tbuckley/cabot-search huggingface dataset:
Widespread duplications in the genomes of laboratory stocks of Dictyostelium discoideum
Authors: Gareth Bloomfield, Yoshimasa Tanaka, Jason Skelton, Alasdair Ivens, Robert R Kay
Journal: Genome biology (2008)

Duplications of stretches of the genome are an important source of individual genetic variation, but their unrecognized presence in laboratory organisms would be a confounding variable for genetic analysis. We report here that duplications of 15 kb or more are common in the genome of the social amoeba Dictyostelium discoideum. Most stocks of the axenic 'workhorse' strains Ax2 and Ax3/4 obtained from different laboratories can be expected to carry different duplications. The auxotrophic strains DH1 and JH10 also bear previously unreported duplications. Strain Ax3/4 is known to carry a large duplication on chromosome 2 and this structure shows evidence of continuing instability; we find a further variable duplication on chromosome 5. These duplications are lacking in Ax2, which has instead a small duplication on chromosome 1. Stocks of the type isolate NC4 are similarly variable, though we have identified some approximating the assumed ancestral genotype. More recent wild-type isolates are almost without large duplications, but we can identify small deletions or regions of high divergence, possibly reflecting responses to local selective pressures. Duplications are scattered through most of the genome, and can be stable enough to reconstruct genealogies spanning decades of the history of the NC4 lineage. The expression level of many duplicated genes is increased with dosage, but for others it appears that some form of dosage compensation occurs. The genetic variation described here must underlie some of the phenotypic variation observed between strains from different laboratories. We suggest courses of action to alleviate the problem.
Oxidized LDL Inhibits Vascular Endothelial Growth Factor–Induced Endothelial Cell Migration by an Inhibitory Effect on the Akt/Endothelial Nitric Oxide Synthase Pathway
Authors: Emmanouil Chavakis, Elisabeth Dernbach, Corinna Hermann, Ulrich F. Mondorf, Andreas M. Zeiher, Stefanie Dimmeler
Journal: Circulation (2001)

Background —Oxidized LDL (oxLDL) inhibits endothelial cell (EC) migration. Stimulating ECs with vascular endothelial growth factor (VEGF) leads to the activation of Akt/protein kinase B, which in turn activates endothelial nitric oxide synthase (eNOS) by phosphorylation on serine 1177. VEGF-induced cell migration is dependent on the generation of nitric oxide (NO). Therefore, we investigated whether oxLDL affects EC migration by an inhibitory effect on the Akt/eNOS pathway. Methods and Results —During an in vitro “scratched wound assay,” oxLDL dose-dependently inhibited the VEGF-induced migration of human umbilical vein endothelial cells. Western blot analysis revealed that oxLDL dose- and time-dependently led to dephosphorylation and thus deactivation of Akt. Moreover, oxLDL inhibited the VEGF-induced generation of NO, as detected and quantified using a fluorescent NO indicator, 4,5-diaminofluorescein diacetate. Overexpression of a constitutively active Akt construct (Akt T308D/S473D) or a phosphomimetic eNOS construct (eNOS S1177D) almost completely reversed the inhibitory effect of oxLDL on VEGF-induced EC migration and NO generation. Conclusions —Our data indicate that oxLDL-induced dephosphorylation of Akt, followed by impaired eNOS activation, reduces the intracellular level of NO and thereby inhibits VEGF-induced EC migration.
A peculiar gallbladder content
Authors: E Caturelli, S Dell'Isola, A M Ialungo, G Ghittoni, P Roselli
Journal: Gut (2007)

A 78-year-old man presented with spastic paraparesis. He had a 6 month history of progressive motor disturbance of the lower limbs. He had a past medical history of unexplained occasional episodes of fever during the few days …
Host-Range Properties of Murine Xenotropic and Ecotropic Type-C Viruses
Authors: Herbert K. Oie, Edward K. Russell, James H. Dotson, John Marc Rhoads, Adi F. Gazdar
Journal: JNCI Journal of the National Cancer Institute (1976)

Host-range properties of xenotropic (x-tropic) and ecotropic mouse type-C viruses were determined. NB-tropic viruses replicated only in mouse and rat cells, whereas x-tropic viruses, which do not exogenously infect mouse cells, grew in cells from various other mammalian species. Great variability in susceptibilities to x-tropic viruses was demonstrated in cells from heterologous species and in cells from a single species (human). Although rat cells were susceptible to both types of viruses, hamster cells were uniformly resistant. In addition, the x-tropic viruses crossed class barriers to infect cells of avian species but not insect, fish, or reptile cells.
Estimation of stroke volume from the pulmonary artery pressure record
Authors: A. A. ZACHAROULIS, C. J. MILLS, I. T. GABE, J. P. SHILLINGFORD
Journal: Cardiovascular Research (1974)

This study describes the estimation of stroke volume in a series of dogs by a pulse contour method applied to the pulmonary artery pressure record. The results correlated well with measurements of stroke volume by an electromagnetic flowmeter and by indicator dilution curves when changes were produced by noradrenaline, isoproterenol, propranolol, haemorrhage, pacing, and respiratory outflow occlusion. However, when saline was rapidly infused, error increased significantly.
Heavy metals and arthritis
Authors: H. A. Bird
Journal: Annals of the Rheumatic Diseases (1983)

The fourth annual day conference in the series 'Growing Points in the Treatment of Arthritis' was held at the Granby Hotel, Harrogate, on 7 April 1983.It was devoted to the topic 'Heavy Metals and Arthritis' and attracted an audience of about 100, both physicians and chemists.
Transcriptome analysis of antigenic variation in Plasmodium falciparum--var silencing is not dependent on antisense RNA.
Authors: Stuart A Ralph, Emmanuel Bischoff, Denise Mattei, Odile Sismeiro, Marie-Agnès Dillies, Ghislaine Guigon, Jean-Yves Coppee, Peter H David, Artur Scherf
Journal: Genome biology (2005)

Abstract Background Plasmodium falciparum , the causative agent of the most severe form of malaria, undergoes antigenic variation through successive presentation of a family of antigens on the surface of parasitized erythrocytes. These antigens, known as Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) proteins, are subject to a mutually exclusive expression system, and are encoded by the multigene var family. The mechanism whereby inactive var genes are silenced is poorly understood. To investigate transcriptional features of this mechanism, we conducted a microarray analysis of parasites that were selected to express different var genes by adhesion to chondroitin sulfate A (CSA) or CD36. Results In addition to oligonucleotides for all predicted protein-coding genes, oligonucleotide probes specific to each known var gene of the FCR3 background were designed and added to the microarray, as well as tiled sense and antisense probes for a subset of var genes. In parasites selected for adhesion to CSA, one full-length var gene ( var2csa ) was strongly upregulated, as were sense RNA molecules emanating from the 3' end of a limited subset of other var genes. No global relationship between sense and antisense production of var genes was observed, but notably, some var genes had coincident high levels of both antisense and sense transcript. Conclusion Mutually exclusive expression of PfEMP1 proteins results from transcriptional silencing of non-expressed var genes. The distribution of steady-state sense and antisense RNA at var loci are not consistent with a silencing mechanism based on antisense silencing of inactive var genes. Silencing of var loci is also associated with altered regulation of genes distal to var loci.
Systematic review of the relative efficacy of non-steroidal anti-inflammatory drugs and opioids in the treatment of acute renal colic
Authors: Anna Holdgate, Tamara Pollock
Journal: BMJ (2004)

<h3>Abstract</h3> <b>Objective</b> To examine the relative benefits and disadvantages of non-steroidal anti-inflammatory drugs (NSAIDs) and opioids for the management of acute renal colic. <b>Data sources</b> Cochrane Renal Group9s specialised register, Cochrane central register of controlled trials, Medline, Embase, and reference lists of retrieved articles. <b>Review methods</b> Randomised controlled trials comparing any opioid with any NSAID in acute renal colic if they reported any of the following outcomes: patient rated pain, time to pain relief, need for rescue analgesia, rate of recurrence of pain, and adverse events. <b>Results</b> 20 trials totalling 1613 participants were identified. Both NSAIDs and opioids led to clinically important reductions in patient reported pain scores. Pooled analysis of six trials showed a greater reduction in pain scores for patients treated with NSAIDs than with opioids. Patients treated with NSAIDs were significantly less likely to require rescue analgesia (relative risk 0.75, 95% confidence interval 0.61 to 0.93). Most trials showed a higher incidence of adverse events in patients treated with opioids. Compared with patients treated with opioids, those treated with NSAIDs had significantly less vomiting (0.35, 0.23 to 0.53). Pethidine was associated with a higher rate of vomiting. <b>Conclusions</b> Patients receiving NSAIDs achieve greater reductions in pain scores and are less likely to require further analgesia in the short term than those receiving opioids. Opioids, particularly pethidine, are associated with a higher rate of vomiting.
Adenosine Restores Angiotensin II–Induced Contractions by Receptor-Independent Enhancement of Calcium Sensitivity in Renal Arterioles
Authors: En Yin Lai, Peter Martinka, Michael Fähling, Ralf Mrowka, Andreas Steege, Adrian Gericke, Mauricio Sendeski, P.B. Persson, A. Erik G. Persson, Andreas Patzak
Journal: Circulation Research (2006)

Adenosine is coupled to energy metabolism and regulates tissue blood flow by modulating vascular resistance. In this study, we investigated isolated, perfused afferent arterioles of mice, which were subjected to desensitization during repeated applications of angiotensin II. Exogenously applied adenosine restores angiotensin II–induced contractions by increasing calcium sensitivity of the arterioles, along with augmented phosphorylation of the regulatory unit of the myosin light chain. Adenosine restores angiotensin II–induced contractions via intracellular action, because inhibition of adenosine receptors do not prevent restoration, but inhibition of NBTI sensitive adenosine transporters does. Restoration was prevented by inhibition of Rho-kinase, protein kinase C, and the p38 mitogen-activated protein kinase, which modulate myosin light chain phosphorylation and thus calcium sensitivity in the smooth muscle. Furthermore, adenosine application increased the intracellular ATP concentration in LuciHEK cells. The results of the study suggest that restoration of the angiotensin II–induced contraction by adenosine is attributable to the increase of the calcium sensitivity by phosphorylation of the myosin light chain. This can be an important component of vascular control during ischemic and hypoxic conditions. Additionally, this mechanism may contribute to the mediation of the tubuloglomerular feedback by adenosine in the juxtaglomerular apparatus of the kidney.
Ethanol facilitates hepatitis C virus replication via up-regulation of GW182 and heat shock protein 90 in human hepatoma cells
Authors: Terence N. Bukong, Wei Hou, Karen Kodys, Gyongyi Szabo
Journal: Hepatology (2012)

Abstract Alcohol use and hepatitis C virus (HCV) infection synergize to cause liver damage, and microRNA-122 (miR-122) appears to play a key role in this process. Argonaute 2 (Ago2), a key component of the RNA-induced silencing complex (RISC), has been shown to be important in modulating miR-122 function during HCV infection. However, GW182, a critical component of processing bodies (GW bodies) that is recruited by Ago2 to target messenger RNA (mRNA), has not been assessed in HCV infection. To characterize the role of GW182 in the pathogenesis of HCV infection, we determined its transcription and protein expression in an HCV J6/JFH1 culture system. Transcript and protein levels of GW182 as well as HCV RNA and protein expression increased with alcohol exposure. Specific silencing of mRNA expression by small interfering RNA against GW182 significantly decreased HCV RNA and protein expression. Overexpression of GW182 significantly increased HCV RNA and protein expression in HCV J6/JFH1 infected Huh7.5 cells. Furthermore, GW182 colocalized and coimmunoprecipitated with heat shock protein 90 (HSP90), which increased upon alcohol exposure with and without HCV infection and enhanced HCV gene expression. The use of an HSP90 inhibitor or knockdown of HSP90 decreased GW182 and miR-122 expression and significantly reduced HCV replication. Conclusion : Overall, our results suggest that GW182 protein that is linked to miR-122 biogenesis and HSP90, which has been shown to stabilize the RISC, are novel host proteins that regulate HCV infection during alcohol abuse. (Hepatology 2013)
Precipitins to dietary proteins in atopic eczema
Authors: R.StC. BARNETSON, HAZEL DRUMMOND, ANNE FERGUSON
Journal: British Journal of Dermatology (1983)

Journal Article Precipitins to dietary proteins in atopic eczema Get access R.StC. BARNETSON, R.StC. BARNETSON Department of Dermatology, Royal Infirmary, Edinburgh and Gastro‐intestinal Unit, Western General Hospital, Edinburgh Dr R.StC.Barnetson, Department of Dermatology, Royal Infirmary, Edinburgh. Search for other works by this author on: Oxford Academic Google Scholar HAZEL DRUMMOND, HAZEL DRUMMOND Department of Dermatology, Royal Infirmary, Edinburgh and Gastro‐intestinal Unit, Western General Hospital, Edinburgh Search for other works by this author on: Oxford Academic Google Scholar ANNE FERGUSON ANNE FERGUSON Department of Dermatology, Royal Infirmary, Edinburgh and Gastro‐intestinal Unit, Western General Hospital, Edinburgh Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 109, Issue 6, 1 December 1983, Pages 653–655, https://doi.org/10.1111/j.1365-2133.1983.tb00544.x Published: 01 December 1983 Article history Accepted: 14 May 1983 Published: 01 December 1983
Early myocardial ischaemia: evaluation of the histochemical haematoxylin-basic fuchsin-picric acid (HBFP) staining technique
Authors: J. V. REEMPTS, M. BORGERS, R. S. RENEMAN
Journal: Cardiovascular Research (1976)

A series of experiments, carried out to evaluate the histochemical method for the morphological diagnosis of early stages of myocardial ischaemia (HBFP) is reported. The experiments were performed on dog hearts in which ischaemia was induced by coronary artery ligation for different periods of time. The original procedure or modifications of the HBFP-technique, including different staining, rinsing, and differentiation times, the use of different commercial brands of chemicals and preparatory changes of routine histological procedures such as fixation, embedding, cutting, and mounting, did not give satisfactory results. False positive and negative staining was frequent. Very equivocal results were obtained on serial sections of ischaemic tissue samples. Therefore this method was regarded as unreliable and non-reproducible.
An Address on the Varieties of Colitis and their Diagnosis by Sigmoidoscopic Examination
Authors: P. L. Mummery
Journal: BMJ (1911)

COLITIS is at the present time a name which is very loosely used to describe a number of quite distinct conditions.Ulcerative colitis is a very distinct and defihite disease, characterized by severe and intractable diarrhoea, profuse haemorrhage, high temperature, and which' seriously
Human Papillomavirus Vaccine and Sexual Activity
Authors: Robert A. Bednarczyk
Journal: JAMA Internal Medicine (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 Internal Medicine 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 Internal Medicine journal
Serum angiogenic profile of patients with glioblastoma identifies distinct tumor subtypes and shows that TIMP-1 is a prognostic factor
Authors: M. Crocker, S. Ashley, I. Giddings, V. Petrik, A. Hardcastle, W. Aherne, A. Pearson, B. Anthony Bell, S. Zacharoulis, M. C. Papadopoulos
Journal: Neuro-Oncology (2010)

Angiogenesis plays a key role in glioblastoma biology and antiangiogenic agents are under clinical investigation with promising results. However, the angiogenic profiles of patients with glioblastoma and their clinical significance are not well understood. Here we characterize the serum angiogenic profile of patients with glioblastoma, and examine the prognostic significance of individual angiogenic factors. Serum samples from 36 patients with glioblastoma were collected on admission and simultaneously assayed for 48 angiogenic factors using protein microarrays. The data were analyzed using hierarchical cluster analysis. Vessel morphology was assessed histologically after immunostaining for the pan-endothelial marker CD31. Tumor samples were also immunostained for tissue inhibitor of metalloproteinase-1 (TIMP-1). Cluster analysis of the serum angiogenic profiles revealed 2 distinct subtypes of glioblastoma. The 2 subtypes had markedly different tumor microvessel densities. A low serum level of TIMP-1 was associated with significantly longer survival independent of patient age, performance status, or treatment. The serum angiogenic profile in patients with glioblastoma mirrors tumor biology and has prognostic value. Our data suggest the serum TIMP-1 level as an independent predictor of survival.
Synorth: exploring the evolution of synteny and long-range regulatory interactions in vertebrate genomes
Authors: Xianjun Dong, David Fredman, Boris Lenhard
Journal: Genome biology (2009)

Genomic regulatory blocks are chromosomal regions spanned by long clusters of highly conserved noncoding elements devoted to long-range regulation of developmental genes, often immobilizing other, unrelated genes into long-lasting syntenic arrangements. Synorth http://synorth.genereg.net/ is a web resource for exploring and categorizing the syntenic relationships in genomic regulatory blocks across multiple genomes, tracing their evolutionary fate after teleost whole genome duplication at the level of genomic regulatory block loci, individual genes, and their phylogenetic context.
Abstract 2870: p28, a cell penetrating peptide fragment of azurin, inhibits COP1 mediated ubiquitination of wild type and mutated p53, but does not alter intracellular levels of <i>c-jun</i>
Authors: Tohru Yamada, Konstantin Christov, Anne Shilkaitis, Laura Bratescu, Albert Green, Simona Santini, Anna Rita Bizzarri, Salvatore Cannistraro, Tapas K. Das Gupta, Craig W. Beattie
Journal: Cancer Research (2012)

Abstract Amino acids (aa) 50-77 of azurin, p28, a 128 aa member of the cupredoxin family of copper containing redox proteins, isolated from the opportunistic pathogen Pseudomonas aeruginosa is a cell penetrating peptide (CPP) that preferentially penetrates a wide variety of human cancer cells. Exposure of p53wt, mut cancer cells to p28 produces a post translational increase in the level of p53, inhibition of the cell cycle at G2/M and apoptosis (Yamada et. al., Mol. Can. Therap., 8:2947-58, 2009). Computer simulation (ClusPro, GROMACS) and domain specific antibodies to p53 suggest p28 binds to motifs that span aa 110–146 in flexible L1 loop and 80 and 276 of the p53 DNA binding domain (DBD), respectively. Western and RT-PCR analyses of human breast cancer, MCF-7 (p53wt), MCF-7 derived MDD2 (p53dom/neg), MDA-MB-231 (p53mut), and melanoma cells, Mel-29 (p53wt), Mel-23 (p53mut) and Mel-6 (p53null) exposed to p28 for 72 hrs showed a significant increase in the levels of p53 and p21 in MCF-7, MDA-MB-231, Mel-29 and Mel-23 cells, while significantly reducing the level of FoxM1 over a 72hr exposure. The level of STMN1 was not altered suggesting the block at G2/M does not involve microtubules. p28 significantly decreased the level of the E3 ligase COP1 in p53wt, mut MCF-7, MDA-MB-231, Mel-29 and Mel-23, but not in p53null Mel-6 cells. In addition, p28 did not significantly decrease the level of E3 ligases TOPORS, Pirh2 or HDM2 which also ubiquitinate p53. The levels of p53, p21, FoxM 1, STMN1, COP1, TOPORS and Pirh2 either remained essentially at control levels (p53, p21) or were elevated (FoxM1, STMN1, COP1, TOPORS, Pirh2) at some point during a 72 hr exposure of p53dom/neg MDD2 cells to p28. In contrast, COP1 has also been reported to negatively regulate cell proliferation in a c-jun-dependent manner and not regulate intracellular levels of p53 (Migliorini et. al., J. Clin. Invest., 121: 1329-43, 2011). The p28 induced decrease in the level of COP1 in p53wt, mut cancer cells was not accompanied by a sustained increase in c-jun, in any cancer cell line, suggesting that COP1 regulates the level of p53 in cancer cells independent of any effect on c-jun. These data also suggest that COP1, but not TOPORS or Pirh2, also binds within this region of p53, and that COP1 is a major regulator of p53 activity. In sum, these data suggest that p28 binds to a specific motif within the p53 DBD where it inhibits COP1 mediated binding to and ubiquitination of p53. 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 2870. doi:1538-7445.AM2012-2870