spears, S Groshen, J A Merritt, M S Mitchell
Journal: Journal of Clinical Oncology (1997)

PURPOSE To determine the toxicity and immunologic activity of an antiidiotype melanoma vaccine that consists of monoclonal antibody I-Mel-2 (MELIMMUNE-2, IDEC Pharmaceuticals, La Jolla, CA) and an immunologic adjuvant SAF-m. PATIENTS AND METHODS Twenty-six patients with metastatic melanoma, 17 of whom had previously received chemotherapy, were given 2 mg of I-Mel-2 and either 100 micrograms (n = 6) or 250 micrograms (n = 20) of SAF-m. Antiidiotype vaccine was given intramuscularly (IM) biweekly for 4 weeks, and then bimonthly until disease progression. Human antimurine antibodies (HAMA), anti-I-Mel-2 antibodies, and specific antibody (Ab)3 against the melanoma epitope mimicked by the vaccine were titrated before treatment, biweekly from weeks 4 to 12, and every 4 to 8 weeks thereafter. Computed tomographic (CT) scans of the chest, abdomen, and pelvis and magnetic resonance imaging (MRI) of the brain were obtained before and bimonthly during treatment to evaluate responses. RESULTS Elevated titers of human antimouse antibodies and anti-I-Mel-2 antibodies were associated with clinical antitumor effect (P = .02 and P = .05, respectively). Ab3 was absent in most patients, but was found in the best clinical responder. Fever, myalgias/arthralgias, fatigue, nausea, and headaches were the most common toxicities. Grade III myalgias/arthralgias and headaches required dose reduction of SAF-m in eight patients at the 250-microgram dose. No treatment-related death occurred. Six patients had an antitumor effect: one complete response in liver and lung, two minor responses, and three stable disease. The patient with a complete response has survived nearly 5 years. CONCLUSION I-Mel-2 antiidiotype vaccine was safe, tolerated best at the 100-microgram dose of SAF-m, and had immunologic and clinical activity.
<i>The Harvest Moon</i>
Authors: Jeanette M. Smith
Journal: JAMA (2015)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
The Contribution of Nutrition Research to the Control of Undernutrition: The Indian Experience
Authors: C Gopalan
Journal: Annual Review of Nutrition (1992)

Since diseases directly related to undernutrition are the major public health problems of India, nutrition research in the country has been largely directed towards elucidating their causes and identifying the most feasible methods for their prevention and control. This effort is an interdisciplinary exercise carried out in the laboratory, the clinic, and the field, with close interaction among biochemists, clinicians, and epidemiologists. Some of the identified solutions have found practical application; but, as in other areas of scientific endeavor, a gap exists between the acquisition of knowledge in the laboratories and its application in the field. Today, thanks to research efforts of the last few decades, we have the knowledge with which most diseases related to undernutrition can be prevented. Unfortunately, however, we do not always have the means of applying this knowledge under real-life conditions in the field. Even so, nutrition research during the last few decades has contributed significantly to the amelioration of undernutrition among poor communities in India.
Progressive Lower Extremity Pain
Authors: Dustin Y. Yoon, Andrew W. Hoel
Journal: JAMA Surgery (2015)

A 39-year-old active woman presented with a progressive 6-month history of bilateral lower extremity pain after walking 1 block or ascending a flight of stairs. The pain was aching, relieved with rest, and primarily in her buttocks and thighs bilaterally. What is your diagnosis?
The Richmond Agitation Sedation Scale was accurate for detecting delirium in older patients in the ED
Authors: Christopher Robert Carpenter
Journal: Annals of Internal Medicine (2015)

Source Citation Han JH, Vasilevskis EE, Schnelle JF, et al. The diagnostic performance of the Richmond Agitation Sedation Scale for detecting delirium in older emergency department patients. Acad Emerg Med. 2015;22:878-82. 26113020