tbuckley/cabot-search huggingface dataset:
PTU-149 Is Pepsin Detected in the Saliva of Healthy Individuals?
Authors: J O Hayat, A Woodcock, P Dettmar, E Yazaki, J-Y Kang, D Sifrim
Journal: Gut (2013)

<h3>Introduction</h3> The presence of pepsin in the oesophagus or more proximally (pharynx or airways) suggests gastro-oesophageal reflux (GOR). However, appropriate normal values and correlation with acid and non acid reflux are still limited. The <b>aim</b> of this study was to measure pepsin in expectorated saliva together with objective assessment of GOR by pH-impedance in a large cohort of healthy asymptomatic subjects. <h3>Methods</h3> 100 healthy subjects, age 30.7 (range 19–55), BMI 23.7 (17.7–32.8) with no typical or atypical reflux symptoms underwent MII-pH monitoring “off” PPI. Oesophageal pH was measured 5 cm above the LOS and impedance sensors were positioned at 3.7.9.12 and 15 cm above LOS. Subjects collected expectorated saliva on waking, one hour after lunch and one hour after dinner. Saliva was collected into tubes containing 0.5 ml of 0.01 M citric acid and analysed for the presence of pepsin using a lateral flow test comprising two unique human monoclonal antibodies to pepsin (Peptest™, RDBiomed Ltd). The cut off value to determine pepsin positivity was 25 ng/ml. <h3>Results</h3> Of 300 saliva samples tested, 19% were +ve for pepsin. 64% of subjects had all three saliva samples negative; 20% had 1 sample positive, 12% had 2 samples positive and 4% had 3 samples positive. A similar percentage of samples were positive after lunch (24%) and dinner (22%), but lower on waking (10%). Median acid exposure time was 0.3% (IQR – 0.1–0.8%, 95<sup>th</sup>centile 3.5%). Median no. of reflux events was 32 (15–42, 77) being acid 11 (5–22.47) and non-acid 15 (8–25, 46). Saliva samples positive for pepsin were preceded by significantly more reflux events during the 60 min interval before sampling compared to negative samples both after lunch and dinner (+ve pepsin 6 reflux (4–9) vs. -ve pepsin 3 reflux (1–5) p &lt; 0.0001). Supine acid exposure and no. of reflux episodes was not significantly different with +ve or -ve morning samples. Subjects with 3 saliva samples +ve for pepsin had a higher ratio of proximal reflux episodes than subjects with no +ve samples (37%(range 29–40%) vs. 19%(12–33%), p &lt; 0.02). Only 6/300 samples contained more than 250 ng/ml pepsin. <h3>Conclusion</h3> Pepsin was found in the expectorated saliva of a proportion of healthy individuals who did not experience reflux symptoms, particularly post-prandially. However, only 4% of healthy subjects had 3 positive samples. An increased number of reflux episodes were found prior to giving saliva samples with detectable levels of pepsin. Our results suggest that the presence of pepsin in saliva can be a potential screening tool for GERD when at least 3 samples throughout a day are positive or samples contain more than 250 ng/ml pepsin. <h3>Disclosure of Interest</h3> None Declared
<i>Into Bondage</i>
Authors: Thomas B. Cole
Journal: JAMA (2016)

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
Abstract 2594: Ciclopirox inhibits lymphatic endothelial cell tube formation by suppressing VEGFR-3-mediated ERK signaling pathway
Authors: Yan Luo, Shile Huang
Journal: Cancer Research (2011)

Abstract Ciclopirox olamine (CPX), an off-patent antifungal agent used to treat mycoses of skin and nails, has recently been demonstrated to be a potential anticancer agent. However, the underlying mechanism is not well understood. Here for the first time we show that CPX inhibited lymphangiogenesis in an in vitro model (tube formation). This effect was in part associated with inhibition of vascular endothelial growth factor receptor 3 (VEGFR-3) expression, as overexpression of VEGFR-3 conferred partial resistance to CPX inhibitory effect on tube formation in lymphatic endothelial cells (LECs), whereas downregulation of VEGFR-3 mimicked the effect of CPX, blocking the tube formation. Further study revealed that CPX did not alter mRNA level, but inhibited protein synthesis and promoted protein degradation of VEGFR-3. In addition, we found that CPX inhibited phosphorylation of the extracellular signal-related kinase 1/2 (ERK1/2), a downstream effector of VEGFR-3. Overexpression of VEGFR-3 attenuated CPX inhibition of ERK1/2 phosphorylation, whereas downregulation of VEGFR-3 inhibited extracellular signal-related kinase 1/2 (ERK1/2) phosphorylation in LECs. Ectopic expression of constitutively active mitogen -activated protein kinase kinase 1 (MKK1) resulted in activation of ERK1/2, and partially prevented CPX inhibition of LEC tube formation. The results suggest that CPX inhibits LEC tube formation at least in part through inhibiting VEGFR-3-mediated ERK signaling pathway. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2594. doi:10.1158/1538-7445.AM2011-2594
Genome-wide Significant Associations for Cannabis Dependence Severity
Authors: James T. R. Walters, Michael J. Owen
Journal: JAMA Psychiatry (2016)

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 Psychiatry HomeNew OnlineCurrent IssueFor Authors Podcast 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 Psychiatry journal
Long-Term Tissue Culture of Neuroblastomas. II. Morphologic Evidence for Differentiation and Maturation&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: Milton N. Goldstein, José A. Burdman, L. J. Journey
Journal: JNCI Journal of the National Cancer Institute (1964)

Neuroblastoma cells were obtained from 13 young children and cultured in vitro for periods of 1 week to over a year. All but one of the biopsies contained undifferentiated masses of immature neuroblasts resembling small lymphocytes. Culture in vitro of the neuroblastoma cells resulted in differentiation and maturation into more mature neural elements within 5 months. The morphologic evidence for maturation of the neuroblastoma cells included an increase in nuclear size, development of a single large nucleolus, accumulation of Nissl ribonucleic acid substance, the formation of neurofibrils, and hypertrophy of axons. Explantation of a more mature-appearing neuroblastoma resulted in the transformation of all the nerve cells into mature ganglion cells within 20 days. The studies in vitro suggest that neuroblastoma may be the result of a biochemical defect which would prevent maturation of the nerve cells or a tumor population whose progeny have the potentialities to differentiate and mature. The factors responsible for these phenomena in vitro are under investigation.
Retinal Hemorrhage at High Altitude
Authors: Regina Frayser, Charles S. Houston, A. Charles Bryan, I. Drummond Rennie, Gary Gray
Journal: New England Journal of Medicine (1970)

IN July, 1968, retinal disorders were found to have developed in two persons working at 17,500 feet on Mount Logan, Yukon Territory: one of them had papilledema and was semicomatose. In July, 1969, as part of the high-altitude studies conducted by the Arctic Institute in its long-term environmental research program, a pilot study of the retinal circulation was undertaken. The purpose of this communication is to report the frequent occurrence of retinal hemorrhage, often asymptomatic, among persons exposed to high altitude. The only previous mention of this condition that we have found is in the report by Singh et al. . . .
Treatment of Malignant Ventricular Arrhythmias with Endocardial Resection and Implantation of the Automatic Cardioverter-Defibrillator
Authors: Edward V. Platia, Lawrence S.C. Griffith, Levi Watkins, Morton M. Mower, Thomas Guarnieri, M. Mirowski, Philip R. Reid
Journal: New England Journal of Medicine (1986)

Although ventricular resection guided by endocardial mapping has been a successful treatment for drug-refractory ventricular arrhythmias, 20 to 30 percent of patients still have postoperative sustained ventricular tachycardia or sudden death. To improve the outcome of the procedure, we implanted an automatic cardioverter-defibrillator in conjunction with endocardial resection in 28 patients, all of whom had had previous myocardial infarctions and between one and five cardiac arrests. There were three perioperative deaths. During follow-up of 8 to 51 months (mean, 25), 4 of the 25 survivors had recurrences of hypotensive ventricular tachycardia, which in all instances were automatically terminated by the implanted device. One patient, whose automatic cardioverter-defibrillator was not functional, died suddenly. We conclude that patients undergoing mapping-directed endocardial resection can be provided with additional protection against recurrent ventricular tachyarrhythmias or sudden death by implantation of an automatic cardioverter-defibrillator.
Abstract 2022: The WAVE3-dependent cancer cell invasion is regulated by miR-31 during cancer progression and metastasis
Authors: Khalid Sossey-Alaoui
Journal: Cancer Research (2010)

Abstract MicroRNAs are small non-coding RNAs that are directly involved in the regulation of gene expression by either translational repression or degradation of target mRNAs. Because of the high level of conservation of the target motifs, known as seed sequences, within the 3′-untranslated regions (UTR), a single microRNA can regulate numerous target genes simultaneously, providing a mechanism for this class of RNAs to serve as master regulators of gene expression. Loss of expression of miR-31 has recently been suggested to be associated with cancer progression and metastasis (1). Our previous studies reported a very significant correlation between the expression levels of WAVE3, an actin cytoskeleton remodeling protein, and advanced stages of breast cancer, clearly supporting the function of WAVE3 as a metastasis promoter protein (2). Here we show that the activity of WAVE3 to promote cancer cell invasion is regulated by miR-31 microRNA. We also show a clear inverse correlation between expression levels of WAVE3 and miR-31in invasive versus non-invasive cancer cells. miR-31 directly targets the 3’-UTR of the WAVE3 mRNA and inhibits its expression in the invasive cancer cells. The miR-31-mediated down-regulation of WAVE3 results in a significant reduction in the invasive phenotype of cancer cells, which is specific to the loss of WAVE3 expression since re-expression of a miR-31-resistant form of WAVE3 reverses miR-31-mediated inhibition of cancer cell invasion. We finally report a correlation between the expression levels of WAVE3 and miR-31 in non-invasive vs highly invasive primary human breast cancer tumors. In conclusion, a novel mechanism for the regulation of WAVE3 expression in cancer cells has been identified, which controls the invasive properties of cancer cells. The present study also identifies a critical role for WAVE3, downstream of miR-31, in at least one of the multiple steps that govern the invasion-metastasis cascade. References: 1-Valastyan et al., A pleiotropically acting microRNA, miR-31, inhibits breast cancer metastasis. Cell 137:1032-1046. 2009. 2-Sossey-Alaoui et al., Down-regulation of WAVE3, a metastasis promoter gene, inhibits invasion and metastasis of breast cancer cells. Am J Pathol. 170:2112-2121. 2007. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2022.
Thrombocytopenic Purpura with Histiocytosis of the Spleen
Authors: Benjamin H. Landing, Lotte Strauss, Allen C. Crocker, Herbert Braunstein, Walter L. Henley, John R. Will, Martin Sanders
Journal: New England Journal of Medicine (1961)

THE recent independent observation, by several of us, of peculiar histiocytosis of the spleens of patients with "idiopathic" thrombocytopenic purpura has prompted the collection and review of the material here presented. The 9 patients†† described have shown no consistent abnormality of other blood elements, and the unusual histiocytes appear limited to the spleen. Only 2 patients had onset of symptoms in middle life, as did 2 similar ones described in the literature.1 , 2 In the majority the symptoms developed in childhood or early adult life. Easy bruising, repeated epistaxis or formation of hematomas after injury tended to precede more severe manifestations. . . .
Abstract 284: FGFR2 is required for growth and survival in a rare subset of <i>FGFR2</i> amplified colorectal cancer
Authors: Anjili Mathur, Lenora Davis, Alessandra Di Bacco, Adi Gazdar, Bart Lutterbach
Journal: Cancer Research (2010)

Abstract FGFR2 amplification has been reported in subsets of gastric cancer and breast cancer. We describe FGFR2 amplification in a cell line derived from a colorectal carcinoma arising in a young patient with ulcerative colitis. The cell line has features of endocrine differentiation, representing a rare (&amp;lt; 1%) subset of colorectal cancer. FGFR2 amplification in this cell line results in an overexpressed and highly activated FGFR2 kinase. The FGFR selective inhibitor PD173074 blocked FGFR2 phosphorylation and inhibited Erk, Akt, and S6 ribosomal protein phosphorylation. FGFR2 inhibition resulted in profound cell death as measured by robust accumulation of cells in subG1 by flow cytometry and PARP cleavage by western analysis. A structurally unrelated FGFR2 inhibitor, MK2461, also caused cell death and inhibited downstream signaling pathways. RTK arrays revealed coactivation of EGFR family kinases, and a functional role for these kinases is being investigated. Interestingly, an FGFR2 isoform in this cell line migrated at 160kD, in contrast to the 140kD isoform observed in SNU16 and other cell lines. However, C-terminal FGFR2 antibodies did not react with the 160kD FGFR2 isoform, suggesting that it has a C-terminal deletion similar to the FGFR2 isoform in OCUM2M and KatoIII cell lines. We are currently defining the frequency of FGFR2 overexpression and activation in colon cancer tissue microarrays. The strong growth inhibition and induction of cell death observed in vitro suggests that colorectal cancer tumor cells harboring FGFR2 amplification / activation may show similar response to FGFR inhibitor therapy. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 284.
Abstract 3018: Identification of genes up-and down-regulated by dermcidin in G-361 malignant melanoma cell line.
Authors: Jose E. Belizario, Marcela Perez
Journal: Cancer Research (2013)

Abstract Dermcidin (DCD) is a human gene mapped to chromosome 12q13 region, only identified in primates and humans, and normally expressed in the eccrine glands of skin and brain. Several studies have confirmed DCD-derived peptides contribute to innate and immune surveillance and in the oncogenic processes of breast, prostate and skin cancers, as revealed by its role as a growth factor and cell survival. We have further explored DCD function and its tumorigenic potential on skin melanocytes by specifically knocking down its expression in G-361 malignant melanoma cells via expressing constitutively short hairpin RNA against DCD mRNA. Biological and biochemical assays showed that the "knockdown" in the expression of DCD in two cell clones decreased significantly the in vitro growth in cell culture and tumor formation in nude mice. Similar results were obtained treating nude mice bearing G-361 melanoma xenografts with rabbit polyclonal antibodies against DCD protein (1 mg/Kg, i.p., once week, and one month). Here, we present a summary of a DNA microarray-based study that identified the genes that are up- and down-regulated in a G-361 pLKO control clone and a clone expressing constitutively short hairpin RNA against DCD mRNA. A total of 213 genes were differentially and repeatedly expressed in the G-361-DCD-RNAi clone IBC-I (&amp;gt;3-fold change and P &amp;lt; 0.005). Relative to pLKO vector control data profiling, 99 genes were up-regulated and 120 genes were down-regulated. Next, we validated various genes by real time-PCR. Systematic functional analysis of the differentially expressed genes using DAVID platform revealed significant enrichment for U1-U5 spliceosomal complex genes (SNORs) required for post-transcriptional processing of rRNA, mRNA and tRNA as well as small nucleolar RNA and non-coding RNAs (ncRNAs). Further studies are on way to prove the functional connections among ncRNAs in DCD-induced the development and progression of melanoma malignancy. Citation Format: Jose E. Belizario, Marcela Perez. Identification of genes up-and down-regulated by dermcidin in G-361 malignant melanoma cell line. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3018. doi:10.1158/1538-7445.AM2013-3018
Abstract 1050: CD109 expression promotes cell activity and enhances EGF signaling in human glioblastoma cells
Authors: Yoshiki Murakumo, Jing-min Zhang, Masahide Takahashi
Journal: Cancer Research (2010)

Abstract CD109 is a glycosylphosphatidylinositol (GPI)-anchored cell surface protein whose expression is predominantly detected in squamous cell carcinomas of esophagus, lung, uterus and oral cavity. In the previous study, we found CD109 expression in cell lines derived from human glioblastomas by Northern blot analysis, however, the role of CD109 expression in glioblastoma cells is unclear. Here, we describe our study on significance of CD109 expression in biology of human glioblastoma cells. CD109-overexpressing glioblastoma cells exhibit upregulation of cell growth, motility and invasion ability compared with control cells. Evaluation of intracellular signaling status revealed that the CD109-overexpressing cells showed enhanced phosphorylation of ERK, AKT, and p38MAPK. After epidermal growth factor (EGF) stimulation, strong and sustained phosphorylation of these molecules and EGF receptor (EGFR) was observed in the CD109-overexpressing cells. In addition, we found an interaction between CD109 and EGFR and colocalization of these molecules without EGF stimulation. However, the interaction and colocalization were abolished after EGF stimulation, and EGFR internalization was not affected by CD109 overexpression. These findings suggest that CD109 facilitates EGF signaling via binding to EGFR and its expression is associated with the malignant behavior of glioblastoma cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1050.
Abstract 3887: A screen for new cancer specific drugs that target centrosome clustering
Authors: Eiko Kawamura, Andrew Fielding, Nagarajan Kannan, Connie Eaves, Michel Roberge, Shoukat Dedhar
Journal: Cancer Research (2012)

Abstract Most normal cells have two centrosomes that form bipolar spindles during mitosis, while cancer cells often contain extra centrosomes. Such cancer cells then achieve bipolar division by clustering centrosomes into two functional poles. Our lab has previously shown that inhibition of Integrin-linked kinase, which is a signaling and scaffold protein in focal adhesion and is also a centrosomal protein, results in scattered centrosomes and multipolar spindles, which leads to cancer specific cell death (Fielding et al., 2011, 30:521-534, Oncogene). A major problem with clinically used anti-mitotic drugs, such as taxol, is their toxicity in normal cells. Our goal is to develop new drugs that act specifically on cancer cells through targeting extra centrosomes without affecting normal cells. To discover new drugs, we established a high-content screen that automatically detects cells with de-clustered centrosomes. BT-549, a breast cancer cell line, was used for the screen, since it is known to effectively cluster centrosomes. The Canadian Chemical Biology Network enabled us to test chemical libraries predicted to have drug-like properties. For screening, cells were grown in 96 well plates, treated with test compounds for 5 hours, and subjected to immunofluorescence to examine centrosome arrangement in mitotic cells. Images were taken and analyzed with an automated fluorescence imager, Cellomics Array Scan VTI. We have thus screened over 6000 compounds from which we identified 18 hits. Fifteen of these were confirmed to inhibit centrosome clustering in the cells cultured under standard conditions, and induce an arrest in mitosis. Three compounds are structurally similar, suggesting a common structural motif as preventing centrosome clustering. To compare the effects of these drugs on normal and cancer cells, the viability of several breast and other cancer cell lines, an immortalized model of normal human mammary epithelial cells (MCF10A), and freshly isolated primary normal human mammary epithelial cells were examined after two days of drug treatment using the MTT assay. These comparisons identified some compounds that selectively reduced the viability of cancer cells, but not normal mammary epithelial cells suggesting their potential for cancer-specific therapy. These small molecules are currently being tested in orthotopic and xenograft models, and will be studied for target identification and mechanism of action for further drug development. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3887. doi:1538-7445.AM2012-3887