tbuckley/cabot-search huggingface dataset:
Obesity and the metabolic response to severe multiple trauma in man.
Authors: M Jeevanandam, D H Young, W R Schiller
Journal: Journal of Clinical Investigation (1991)

In the obese state profound metabolic disturbances exist and it is not known how this disrupted metabolism in obese subjects (body mass index greater than 30) may change their ability to respond to the superimposed, injury-induced stress. Understanding the mechanisms that modify the metabolic parameters in traumatized obese patients is essential in their nutritional assessment and further treatment. We have investigated in 7 obese and 10 nonobese multiple trauma patients, on a whole-body level, the energy metabolism, protein kinetics, and lipolysis in the early catabolic "flow phase" of severe injury when they were receiving maintenance fluids without calories or nitrogen. Traumatized obese patients mobilized relatively more protein and less fat compared with nonobese subjects. A relative block both in lipolysis and fat oxidation is experienced by injured obese patients that results in a shift to preferential use of proteins and carbohydrates. Reduced endogenous protein synthetic efficiency observed in obese patients implies increased protein recycling. Thus obese patients could not effectively use their most abundant fat fuel sources and have to depend on other fuel sources. The nutritional management of obese trauma victims should therefore be tailored towards provision of enough glucose calories to spare protein.
Abnormal Kinetics of Degranulation in Chronic Granulomatous Disease
Authors: Sondra Barrett Gold, Deanne M. Hanes, Daniel P. Stites, H. Hugh Fudenberg
Journal: New England Journal of Medicine (1974)

The rate of degranulation by neutrophils from three male patients with X-linked chronic granulomatous disease was studied with use of non-ingestable heat-aggregated human IgG as the phagocytic stimulus. Both the spontaneous and the stimulated release of two lysosomal enzymes (acid phosphatase and β-glucuronidase) was measured at various times. The difference between these two measurements, called the net release, was compared to that from 25 control subjects. For the first 15 minutes after phagocytic stimulation the net release of lysosomal enzymes was significantly reduced in neutrophils from the patients and their mothers in comparison to controls. By 30 minutes, the net release became normal. The total content of acid phosphatase and β-glucuronidase in polymorphonuclear leukocytes from patients was normal. These data suggest impaired lysosomal degranulation during the early stages of phagocytosis in X-linked chronic granulomatous disease. (N Engl J Med 291:332–337, 1974)
The effect of Chinese herbal medicine, xiao‐qing‐long tang (XQLT), on allergen‐induced bronchial inflammation in mite‐sensitized mice
Authors: S. T. Kao, S. T. Wang, C. K. Yu, H. Y. Lei, J. Y. Wang
Journal: Allergy (2000)

Background: There are detailed descriptions of the clinical experiences and prescriptions of asthma in traditional Chinese medicine. Xiao‐qing‐long tang (XQLT), or sho‐seiryo‐to by its Japanese name, is one of the Chinese herbal medicines used to treat bronchial asthma and allergic rhinitis for centuries. However, the therapeutic mechanisms of this medication are still far from clear. In this study, a house‐dust‐mite ( Dermatophagoides pteronyssinus [Der p])‐sensitized murine model of asthma was used to evaluate the immunomodulatory effect of XQLT on the allergen‐induced airway inflammation in asthma. Methods: Three different protocols were designed to evaluate the treatment and/or long‐term prophylactic effect of XQLT in Der p‐sensitized mice. XQLT extracts (1 gm/kg) were administered to sensitized mice 1 h before allergen challenge (AC) (group A), 24 h after AC (group B), and every other day six times before AC (group C), respectively. Cellular infiltration and T‐cell subsets in the bronchoalveolar lavage fluid (BALF) of allergen‐challenged mice were analyzed. Intrapulmonary lymphocytes were also isolated to evaluate their response to allergen stimulation. Results: When XQLT was administered to the sensitized mice before AC (groups A and C), it suppressed airway inflammation by decreasing the number of total cells and eosinophil infiltration in the BALF, and downregulated the allergen‐ or mitogen‐induced intrapulmonary lymphocyte response of sensitized mice as compared to those of controls. This immunomodulatory effect of XQLT may be exerted through the regulation of T‐cell subsets by elevation or activation of the CD8 + and double‐negative T‐cell population in the lung. However, the administration of XQLT to sensitized mice 24 h after AC (group B) did not have the same inhibitory effect on the airway inflammation as XQLT given before AC. Conclusions: The administration of XQLT before AC has the immunomodulatory effect of reducing bronchial inflammation in the allergen‐sensitized mice.
Reply to Pascal Mouracade's Letter to the Editor re: Thomas F. Chromecki, Eugene K. Cha, Harun Fajkovic, et al. The Impact of Tumor Multifocality on Outcomes in Patients Treated with Radical Nephroureterectomy. Eur Urol 2012;61;245–53
Authors: Shahrokh F. Shariat
Journal: European Urology (2012)
Abstract 2033: Regulatory role of miR-203 in prostate cancer
Authors: Sharanjot Saini, Shahana Majid, Guoren Deng, Soichiro Yamamura, Koji Ueno, Yi Chen, Saif Zaman, Rajvir Dahiya
Journal: Cancer Research (2010)

Abstract MicroRNAs (miRNAs) constitute an evolutionarily conserved class of small non-coding RNAs that primarily regulate gene expression at the post-transcriptional level via sequence-specific interaction with the 3’-untranslated regions (UTRs) of cognate mRNA targets. It is being increasingly recognized that miRNAs play roles in the establishment and progression of human malignancies. Several recent studies have shown that microRNAs are significantly altered in prostate cancer. Here we explored the role of miR-203 in prostate cancer progression and metastasis. RT-PCR analysis of prostate carcinoma cell lines showed that miR-203 expression is attenuated in prostate cancer. This attenuation was validated by in situ hybridization analysis of miR-203 in clinical specimens. To evaluate the functional significance of miR-203, miR-203 was reintroduced in prostate cancer cell lines followed by functional assays. Overexpression of miR-203 in prostate cancer cell line leads to decreases in cell growth, clonability, invasiveness and migratory properties. miR-203 reexpression in prostate carcinoma cell line induces cell cycle arrest at the G0-G1 phase of the cell cycle with a concomitant alteration of cell cycle regulators such as p21, p27, cyclin E and cdk2. Also, miR-203 transfection leads to a significant increase in apoptosis in prostate cancer cells pointing to the pleiotropic roles of this miR in prostate cancer. Further, analysis of putative miR-203 targets showed that miR-203 regulates the expression of survivin, a small inhibitor of apoptosis (IAP) protein that plays a key role in prostate cancer progression. In conclusion, our data suggests a crucial tumor suppressive role for miR-203 in prostate cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2033.
Choledochoduodenal Fistula Due to Tuberculosis
Authors: B. Al Nakib, G.S. Jacob, H. Al Liddawi, J. Commen
Journal: Endoscopy (1982)

Occurrence of choledochoduodenal fistula is rare. Tuberculosis as its etiology has never been reported in the literature to our knowledge. We report a case of tuberculous choledochoduodenal fistula in an adult.
Re: Sigurdur Gudjónsson, Björn L. Isfoss, Kerstin Hansson, et al. The Value of the UroVysion® Assay for Surveillance of Non–Muscle-Invasive Bladder Cancer. Eur Urol 2008;54:402–8
Authors: Shiu-Dong Chung, Ming-Kuen Lai, Hong-Jeng Yu, Shih-Chieh Chueh
Journal: European Urology (2008)
C-terminal truncated hepatitis B virus x protein is associated with metastasis and enhances invasiveness by c-jun/matrix metalloproteinase protein 10 activation in hepatocellular carcinoma
Authors: Karen M.F. Sze, Glanice K.Y. Chu, Joyce M.F. Lee, Irene O.L. Ng
Journal: Hepatology (2012)

Random integration of hepatitis B virus (HBV) DNA into the host genome is frequent in human hepatocellular carcinoma (HCC) and this leads to truncation of the HBV DNA, particularly at the C-terminal end of the HBV X protein (HBx). In this study, we investigated the frequency of this natural C-terminal truncation of HBx in human HCCs and its functional significance. In 50 HBV-positive patients with HCC, full-length HBx was detected in all nontumorous livers. However, full-length HBx was found in only 27 (54%) of the HCC tumors, whereas natural carboxylic acid (COOH)-truncated HBx was found in the remaining 23 (46%) tumors. Upon clinicopathological analysis, the presence of natural COOH-truncated HBx significantly correlated with the presence of venous invasion, a hallmark of metastasis (P = 0.005). Inducible stable expression of the COOH-truncated HBx protein (with 24 amino acids truncated at the C-terminal end) enhanced the cell-invasive ability of HepG2 cells, as compared to full-length HBx, using the Matrigel cell-invasion assay. It also resulted in increased C-Jun transcriptional activity and enhanced transcription of matrix metalloproteinase 10 (MMP10), whereas activation of the MMP10 promoter by COOH-truncated HBx was abolished when the activator protein 1–binding sites on the MMP10 promoter were mutated. Furthermore, silencing of MMP10 by short interfering RNA in HBxΔC1-expressing HepG2 cells resulted in significant reduction of cell invasiveness. Conclusions: Our data suggest that COOH truncation of HBx, particularly with 24 amino acids truncated at the C-terminal end, plays a role in enhancing cell invasiveness and metastasis in HCC by activating MMP10 through C-Jun. (HEPATOLOGY 2013)
Abciximab associated thrombocytopenia: evidence for a complex interaction with heparin
Authors: D.J. Kereiakes, S.D. Berkowitz, K. Anderson, M. Simoons, A. Vahanian, A.M. Lincoff, J.E. Tcheng, H. Weisman, R.M. Califf, E.J. Topol
Journal: Journal of the American College of Cardiology (1998)
Pharmacologic characterization of a novel histamine receptor on human eosinophils.
Authors: D G Raible, T Lenahan, Y Fayvilevich, R Kosinski, E S Schulman
Journal: American Journal of Respiratory and Critical Care Medicine (1994)

There is increased recognition that lung mast cell mediators not only produce the symptoms of acute asthma, but also result in the recruitment and activation of additional proinflammatory cells, such as eosinophils. Histamine, one of the major mast cell mediators, is known to have numerous effects on eosinophil function. These effects of histamine are mediated by distinct receptors on the surface of eosinophils, only some of which have been characterized. Prior studies have suggested that eosinophils have non-H1, non-H2 histamine receptors which mediate the chemotactic effects of histamine. We observed previously that the histamine-induced increase in cytosolic calcium in human eosinophils could not be blocked by classic H1 or H2 antagonists, but could be inhibited by the H3 antagonist thioperamide. The purpose of this study was to further characterize the pharmacologic properties of this calcium-linked histamine receptor. Using Fura-2 loaded eosinophils to measure the concentration of cytosolic calcium, we examined the effect of additional histamine receptor antagonists and agonists. We found that the pKb for the H3 antagonists thioperamide, impromidine, and burimamide (8.1, 7.6, and 7.2, respectively), were similar to those reported for H3 receptors in the central nervous system, suggesting that the eosinophil histamine receptor was similar to H3 receptors. However, when the known H3 agonists were tested for activity ([R]-alpha-methylhistamine, N alpha-methylhistamine), the potencies of these compounds were much less than the potency of histamine itself, indicating a significant difference between H3 receptors and this eosinophil histamine receptor.(ABSTRACT TRUNCATED AT 250 WORDS)
Abstract 4437: Regulation of FANCD2 by the mTOR pathway contributes to the resistance of cancer cells to DNA double strand breaks.
Authors: Changxian Shen, Duane Oswald, Doris Phelps, hakan cam, Christopher E. Pelloski, Qishen Pang, Peter J. Houghton
Journal: Cancer Research (2013)

Abstract Deregulation of the mTOR pathway is closely associated with tumorigenesis. Accordingly mTOR inhibitors such as rapamycin and mTOR-selective kinase inhibitors have been tested as cancer therapeutic agents. Inhibition of mTOR results in sensitization to DNA damaging agents, however the molecular mechanism is not well understood. We found that a mTOR-selective kinase inhibitor, AZD8055, significantly enhanced sensitivity of a pediatric rhabdomyosarcoma xenograft to radiotherapy and sensitized rhabdomyosarcoma cells to interstrand crosslinker (ICL) melphalan. Sensitization correlated with drug-induced downregulation of a key component of the Fanconi anemia (FA) pathway, FANCD2 through mTOR regulation of FANCD2 gene transcripts via mTORC1-S6K1. Importantly, we show that FANCD2 is required for the proper activation of ATM-Chk2 checkpoint in response to ICL and that mTOR signaling promotes ICL-induced ATM-Chk2 checkpoint activation by sustaining FANCD2. In FANCD2 deficient lymphoblasts, FANCD2 is essential to suppress endogenous and induced DNA damage, and FANCD2-deficient cells demonstrated impaired ATM-Chk2 and ATR-Chk1 activation, which was rescued by re-introduction of wild type FANCD2. Pharmacological inhibition of PI3K-mTOR-Akt pathway in Rh30 rhabdomyosarcoma cells attenuated ICL-induced activation of ATM, accompanied with the decrease of FANCD2. These data suggest that the mTOR pathway may promote the repair of DNA double strand breaks by sustaining FANCD2 and provide a novel mechanism of how the FA pathway modulates DNA damage response and repair. Citation Format: Changxian Shen, Duane Oswald, Doris Phelps, hakan cam, Christopher E. Pelloski, Qishen Pang, Peter J. Houghton. Regulation of FANCD2 by the mTOR pathway contributes to the resistance of cancer cells to DNA double strand breaks. [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 4437. doi:10.1158/1538-7445.AM2013-4437
REAPPEARANCE OF A POSITIVE DICK TEST
Authors: John A. Toomey
Journal: JAMA (1926)

Ferry<sup>1</sup>recently called attention to the reappearance of a positive Dick test in a patient who contracted measles. About eighteen months ago, fifty-five nurses were divided into two groups, one of twenty, actively immunized against scarlet fever, and the remaining thirty-five, not protected, serving as a control series. All of the latter have subsequently developed scarlet fever, while nineteen of the twenty protected nurses have continued negative although frequently exposed to the disease. Fifteen of the nurses who developed scarlet fever developed redness at the site of the old Dick test. The longest interval between the reappearance of the redness with scarlet fever and the primary Dick test was one year, in two instances. All other nurses who had local redness had their scarlet fever within from two to three weeks after their test. In two instances, the redness occurred around the Dick test before
Detection of Cecal Adenocarcinoma by Tc-99m Pertechnetate Scintigram
Authors: RICHARD C. GARDNER, PAUL A. KANTROWITZ, HAROLD L. CHANDLER
Journal: Clinical Nuclear Medicine (1984)

A 23-year-old male presented with occult gastrointestinal bleeding and iron deficiency anemia. A Tc-99m pertechnetate abdominal scan was positive and surgery revealed an adenocarcinoma of the cecum. No Meckel's diverticulum was identified. This is the first reported association of an abnormal Tc-99m pertechnetate scan in adenocarcinoma. Carcinoma of the right colon should be considered in any patient with a positive pertechnetate scan for Meckel's diverticulum and suggestive clinical features.
Proarrhythmic effects of the class III agent almokalant: importance of infusion rate, QT dispersion, and early afterdepolarisations
Authors: L. Carlsson, C. Abrahamsson, B. Andersson, G. Duker, G. Schiller-Linhardt
Journal: Cardiovascular Research (1993)

The aim was to study factors contributing to torsade de pointes in the acquired long QT syndrome.Anaesthetised rabbits or cats were given a continuous infusion of methoxamine and the class III agent almokalant (at a rate of 5 or 25 nmol.kg-1.min-1, respectively) and the effects on incidence of torsade de pointes and QT dispersion were examined. Effects of almokalant on action potentials recorded from Purkinje fibres and ventricular cells of rabbits and cats were also studied."High rate" infusion of almokalant prolonged the QTc interval [from 162(SEM 6.2) ms to 211 (5.3) ms, p < 0.001] and initiated torsade de pointes in 9/10 rabbits after a dose of 391(116.3) nmol.kg-1. During "low rate" infusion, 1/8 rabbits developed torsade de pointes (p = 0.0029) despite infusion of 900 nmol.kg-1 almokalant and QTc prolongation from 162(3.6) ms to 230(12.6) ms (p < 0.01). In eight separate rabbits given the high rate infusion of almokalant, seven developed torsade de pointes and the QTc dispersion increased from 15(1.7) ms to 32(5.6) ms (p < 0.05). In six rabbits given the low rate infusion, none developed torsade de pointes (p = 0.0023), and the QTc dispersion was unaltered. In six cats, high rate infusion induced a QT interval lengthening from 241(6.0) ms to 349(8.0) ms (p < 0.001), but in only one cat was torsade de pointes initiated and preceded by a marked increase in QT dispersion (from 22 ms to 78 ms). In vitro, almokalant caused a marked lengthening of the action potential duration and early afterdepolarisations in Purkinje fibres but not in ventricular muscle cells of the rabbit. In the cat, however, almokalant induced a homogeneous prolongation of the action potential duration in both cell types, and early afterdepolarisations were never observed.The rate of infusion of repolarisation delaying agents may influence the dispersion of repolarisation and play a decisive role in the initiation of torsade de pointes.
Quinolines Attenuate PAF-induced Pulmonary Pressor Responses and Edema Formation
Authors: SIGRID FALK, ROLF GÖGGEL, ULRICH HEYDASCH, FRANK BRASCH, KLAUS-MICHAEL MÜLLER, ALBRECHT WENDEL, STEFAN UHLIG
Journal: American Journal of Respiratory and Critical Care Medicine (1999)

In the present study we have investigated the mechanisms of pulmonary edema caused by platelet-activating factor (PAF) in isolated rat lungs as well as in mice in vivo. In blood-free perfused and ventilated rat lungs, PAF increased lung weight by 0.59 +/- 0.18 g. The cyclooxygenase inhibitor aspirin (500 microM) blocked this response by one-third, and the quinolines quinine (330 microM), quinidine (100 microM), and chloroquine (100 microM) by two-thirds. Lipoxygenase inhibition (10 microM AA861) alone or in combination with thromboxane receptor antagonism (10 microM SQ29548) had no effect on PAF-induced weight gain. In combination with aspirin, quinine or quinidine completely prevented PAF-induced weight gain and the concomitant increase of the capillary filtration coefficient (K(f,c)). Pretreatment with quinine in vivo prevented not only PAF-, but also endotoxin-induced edema formation as assessed by Evans Blue extravasation. In addition, in vivo quinine prevented the endotoxin-induced release of tumor neurosis factor (TNF). Furthermore, in perfused lungs quinine reduced the PAF-induced increases in airway and vascular resistance, as well as thromboxane release. These findings demonstrate the following anti-inflammatory properties of quinolines: reduction of thromboxane and TNF formation; reduction of PAF-induced vasoconstriction and bronchoconstriction; and attenuation of PAF- and lipopolysaccharide (LPS)-induced edema formation. We conclude that the PAF- induced edema consists of two separate mechanisms, one dependent on an unknown cyclooxygenase metabolite, the other one sensitive to quinolines.
Vital follow-up of atypical cervical smears.
Authors: L T Newman
Journal: BMJ (1977)

Poor energy intake is certainly not the only cause of growth retardation in chronic renal failure and may indeed not be the most im- portant, for, while growth may improve with supplements, many children still grow poorly in spite of apparently adequate intakes.3Provided the children accept them, feeding energy supplements would still seem to be justified.
Reform of Medical Education: The Effect of Student Unrest
Authors: Norman B. Roberg
Journal: JAMA (1970)

This symposium, sponsored by the National Institutes of Health, contains 12 brief, excellent essays by students and educators of diverse nationality, background, and opinion. The subjects include medical educational reform in France, Japan, and Latin America; new medical schools in Germany and New Zealand; the views of medical students of different countries concerning medical reform and their participation in curricular revision; and the relationships of welfare systems and of biomedical research groups to the reorganization of medical schools. The book includes discussions as well as formal papers, and the sharp debates and critical analyses are of particular value. The historical influences upon medical education and practice, often neglected in the United States, are well presented. The problems of Latin America are predominantly those of a feudalistic social and university organization, while the rigid academic and administrative hierarchies of France have Renaissance and Napoleonic origin. Belgium is trapped in the nationalistic,
Major antigen of liver kidney microsomal autoantibodies in idiopathic autoimmune hepatitis is cytochrome P450db1.
Authors: M P Manns, E F Johnson, K J Griffin, E M Tan, K F Sullivan
Journal: Journal of Clinical Investigation (1989)

Type 1, liver kidney microsomal autoantibodies (LKM-1) are associated with a subgroup of idiopathic autoimmune type, chronic active hepatitis (CAH). The antigenic specificity of LKM-1 autoantibodies from 13 patients was investigated by immunoblot analysis of human liver microsomal proteins. Polypeptides of 50, 55, and 64 kD were detected with these antisera. A high titer LKM-1 serum was selected to screen a human liver lambda gt11 cDNA expression library, resulting in the isolation of several complementary (c)DNA clones. Autoantibodies affinity purified from proteins expressed by two of the immunopositive cDNA clones, HLD8.2 and HLD13.2, specifically react with a 50-kD protein of human liver microsomes and display immunofluorescence staining of the proximal renal tubular epithelia characteristic of LKM-1 sera. Determination of the sequence of HLD8.2 revealed that it encodes a recently described cytochrome P450db1. A bacterial fusion protein constructed from HLD8.2 proved to be a specific and sensitive diagnostic reagent. All sera from patients with LKM-1 positive liver disease react with this fusion protein. No reaction was seen, however, for sera from patients with other types of autoimmune liver diseases, viral hepatitis, systemic immunological disorders, or healthy controls.
SMALL DOSES OF SUBCUTANEOUS SODIUM HEPARIN IN PREVENTING DEEP VENOUS THROMBOSIS AFTER MAJOR SURGERY
Authors: A.N. Nicolaides, S. Desai, J.N. Douglas, G. Fourides, P.A. Dupont, J.D. Lewis, Helen Dodsworth, R.J. Luck, C.W. Jamieson
Journal: The Lancet (1972)