tbuckley/cabot-search huggingface dataset:
Changes in Renal Function and in the Renal Circulation in Cirrhosis.
Authors: W. P. Baldus
Journal: Annals of Internal Medicine (1963)

s1 April 1963Changes in Renal Function and in the Renal Circulation in Cirrhosis.W. P. Baldus, M.D., R. A. Feichter, M.D., W. H. J. Summerskill, M.D., J. C. Hunt, M.D., F.A.C.P.W. P. Baldus, M.D.Search for more papers by this author, R. A. Feichter, M.D.Search for more papers by this author, W. H. J. Summerskill, M.D.Search for more papers by this author, J. C. Hunt, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-58-4-741_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptAzotemia of unknown cause is becoming increasingly significant as a terminal event in patients with cirrhosis who have no evidence of primary renal disease from history, urinalysis, or renal histology. Clinical observations in 25 patients indicated that azotemia preceded hypotension or oliguria and that it developed in patients with resistant ascites and poor hepatic function.Extensive studies of renal function (clearances of inulin, PAH, creatinine, urea, sodium, potassium, water, and total osmolar substances) were therefore determined in 39 patients with cirrhosis. Progressive impairment of certain functions preceded the development of azotemia, and was related particularly to the presence and severity... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Rochester, Minn. (CI) PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 April 1963Volume 58, Issue 4Page: 741-741KeywordsAscitesCirrhosisCreatinineHistologyHypotensionPotassiumRenal circulationRenal diseasesSodiumUrea Issue Published: 1 April 1963 PDF downloadLoading ...
ADP inhibits the sliding velocity of fluorescent actin filaments on cardiac and skeletal myosins.
Authors: H Yamashita, M Sata, S Sugiura, S Momomura, T Serizawa, M Iizuka
Journal: Circulation Research (1994)

We studied the effect of MgADP on the mechanical interaction of actomyosin in cardiac and skeletal muscles using an in vitro motility assay. The sliding velocities of fluorescently labeled actin filaments on rat cardiac and skeletal myosins were measured at various MgATP and MgADP concentrations. The filament velocity depended on MgATP concentration according to classic Michaelis-Menten kinetics with apparent Michaelis constants (Km) of 43 and 137 mumol/L and maximum velocity of 5.6 and 8.6 microns/s for cardiac and skeletal myosins, respectively. The presence of 2 mmol/L MgADP decreased the filament velocity and shifted the substrate concentration dependence of the velocity toward higher MgATP concentrations, yielding the inhibition constants of 194 and 478 mumol/L for cardiac and skeletal myosins, respectively. The activation energies determined by the temperature dependence of the velocity were 61 and 83 kJ/mol for rat V1 and rabbit cardiac myosins, which were similar to those of the dissociation rate constant of actomyosin-ADP complex reported in a solution study. The inhibition of the velocity by MgADP can be explained by the crossbridge scheme in which MgADP competes with MgATP for the substrate site on myosin molecules. In cardiac myosin, addition of a concentration of MgADP as low as 25 mumol/L significantly inhibited the velocity in the presence of 2 mmol/L MgATP, suggesting that increased intracellular MgADP may reduce the rate of crossbridge detachment, resulting in a decreased ATP consumption and an increased economy of force production under ischemic conditions. The present results support the idea that MgADP may be a physiologically important modulator of contraction in cardiac muscle.
Crucial Role of Group IIA Phospholipase A<sub>2</sub> in Oleic Acid–Induced Acute Lung Injury in Rabbits
Authors: SHINGO FURUE, KENJI KUWABARA, KATSUYA MIKAWA, KAHORU NISHINA, MAKOTO SHIGA, NOBUHIRO MAEKAWA, MASAHIKO UENO, YUKIKO CHIKAZAWA, TAKASHI ONO, YOZO HORI, AKIHIRO MATSUKAWA, MASARU YOSHINAGA, HIDEFUMI OBARA
Journal: American Journal of Respiratory and Critical Care Medicine (1999)

Group IIA secretory phospholipase A2 (sPLA2) has been implicated in a variety of inflammatory diseases including acute lung injury (ALI); however, the role of sPLA2 in this disorder remains unclear. The aim of the present investigation was to examine the role of this enzyme in a model of ALI induced by oleic acid (OA) in rabbits by testing human group IIA phospholipase A2 (PLA2) inhibitor, S-5920/LY315920Na. Experimental groups consisted of a saline control group (n = 8), an OA control group (n = 10) infused intravenously with OA (0.1 ml/kg/h for 2 h), and three groups given OA + S-5920/LY315920Na (three different doses, n = 8, respectively). Infusion of OA provoked pulmonary hemorrhage and edema formation, protein leakage, and massive neutrophil infiltration, resulting in severe hypoxemia and impaired lung compliance. PLA2 activity was detected in the bronchoalveolar lavage fluid (BALF), but not plasma, which correlated well with severity of lung injury in this model. Pretreatment with S-5920/LY315920Na diminished the OA-induced PLA2 activity in the BALF and dose-dependently attenuated the previously described lung injury induced by OA, accompanied by protection against lung surfactant degradation and production of thromboxane A2 (TXA2) and leukotriene B4 (LTB4). S-5920/LY315920Na also inhibited the OA-induced production of interleukin-8 (IL-8), both in plasma and BALF. Thus, sPLA2 appears to play a key role in OA-induced lung injury, suggesting that the group IIA PLA2 inhibitor may be a promising agent for patients with acute respiratory distress syndrome (ARDS).
Tie1 attenuation reduces murine atherosclerosis in a dose-dependent and shear stress–specific manner
Authors: Kel Vin Woo, Xianghu Qu, Vladimir R. Babaev, MacRae F. Linton, Raul J. Guzman, Sergio Fazio, H. Scott Baldwin
Journal: Journal of Clinical Investigation (2011)

Although the response of endothelial cells to the disturbed blood flow in the vicinity of atherosclerotic lesions is known to be distinct from that elicited by nonatherogenic laminar flow, the mechanisms involved are poorly understood. Our initial studies confirmed that expression of the endothelial receptor tyrosine kinase Tie1 was evident at regions of atherogenic flow in mature animals. We therefore hypothesized that Tie1 plays a role in the endothelial response to atherogenic shear stress. Consistent with this, we found that Tie1+/- mice bred to the apoE-deficient background displayed a 35% reduction in atherosclerosis relative to Tie1+/+;Apoe-/- mice. Since deletion of Tie1 results in embryonic lethality secondary to vascular dysfunction, we used conditional and inducible mutagenesis to study the effect of endothelial-specific Tie1 attenuation on atherogenesis in Apoe-/- mice and found a dose-dependent decrease in atherosclerotic lesions. Analysis of primary aortic endothelial cells indicated that atheroprotective laminar flow decreased Tie1 expression in vitro. Attenuation of Tie1 was associated with an increase in eNOS expression and Tie2 phosphorylation. In addition, Tie1 attenuation increased IkBα expression while decreasing ICAM levels. In summary, we have found that shear stress conditions that modulate atherogenic events also regulate Tie1 expression. Therefore, Tie1 may play a novel proinflammatory role in atherosclerosis.
Emigration of doctors: a problem for the developing and the developed countries. Part I.
Authors: B Senewiratne
Journal: BMJ (1975)

2 Blackwood, W., et al, Brain, 1969, 92, 897. 3 Harrison, M. J. G., in Tenth Symposium on Advanced Medicine, p. 215, ed. J. G. G. Ledingham, p. 215. London, Pitman Medical, 1974. 4 Fields, W. S., et al, Journal of the American Medical Association, 1970, 211, 1993. 5 Thompson, J. E., Annals of Surgery, 1973, 178, 263. 6 Millikan, C. H., Stroke, 1971, 2, 201. 7 Fisher, C. M., Archives of Ophthalmology, 1952, 47, 167. 8 Skinh^j, E., H^edt-Rasmussen, K., and Paulson, O. B., Neurology, (Minneapolis), 1970, 20, 485. 9 Du Boulay, G. H., British Journal of Hospital Medicine, 1973, 10, 258. 10 Marshall, J., Lancet, 1971, 1, 719. 11 Walter, P. F., Reid, S. D., and Kass Wenger, N., Annals of Internal Medicine, 1970, 72, 471.
Do infiltrating neutrophils contribute to the pathogenesis of indomethacin induced ulceration of the rat gastric antrum?
Authors: M A Trevethick, N M Clayton, P Strong, I W Harman
Journal: Gut (1993)

The potential involvement of neutrophils in the pathogenesis of indomethacin induced ulceration of the gastric antrum in the re-fed rat was studied. Indomethacin was associated with a time dependent increase in the extent and severity of ulceration, blood neutrophilia, neutrophil infiltration into the gastric antrum, and calcium ionophore induced immunoreactive leukotriene B4 (LTB4) release from the antrum ex vivo. Neutrophil infiltration into the antrum was detectable 1 hour after dosing with indomethacin, at which time damage was apparent microscopically but not macroscopically. Thus, cell infiltration may contribute to the development, if not the initiation, of ulceration. Consistent with this suggestion, oral dexamethasone (5 mg/kg) significantly attenuated indomethacin induced ulceration, the associated neutrophil infiltration, and calcium ionophore induced immunoreactive leukotriene B4 release from the gastric antrum and whole blood ex vivo, although the blood neutrophilia was unaffected. These results suggest that indomethacin induced ulceration of the rat gastric antrum may have a dependence on neutrophil infiltration for its pathogenesis.
Hepatitis C virus replication in chronic liver disease
Authors: S. Magrin, A. Craxì, C. Fabiano, G. Fiorentino, P. Almasio, V. Di Marco, O. Lo Iacono, R. Bruno, G.B. Pinzello, U. Palazzo, L. Marino, G. Provenzano, M. Vitale, A. Maggio, L. Pagliaro
Journal: Journal of Hepatology (1991)
Gender differences in the bronchoalveolar lavage cell proteome of patients with chronic obstructive pulmonary disease
Authors: Maxie Kohler, AnnSofi Sandberg, Sanela Kjellqvist, Andreas Thomas, Reza Karimi, Sven Nyrén, Anders Eklund, Mario Thevis, C. Magnus Sköld, Åsa M. Wheelock
Journal: Journal of Allergy and Clinical Immunology (2012)
O68 SOFOSBUVIR AND RIBAVIRIN FOR THE TREATMENT OF CHRONIC HCV WITH CIRRHOSIS AND PORTAL HYPERTENSION WITH AND WITHOUT DECOMPENSATION: EARLY VIROLOGIC RESPONSE AND SAFETY
Authors: N. Afdhal, G. Everson, J.L. Calleja, G. McCaughan, W.T. Symonds, J. Denning, L. McNair, J.G. McHutchison, S. Arterburn, M. Charlton, R. Reddy, T. Asselah, E. Gane, X. Forns
Journal: Journal of Hepatology (2014)
Phase II Study of Induction Cisplatin and Irinotecan Followed by Concurrent Carboplatin, Etoposide, and Thoracic Radiotherapy for Limited-Stage Small-Cell Lung Cancer, CALGB 30206
Authors: Michael J. Kelley, Jeffrey A. Bogart, Lydia. D. Hodgson, Rafat H. Ansari, James N. Atkins, Herbert Pang, Mark R. Green, Everett E. Vokes
Journal: Journal of Thoracic Oncology (2012)
Abstract B26: Melanoma cells induce stem cells like fenotype of normal human keratinocytes
Authors: Ondrej Kodet, Lukas Lacina, Barbora Dvorankova, Michal Kolar, Hynek Strnad, Karel Smetana
Journal: Cancer Research (2013)

Abstract Introduction: Nodular melanoma is one of the most life threatening tumors with frequently poor therapeutic outcome. Similarly to other the tumors, the intercellular interactions may be of crucial importance for biological properties of melanoma and course of the disease. This study is mapping the effect of melanoma cells and melanoma associated fibroblasts on keratinocytes as compared with effect of neural crest stem cells. Methods: 100 samples removed during radical melanoma resection were analyzed by histology and 20 of them by immunohistochemistry and compared with in vitro models. For in vitro models of intercellular interactions we co-cultured in transwell systems melanoma cells or neonatal melanocytes or neural crest stem cells respectively with human normal keratinocytes. Further, we employed also melanoma associated fibroblasts and normal human dermal fibroblasts respectively in above mentioned culture system. Transcriptional analysis of these models was carried out in collaboration with the Institute of Molecular Genetics of the ASCR on the whole genome level by using Illumina microarrays. Results: In tissue surrounding nodular melanoma we have observed significant hyperplasia of epithelial layer with aberrant suprabasal expression of keratin 14 (K14) along with absence of K10 - marker of differentiated epidermal keratinocytes. In vitro models revealed that melanoma cells, neural crest stem cells and also melanoma associated fibroblasts were able to influence expression of K14, but also expression of K19 and K8 as well as of vimentin in cocultured keratinocytes. Cytokines and growth factors such as FGF2, CXCL1, IL8 and VEGFA seem to participate in this activity of melanoma cell to keratinocytes. Conclusion: Melanoma cells as well as melanoma associated fibroblasts are able to modify the landscape of tissue surrounding the proliferating malignant clone. These interactions result in maintenance of low differentiation status of keratinocytes in vivo as well as in vitro. This interaction further highlights the role of intercellular interactions in melanoma, but the functional significance for melanoma biology requires further analysis. This study was supported by the Charles University project PRVOUK 27-1 and by the Grant Agency of the Czech Republic project no 304/121/333. Citation Format: Ondrej Kodet, Lukas Lacina, Barbora Dvorankova, Michal Kolar, Hynek Strnad, Karel Smetana, Jr.. Melanoma cells induce stem cells like fenotype of normal human keratinocytes. [abstract]. In: Proceedings of the Third AACR International Conference on Frontiers in Basic Cancer Research; Sep 18-22, 2013; National Harbor, MD. Philadelphia (PA): AACR; Cancer Res 2013;73(19 Suppl):Abstract nr B26.
Framework for analysing risk and safety in clinical medicine
Authors: C. Vincent, S. Taylor-Adams, N. Stanhope
Journal: BMJ (1998)

Adverse events are incidents in which a patient is unintentionally harmed by medical treatment. Awareness while under anaesthetic, deaths during surgery, and missed cases of meningitis are tragic for both patients and staff, and may lead to complaints or litigation. Investigations usually focus on the actions of individual doctors and seldom examine the background to these events.

In a recent case of a patient whose bowel was perforated during surgery, examination of the medical records led to criticism of the surgeon. Only later did it emerge that the operation had been carried out in near darkness because of several equipment and power problems. Adverse events usually originate in a variety of systemic features operating at different levels—the task, the team, the work environment, and the organisation. We present a framework that aims to encompass the many factors influencing clinical practice. It can be used to guide the investigation of incidents, to generate ways of assessing risk, and to focus research on the causes and prevention of adverse outcomes.



The original model for accident assessment was developed for use in complex industrial settings such as offshore drilling platforms



#### Summary points

Adverse events in which patients are harmed by medical treatment are common

Investigations which consider only actions or omissions of individual clinicians are incomplete and misleading

Psychological research shows that liability to error is strongly affected by adverse conditions of work

These conditions include high workload, inadequate supervision, poor communication, rapid change within an organisation

A framework of risk factors allows a systematic approach to safety and error reduction

In spite of increased attention to quality, errors and adverse outcomes are still frequent in clinical practice.1 The risk of iatrogenic injury to patients in acute hospitals remains high, with studies reporting rates of 4-17%.2-4 A recent American observational study found that …
Bcr-Abl signaling through the PI-3/S6 kinase pathway inhibits nuclear translocation of the transcription factor Bach2, which represses the antiapoptotic factor heme oxygenase-1
Authors: Chikashi Yoshida, Fumiko Yoshida, Daniel E. Sears, Stephen M. Hart, Dai Ikebe, Akihiko Muto, Subham Basu, Kazuhiko Igarashi, Junia V. Melo
Journal: Blood (2006)
Medical Student Loans Defaulted by Death
Authors: Stephen J. Galla
Journal: JAMA (1972)

ABSTRACT To the Editor.— I was appalled after reading the EDITORIAL Loans Defaulted by Death (218:1566, 1971). Indeed, I was surprised that you would reveal to physicians that any of the money they had contributed to the AMA-ERF was being used inefficiently.Whenever I have taken out a loan, I have been required to purchase life insurance to cover the loan in the event of death. Why does not the AMA-ERF require all recipients of loan funds to cover their obligations with life insurance?
Use of the Diagnostic Criteria for Psychosomatic Research in Oncology
Authors: Luigi Grassi, Silvana Sabato, Elena Rossi, Bruno Biancosino, Luciana Marmai
Journal: Psychotherapy and Psychosomatics (2005)

Psycho-oncology literature has shown that 30-50% of cancer patients meet the criteria for a psychiatric diagnosis, according to the usual nosographic classification (e.g. DSM). The Diagnostic Criteria for Psychosomatic Research (DCPR) have been shown to be useful in identifying psychological constellations in patients with medical illness. The aims of the study were to compare the DSM-IV and the DCPR in their application to cancer patients.One hundred and forty-six patients with cancer underwent semistructured interviews to assess psychiatric morbidity and psychosocial syndromes according to the DSM-IV and the DCPR, respectively. The Brief Symptom Inventory (BSI) was also used to assess psychological stress symptoms.Sixty-five subjects (44.5%) met the criteria for a DSM-IV diagnosis (DSM cases), while 104 patients (71.2%) presented symptoms meeting the criteria for at least one DCPR syndrome. Three DCPR dimensions were more frequent than others, specifically Health Anxiety (37.7%), Demoralization (28.8%) and Alexithymia (26%). Among the subjects with no formal DSM-IV diagnosis (n = 81), 58% had at least one DCPR syndrome. DSM-IV cases had higher scores on several BSI subscales in comparison with patients with only one DCPR syndrome, while no difference was found in patients with more than one DCPR diagnosis.The DCPR system was found to be useful in oncology in investigating psychological conditions which are not identified by the DSM-IV alone. Assessment of more specific constructs, other than intensity of general stress symptoms, may give more specific information and help in tailoring psychological intervention for patients with cancer.
Effects of propafenone on the median frequency of ventricular fibrillation in Langendorff perfused guinea-pig hearts
Authors: U. Eggenreich, P. H Fleischmann, G. Stark, P. Wach
Journal: Cardiovascular Research (1996)

Objective: The aim was to investigate the antifibrillatory effects of two concentrations of propafenone by means of signal analysis of epicardial ECG recordings in isolated, Langendorff-perfused guinea-pig hearts. Methods: Isolated Langendorff-perfused guinea-pig hearts were used as a model for sustained ventricular fibrillation (VF) during reperfusion after global ischaemia. ECG signals were recorded for the first 20 min of reperfusion. The recording was divided into episodes of 1 s and the median frequency (FM) of the dynamic power spectrum was computed for each episode. Cardiac electrical activity was monitored for an additional 10 min. Additionally steady state conditions (i.e. constant FM values for the remaining observation period) were analysed and the effects of 0.1 μM and 1.0 μM propafenone added at reperfusion on the FM were examined. Results: After initial irregularities, FM remained on a high steady state level in the control group. The addition of propafenone altered the steady state value of FM in a dose-dependent and significant manner but had no effects on the time until steady state was reached. During reperfusion without propafenone, 1 out of 6 hearts spontaneously converted to a stable sinus rhythm. Reperfusion with 0.1 μM propafenone caused spontaneous conversion to stable sinus rhythm in 1 out of 6 hearts and intermittent periods of sinus rhythms in 2 additional hearts. During the first 30 min of reperfusion with 1.0 μM propafenone, 5 out of 6 hearts spontaneously converted to stable sinus rhythm. The sixth heart showed repeated switching between VF and periods of non-sustained sinus rhythm. Conclusion: Propafenone caused a dose-dependent decrease of FM at steady state conditions. The rate of spontaneous termination of VF appeared to be dose dependent and the stability of the sinus rhythm was correlated inversely with the FM immediately before spontaneous defibrillation. Therefore, in this model the FM value prior to spontaneous termination of VF may be useful in the estimation of defibrillation success.
MicroRNA Signature of Primary Pigmented Nodular Adrenocortical Disease: Clinical Correlations and Regulation of <i>Wnt</i> Signaling
Authors: Dimitrios Iliopoulos, Eirini I. Bimpaki, Maria Nesterova, Constantine A. Stratakis
Journal: Cancer Research (2009)

Abstract MicroRNAs comprise a novel group of gene regulators implicated in the development of different types of cancer; however, their role in primary pigmented nodular adrenocortical disease (PPNAD) has not been investigated. PPNAD is a bilateral adrenal hyperplasia often associated with Carney complex, a multiple neoplasia syndrome; both disorders are caused by protein kinase A (PKA) regulatory subunit type 1A (PRKARIA)–inactivating mutations. We identified a 44-microRNA gene signature of PPNAD after comparing PPNAD with normal adrenal samples. Specifically, 33 microRNAs were up-regulated and 11 down-regulated in PPNAD relative to normal tissues. These results were validated by stem loop real-time PCR analysis. Comparison of microRNA microarray data with clinicopathologic variables revealed a negative correlation (r = −0.9499) between let-7b expression and cortisol levels in patients with PPNAD. Integration of microRNA microarray with serial analysis of gene expression data together with bioinformatic algorithm predictions revealed nine microRNA-gene target pairs with a potential role in adrenal pathogenesis. Using a PPNAD cell line, we showed that miR-449 was up-regulated and identified its direct target, WNT1-inducible signaling pathway protein 2 (WISP2); in addition, pharmacologic inhibition of PKA resulted in the up-regulation of miR-449 leading to the suppression of WISP2. Overall, we investigated, for the first time, the microRNA profile and its clinical significance in PPNAD; these data also suggest that PKA, via microRNA regulation, affects the Wnt signaling pathway, which through expression and clinical studies is suspected to be a primary mediator of PRKAR1A-related tumorigenesis. [Cancer Res 2009;69(8):3278–82]
A CASE OF ANGINA AND DYSPHAGIAILLUSTRATING THE VALUE OF ANTISYPHILITIC TREATMENT IN A CONDITION MISTAKEN FOR EPITHELIOMA.
Authors: FRANK WOODBURY
Journal: JAMA (1904)

<h3>History.</h3> —Mrs. X., a widow, about 35 years of age. Her husband died of pulmonary tuberculosis about 18 months before I saw her. She nursed him during his illness, and in consequence of much loss of rest, and of the great physical and mental strain, her health had been much impaired. In the year following, however, she had apparently regained her health and strength. She was a brunette, well nourished, and physically well developed, of a bilious temperament and of active habits. The account of her ailment, for which she sought the advice of the late Dr. Thomas G. Morton, was that for the last six months she had experienced great pain in swallowing, even on the attempt to drink a little milk or water. Otherwise her health had been good. She thought that she had lost a few pounds in weight, which she attributed to her inability to take