tbuckley/cabot-search huggingface dataset:
THE RELATION OF THE SPLEEN TO BLOOD DESTRUCTION AND REGENERATION AND TO HEMOLYTIC JAUNDICE
Authors: Richard M. Pearce, Max Minor Peet
Journal: The Journal of Experimental Medicine (1913)

The increased resistance of the red blood corpuscles characteristic of the splenectomized animal is as evident one year after removal of the spleen as it is at earlier periods. So also is the decreased tendency to jaundice after the administration of hemolytic serum. The increase in resistance of the red cells cannot be explained on the basis of an increase in reticulated cells in the circulating blood.
Properties of strains of Escherichia coli carried in different phases of ulcerative colitis
Authors: E. M. Cooke, S. P. Ewins, J. Hywel-Jones, J. E. Lennard-Jones
Journal: Gut (1974)

Strains of E. coli from the faeces of patients with active ulcerative colitis and with colitis in remission were examined for haemolysin and necrotoxin production. Cultures from 63 patients with active colitis grew haemolytic E. coli in 23 (37%) as compared with 24 (21%) from 115 patients whose disease was in remission (p < 0.05). The corresponding proportions for necrotoxin-producing strains were 22% and 12%. Of 35 patients investigated both in relapse and remission of the colitis, 14 changed their carriage of haemolytic E. coli. Thirteen of these carried haemolytic organisms in relapse but not in remission, and one carried haemolytic organisms in remission but not in relapse (p < 0.01). Strains of E. coli were also examined from specimens of faeces obtained at weekly intervals for 28 weeks from 19 patients. The acquisition of haemolytic or necrotoxic E. coli strains tended to follow rather than precede the onset of the attack in the four patients who developed a relapse of the disease during this period. Among these 19 patients haemolytic and necrotoxic strains were found most commonly when blood was regularly present in the faeces. These facts suggest that conditions in the bowel during a relapse of colitis tend to favour the presence of haemolysin- and necrotoxin-producing organisms, rather than that these organisms cause the relapse. Of 50 strains of E. coli from patients treated with sulphasalazine tested for sensitivity to sulphapyridine 49 were resistant. There was no clear relation between the activity of the colitis and the presence of any of the 27 serotypes of E. coli examined.
A Bicistronic <i>CYCLIN D1-TROP2</i> mRNA Chimera Demonstrates a Novel Oncogenic Mechanism in Human Cancer
Authors: Emanuela Guerra, Marco Trerotola, Roberta Dell' Arciprete, Veronica Bonasera, Barbara Palombo, Tarek El-Sewedy, Tommaso Ciccimarra, Carlo Crescenzi, Franco Lorenzini, Cosmo Rossi, Giovanna Vacca, Rossano Lattanzio, Mauro Piantelli, Saverio Alberti
Journal: Cancer Research (2008)

Abstract A chimeric CYCLIN D1-TROP2 mRNA was isolated from human ovarian and mammary cancer cells. The CYCLIN D1-TROP2 mRNA was shown to be a potent oncogene as it transforms naïve, primary cells in vitro and induces aggressive tumor growth in vivo in cooperation with activated RAS. Silencing of the chimeric mRNA inhibits the growth of breast cancer cells. The CYCLIN D1-TROP2 mRNA was expressed by a large fraction of the human gastrointestinal, ovarian, and endometrial tumors analyzed. It is most frequently detected in intestinal cell aneuploid cancers and it is coexpressed with activated RAS oncogenes, consistent with a cooperative transforming activity in human cancers. The chimeric mRNA is a bicistronic transcript of post transcriptional origin that independently translates the Cyclin D1 and Trop-2 proteins. This is a novel mechanism of CYCLIN D1 activation that achieves the truncation of the CYCLIN D1 mRNA in the absence of chromosomal rearrangements. This leads to a higher CYCLIN D1 mRNA stability, with inappropriate expression during the cell cycle. The stabilized CYCLIN D1 mRNA cooperates with TROP2 in stimulating the growth of the expressing cells. These findings show a novel epigenetic, oncogenic mechanism, which seems to be widespread in human cancers. [Cancer Res 2008;68(19):8113–21]
Double-blind Placebo-Controlled Trial of Oral Acyclovir in First-Episode Genital Herpes Simplex Virus Infection
Authors: Gregory J. Mertz
Journal: JAMA (1984)

One hundred nineteen patients with primary and 31 patients with nonprimary first-episode genital herpes were treated for ten days with 200 mg of acyclovir capsules or placebo capsules orally five times daily. Among acyclovir recipients with primary genital herpes, the median duration of viral shedding (two days), time to crusting of all lesions (seven days), time to healing of all lesions (12 days), and duration of local pain (five days) and constitutional symptoms (three days) were shorter than among placebo recipients (9, 10, 16, 7, and 6 days, respectively). Among patients with nonprimary first-episode genital herpes, oral acyclovir shortened the median duration of viral shedding but had no significant effect on the duration of lesions or symptoms. The time to first recurrence and frequency of recurrences were similar in acyclovir- and placebo-treated patients. Oral acyclovir treatment of primary first-episode genital herpes shortens the duration of viral shedding and symptoms and accelerates healing, but it does not appear to influence subsequent genital recurrences.
Incidence Proportions of Brain Metastases in Patients Diagnosed (1973 to 2001) in the Metropolitan Detroit Cancer Surveillance System
Authors: Jill S. Barnholtz-Sloan, Andrew E. Sloan, Faith G. Davis, Fawn D. Vigneau, Ping Lai, Raymond E. Sawaya
Journal: Journal of Clinical Oncology (2004)

Population-based estimates of the incidence of brain metastases are not generally available. The purpose of this study was to calculate population-based incidence proportions (IPs) of brain metastases from single primary lung, melanoma, breast, renal, or colorectal cancer.Patients diagnosed with single primary lung, melanoma, breast, renal, or colorectal cancer (1973 to 2001) in the Metropolitan Detroit Cancer Surveillance System (MDCSS) were used for analysis. IP of brain metastases by primary site and variable of interest (race, sex, age at diagnosis of primary cancer, and Surveillance, Epidemiology, and End Results [SEER] stage of primary cancer) was calculated with 95% CIs.Total IP percentage (IP%) of brain metastases was 9.6% for all primary sites combined, and highest for lung (19.9%), followed by melanoma (6.9%), renal (6.5%), breast (5.1%), and colorectal (1.8%) cancers. Racial differences were seen with African Americans demonstrating higher IP% of brain metastases compared with other racial groups for most primary sites. IP% was significantly higher for female patients with lung cancer, and significantly higher for male patients with melanoma. The highest IP% of brain metastases occurred at different ages at diagnoses: age 40 to 49 years for primary lung cancer; age 50 to 59 years for primary melanoma, renal, or colorectal cancers; and age 20 to 39 for primary breast cancer. IP% significantly increased as SEER stage of primary cancer advanced for all primary sites.Total IP% of brain metastases was lower than previously reported, and it varied by primary site, race, sex, age at diagnosis of primary cancer, and SEER stage of primary cancer.
Complement Activation Selectively Potentiates the Pathogenicity of the IgG2b and IgG3 Isotypes of a High Affinity Anti-Erythrocyte Autoantibody
Authors: Samareh Azeredo da Silveira, Shuichi Kikuchi, Liliane Fossati-Jimack, Thomas Moll, Takashi Saito, J. Sjef Verbeek, Marina Botto, Mark J. Walport, Michael Carroll, Shozo Izui
Journal: The Journal of Experimental Medicine (2002)

By generating four IgG isotype-switch variants of the high affinity 34–3C anti-erythrocyte autoantibody, and comparing them to the IgG variants of the low affinity 4C8 anti-erythrocyte autoantibody that we have previously studied, we evaluated in this study how high affinity binding to erythrocytes influences the pathogenicity of each IgG isotype in relation to the respective contributions of Fcγ receptor (FcγR) and complement. The 34–3C autoantibody opsonizing extensively circulating erythrocytes efficiently activated complement in vivo (IgG2a = IgG2b &amp;gt; IgG3), except for the IgG1 isotype, while the 4C8 IgG autoantibody failed to activate complement. The pathogenicity of the 34–3C autoantibody of IgG2b and IgG3 isotypes was dramatically higher (&amp;gt;200-fold) than that of the corresponding isotypes of the 4C8 antibody. This enhanced activity was highly (IgG2b) or totally (IgG3) dependent on complement. In contrast, erythrocyte-binding affinities only played a minor role in in vivo hemolytic activities of the IgG1 and IgG2a isotypes of 34–3C and 4C8 antibodies, where complement was not or only partially involved, respectively. The remarkably different capacities of four different IgG isotypes of low and high affinity anti-erythrocyte autoantibodies to activate FcγR-bearing effector cells and complement in vivo demonstrate the role of autoantibody affinity maturation and of IgG isotype switching in autoantibody-mediated pathology.
Early surgery versus initial conservative treatment in patients with spontaneous supratentorial intracerebral haematomas in the International Surgical Trial in Intracerebral Haemorrhage (STICH): a randomised trial
Authors: A David Mendelow, Barbara A Gregson, Helen M Fernandes, Gordon D Murray, Graham M Teasdale, D Terence Hope, Abbas Karimi, M Donald M Shaw, David H Barer
Journal: The Lancet (2005)
969 UCP2 OVEREXPRESSION SENSITIZES NASH LIVER TO ISCHEMIA/REPERFUSION INJURY BY INCREASING MITOCHONDRIAL PROTON LEAK
Authors: G. Serviddio, F. Bellanti, A.D. Romano, R. Tamborra, T. Rollo, D. Bruno, A. Petrella, E. Altomare
Journal: Journal of Hepatology (2008)
A Prospective Study of Impairment in Glucose Control Caused by Clozapine Without Changes in Insulin Resistance
Authors: Oliver D. Howes, Ajay Bhatnagar, Fiona P. Gaughran, Stephanie A. Amiel, Robin M. Murray, Lyn S. Pilowsky
Journal: American Journal of Psychiatry (2004)

This prospective study examines the effect of clozapine on glucose control and insulin sensitivity.
Visfatin/NAMPT: A Multifaceted Molecule with Diverse Roles in Physiology and Pathophysiology
Authors: Tuva B. Dahl, Sverre Holm, Pål Aukrust, Bente Halvorsen
Journal: Annual Review of Nutrition (2012)

Visfatin/NAMPT (nicotinamide phosphoribosyltransferase) is a protein with several suggested functions. Although the first discovery of this molecule as a pre-B-cell colony-enhancing factor suggested primarily a cytokine function, its rediscovery as the key enzyme in nicotinamide adenine dinucleotide generation has considerably widened its potential biological activities. Although originally thought to be produced in adipose tissue (i.e., adipocytes and infiltrating macrophages), its production seems to involve other cells and tissues such as skeletal muscle, liver, immune cells, cardiomyocytes, and the brain. Visfatin/NAMPT has both intracellular and extracellular effects influencing several signaling pathways. Its broad spectrum of effects is mirrored by its potential involvement in a wide range of disorders including human immunodeficiency virus infection, septicemia, myocardial failure, atherosclerosis, metabolic disorders, inflammatory diseases, malignancies, and neurodegenerative disorders and aging. Moreover, studies on visfatin/NAMPT in atherosclerotic disorders suggest a rather complex role of this molecule in pathophysiology, potentially mediating both adaptive and maladaptive responses.
Small intestinal structure and passive permeability in systemic sclerosis.
Authors: I Cobden, J Rothwell, A T Axon, M F Dixon, D J Lintott, N R Rowell
Journal: Gut (1980)

Seventeen patients with proven systemic sclerosis had a peroral jejunal biopsy performed. Four biopsies were regarded as showing abnormalities, which were mostly confined to the deeper structures, although in two there was a minimal degree of villous atrophy without epithelial cell changes. Passive intestinal permeability, as assessed by the cellobiose/mannitol test, was normal in all patients. In contrast, seven patients had a low xylose test result, which in five of them could be accounted for by impaired renal function, small intestinal bacterial contamination, or altered gastrointestinal transit. These results indicate that passive intestinal permeability is unaltered in systemic sclerosis, and that malabsorption, when it occurs, is caused by other factors.
Rare Cause of Recurrent Small-Bowel Obstruction
Authors: June-Ho Kim, Mimmie Kwong, James Griffin, Diane Schwartz
Journal: JAMA Surgery (2014)

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Appearance of peroxidase reactivity within the rough endoplasmic reticulum of blood monocytes after surface adherence.
Authors: P T Bodel, B A Nichols, D F Bainton
Journal: The Journal of Experimental Medicine (1977)

Rabbit blood monocytes, which contain no cytochemically demonstrable peroxidase, develop peroxidatic activity in the RER and perinuclear cisternae within 2 h after adherence to serum- or fibrin-coated surfaces. A similar reactivity appears in surface-adherent human and rat blood monocytes. In both localization and characteristics, this enzyme reactivity in monocytes resembles that normally seen in the resident peritoneal macrophages of the rabbit, as well as in several types of tissue macrophages in other species. Thus this observation supports the concept, presently based on the kinetic data of other investigators, that blood monocytes are the precursors of such cells. Moreover, the appearance of new enzyme activity after adherence may reflect alterations in cellular metabolism resulting from plasma membrane:surface interactions.
A human T‐cell antigen defined by xenoantiserum to sézary leukemic cells: Immunochemical and functional studies
Authors: Minoru Ogasawara, Yoshifumi Ishii, Hirofumi Kamiya, Kokichi Kikuchi
Journal: American Journal of Hematology (1982)

Abstract Xenoantiserum to Sézary cell leukemia cells (ASS) was developed by immunizing rabbits with those cells and was absorbed with human red cells, liver, tonsil B cells, and cultured Raji cells. This reagent reacted by immunofluorescence with virtually all human thymus and T cells. In the thymus, medullary cells reacted more strongly with ASS than did cortical thymocytes. When immunoprecipitates that formed between ASS and 125 I‐labeled lymphocyte surface glycoproteins were analyzed by sodium dodecyl sulfate‐polyacrylamide gel electrophoresis, it was found that ASS precipitated a 72K molecular weight (MW) glycoprotein from T cells but not from B cells. On the one hand, it was shown by functional studies that T cells sensitive to the cytotoxic effect of ASS contained T cells that could aid the immunoglobulin synthesis of B cells induced by pokeweed mitogen. On the other hand, suppressor T cells induced by concanavalin A resided in those cells rather resistant to its cytotoxic effect. These data support the idea that the 72K MW glycoprotein on human thymus and T cells might be homologous to mouse Lyt‐1 antigens.
Activating Mutations in the<i>ABCC8</i>Gene in Neonatal Diabetes Mellitus
Authors: Andrey P. Babenko, Michel Polak, Hélène Cavé, Kanetee Busiah, Paul Czernichow, Raphael Scharfmann, Joseph Bryan, Lydia Aguilar-Bryan, Martine Vaxillaire, Philippe Froguel
Journal: New England Journal of Medicine (2006)

The ATP-sensitive potassium (KATP) channel, composed of the beta-cell proteins sulfonylurea receptor (SUR1) and inward-rectifying potassium channel subunit Kir6.2, is a key regulator of insulin release. It is inhibited by the binding of adenine nucleotides to subunit Kir6.2, which closes the channel, and activated by nucleotide binding or hydrolysis on SUR1, which opens the channel. The balance of these opposing actions determines the low open-channel probability, PO, which controls the excitability of pancreatic beta cells. We hypothesized that activating mutations in ABCC8, which encodes SUR1, cause neonatal diabetes.
The first reported UK fatality related to gamma-butyrolactone (GBL) ingestion
Authors: Paul I Dargan, Jenny Button, Susie Davies, John Ramsey, Simi George, David W Holt, David M Wood
Journal: Journal of the Royal Society of Medicine (2009)

Gamma-butyrolactone (GBL) is rapidly metabolized to gamma-hydroxybutyrate (GHB) in vivo following ingestion. GBL and GHB cause similar clinical features in users, and both of these agents are widely used as recreational drugs due to their mood-enhancing, stimulant and prosexual effects, particularly on the nightclub scene.1,2

In 2003, GHB was classified in the UK as a Class C controlled substance under the Home Office Misuse of Drugs Act (1971). GBL is currently not classified in the UK and many other countries in the world; the UK Home Office Advisory Council on the Misuse of Drugs is currently consulting on proposed changes to the legal status of GBL, and the related compound 1,4-butanediol (1,4BD).

There are numerous reported fatalities related to GHB ingestion.3 However, although there has been media coverage in the lay press of potential GBL-related fatalities in the UK,4,5 there have only been three previous reports of GBL-related fatality, two in Germany and one in the USA.6,7 We report here the first case of a fatality related to isolated GBL toxicity in the UK, which we feel supports the case for classifying GBL similar to that of GHB.
Recovery after "lethal" quantity of paint remover.
Authors: C J Roberts, F P Marshall
Journal: BMJ (1976)

<b>Background:</b> The chest X–ray (CXR) is part of the current ARDS definition (JAMA 2012; 307:2526) but detains poor interobserver reliability. The RALE score was recently proposed to evaluate lung edema on CXR in ARDS patients (Thorax 2018; 73: 840; figure 1A). The current study determined its diagnostic accuracy for ARDS in a cohort of ICU patients expected to need invasive ventilation for &gt;24 hours. <b>Methods:</b> The current ARDS definition was used as the gold standard. The RALE score was calculated for the first available CXR. ROC curves were constructed, and the optimal cutoff was used to determine sensitivity, specificity, negative and positive predictive value of the RALE score for ARDS. <b>Results:</b> The study included 144 patients, of whom 33 had ARDS according to the current ARDS definition. A higher RALE score was found in patients with ARDS compared to patients without ARDS (23 [16–33] vs 7 [3–11]; P&lt;0.001). The optimal RALE score cutoff was 9 (figure 1B). Agreement on the RALE score between two independent researchers was excellent, with an interclass coefficient of 0.95 (95%CI 0.92–0.96). <b>Conclusions:</b> In this cohort of invasively ventilated ICU patients, the RALE score had an excellent diagnostic accuracy for ARDS, was easy to calculate, feasible and reliable. Additional validation of the cutoff and RALE performance is needed in larger cohorts.
Cell Cycle Checkpoint Function in Bladder Cancer
Authors: Sharon C Doherty, Stephanie R McKeown, Valerie McKelvey-Martin, C Stephen Downes, Anthony Atala, James J Yoo, Dennis A Simpson, William K Kaufmann
Journal: JNCI Journal of the National Cancer Institute (2003)

Background: Cell cycle checkpoints function to maintain genetic stability by providing additional time for repair of DNA damage and completion of events that are necessary for accurate cell division. Some checkpoints, such as the DNA damage G1 checkpoint, are dependent on p53, whereas other checkpoints, such as the decatenation G2 checkpoint, are not. Because bladder transitional cell carcinomas (TCCs) often contain numerous chromosomal aberrations and appear to have highly unstable genomes, we analyzed cell cycle checkpoint functions in a panel of TCC lines. Methods: Cell cycle arrest was induced in normal human fibroblasts (NHF1-hTERT) and normal human uroepithelial cells (HUCs), and TCC lines and checkpoint functions were quantified using flow cytometry and fluorescence microscopy. The inducers and checkpoints were ionizing radiation (i.e., DNA damage) (G1 and G2 checkpoints), the mitotic inhibitor colcemid (polyploidy checkpoint), or the topoisomerase II catalytic inhibitor ICRF-193 (decatenation G2 checkpoint). Four of the five TCC lines expressed mutant p53. Results: HUCs had an effective G1 checkpoint response to ionizing radiation, with 68% of cells inhibited from moving from G1 into S phase. By contrast, G1 checkpoint function was severely attenuated (<15% inhibition) in three of the five TCC lines and moderately attenuated (<50% inhibition) in the other two lines. NHF1-hTERT had an effective polyploidy checkpoint response, but three of five TCC lines were defective in this checkpoint. HUCs had effective ionizing radiation and decatenation G2 checkpoint responses. All TCC lines had a relatively effective G2 checkpoint response to DNA damage, although the responses of two of the TCC lines were moderately attenuated relative to HUCs. All TCC lines had a severe defect in the decatenation G2 checkpoint response. Conclusion: Bladder TCC lines have defective cell cycle checkpoint functions, suggesting that the p53-independent decatenation G2 checkpoint may cooperate with the p53-dependent G1 checkpoints to preserve chromosomal stability and suppress bladder carcinogenesis.