tbuckley/cabot-search huggingface dataset:
PMO-044 Mortality post percutaneous endoscopic gastrostomy insertion: a root-cause analysis: Abstract PMO-044 Table 1
Authors: J Barker, S Ooi, L McEvoy, J Mawdsley, C E Collins, I Beveridge, K Sundaram, K J Monahan
Journal: Gut (2012)

Introduction Meta-analysis has demonstrated a 19% 30-day mortality following Percutaneous Endoscopic Gastrostomy (PEG) insertion.1 The 2008 National Confidential Enquiry into Patient Outcome and Death (NCEPOD)2 retrospectively audited inpatient death, demonstrating poor patient selection and use of multidisciplinary assessment. The figures demonstrated the need for endoscopy units to engage in regular audit of PEG insertion and suggested reviewing all cases of mortality within 30 days of procedure. Methods A root-cause analysis of mortality after inpatient PEG insertion was undertaken from over 1 year from June 2010 to May 2011 at West Middlesex University Hospital, London. Results 45 patients underwent PEG insertion with an average age of 72.66 years (range 33–100; 19 females; 26 males). Indications were neurological in 96% (43). Six were for PEG re-insertion following tube failure. Most were American Society of Anaesthesiologists (ASA) grade II (56%). The one ASA IV case was an intensive care unit inpatient. The 30-day mortality was 20%, with an average age of 82.9 years and average survival of 14.4 days. All indications for insertion were for poor swallow post stroke. The majority of patients were ASA-II. All causes of death were all attributed to pneumonia on their death certificates. None of the deaths were procedure related. However, these patients demonstrated multiple co-morbidities and a poor functional baseline level pre-procedure. 20 patients died within 365 days (44.4% 1 year mortality) with an average age at insertion of 81.8 years. Conclusion The 30-day mortality rate in this study mirrors that found in previous published data, with all known deaths due to respiratory disease; none were found to be procedure related deaths. This is despite careful patient selection, assessment by a multidisciplinary team and the application of other recommendations of the NCEPOD report. It would be prudent for further review and audit of careful selection of appropriateness for PEG particularly in cases with multiple comorbidities with consideration into the futility of the procedure. Thus patient selection for PEG insertion remains a difficult problem. View this table: Abstract PMO-044 Table 1 Competing interests None declared. References 1. Mitchell SL, Tetroe JM. Survival after percutaneous endoscopic gastrostomy placement in older persons. J Gerontol A Biol Sci Med Sci 2000; 55 :M735–9. 2. Johnston S, Tham T, Mason M. Death after PEG: results of the national confidential enquiry into patient outcome and death. Gastrointestinal Endoscopy 2008; 68 :223–7.
Abstract 867: IGF-I receptor targeting therapy for esophageal carcinomas.
Authors: Yasushi Adachi, Hiroyuki Yamamoto, Hirokazu Ohashi, Yasutaka Matsunaga, Katsuhiko Nosho, Hiromu Suzuki, Hiroaki Taniguchi, Yoshiaki Arimura, Takao Endo, Yasuo Kato, Kohzoh Imai, David P. Carbone, Yasushisa Shinomura
Journal: Cancer Research (2013)

Abstract Insulin-like growth factor (IGF)-I receptor (IGF-IR) signaling is required for tumorigenicity and cancer development of many malignancies, however this pathway has not been well studied in human esophageal carcinomas. Esophageal cancer is one of worst prognostic disease, main types of which are squamous cell carcinomas (ESCC) and adenocarcinoma (EAC). Previously we have reported that the IGF axis may play a key role in tumor progression of ESCC and its detection may be useful for the prediction of recurrence and poor prognosis and possibly for selecting patients for targeting therapy for IGF-IR. We have previously shown successful therapy for several gastrointestinal cancers using recombinant adenoviruses expressing dominant negative forms of IGF-IR (Ad-IGF-IR/dn). In this study, we wanted to develop potential targeted therapeutics to IGF-1R; therefore, we assessed the effect of IGF-IR blockade in both types of esophageal cancer. We analyzed immunohistochemical expression of IGF-IR in a tissue array. A tyrosine kinase inhibitor, BMS-536924, and Ad-IGF-IR/dn were used to treat several ESCC lines, such as TE1, TE8, TT, TTn, and EAC lines, including OE19 and OE33. We assessed the effect of both IGF-IR blockade on signal transduction, growth, and apoptosis. IGF-IR is expressed frequently in esophageal tumors, but not in normal mucosa. IGF-IR was produced in ESCC more than EAC, and is detected in metastasized similar to the primary site. IGF-IR inhibition suppressed proliferation and colony formation in both types of cancer. Blockade of IGF-IR up-regulated both stress- and chemotherapy-induced apoptosis in both esophageal tumor type. Although IGF-IR/dn blocked ligand-induced activation of Akt-1 mainly, BMS-536924 effectively blocked both activation of Akt and MAPK. Thus, the IGF axis may play a key role in tumor progression of human esophageal carcinomas. The IGF-IR targeting strategies might be useful anticancer therapeutics which can be used widely for human esophageal malignancies. Citation Format: Yasushi Adachi, Hiroyuki Yamamoto, Hirokazu Ohashi, Yasutaka Matsunaga, Katsuhiko Nosho, Hiromu Suzuki, Hiroaki Taniguchi, Yoshiaki Arimura, Takao Endo, Yasuo Kato, Kohzoh Imai, David P. Carbone, Yasushisa Shinomura. IGF-I receptor targeting therapy for esophageal carcinomas. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 867. doi:10.1158/1538-7445.AM2013-867
Lysosomal elastase and cathepsin G in beige mice. Neutrophils of beige (Chediak-Higashi) mice selectively lack lysosomal elastase and cathepsin G.
Authors: K Takeuchi, H Wood, R T Swank
Journal: The Journal of Experimental Medicine (1986)

A profound decrease in activities of the two lysosomal serine proteinases, elastase, and cathepsin G, was found in neutrophils of four independent beige mutants. Elastase and cathepsin G activities were assayed with the specific synthetic substrates MeO-Suc-Ala-Ala-Pro-Val-MCA and Suc-Ala-Ala-Pro-Phe-pNA, respectively. The defect is intrinsic to cells of beige mice, since transplantation of bone marrow from normal to mutant mice restored normal proteinase activity, and normal mice transplanted with beige marrow produced neutrophils with a deficiency of proteinase activity. The loss of elastase and cathepsin G activity was confirmed by separation of [3H]diisopropylfluorophosphate-labeled proteins on denaturing gels, which also revealed that other serine proteinases are at normal levels in beige neutrophil extracts. The deficiency of lysosomal proteinase activity appears specific, in that four other common neutrophil lysosomal enzymes, plus the spectrum of major neutrophil proteins are not affected by the beige mutation. The deficiency of proteinase activity is likely not the primary genetic alteration of the beige mutation, since more than one proteinase is affected, and heterozygous F1 mice have normal rather than intermediate levels of both proteinases. The lowered proteinase activity may contribute to the high susceptibility of beige mice and Chediak-Higashi patients to infection.
Acute Pancreatitis With Infectious Hepatitis
Authors: James L. Achord
Journal: JAMA (1968)

Four patients had evidence of acute pancreatitis occurring during infectious hepatitis. Paper electrophoresis of serum and urine of one patient revealed migration patterns of amylolytic activity identical to those of saline extracts of human pancreas. Definite gross and histologic pancreatitis was seen at autopsy in two patients who died of acute fulminant hepatitis. The fourth patient had only mild increases in the level of urine amylase but a classical "reversed 3 sign" on roentgenograms of the uppergastrointestinal tract, that largely disappeared in eight days.
Première expérience Française de cholangioscopie et de wirsungoscopie utilisant un appareil à usage unique (Spyglass) à travers un duodénoscope thérapeutique standard
Authors: R Laugier, A Laquiere
Journal: Endoscopy (2008)

Introduction: Dans certaines circonstances, l'efficacité diagnostique ou thérapeutique du cathétérisme rétrograde de la papille n'est pas optimale: une visualisation directe des lésions pourrait être préférable.
Medicare and Medical Students
Authors: James R. Scholten
Journal: JAMA (1966)

Of 1,500 medical students at four medical schools, 1,053 anonymously and voluntarily completed questionnaires eliciting information on their knowledge and attitudes toward the Medicare program. Their responses indicate that 80% of them have little or no knowledge regarding the details of the program. Despite this lack of information, a large majority of the students have opinions which are, in general, negative. The attitudes and opinions expressed were remarkably homogeneous in each of the four classes at each school. There were differences between the schools which may depend upon the ecology of the school, ie, socioeconomic background of students and types of careers pursued by the graduates. On the basis of data available, it would seem that a significant proportion of medical students believe that their career plans have been altered by this legislation. This ranges from a high of 24.6% in the fourth-year class of school C to a low of 3.5% of the first-year class in school B.
A CASE OF GRANULOPENIA FOLLOWING AMIDOPYRINE, WITH TWO RECURRENCES
Authors: Wingate M. Johnson
Journal: JAMA (1934)

Mrs. B. N. J., aged 41, the wife of a physician, had a left supra-orbital neuralgia for which she took amidopyrine in 5 grain (0.3 Gm.) doses from one to four times a day for about two weeks. On May 6 she began to ache and had a temperature of 100 to 101 F. The next day her gums became moderately inflamed. May 8 she was chilly, the aching became worse, and she began to feel prostrated. The prostration became more marked, the temperature elevation continued, and the gums became swollen and spongy. On May 10 a leukocyte count was 1,400, with no granulocytes. She was taken to the North Carolina Baptist Hospital and given 8 minims (0.5 cc.) of turpentine into the deltoid muscle of the left arm, as suggested by Roberts and Kracke.1 In addition she was given 10 cc. of pentnucleotide, in the buttocks, twice a day
Vitamin E supplementation and oxidative damage to DNA and plasma LDL in type 1 diabetes.
Authors: S Astley, A Langrish-Smith, S Southon, M Sampson
Journal: Diabetes Care (1999)

OBJECTIVE: To determine the effect of 400 IU/day of the antioxidant vitamin E on the susceptibility of plasma LDL and lymphocyte DNA to oxidative damage in type 1 diabetes. RESEARCH DESIGN AND METHODS: We studied 42 patients with type 1 diabetes and 31 age- and sex-matched control subjects in a randomized prospective double-blind placebo-controlled trial by using 400 IU/day of oral vitamin E for 8 weeks. Measurements were made of single-strand breaks in lymphocyte DNA at baseline and after hydrogen peroxide-induced stress (comet assay) and of copper-induced LDL oxidization and plasma antioxidant profiles. RESULTS: Plasma LDL and lymphocyte DNA were more resistant to induced oxidative change in the type 1 diabetes group than in control subjects. Vitamin E supplementation reduced LDL oxidizability in the control subjects but not in the type 1 diabetes group and had no effect on oxidative DNA damage in either group. The type 1 diabetes group had a significantly poorer plasma antioxidant profile with lower mean serum concentrations of alpha-tocopherol and most carotenoids than control subjects. CONCLUSIONS: Plasma LDL and lymphocyte DNA appear to be more resistant to oxidative change in type 1 diabetic subjects than in control subjects, and there was no evidence of oxidatively induced DNA or LDL change in type 1 diabetes. This study does not support the hypothesis of oxidative damage in these patients, and a dose of vitamin E (400 IU/day) that reduced LDL oxidative susceptibility in control subjects did not do so in patients with type 1 diabetes.
Aminopyrine in Hodgkin's Disease
Authors: Paul W. Spear
Journal: JAMA (1963)

<h3>To the Editor:</h3> —Dr. Trimble's somewhat acidulous remarks concerning the hazards of aminopyrine serve only to call attention to the inconsistencies of our profession. I am sure that Dr. Trimble's own staff uses butazolidin, corticosteroids, apresoline, and many other drugs of current vintage whose effects are purely symptomatic but which, nevertheless, cause frequent and serious reactions. Despite these hazards, we all countenance the use of such drugs under proper supervision. I know of no good reason for not doing the same with aminopyrine. One of our eminent consultants, Dr. William Dock, drawing on his own experience and that of another equally eminent consultant, Dr. Isadore Snapper, has stated, "We are not only familiar with the literature which Dr. Wintrobe quotes but both have been using this drug for a total of nearly 90 years. Neither happens to have had a case of agranulocytosis so far, so we regard Damashek's figure
Findings of 123I-Iomazenil SPECT During and After Stroke-Like Episodes in a Patient With MELAS
Authors: Yoshiharu Taguchi, Shutaro Takashima, Kyo Noguchi, Kortaro Tanaka
Journal: Clinical Nuclear Medicine (2013)

Reduced cortical benzodiazepine receptor binding potential in late images of I-iomazenil SPECT indicates neuronal damage in the cortex. We present the case of a 31-year-old woman with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) who had focal seizures in the right hand. FLAIR imaging in the ictal state revealed a high-intensity lesion in the left post-central gyrus, while I-iomazenil SPECT showed decreased tracer uptake in this lesion. The lesion completely disappeared on FLAIR imaging performed 1 month after the focal seizures; in contrast, I-iomazenil SPECT still revealed a significant decrease in tracer uptake in this lesion.
Congenital Thrombophilic States Associated with Venous Thrombosis: A Qualitative Overview and Proposed Classification System
Authors: Mark A. Crowther, John G. Kelton
Journal: Annals of Internal Medicine (2003)

Congenital causes of venous thrombosis have gained increasing prominence with the description of the factor V Leiden mutation and the prothrombin gene mutation. More recently, the description of the association between increased levels of coagulation factors and venous thrombosis and the finding that patients with thrombophilia can harbor more than one prothrombotic state have further increased the clinical relevance of the congenital thrombophilic states. In this qualitative review, we summarize current knowledge of the congenital prothrombotic states and propose a simple classification system that divides the states into two broad groups: those associated with reduced levels of the inhibitors of the coagulation cascade and those associated with increased levels or function of the coagulation factors. The first group is less common than the second, but it is associated with a much higher risk for venous thrombosis. This review provides clinicians with an evidence-based, practical guide to the congenital prothrombotic states.
Abstract 4933: In vivo visualization of heterogeneous cancer cell populations by fluorescence molecular tomography
Authors: Ciro Zanca, Maria del Mar Inda, Rudy Bonavia, Jill Wykosky, Vladislav Verkhusha, Webster Cavenee, Frank Furnari
Journal: Cancer Research (2014)

Abstract Glioblastoma is the most common and aggressive tumor type that affects the central nervous system in adults. Despite advances in treatment strategies, its prognosis remains poor. EGFR and its mutant form EGFRvIII are amplified in a subset of clinical cases and interaction between cell populations expressing each receptor has been shown to enhance overall tumor growth. For instance, EGFRvIII induces expression of several secreted oncogenic factors, such as IL6 and LIF, which in turn stimulate the growth of EGFR expressing cells through an IL6 receptor (gp130)/EGFR cross-talk interaction. Therapy directed towards EGFR or EGFRvIII inhibition has been ineffective because of mechanisms that inhibit cell death. We hypothesize that these factors secreted by EGFRvIII expressing cells, in addition to promoting tumor growth, play a role in the failure of EGFR-directed therapies reported for glioblastoma. Preliminary data indicate that EGFRvIII-expressing cells prompt an IL6/LIF-mediated paracrine and autocrine antiapoptotic signaling cascade, leading to upregulation of the pro-survival protein, Survivin. RNAi-mediated downregulation of Survivin reverts this phenotype. To determine the effect of identified signaling effectors and cytokines in promoting EGFR tyrosine kinase inhibitor resistance, an in vivo model system of heterogeneous tumor growth was established and imaged using fluorescence molecular tomography (FMT) technology. Survivin, upstream pathways and cytokines were ablated in EGFR or EGFRvIII-expressing glioma cell lines tagged with different near infrared fluorescent proteins (turboFP635 or iRFP713). Orthotopically engrafted tumors of mixed EGFR/EGFRvIII populations were then evaluated for their tumor growth and cellular composition when challenged with EGFR tyrosine kinase inhibitors. In conclusion, this system allows for the validation of molecular mechanisms that promote cancer cell survival and establishes the basis for alternative treatment strategies. Citation Format: Ciro Zanca, Maria del Mar Inda, Rudy Bonavia, Jill Wykosky, Vladislav Verkhusha, Webster Cavenee, Frank Furnari. In vivo visualization of heterogeneous cancer cell populations by fluorescence molecular tomography. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4933. doi:10.1158/1538-7445.AM2014-4933
An Intervention to Reduce HIV Risk Behavior of Substance-Using Men Who Have Sex with Men: A Two-Group Randomized Trial with a Nonrandomized Third Group
Authors: Gordon Mansergh, Beryl A. Koblin, David J. McKirnan, Sharon M. Hudson, Stephen A. Flores, Ryan E. Wiegand, David W. Purcell, Grant N. Colfax
Journal: PLoS Medicine (2010)

In a randomized trial of a behavioral intervention among substance-using men who have sex with men, aimed at reducing sexual risk behavior, Mansergh and colleagues fail to find evidence of a reduction in risk from the intervention.
The Control of the Cerebral Circulation
Authors: Henry A. Shenkin
Journal: JAMA (1961)

The cerebral circulation is broadly limited by factors extrinsic to the brain, namely the general arterial blood pressure and the cardiac output. The cerebral blood flow will be maintained until the cardiac output is decreased by more than a third or the blood pressure is lowered to half or less of the normal value. Within these broad limits the cerebral blood flow is regulated by intrinsic factors, principally the cerebrovascular tone, which in turn is markedly influenced by chemical factors, chiefly the respiratory gases, and only slightly affected by neurogenic factors.
Different Roles of Interleukin-23 During the Epicutaneous Sensitization and the Antigen Exposure to the Airways On Airway Inflammation and Responsiveness in Mice
Authors: Katsunori Masaki, Yusuke Suzuki, Shizuko Kagawa, Motohiro Kodama, Hiroki Kabata, Jun Miyata, Kyuto Tanaka, Koichi Fukunaga, Tsuyoshi Oguma, Tomoko Betsuyaku, Koichiro Asano
Journal: Journal of Allergy and Clinical Immunology (2013)
Nerve Growth in Neurofibromatosis
Authors: Solomon H. Snyder
Journal: New England Journal of Medicine (1974)

Nerve-growth factor is a remarkable protein, discovered more than 20 years ago as a substance that dramatically stimulates the outgrowth of neurites from sympathetic and sensory ganglions of embryos and characterized extensively by Rita Levi-Montalcini.1 Screening of many tissues disclosed the major sources of nerve-growth factor as salivary glands of mice (but not of rats), snake venom and some tumors — a bizarre distribution that still makes little sense to most investigators. Once the factor was extensively purified and antibodies prepared, it was found that treatment of young animals with anti-nerve-growth factor could virtually destroy their sympathetic nervous system, a . . .
The alpha1 Na,K-ATPase gene is a susceptibility hypertension gene in the Dahl salt-sensitiveHSD rat.
Authors: V L Herrera, H X Xie, L V Lopez, N J Schork, N Ruiz-Opazo
Journal: Journal of Clinical Investigation (1998)

Despite the prevalence of essential hypertension, its underlying genetic basis has not been elucidated due to the complexities of its determinants. To identify a hypertension susceptibility gene, we used an approach that integrates molecular, transgenic, and genetic analysis using Dahl salt-sensitive (S) and Dahl salt-resistant (R) rats ascertained for genotype and phenotype. To determine the role of the Dahl S Q276L alpha1 Na,K-ATPase gene variant, we developed transgenic Dahl S rats bearing the Dahl R wild-type (wt) alpha1 Na, K-ATPase cDNA directed by the cognate wt promoter region, Tg[wtalpha1]. Transgenic Dahl S rats exhibited less salt-sensitive hypertension, less hypertensive renal disease, and longer life span when compared with non-transgenic Dahl S controls. Total chromosome 2 linkage analysis of F2(SxR) male rats detects cosegregation of the alpha1 Na,K-ATPase locus with salt-sensitive hypertension. These data support the alpha1 Na,K-ATPase gene as a susceptibility gene for salt-sensitive hypertension in the Dahl S rat model, and provide the basis for the study of the alpha1 Na,K-ATPase locus in human hypertension.
Normal hearing tests: is a further appointment really necessary?
Authors: G. Kumar, F. Amen, D. Roy
Journal: Journal of the Royal Society of Medicine (2007)

By couching the discussion of Blair and Bush in terms of hubris and nemesis, Lord Owen 1 has avoided the pitfall of diagnosis from afar while still highlighting serious problems with the two world leaders (JRSM November 2006).He does dip his toe into psychodynamics citing Freud and Justin Frank, but, by and large, he sticks to discussing behaviour and its relation to hubris and power.As a politician, Lord Owen is qualified to discuss the political leaders he has encountered.As a physician, should he be making medical judgments on political leaders?Simon Wessely has questions about this and about whether or not psychiatrists should venture beyond the consulting room. 2 Should psychiatrists limit their judgments to patients they have examined?The American Psychiatric Association says 'yes' and Dr Wessely cites data to support that view.But the question remains, can psychiatrists and neuroscientists, with the help of philosophers, provide useful insights that contribute to the understanding of leaders and their followers?I believe that we should try.We should bring whatever scientific data there may be to counter ideology, blind faith and the intoxicating effects of power.It is true hubris often comes with power.Even though we do not have a psychiatric diagnosis for hubris, it is a psychological entity and as such should potentially be understood by science, as are other psychological phenomena.We do not diagnose those that we have not personally examined and we cannot diagnose an entire population, but perhaps we can bring clinical and scientific insights to help understand destructive behaviour As scientists and clinicians, we too must guard against hubris.Hopefully our colleagues will help us with that.JRMS should be applauded for exploring the issue.