tbuckley/cabot-search huggingface dataset:
Hypoprothrombinemia and Bleeding Due to Cefoperazone
Authors: JAMES C. OSBORNE
Journal: Annals of Internal Medicine (1985)

Letters and Corrections1 May 1985Hypoprothrombinemia and Bleeding Due to CefoperazoneJAMES C. OSBORNE, M.D.JAMES C. OSBORNE, M.D.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-102-5-721_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The use of third-generation cephalosporins to treat infections in seriously ill patients is increasing. Widespread use of these agents necessitates recognition of the potential complications that have become more evident as larger numbers of patients are treated with these agents. We have recently seen two patients who developed moderately severe hemorrhages due to a vitamin-K-correctable hypoprothrombinemia during treatment with cefoperazone sodium.A 67-year-old man had cryptococcal meningitis and diffuse mixed lymphoma. He developed peritonitis and, after surgery to repair a perforated duodenal ulcer, was treated with cefoperazone sodium, 2 g every 12 hours. He had mild renal...References1. COHENWASHTONBARRANCO MHS. Multicenter clinical trial of cefoperazone sodium in the United States. Am J Med. 1984;77:35-41. CrossrefMedlineGoogle Scholar2. SMITHLIPSKY CJ. Hypoprothrombinemia and platelet dysfunction caused by cephalosporin and oxalactam antibiotics. J Antimicrob Chemother. 1983;11:496-9. CrossrefMedlineGoogle Scholar3. HOCHMANCLARKROLLATHOMASKALDANYD'ELIA RJASAJ. Bleeding in patients with infections: are antibiotics helping or hurting? Arch Intern Med. 1982;142:1440-2. Google Scholar4. LIPSKY J. N-methyl-thio-tetrazole inhibition of the gamma carboxylation of glutamic acid: possible mechanism for antibiotic-associated hypoprothrombinemia. Lancet. 1983;2:192-3. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByBeta-Lactam AntibioticsBeta-Lactam AntibioticsINTERACTIONS OF WARFARINCephalosporin-Associated Hypoprothrombinemia: Case and Review of the LiteratureCefoperazone plus mezlocillin for empiric therapy of febrile cancer patientsVitamin K Reversible Hypoprothrombinemia in Rats II. Efficacy of Vitamin K on Latamoxef-Induced Coagulopathy in RatsDeterminants of Antibiotic-associated HypoprothrombinemiaSingle-dose cephalosporin prophylaxis of 929 surgical procedures in a prepaid group practice: A prospective, randomized comparison of cefoperazone and cefotaximeCefoperazone-Induced Coagulopathy 1 May 1985Volume 102, Issue 5Page: 721-722KeywordsCryptococcal meningitisDuodenal ulcersHemorrhageLymphomaPeritonitisSodiumSurgery Issue Published: 1 May 1985 PDF DownloadLoading ...
Lysosomal Transmembrane Protein LAPTM4B Promotes Autophagy and Tolerance to Metabolic Stress in Cancer Cells
Authors: Yang Li, Qing Zhang, Ruiyang Tian, Qi Wang, Jean J. Zhao, J. Dirk Iglehart, Zhigang Charles Wang, Andrea L. Richardson
Journal: Cancer Research (2011)

Abstract Amplification of chromosome 8q22, which includes the gene for lysosomal associated transmembrane protein LAPTM4B, has been linked to de novo anthracycline resistance in primary breast cancers with poor prognosis. LAPTM4B overexpression can induce cytosolic retention of anthracyclines and decrease drug-induced DNA damage. In this study, we tested the hypothesis that LAPTM4B may contribute to tumor cell growth or survival in the absence of a chemotherapeutic exposure. In mammary cells, LAPTM4B protein was localized in lysosomes where its depletion increased membrane permeability, pH, cathepsin release, and cellular apoptosis. Loss of LAPTM4B also inhibited later stages of autophagy by blocking maturation of the autophagosome, thereby rendering cells more sensitive to nutrient deprivation or hypoxia. Conversely, enforced overexpression of LAPTM4B promoted autophagic flux and cell survival during in vitro starvation and stimulated more rapid tumor growth in vivo. Together, our results indicate that LAPTM4B is required for lysosome homeostasis, acidification, and function, and that LAPTM4B renders tumor cells resistant to lysosome-mediated cell death triggered by environmental and genotoxic stresses. Cancer Res; 71(24); 7481–9. ©2011 AACR.
COMPARATIVE OUTCOMES OF CATHETER–DIRECTED THROMBOLYSIS WITH ANTICOAGULATION VERSUS ANTICOAGULATION ALONE IN CANCER PATIENTS WITH DEEP VENOUS THROMBOSIS
Authors: Yevgeniy Brailovsky, Vladimir Lakhter, Chad Zack, John Gaughan, Alfred Bove, Riyaz Bashir
Journal: Journal of the American College of Cardiology (2013)
ACCIDENTS IN EYE OPERATIONS.
Authors: F. C. HEATH
Journal: JAMA (1898)

While it is more flattering to one's vanity to record successes, it is often quite as profitable to study failures and embarrassments, with a view to learning how to avoid or master them in the future. It will be the aim of this paper to consider briefly a few accidents occurring in eye operations. Some years ago, as I was making a paracentesis on an Irishman's eye with a Graefe knife, the patient made a sudden violent movement on the entrance of the knife point into the anterior chamber. A serious accident in this case was avoided by depressing the handle of the knife quickly so that the point could not injure the lens, but a good lesson was learned—not to operate too soon after instilling cocain. A more serious accident occurred on attempting to do an iridectomy, without an assistant, on an intractable patient who moved her eye
THE ANTIRACHITIC ACTIVITY OF MONOCHROMATIC AND REGIONAL ULTRAVIOLET RADIATIONS
Authors: ALFRED F. HESS
Journal: JAMA (1927)

In 1923, experiments were carried out to ascertain the length of the ultraviolet waves which are endowed with the remarkable property of preventing or curing rickets. It was found that, in order to be of value, "ultraviolet waves must have a length not longer than 302 or possibly 313 millimicrons."<sup>1</sup>This conclusion was arrived at by means of an extended series of experiments which made use of selective glass filters and has been confirmed by the recent work of Luce.<sup>2</sup>The study served to emphasize the remarkable specificity of waves of light in relation to rickets, showing that a difference of about 20 millionths of a millimeter determined whether ultraviolet radiation was either effective or ineffective in this respect. The data, however, were not sufficiently refined, the analysis of the spectrum not precise enough to warrant a definite conclusion as to whether the intense waves of the mercury
Spurious leukocytosis and thrombocytopenia. A dual phenomenon caused by clumping of platelets in vitro
Authors: D. L. Solanki
Journal: JAMA (1983)

Three patients with spurious thrombocytopenia caused by in vitro clumping of platelets also had leukocytosis that was inappropriate for their clinical state and could not be verified on examination of a blood smear. Serial blood counts and analysis of the platelet and WBC histograms proved the "leukocytosis" to be spurious and caused by platelet clumps erroneously "recognized" by the counter as white blood cells. In three additional patients, the WBC counts increased concomitantly with a decrease in their platelet counts but remained within the normal range. Abnormal platelet and WBC counts generated by automated cell counters must be verified by examination of a blood smear before patients are subjected to unwarranted investigations and therapy. (<i>JAMA</i>1983;250:2514-2515)
DNA Fingerprints Come to Court
Authors: Beverly Merz
Journal: JAMA (1988)

COMB SEARCHES may be on the way to replacing strip searches in criminals' nightmares, thanks to a new technique known as DNA fingerprinting.  The technique, which produces a visual representation of a person's genome, enables the identification of perpetrators from as little as a single hair root, providing they have left some biologic evidence—hair, skin cells, blood, or semen—at the scene of the crime.  DNA fingerprinting was developed by British geneticist Alec Jeffreys, PhD, in 1985. Jeffreys, professor of genetics at the University of Leicester, built upon a discovery, five years earlier, of certain hypervariable regions called minisatellites in unexpressed areas of DNA.  The hypervariability was evidenced in the number of repetitions of certain sequences of base pairs. For example, in a given minisatellite, a certain 32-base pair segment may appear 28 times in one person's DNA, 22 times in another's, and 19 times in a third person's.  It was
Abstract 5476: Small molecule activation of BAX-mediated apoptosis through direct engagement of the BAX trigger site
Authors: Evripidis Gavathiotis, Denis Reyna, Loren Walensky
Journal: Cancer Research (2011)

Abstract BCL-2 family proteins are key regulators of the mitochondrial apoptotic pathway in health and disease. Anti-apoptotic members such as BCL-2 and BCL-XL have been implicated in the initiation, progression, and chemoresistance of human cancer. The anti-apoptotic BCL-2/BCL-XL groove that binds and sequesters pro-apoptotic BH3 death helices has been successfully targeted by small molecules and peptides. Such compounds induce tumor cell apoptosis and are being advanced in clinical trials as promising next-generation cancer therapeutics. We recently localized a distinct BH3 binding groove on pro-apoptotic BAX and demonstrated that engagement of the novel site by a triggering BIM BH3 helix directly activates BAX (Gavathiotis et al. Nature, 2008), unleashing a succession of key conformational changes that culminates in the formation of a toxic mitochondrial pore (Gavathiotis et al. Mol Cell, 2010). Here we applied these new structural insights in a computational screen to identify small molecules capable of directly engaging the BAX trigger site for therapeutic induction of BAX-mediated apoptosis in human cancer. We confirmed by NMR analysis that a series of identified small molecules indeed bound to the BAX trigger site and in fluorescence polarization assays were strikingly selective for the BH3-binding groove of BAX as compared to that of anti-apoptotic targets. We demonstrate that molecular binding triggers dose-responsive BAX activation, as assessed by in vitro oligomerization, membrane permeabilization, and cell death assays. Importantly, the small molecule BAX activators induce apoptosis of cancer cells in a BAX-dependent manner, highlighting both the selectivity and pharmacologic potential of direct BAX activation as a novel strategy for cancer therapy. 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 5476. doi:10.1158/1538-7445.AM2011-5476
Is There a Role for Cetuximab in Non–Small Cell Lung Cancer?
Authors: Daniel Morgensztern, Ramaswamy Govindan
Journal: Clinical Cancer Research (2007)

Abstract The epidermal growth factor receptor (EGFR) is commonly overexpressed in non–small cell lung cancer (NSCLC). In addition, activating mutations in the EGFR tyrosine kinase domain have been described almost exclusively in NSCLC. Cetuximab, a monoclonal antibody against EGFR, has only modest single-agent activity in advanced NSCLC. A few phase II studies conducted in advanced NSCLC show no significant benefit from adding cetuximab to chemotherapy. However, in vitro observations of synergy between EGFR inhibitors and radiation therapy have been confirmed in the clinical setting of head and neck cancer. The addition of cetuximab to radiotherapy improves survival in patients with locally advanced unresectable squamous cell cancer of the head and neck compared with radiotherapy alone and this combination is being actively studied in locally advanced NSCLC. Research is also ongoing to define the role of cetuximab in combination with other targeted agents. This review will summarize the results of recently published studies on cetuximab and outline current research with this agent in NSCLC.
Evolving concepts of sleep cycle generation: From brain centers to neuronal populations
Authors: J. A. Hobson, R. Lydic, H. A. Baghdoyan
Journal: Behavioral and Brain Sciences (1986)

Abstract As neurophysiological investigations of sleep cycle control have provided an increasingly detailed picture of events at the cellular level, the concept that the sleep cycle is generated by the interaction of multiple, anatomically distributed sets of neurons has gradually replaced the hypothesis that sleep is generated by a single, highly localized neuronal oscillator. Cell groups that discharge during rapid-eye-movement (REM) sleep (REM-on) and neurons that slow or cease firing during REM sleep (REM-off) have long been thought to comprise at least two neurochemically distinct populations. The fact that putatively cholinoceptive and/or cholinergic (REM-on) and putatively aminergic (REM-off) cell populations discharge reciprocally over the sleep cycle suggests a causal interdependence. In some brain stem areas these cell groups are not anatomically segregated and may instead be neurochemically mixed (interpenetrated). This finding raises important theoretical and practical issues not anticipated in the original reciprocal-interaction model. The electrophysiological evidence concerning the REM-on and REM-off cell groups suggests a gradient of sleep-dependent membrane excitability changes that may be a function of the connectivity strength within an anatomically distributed neuronal network. The connectivity strength may be influenced by the degree of neurochemical interpenetration between the REM-on and REM-offcells. Recognition of these complexities forces us to revise the reciprocal-interaction model and to seek new methods to test its tenets. Cholinergic microinjection experiments indicate that some populations of REM-on cells can execute specific portions of the REM sleep syndrome or block the generation of REM sleep. This observation suggests that the order of activation within the anatomically distributed generator populations may be critical in determining behavioral outcome. Support for the cholinergic tenets of the reciprocal-interaction model has been reinforced by observations from sleep-disorders medicine. Specific predictions of the reciprocal-interaction model and suggestions for testing these predictions are enumerated for future experimental programs that aim to understand the cellular and molecular basis of the mammalian sleep cycle.
Significance of increased plasma adrenomedullin concentration in patients with cirrhosis
Authors: Hideyuki Kojima, Tatsuhiro Tsujimoto, Masahito Uemura, Akira Takaya, Shingo Okamoto, Shirou Ueda, Kenji Nishio, Seiji Miyamoto, Atsushi Kubo, Naoto Minamino, Kenji Kangawa, Hisayuki Matsuo, Hiroshi Fukui
Journal: Journal of Hepatology (1998)
BUN/Creatinine Ratios: Aid to Decision Making About Delayed Imaging in Tc-99m Red Blood Cell Scans for Gastrointestinal Hemorrhage
Authors: DAVID H. LEWIS, ARNOLD F. JACOBSON
Journal: Clinical Nuclear Medicine (1998)

In patients with gastrointestinal hemorrhage, delayed or late scans with Tc-99m labeled red blood cells are readily performed and have prognostic impact when early images are negative. Nevertheless, there have been no indicators for the likelihood of detecting bleeding on such images. In a review of all gastrointestinal bleeding scans over an 8-year period, 73 patients had delayed images (>3 hours) following early negative exams. For these patients, determinations of serum blood urea nitrogen (BUN) and creatinine (Cr) were evaluated as the BUN/Cr ratio and were compared against delayed scan findings and confirmed diagnoses. Patients with significant renal failure were excluded from analysis. There were 34 late positive (46%) and 39 late negative (54%) studies. Mean BUN/Cr was 26.5 and 20.0 in patients with late positive and late negative scans, respectively (p < 0.05). Occurrence of late positive scans was 38% (19/50) for BUN/Cr <25.0 vs. 65% (15/23) for BUN/Cr >25.0 (p < 0.05). Patients with early negative images and a BUN/Cr ratio of 25 or greater have a greater likelihood of a positive delayed image. Late imaging should be encouraged in patients with elevated BUN/Cr and early negative scintigraphy.
Herpes Zoster after Fractured Spine Complicating E.C.T
Authors: A. I. Roith
Journal: BMJ (1956)

In the supraorbital case it has so far lasted for over three years, but in the others it tended to remit within 18 months.Two of these five had severe pre-herpetic pain, the other three had none.No effective treatment for post-herpetic pain was discovered.The methods tried were analgesics, including aspirin and its compounds, opium, nepenthe, levorphanol tartrate, pethidine, local injections of procaine, deep x rays (two cases), short-wave therapy, ultra-violet rays, ultrasonics (one case), E.C.T. (one case), liver, posterior pituitary injec-
Human infections with Microsporum gypseum in Denmark
Authors: PER ONSBERG
Journal: British Journal of Dermatology (1978)

Ninety cases of Microsporum gypseum infection in Denmark during the period 1933-1977 are reviewed. The sex ratio, age distribution, and anatomical sites are started. A case of onychomycosis in a 1-year-old child is reported, and the cases of M. gypseum onychomycosis in the literature are reviewed.
Depletion of stratum corneum intercellular lipid lamellae and barrier function abnormalities after long-term topical corticosteroids
Authors: H.-M. SHEU, J.Y.-Y. LEE, C.-Y. CHAI, K.-W. KUO
Journal: British Journal of Dermatology (1997)

The intercellular lipid lamellae of the stratum corneum (SC) is believed to provide the permeability barrier of the epidermis. Previous functional studies have demonstrated an increase in the transepidermal water loss (TEWL) after long‐term use of topical corticosteroids (TCS); however, direct morphological confirmation of this barrier abnormality is still lacking. The aim of this study was to determine whether any abnormality could be detected in the structure of the SC intercellular lipid lamellae in patients after long‐term TCS. Atrophic skin and untreated normal skin of 10 patients after long‐term TCS were examined by transmission electron microscopy using ruthenium tetroxide‐ fixed tissue for the multilamellar lipid sheets of SC, and oil red O stain for neutral lipids of the SC. Layers of the SC were evaluated by 0·1% methylene blue stain after alkaline expansion, and TEWL was measured by Evaporimeter EPI. The TCS‐treated atrophic skin had fewer layers of horny cells, mean 9–4 layers, than the normal control skin, 18 layers (P<0·001) and increased TEWL of 21·3g/m2 compared with the control skin TEWL of 6·7 g/m2(P<0·01). The mean neutral lipid content of the SC was also significantly lower (P<0·001). Moreover, ultrastructural studies revealed a marked decrease in both the numbers of intercellular lipid lamellae of SC and membrane‐coating granules of stratum granulosum in the atrophic skin. These results suggest that the diminution in the SC intercellular lipid lamellae and SC cell layers play an important part in the pathogenesis of barrier dysfunction after long‐term use of TCS.
Transforming growth factor-β2 upregulates sphingosine kinase-1 activity, which in turn attenuates the fibrotic response to TGF-β2 by impeding CTGF expression
Authors: Shuyu Ren, Andrea Babelova, Kristin Moreth, Cuiyan Xin, Wolfgang Eberhardt, Anke Doller, Hermann Pavenstädt, Liliana Schaefer, Josef Pfeilschifter, Andrea Huwiler
Journal: Kidney International (2009)
Anti-Adrenergic Effects of Nitroglycerin on the Heart
Authors: W. RAAB, E. LEPESCHKIN
Journal: Circulation (1950)

The therapeutic effect of nitroglycerin is generally attributed to its coronary dilator effect alone. In contrast, it could be shown that nitroglycerin also counteracts the chronotropic as well as the electrocardiographic T-wave depressing effects of epinephrine, arterenol and cardiac sympathin upon the heart. Accordingly, its therapeutic action in angina pectoris is suspected as being largely due to a chemical protection of the heart muscle against the chemically anoxia-producing effects of sympathomimetic amines.
No ladies or girls please--just women
Authors: J. Robinson
Journal: BMJ (1984)

<h3>Abstract</h3> The nautiloid lineage extends back nearly 500 million years but today, is represented by only two living genera, <i>Nautilus</i> and <i>Allonautilus</i>. Behavioral observations of these living nautiluses have improved our understanding of how nautiloids, and ammonoids, behaved and interacted in their environment. These behaviors may also help to inform conservation practices. Here, we describe feeding and mating behaviors in wild nautiluses not reported from any other population. In Palau, <i>Nautilus belauensis</i> was observed actively preying on a large, living crab (<i>Chaceon</i> sp.) and performing courtship-like behaviors prior to mating. These behaviors occurred across multiple nights and from different nautiluses, suggesting that the behaviors are characteristic of at least a subset of the population, if not the entire population. Perhaps the behaviors exhibited by the Palauan nautiluses are an outlier and simply a localized characteristic of a far-removed population. Or, perhaps these apparent abnormal behaviors of Palauan nautiluses are what all nautiluses across the Indo-Pacific should be exhibiting. If the latter explanation is correct, we can start to address the potential causes of the behavioral differences, such as population size, habitat type, and prey availability. In either case, this apparent behavioral plasticity may have also been a reason that the nautiloid lineage has been able to survive throughout millions of years of environmental changes. Today, these behavioral observations could prove to be a valuable conservation tool to protect species and environments, especially in the deep-sea ecosystem the nautiluses inhabit.
THE INITIAL LESION IN EXPERIMENTAL ALLERGIC NEURITIS
Authors: Karl E. Åström, Henry de F. Webster, Barry G. Arnason
Journal: The Journal of Experimental Medicine (1968)

Experimental allergic neuritis (EAN) was produced in rats by the intradermal injection of an emulsion of peripheral nerve in Freund's adjuvant. Early lesions in perfused sciatic nerves were studied by phase, light, and electron microscopy at intervals up to 15 days following immunization. Circulating lymphocytes attached focally to the inner surface of blood vessels, primarily venules, to initiate parenchymal lesion formation. Attached cells had the hand mirror configuration typical of the motile lymphocyte. They subsequently flattened against the endothelial surface and then traversed the vascular wall by sinking into and passing through the cytoplasm of endothelial cells. The transgressor and transgressed cell membranes were intact and both cells retained their integrity. Lymphocytes began to transform and divide intravascularly; these events accelerated extravascularly. Although the migrating cells became larger and more pleomorphic in the perivascular regions, their essential character was in keeping with an origin from circulating lymphocytes. In many lesions, there was fluid with protein, possibly produced by the transformed extravascular cells. The described cellular events precede tissue damage and are likely instrumental in the myelin destruction which follows