tbuckley/cabot-search huggingface dataset:
THE INTESTINAL FLORA IN MOUSE TYPHOID INFECTION
Authors: Leslie T. Webster
Journal: The Journal of Experimental Medicine (1923)

The normal flora of laboratory mice at The Rockefeller Institute, fed on a bread and milk diet, was determined. Bacillus acidophilus and Bacillus bifidus outnumber the Bacillus coli, Bacillus acidi lactici, and Bacillus coli communior group about twenty-five to one. White and yellow cocci which may or may not liquefy gelatin are occasionally noted; spirochetal and vibrio forms and yeasts are usually seen in stained preparations. This flora does not change when mice are artificially infected per os with a strain of mouse typhoid bacilli (Bacillus pestis cavice) and is the same in the animals which resist the infection as in those which succumb. Mice fed on a meat diet and showing a colon, Bacillus diffluens, and Bacillus welchii flora do not differ in susceptibility to mouse typhoid from the normal mice fed on bread and milk and showing the above acidophilus flora.
CHOLERA—ITS DISASTROUS PAST AND ITS MORE HOPEFUL FUTURE.
Authors: H. RAYMOND ROGERS
Journal: JAMA (1884)

The absolute failure in the past to read aright the clearly defined symptoms of this disease has left it, as found to-day, one of the most obscure and incomprehensible of all diseases. The wrong reading of symptoms is indicated by the fact that the rate of mortality is virtually the same, whether nature alone is trusted for the cure, or whether the treatment is according to the best lights in medical science; viz.: 50 per cent. of those who are attacked. Such being the fact, it is discreditable, not to say criminal, longer to entertain the theories or to employ the modes of treatment belonging to such a past. Our profession will be held to a rigid accountability by a world of growing intelligence. This disease will be studied by those outside of the profession who have faith in a better state of things as being possible. The hope for
Thromboxane synthetase inhibitors reduce infarct size by a platelet-dependent, aspirin-sensitive mechanism.
Authors: K M Mullane, D Fornabaio
Journal: Circulation Research (1988)

Platelets are suggested to exacerbate ischemia-induced myocardial injury, which has led to the study of various antiplatelet therapies including thromboxane synthetase inhibitors (TXSI). Two such agents, benzylimidazole and OKY-046, reduce infarct size commensurate with a diminution in serum thromboxane B2 formation in anesthetized dogs subjected to 90 minutes of coronary artery occlusion followed by 5 hours of reperfusion. In contrast, platelet depletion with specific antiserum does not reduce infarct size but prevents the cardioprotection afforded by the TXSI. Platelet-derived prostaglandin endoperoxides (PGG2 and PGH2), which cannot be converted to thromboxane A2 in the inhibited platelet, can be transformed to PGE2 and PGD2 in plasma and to PGI2 by the blood vessel wall. These prostaglandins are considered "cardioprotective." Consequently, a low dose of aspirin (3-5 mg/kg) given 24 hours before coronary occlusion was used to selectively block the platelet cyclooxygenase enzyme. Aspirin, by itself, does not reduce infarct size, but it suppresses the myocardial salvage induced by OKY-046. Thus, TXSI reduce infarct size by platelet-dependent, aspirin-sensitive mechanism that depends on the redirection of platelet-derived PGG2 and PGH2 to protective metabolites, rather than inhibition of thromboxane A2 per se. Moreover, myocardial salvage induced by the TXSI is accompanied by a reduction in neutrophil accumulation in the myocardium, as indicated by the levels of the neutrophil-specific myeloperoxidase enzyme. Platelet depletion or pretreatment with aspirin prevents the TXSI-induced suppression of neutrophil accumulation. Consequently, it is proposed that the prostaglandin-mediated protective effects of TXSI can be resolved, at least in part, in terms of a braking action on neutrophil activation to prevent leukocyte-dependent tissue injury.
Polymyxin B with dual carbapenem combination therapy against carbapenemase-producing Klebsiella pneumoniae
Authors: Nathalie Grace Chua, Yvonne Peijun Zhou, Thuan Tong Tan, Pushpalatha Bangalore Lingegowda, Winnie Lee, Tze Peng Lim, Jocelyn Teo, Yiying Cai, Andrea L. Kwa
Journal: Journal of Infection (2014)
Processing of endoplasmic reticulum luminal antigens associated with halothane hepatitis in rat hepatocytes
Authors: Hamid R. Amouzadeh, Lance R. Pohl
Journal: Hepatology (1995)

In this study we have investigated the mechanism of the processing of trifluoroacetylated liver microsomal protein antigens associated with halothane hepatitis to learn how the immune system might come in contact with these proteins to form antibodies directed against them. Rats were treated with halothane and parenchymal (PC) and non-parenchymal cells (NPC) were isolated 16 hours later. Immunoblotting of the cell lysates with antisera directed against the trifluoroacetyl hapten showed the presence of high levels of trifluoroacetylated proteins in parenchymal cells, whereas none of these proteins were detected in endothelial or Kupffer cells that were isolated by centrifugal elutriation. The half-lives of 100-, 82-, 80-, 63-, 59-, 58-, and 57-kd trifluoroacetylated and native carrier proteins of the trifluoroacetyl hapten in cultures of rat primary parenchymal cells were approximately 1 day. The turnovers of all of these trifluoroacetylated proteins, except for that of the trifluoroacetylated 100-kd protein, were inhibited by treatment of the cells with ammonium chloride, leupeptin, 4-(2-aminoethyl)-benzenesulfonyl fluoride, or 3-methyl-adenine (3-MA). These results indicate that, in liver, the major source of the formation of trifluoroacetylated antigens associated with halothane hepatitis is the parenchymal cells, It appears that most of the trifluoroacetylated antigens and possibly the native carrier protein of the trifluoroacetyl haptens are transferred from the endoplasmic reticulum (ER) to an acidic compartment of PCs, where they are enzymatically degraded. The processing of the trifluoroacetylated proteins by this pathway may be a protective mechanism that prevents these covalently altered proteins from inducing an antibody response in most patients who are administered halothane.
Linking genotoxic responses and reproductive success in ecotoxicology.
Authors: S L Anderson, G C Wild
Journal: Environmental Health Perspectives (1994)

The potential of genotoxicity biomarkers as predictors of detrimental environmental effects, such as altered reproductive success of wild organisms, must be rigorously determined. Recent research to evaluate relationships between genotoxic responses and indicators of reproductive success in model animals is described from an ecotoxicological perspective. Genotoxicity can be correlated with reproductive effects such as gamete loss due to cell death; embryonic mortality; and heritable mutations in a range of model animals including polychaete worms, nematodes, sea urchins, amphibians, and fish. In preliminary studies, the polychaete worm, Neanthes arenaceodentata, and the nematode, Caenorhabditis elegans, have also shown the potential for cumulative DNA damage in gametes. If DNA repair capacity is limited in gametes, then selected life history traits such as long and synchronous periods of gametogenesis may confer vulnerability to genotoxic substances in chronic exposures. Recommendations for future research include strategic development of animal models that can be used to elucidate multiple mechanisms of effect (multiend point) at varying levels of biological organization (multilevel).
Kidney Function, Proteinuria, and Adverse Outcomes—Reply
Authors: Brenda R. Hemmelgarn
Journal: JAMA (2010)

In Reply: We agree with Dr Nonoguchi and colleagues that there are several potential metrics for assessing the rate of kidney function loss, including those based on absolute changes in eGFR. Because of space limitations, we were not able to present or discuss all of them in our article.
Transient Nutlin-3a Treatment Promotes Endoreduplication and the Generation of Therapy-Resistant Tetraploid Cells
Authors: Hong Shen, Diarmuid M. Moran, Carl G. Maki
Journal: Cancer Research (2008)

Abstract p53 activity is controlled in large part by MDM2, an E3 ubiquitin ligase that binds p53 and promotes its degradation. The MDM2 antagonist Nutlin-3a stabilizes p53 by blocking its interaction with MDM2. Several studies have supported the potential use of Nutlin-3a in cancer therapy. Two different p53 wild-type cancer cell lines (U2OS and HCT116) treated with Nutlin-3a for 24 hours accumulated 2N and 4N DNA content, suggestive of G1 and G2 phase cell cycle arrest. This coincided with increased p53 and p21 expression, hypophosphorylation of pRb, and depletion of Cyclin B1, Cyclin A, and CDC2. Upon removal of Nutlin-3a, 4N cells entered S phase and re-replicated their DNA without an intervening mitotic division, a process known as endoreduplication. p53-p21 pathway activation was required for the depletion of Cyclin B1, Cyclin A, and CDC2 in Nutlin-3a–treated cells and for endoreduplication after Nutlin-3a removal. Stable tetraploid clones could be isolated from Nutlin-3a treated cells, and these tetraploid clones were more resistant to ionizing radiation and cisplatin-induced apoptosis than diploid counterparts. These data indicate that transient Nutlin-3a treatment of p53 wild-type cancer cells can promote endoreduplication and the generation of therapy-resistant tetraploid cells. These findings have important implications regarding the use of Nutlin-3a in cancer therapy.[Cancer Res 2008;68(20):8260–8]
Worldwide Barriers to Organ Donation
Authors: Ivan Rocha Ferreira Da Silva, Jennifer A. Frontera
Journal: JAMA Neurology (2014)

The disparity between patients awaiting organ transplantation and organ availability increases each year. As a consequence, organ trafficking has emerged and developed into a multibillion-dollar-a-year industry.To identify and address barriers to organ donation in the United States and globally.Evidence-based peer-reviewed articles, including prospective and retrospective cohort studies, as well as case series and reports were identified in a PubMed search of organ donation, barriers to organ donation, brain death, donation after cardiac death, and organ trafficking. Additional Internet searches were conducted of national and international transplant and organ donation websites and US Department of Health of Health and Human Services websites. Citation publication dates ranged from August 1, 1968, through June 28, 2014.The lack of standardization of brain death and organ donation criteria worldwide contributes to a loss of potential donors. Major barriers to donation include variable clinical and legal definitions of brain death; inconsistent legal upholding of brain death criteria; racial, ethnic, and religious perspectives on organ donation; and physician discomfort and community misunderstanding of the process of donation after cardiac death. Limited international legislation and oversight of organ donation and transplant has contributed to the dilemma of organ trafficking.An urgent need exists for a global standard on the definition of brain death and donation after death by cardiac criteria to better regulate organ donation and maximize transplantation rates. Unified standards may have a positive effect on limiting organ trafficking.
Similarity of Folate Receptor Expression in UMSCC 38 Cells to Squamous Cell Carcinoma Differentiation Markers
Authors: R. B. Orr, A. R. Kreisler, B. A. Kamen
Journal: JNCI Journal of the National Cancer Institute (1995)

Journal Article Similarity of Folate Receptor Expression in UMSCC 38 Cells to Squamous Cell Carcinoma Differentiation Markers Get access Rebecca B. Orr, Rebecca B. Orr Departments of Pediatrics and Pharmacology, University of Texas Southwestern Medical CenterDallas Search for other works by this author on: Oxford Academic PubMed Google Scholar Amy R. Kreisler, Amy R. Kreisler Departments of Pediatrics and Pharmacology, University of Texas Southwestern Medical CenterDallas Search for other works by this author on: Oxford Academic PubMed Google Scholar Barton A. Kamen Barton A. Kamen * Departments of Pediatrics and Pharmacology, University of Texas Southwestern Medical CenterDallas * Correspondence to. Barton A. Kamen, M.D., Ph.D., Departments of Pediatrics and Pharmacology, University of Texas Southwestern MedicaJ Center, 5323 Harry Hines Blvd., Dallas, TX 75235. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 87, Issue 4, 15 February 1995, Pages 299–303, https://doi.org/10.1093/jnci/87.4.299 Published: 15 February 1995 Article history Received: 12 April 1994 Revision received: 14 November 1994 Accepted: 15 November 1994 Published: 15 February 1995
KERATOCENTESIS IN INFECTED WOUNDS OF THE EYEBALL.
Authors: M. F. WEYMANN
Journal: JAMA (1899)

Thanks to antiseptic and aseptic treatment, we are now pretty well enabled to eliminate wound infection. Still, there are parts of the body, chiefly cavities, where, even with the greatest care and most rigorous asepsis, this can not be accomplished. Then, too, there occur wounds that become badly infected before the physician is able to see them. What should be done in such instances? Antisepsis is certainly not the principal thing, though we do not care to entirely deny its usefulness. It must be borne in mind, however, that antiseptics are, as a rule, severe tissue irritants and only help to increase the discharge, which, in itself, opposes healing. Furthermore, in many cavities the application of antiseptics would be an actual menace to life, by absorption. What, under these conditions, is the most vital point? Drainage, no doubt. We know that the dangers of local infection are twofold: 1, irritation
Association with FcRγ Is Essential for Activation Signal through NKR-P1 (CD161) in Natural Killer (NK) Cells and NK1.1+ T Cells
Authors: Noriko Arase, Hisashi Arase, Seung Yong Park, Hiroshi Ohno, Chisei Ra, Takashi Saito
Journal: The Journal of Experimental Medicine (1997)

Natural killer (NK) cells exhibit cytotoxicity against variety of tumor cells and virus-infected cells without prior sensitization and represent unique lymphocytes involved in primary host defense. NKR-P1 is thought to be one of NK receptors mediating activation signals because cross-linking of NKR-P1 activates NK cells to exhibit cytotoxicity and IFN-γ production. However, molecular mechanism of NK cell activation via NKR-P1 is not well elucidated. In this study, we analyzed the cell surface complex associated with NKR-P1 on NK cells and found that NKR-P1 associates with the FcRγ chain which is an essential component of Fc receptors for IgG and IgE. The association between FcRγ and NKR-P1 is independent of Fc receptor complexes. Furthermore, NK cells from FcRγ-deficient mice did not show cytotoxicity or IFN-γ production upon NKR-P1 cross-linking. Similarly, NK1.1+ T cells from FcRγ-deficient mice did not produce IFN-γ upon NKR-P1 crosslinking. These findings demonstrate that the FcRγ chain plays an important role in activation of NK cells via the NKR-P1 molecule.
A CASE OF LACRYMAL CONCRETIONS
Authors: G. Maxted
Journal: BMJ (1915)

LACUIYAL CUOINC1EETONE. [MAY I5, 19I5 been rigorously excluded as peccanit causes of tlle neuralgias.Fromii othier associate(d symptoms of hypo- tlyroidism I recelitly determiiined to place thle patient on tlhyroid medi6ation, yielding withlinl the shiort period un- expectedlly gratifying results.REFE;REINCES.
Pathology and cost effectiveness of endoscopy surveillance for premalignant gastric lesions
Authors: M Rugge
Journal: Gut (2003)

We read with great interest the article by Whiting et al ( Gut2002;50:378–81 [OpenUrl][1][Abstract/FREE Full Text][2] ). The Birmingham experience shows how the prevalence of gastric cancers detected at an early stage is significantly higher in the endoscopically surveyed population than in non-surveyed patients. As a result, this study demonstrates that, in the secondary prevention of gastric malignancy, the “once in a lifetime” strategy (suggested for colorectal cancer) is not cost effective while repeated endoscopies (in selected patients) seem most appropriate. This conclusion however raises two cardinal questions. Firstly, are there “special” requirements (that is, a protocol of gastric biopsy sampling) to be satisfied when carrying out the upper endoscopy procedure? Secondly, are there evidence based criteria for selecting patients to be included in surveillance programmes? The authors do not provide detailed information on the number of … [1]: {openurl}?query=rft.jtitle%253DGut%26rft.stitle%253DGut%26rft.issn%253D0017-5749%26rft.aulast%253DWhiting%26rft.auinit1%253DJ%2BL%26rft.volume%253D50%26rft.issue%253D3%26rft.spage%253D378%26rft.epage%253D381%26rft.atitle%253DThe%2Blong%2Bterm%2Bresults%2Bof%2Bendoscopic%2Bsurveillance%2Bof%2Bpremalignant%2Bgastric%2Blesions%26rft_id%253Dinfo%253Adoi%252F10.1136%252Fgut.50.3.378%26rft_id%253Dinfo%253Apmid%252F11839718%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [2]: /lookup/ijlink?linkType=ABST&journalCode=gutjnl&resid=50/3/378&atom=%2Fgutjnl%2F52%2F3%2F453.atom
LONG-TERM CLINICAL IMPACT OF ACUTE STENT MALAPPOSITION: AN ADAPT-DES IVUS SUBSTUDY
Authors: Cristiano Souza, Gary Mintz, Bernhard Witzenbichler, Christopher Metzger, Michael Rinaldi, Peter Duffy, Giora Weisz, Ernest Mazzaferri, Thomas Stuckey, Bruce Brodie, Ke Xu, Ajay Kirtane, Gregg Stone, Akiko Maehara
Journal: Journal of the American College of Cardiology (2014)
Serotonin as a mediator of cyclic flow variations in stenosed canine coronary arteries.
Authors: J H Ashton, C R Benedict, C Fitzgerald, S Raheja, A Taylor, W B Campbell, L M Buja, J T Willerson
Journal: Circulation (1986)

The data obtained in this study demonstrate that the concentration of serotonin is markedly elevated (18- to 27-fold) at the site of a coronary arterial stenosis in open-chest, anesthetized dogs with cyclic flow variations. Cyclic flow variations in this experimental preparation were abolished by ketanserin, a 5-hydroxytryptamine antagonist, but serotonin concentration at the site of the coronary stenosis remained elevated. The intra-atrial administration of serotonin (0.16 to 1 mg/min) restored cyclic flow variations after they had been abolished by ketanserin. Taken together, these data suggest that serotonin may be one of the important mediators of cyclic flow variations in this experimental preparation.
Diastolic Heart Sounds and Filling Waves in Coronary Artery Disease
Authors: PETER F. COHN, PANTEL S. VOKONAS, RICHARD A. WILLIAMS, MICHAEL V. HERMAN, RICHARD GORLIN
Journal: Circulation (1971)

One hundred thirty selected patieints with chest pain syndromes were studied by apex- and phonocardiography as well as by cardiac catheterization, selective cine coronary arteriography, and cine left ventriculography. Ninety-three patients had coronary artery disease; 37 did not. Abnormal graphic studies were found in 42 patients with coronary artery disease and three patients with normal coronary arteriograms. These abnormalities correlated well with the presence of elevated left ventricular end-diastolic pressure. Third heart sounds were found less frequently than fourth heart sounds and/or abnormal apexcardiographic a waves, but when present were usually associated with a depressed cardiac index. Diagnostically, over 90% of all patients with chest pain who exhibited graphic abnormalities had significant coronary atherosclerosis. Normal graphic studies did not rule out coronary artery disease, but did indicate adequate left ventricular function since only 5% of patients with normal graphic studies had elevated left ventricular end-diastolic pressure combined with a low cardiac index.
Giant Hepatic Hemangioma Studied With Intravenous Total Body Arteriography Technique
Authors: GOVINDARAJAN NARAYANAN, DAVID C. YANG, KENG G. TAI, LESLIE WISE, JOSEPH GIOVANNIELLO
Journal: Clinical Nuclear Medicine (1996)

Hepatic hemangiomas are the most common benign tumors of the liver. They are usually single, small, and asymptomatic. However, giant hepatic hemangiomas have been reported in the past, usually detected as incidental findings. Radionuclide blood pool imaging studies are used to confirm the presence of a hemangioma. This report describes a case of a giant hepatic hemangioma detected using intravenous total-body arteriography, done as a part of radionuclide blood pool hemangioma study. This simple addition to the regular RBC blood pool hemangioma study helps to determine the size of the liver in the early arterial phase and shows obvious increased blood pool activity in the delayed phase. It is also useful in detecting lesions in other parts of the body when present.
Interaction between plasminogen activator inhibitor type 1 (PAI-1) bound to fibrin and either tissue-type plasminogen activator (t-PA) or urokinase-type plasminogen activator (u-PA). Binding of t-PA/PAI-1 complexes to fibrin mediated by both the finger and the kringle-2 domain of t-PA.
Authors: O F Wagner, C de Vries, C Hohmann, H Veerman, H Pannekoek
Journal: Journal of Clinical Investigation (1989)

Plasminogen activation is catalyzed both by tissue-type-(t-PA) and by urokinase-type plasminogen activator (u-PA). This reaction is controlled by plasminogen activator inhibitor type 1 (PAI-1) that is either present in plasma or bound to fibrin, present in a thrombus. We studied the mechanism of in vitro inhibition of both t-PA and u-PA activity by PAI-1 bound to fibrin. It is shown that activation of latent PAI-1 unmasks a specific fibrin-binding site that is distinct from its reactive site. This reactive site of activated PAI-1 bound to fibrin is fully exposed to form complexes with t-PA and u-PA, that are unable to activate plasminogen. Upon complex formation with either one of the plasminogen activators, PAI-1 apparently undergoes a conformational change and loses its affinity for fibrin. Consequently, complexes of u-PA and PAI-1 dissociate from the fibrin matrix and are encountered in the fluid phase. In contrast, t-PA/PAI-1 complexes remain bound to fibrin. By employing recombinant t-PA deletion-mutant proteins, that precisely lack domains involved in fibrin binding, we demonstrate that binding of t-PA/PAI-1 complexes is mediated by both the "finger" (F) and the "kringle-2" (K2) domain of t-PA. A model is proposed that explains inhibition of the fibrinolytic process, at the level of plasminogen activation by t-PA, directed by PAI-1 bound to fibrin. An implication of the proposed model is that t-PA/PAI-1 complexes and free t-PA compete for the same binding sites on fibrin.