tbuckley/cabot-search huggingface dataset:
ACTION ON FIBROBLASTS OF THE PROTEIN FRACTION OF EMBRYONIC TISSUE EXTRACT
Authors: Lillian E. Baker, Alexis Carrel
Journal: The Journal of Experimental Medicine (1926)

The above experiments indicate that the growth-stimulating substance found in embryonic tissue extract, which has been responsible for the continuous growth of fibroblasts in vitro for 14 years, is either protein in nature or closely associated with the protein of the extract and adsorbed by it. If any specific hormone responsible for cell division is present, it is united to the protein or carried along with it in its first precipitation. It seems probable that the tissues utilize this protein for the nitrogen which they build into protoplasm. Whether it is first hydrolyzed before adsorption by the tissues has not been ascertained as yet. It has been shown in other experiments reported in the following paper that the amino acids of the tissue juice do not suffice for the growth of fibroblasts and that hydrolyzed tissue juice is toxic in the same way that a too concentrated mixture of amino acids is toxic. The results of the foregoing experiments may be summarized as follows: 1. Fractionation of embryo tissue juice has shown that it is the protein fraction that contains the activating substance. 2. Tissues continue to grow for a long time in the protein of the extract precipitated by CO2 and at a rate approximately equal to that in the original extract diluted to the same nitrogen concentration. 3. The non-protein nitrogen gives slight stimulation to growth. 4. Purification of the protein by repeated precipitation destroys its growth-promoting properties, but whether this is due to a denaturing of the protein,—which occurs very readily,—or to loss of some substance possibly an enzyme attached to it, has not been ascertained. 5. Preparations of purified proteins from embryonic tissue and egg white have shown no marked nutritive or stimulating action. A number of other pure substances have been tried without effect.
Normalization of obesity-associated insulin resistance through immunotherapy
Authors: Shawn Winer, Yin Chan, Geoffrey Paltser, Dorothy Truong, Hubert Tsui, Jasmine Bahrami, Ruslan Dorfman, Yongqian Wang, Julian Zielenski, Fabrizio Mastronardi, Yuko Maezawa, Daniel J Drucker, Edgar Engleman, Daniel Winer, H.-Michael Dosch
Journal: Nature Medicine (2009)
Autocrine stimulation of VEGFR-2 activates human leukemic cell growth and migration
Authors: Sergio Dias, Koichi Hattori, Zhenping Zhu, Beate Heissig, Margaret Choy, William Lane, Yan Wu, Amy Chadburn, Elizabeth Hyjek, Muhammad Gill, Daniel J. Hicklin, Larry Witte, M.A.S. Moore, Shahin Rafii
Journal: Journal of Clinical Investigation (2000)

Emerging data suggest that VEGF receptors are expressed by endothelial cells as well as hematopoietic stem cells. Therefore, we hypothesized that functional VEGF receptors may also be expressed in malignant counterparts of hematopoietic stem cells such as leukemias. We demonstrate that certain leukemias not only produce VEGF but also express functional VEGFR-2 in vivo and in vitro, resulting in the generation of an autocrine loop that may support leukemic cell survival and proliferation. Approximately 50% of freshly isolated leukemias expressed mRNA and protein for VEGFR-2. VEGF(165) induced phosphorylation of VEGFR-2 and increased proliferation of leukemic cells, demonstrating these receptors were functional. VEGF(165) also induced the expression of MMP-9 by leukemic cells and promoted their migration through reconstituted basement membrane. The neutralizing mAb IMC-1C11, specific to human VEGFR-2, inhibited leukemic cell survival in vitro and blocked VEGF(165)-mediated proliferation of leukemic cells and VEGF-induced leukemic cell migration. Xenotransplantation of primary leukemias and leukemic cell lines into immunocompromised nonobese diabetic mice resulted in significant elevation of human, but not murine, VEGF in plasma and death of inoculated mice within 3 weeks. Injection of IMC-1C11 inhibited proliferation of xenotransplanted human leukemias and significantly increased the survival of inoculated mice. Interruption of signaling by VEGFRs, particularly VEGFR-2, may provide a novel strategy for inhibiting leukemic cell proliferation.
Multiple liver lesions in a smoker
Authors: J Sharkey, K R Palmer, I D R Arnott, S Glancy
Journal: Gut (2007)

A 39-year-old female smoker presented to the gastrointestinal unit with a 6-month history of increasing right upper quadrant pain, abdominal distension, nausea and anorexia. There was a history of dysmenorrhoea but no …
Anemia and Chronic Heart Failure
Authors: Andrew L. Clark, John G.F. Cleland
Journal: Circulation (2005)

he treatment of patients with chronic heart failure is one of the great successes of modern medical therapy.Good medical management can approximately double life expectancy for patients with significant left ventricular systolic dysfunction, 1 and for some patients at least, induce a state of remission. 2Mortality remains high, however, and many patients remain symptom limited.
RECK gene expression in hepatocellular carcinoma: Correlation with invasion-related clinicopathological factors and its clinical significance
Authors: Katsuyoshi Furumoto, Shigeki Arii, Akira Mori, Hiroaki Furuyama, Manuel J. Gorrin Rivas, Teizou Nakao, Naoki Isobe, Toru Murata, Chiaki Takahashi, Makoto Noda, Masayuki Imamura
Journal: Hepatology (2001)

The RECK (reversion-inducing-cysteine-rich protein with Kazal motifs) gene was initially isolated as a transformation suppressor gene. It encodes a membrane-anchored glycoprotein with multiple serine protease inhibitor-like domains. The RECK gene is expressed widely in normal organs but is undetectable in many tumor-derived cell lines. When artificially expressed in such cell lines, RECK suppresses their invasive and metastatic activities. Clinical implications of these findings, however, remained undefined because of the lack of studies using fresh human tumor samples. In the present study, we have addressed this issue by analyzing the levels of RECK gene expression in hepatocellular carcinoma (HCC). RECK mRNA was detectable by RNA blot hybridization in all the tumorous and contiguous nontumorous tissues obtained from 64 patients with HCC. In 26 cases, the RECK expression in tumorous tissues was higher than that in nontumorous tissues. The expression of RECK protein in these tissues could also be demonstrated by immunohistochemistry. Patients with high RECK mRNA expression in tumorous tissues tended to show better survival (P =.02), and such tumors had a tendency to be less invasive. Univariate and multivariate analysis revealed that the RECK mRNA expression is a novel and independent variable affecting overall survival (P =.01). These findings support the hypothesis that RECK has negative effects on the invasiveness of HCC cells and suggest the feasibility of RECK mRNA as a promising prognostic molecular marker for HCC.
Interleukin-1β causes excitotoxic neurodegeneration and multiple sclerosis disease progression by activating the apoptotic protein p53
Authors: Silvia Rossi, Caterina Motta, Valeria Studer, Giulia Macchiarulo, Elisabetta Volpe, Francesca Barbieri, Gabriella Ruocco, Fabio Buttari, Annamaria Finardi, Raffaele Mancino, Sagit Weiss, Luca Battistini, Gianvito Martino, Roberto Furlan, Jelena Drulovic, Diego Centonze
Journal: Molecular Neurodegeneration (2014)

Understanding how inflammation causes neuronal damage is of paramount importance in multiple sclerosis (MS) and in other neurodegenerative diseases. Here we addressed the role of the apoptotic cascade in the synaptic abnormalities and neuronal loss caused by the proinflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor (TNF-α) in brain tissues, and disease progression caused by inflammation in relapsing-remitting MS (RRMS) patients. The effect of IL-1β, but not of TNF-α, on glutamate-mediated excitatory postsynaptic currents was blocked by pifithrin-α (PFT), inhibitor of p53. The protein kinase C (PKC)/transient receptor potential vanilloid 1 (TRPV1) pathway was involved in IL-1β-p53 interaction at glutamatergic synapses, as pharmacological modulation of this inflammation-relevant molecular pathway affected PFT effects on the synaptic action of IL-1β. IL-1β-induced neuronal swelling was also blocked by PFT, and IL-1β increased the expression of p21, a canonical downstream target of activated p53. Consistent with these in vitro results, the Pro/Pro genotype of p53, associated with low efficiency of transcription of p53-regulated genes, abrogated the association between IL-1β cerebrospinal fluid (CSF) levels and disability progression in RRMS patients. The interaction between p53 and CSF IL-1β was also evaluated at the optical coherence tomography (OCT), showing that IL-1β-driven neurodegenerative damage, causing alterations of macular volume and of retinal nerve fibre layer thickness, was modulated by the p53 genotype. Inflammatory synaptopathy and neurodegeneration caused by IL-1β in RRMS patients involve the apoptotic cascade. Targeting IL-1β-p53 interaction might result in significant neuroprotection in MS.
HDAC6 inhibitors reverse axonal loss in a mouse model of mutant HSPB1–induced Charcot-Marie-Tooth disease
Authors: Constantin d'Ydewalle, Jyothsna Krishnan, Driss M Chiheb, Philip Van Damme, Joy Irobi, Alan P Kozikowski, Pieter Vanden Berghe, Vincent Timmerman, Wim Robberecht, Ludo Van Den Bosch
Journal: Nature Medicine (2011)
Effect of a Preoperative Intervention on Preoperative and Postoperative Outcomes in Low-Risk Patients Awaiting Elective Coronary Artery Bypass Graft Surgery
Authors: Heather M. Arthur
Journal: Annals of Internal Medicine (2000)

Background: In publicly funded health care systems, a waiting period for such services as coronary artery bypass graft surgery (CABG) is common. The possibility of using the waiting period to improve patient outcomes should be investigated. Objective: To examine the effect of a multidimensional preoperative intervention on presurgery and postsurgery outcomes in low-risk patients awaiting elective CABG. Design: Randomized, controlled trial. Setting: A regional cardiovascular surgery center in a tertiary care hospital, southwestern Ontario, Canada. Patients: 249 patients on a waiting list for elective CABG whose surgeries were scheduled for a minimum of 10 weeks from the time of study recruitment. Intervention: During the waiting period, the treatment group received exercise training twice per week, education and reinforcement, and monthly nurse-initiated telephone calls. After surgery, participation in a cardiac rehabilitation program was offered to all patients. Measurements: Postoperative length of stay was the primary outcome. Secondary outcomes were exercise performance, general health-related quality of life, social support, anxiety, and utilization of health care services. Results: Length of stay differed significantly between groups. Patients who received the preoperative intervention spent 1 less day [95% CI, 0.0 to 1.0 day] in the hospital overall (P = 0.002) and less time in the intensive care unit (median, 2.1 hours [CI, −1.2 to 16 hours]; P = 0.001). During the waiting period, patients in the intervention group had a better quality of life than controls. Improved quality of life continued up to 6 months after surgery. Mortality rates did not differ. Conclusion: The waiting period for elective procedures, such as CABG, may be used to enhance in-hospital and early-phase recovery, improving patients' functional abilities and quality of life while reducing their hospital stay.
Does the healthy hepatitis C virus carrier state really exist? an analysis using polymerase chain reaction
Authors: Martín Prieto, Vicente Olaso, Clara Verdú, Juan Córdoba, Concepción Gisbert, Miguel Rayón, Domingo Carrasco, Marina Berenguer, María Dolores Higón, Joaquín Berenguer
Journal: Hepatology (1995)

To determine whether the presence of hepatitis C virus (HCV) viremia correlates with the severity of liver disease in anti-HCV-positive apparently healthy blood donors, we studied 98 blood donors found positive for anti-HCV using enzyme-linked immunosorbent assay (ELISA). Each subject underwent a liver biopsy, a test for HCV RNA in the serum by polymerase chain reaction (PCR), and a panel of liver injury tests. As a result, 97% of the anti-HCV-positive blood donors had some type of histological abnormality:22 (22%) had minimal changes, 1 (1%) had chronic lobular hepatitis, 40 (41%) had chronic persistent hepatitis (CPH), and 32 (33%) had chronic active hepatitis (CAH). Only 3 subjects had a normal liver histology. HCV RNA was detectable in the serum in 65% of the anti-HCV-positive donors. HCV RNA in serum was detectable in none of the donors with a normal liver histology, in 36% (confidence interval [CI], 17% to 59%) of those with minimal changes, in 70% (CI, 53% to 83%) of those with CPH, and in 87% (CI, 71% to 96%) of those with CAH (P = .00001). HCV RNA was detectable in 75% of the donors with elevated (> 45 U/L) alanine transaminase (ALT) values and in 59% of those with normal ALT levels (P = not significant). The incidence of chronic hepatitis was higher in HCV RNA-positive than in HCV RNA-negative donors (88% vs. 50%; P = .00005).(ABSTRACT TRUNCATED AT 250 WORDS)
Mucosal Uric Acid Induces Interleukin 33 and Initiates Type 2 Immune Responses To Inhaled Protease Allergens
Authors: Kenichiro Hara, Koji Iijima, Takao Kobayashi, Satoshi Seno, Ichiro Tojima, Gail Kephart, Manabu Ueno, Toshitaka Maeno, Masahiko Kurabayashi, Hirohito Kita
Journal: Journal of Allergy and Clinical Immunology (2014)
P213 Never events &amp; the checklist manifesto for intercostal chest drains
Authors: B Khan
Journal: Thorax (2013)

<h3>Background</h3> In the complex medical environment, clinicians commonly face varying challenges especially when undertaking invasive procedure with the risk of potential to harm patients. Checklists have a role in not only helping overcome human fallibility, but also ensuring that key steps are adhered to in order to ensure patient safety. Intercostal chest drains are amongst the most invasive procedure undertaken in Internal Medicine, often out of hours and in emergent clinical situations, and possibly in less than ideal environments and with limited or no supervision. All of these factors have been highlighted in the 2008 UK National Patient Safety Agency (NPSA) report highlighting 780 events of harm including 12 deaths from intercostal chest drain insertions1. The NPSA Never Events2 list includes wrong site surgery, and in the respiratory discipline this encompasses the inserting of a chest drain on the wrong side. Never Events are preventable because: there is guidance that explains what the care or treatment should be; there is guidance to explain how risks and harm can be prevented; and there has been adequate notice and support to put systems in place to prevent them from happening. <h3>Methodology</h3> A systematic review of available literature around chest drain insertion, proformas and checklists was conducted. Other relevant checklists e.g. WHO surgical safety checklist were also reviewed. After an iterative design process involving chest physicians, general physicians, trainees and nurses, a checklist was devised, piloted and introduced into practice. <h3>Conclusion</h3> The Chest drain safety checklist was introduced in August 2011, and has since been adopted by the A&amp;E Department and also neighbouring hospitals. Since its introduction, there have not been any adverse incidents in the Medical Department involving intercostal chest drain insertions. There is more confidence amongst nursing staff as they feel more involved and engaged. Trainees find the structured approach particularly helpful in ensuring key steps are not missed and patient safety ensured, and seek supervision and assistance more readily. <h3>References</h3> NPSA Rapid Response Report 2008 NPSA/2008/RRR003 The NPSA 'never events' 2011/2012, Department of Health
Distribution, functional impact, and origin mechanisms of copy number variation in the barley genome
Authors: María Muñoz-Amatriaín, Steven R Eichten, Thomas Wicker, Todd A Richmond, Martin Mascher, Burkhard Steuernagel, Uwe Scholz, Ruvini Ariyadasa, Manuel Spannagl, Thomas Nussbaumer, Klaus FX Mayer, Stefan Taudien, Matthias Platzer, Jeffrey A Jeddeloh, Nathan M Springer, Gary J Muehlbauer, Nils Stein
Journal: Genome biology (2013)

Abstract Background There is growing evidence for the prevalence of copy number variation (CNV) and its role in phenotypic variation in many eukaryotic species. Here we use array comparative genomic hybridization to explore the extent of this type of structural variation in domesticated barley cultivars and wild barleys. Results A collection of 14 barley genotypes including eight cultivars and six wild barleys were used for comparative genomic hybridization. CNV affects 14.9% of all the sequences that were assessed. Higher levels of CNV diversity are present in the wild accessions relative to cultivated barley. CNVs are enriched near the ends of all chromosomes except 4H, which exhibits the lowest frequency of CNVs. CNV affects 9.5% of the coding sequences represented on the array and the genes affected by CNV are enriched for sequences annotated as disease-resistance proteins and protein kinases. Sequence-based comparisons of CNV between cultivars Barke and Morex provided evidence that DNA repair mechanisms of double-strand breaks via single-stranded annealing and synthesis-dependent strand annealing play an important role in the origin of CNV in barley. Conclusions We present the first catalog of CNVs in a diploid Triticeae species, which opens the door for future genome diversity research in a tribe that comprises the economically important cereal species wheat, barley, and rye. Our findings constitute a valuable resource for the identification of CNV affecting genes of agronomic importance. We also identify potential mechanisms that can generate variation in copy number in plant genomes.
Circulating nitrated N-telopeptide of type III collagen (IIINys) as a biochemical marker of oxidative-related synovial tissue metabolism in rheumatoid arthritis: Figure 1
Authors: N Charni-Ben Tabassi, P Richardot, L Toh, H Marotte, A-C Bay-Jensen, P Miossec, P Garnero
Journal: Annals of the Rheumatic Diseases (2009)

Synovial tissue inflammation plays a major role in mediating joint damage in rheumatoid arthritis (RA).1 An important mediator of inflammation is nitric oxide (NO)2 which is produced by different cells in joint tissues including synoviocytes.3 NO leads to nitration of tyrosine residues producing the post-translational modified nitrotyrosine (Y*).4 Increased immunoreactivity against nitrotyrosine has been shown in synovial tissue from patients with RA although the nature of the proteins and amino acid sequences involved has not been characterised.5 6

We generated a polyclonal antibody directed against the synthetic sequence QY\*DSY\*DVKSG (IIINys) from the …
Electrocardiographs in general practice.
Authors: A. Davies
Journal: BMJ (1989)

amphotericin B. Efficacy in sporotrichosis, paracoccidioido- mycosis, and histoplasmosis is likely but still not proved: the drug has been effective in patients with candidal oesophagitis, peritonitis, and chronic mucocutaneous candidiasis.Relapse rates with both iatroconazole and fluconazole are presently under study as the numbers of successfully treated patients increase.Before AIDS, treatment of cryptococcal meningitis failed in about a quarter of cases and many survivors were left with appreciable residual neurological damage.6This outcome with amphotericin B with or without flucytosine is not good enough, and toxicity is high.Among patients with AIDS the mortality from cryptococcal meningitis varies from 25-58% during the first episode despite treatment with amphotericin B,78 and neurological sequelae
Prostaglandins and the gastric epithelium: effects of misoprostol on gastric epithelial cell proliferation in the dog.
Authors: R A Goodlad, A J Madgwick, M R Moffatt, S Levin, J L Allen, N A Wright
Journal: Gut (1989)

The effects of the methyl ester analogue of prostaglandin E1, misoprostol, on gastric epithelial cell proliferation were investigated in six dogs given 300 micrograms/kg/day of misoprostol orally for 11 weeks and in six control dogs given placebo for 11 weeks. Misoprostol treatment resulted in a 36% increase in stomach weight (p less than 0.01) and a 30% increase in the length (measured as the cell column count from the base/neck junction to the surface) of the fundic gastric glands (p less than 0.01). This mucosal hyperplasia was predominantly caused by enlargement of the foveolar region of the gland, with little change occurring in the neck or in the isthmus. The hyperplasia was the result of an increased number of mitotic (p less than 0.01) and DNA synthesising cells (p less than 0.05) in each gastric gland, which resulted in a significant increase in the gland cell production rate, from 22.5 to 42.6 cells per gland per day (p less than 0.05).
Biased immunoglobulin light chain use in the <i>Chlamydophila psittaci</i> negative ocular adnexal marginal zone lymphomas
Authors: Daxing Zhu, Chen Lossos, Jennifer R. Chapman‐Fredricks, Izidore S. Lossos
Journal: American Journal of Hematology (2013)

Ocular adnexal mucosa associated lymphoid tissue lymphomas (OAMALTL) are the most common lymphomas of the eye. The potential roles for specific antigens in these lymphomas are still controversial. Previously we examined IGHV usage and mutations in Chlamydophila (C) psittaci-negative OAMALTL, demonstrating biased use of the IGHV4 family and IGHV4-34 gene and evidence for antigen selection. Herein, we examined the IGKV/IGLV gene usage and mutations in 34 C. psittaci-negative OAMALTL originating from the orbit (15), conjunctivae (14), and lacrimal gland (5). Clonal potentially functional IGKV/IGLV gene sequences were identified in 30 tumors (18 kappa and 12 lambda). An overrepresentation of the IGKV4 family (P < 0.01) was observed. The IGKV3-20*01 allele was used at a greater frequency than in normal peripheral blood B-lymphocytes (P = 0.02) and commonly paired with the IGHV4-34 allele. Twenty-seven of the 30 unique light chain sequences displayed mutations from germline and evidence for antigen selection. Overall our findings demonstrate that in C. psittaci-negative OAMALTL there is a biased usage of IGKV families and genes, which harbor somatic mutations. These findings and the specific paring between the IGKV3-20*01 and IGHV4-34 alleles suggest that specific antigens could play an important role in the pathogenesis of these lymphomas.
Hodgkin's Disease in the Elderly: Improved Treatment Outcome With a Doxorubicin-Containing Regimen
Authors: Colin D. Weekes, Julie M. Vose, Jim C. Lynch, Dennis D. Weisenburger, Philip J. Bierman, Timothy Greiner, Gregory Bociek, Charles Enke, Martin Bast, Wing C. Chan, James O. Armitage
Journal: Journal of Clinical Oncology (2002)

PURPOSE: Hodgkin’s disease (HD) is a malignancy that displays a bimodal age distribution. Previous reports of treatment in patients ≥ 60 years have found a poor outcome, particularly in patients with advanced disease. Because of an improved side-effect profile, the regimen of chlorambucil, vinblastine, procarbazine, and prednisone (ChlVPP) has been proposed for use in elderly patients. PATIENTS AND METHODS: From September 1982 to May 1998, 262 patients with previously untreated HD received either ChlVPP (n = 176) or ChlVPP plus doxorubicin/bleomycin/vincristine (ChlVPP/ABV hybrid; n = 86). Fifty-six patients were ≥ 60 years old, and 206 were younger than 60 years. RESULTS: The 5-year overall survival (OS; 87% v 39%) and the 5-year event-free survival (EFS; 75% v 31%) favored patients younger than 60 years of age. Prognostic factors analyzed in patients ≥ 60 years of age, other than type of therapy, included sex, stage, Karnofsky performance score, lactic dehydrogenase, number of extranodal sites, B sympto...