tbuckley/cabot-search huggingface dataset:
Serratia arthritis. Medical eradication of infection in a patient with rheumatoid arthritis
Authors: B. B. Dorwart
Journal: JAMA (1973)

<i>We treated a patient with</i>Serratia<i>pyarthrosis who also had rheumatoid arthritis. With prompt diagnosis, vigorous needle aspiration of joint exudate, intravenous but not intra-articular administration of antibiotics, and appropriate splinting, surgical treatment may not be necessary in all cases of</i>Serratia<i>joint infection</i>.
Clinical Signs of Dehydration and Extracellular Fluid Loss
Authors: Jack Lapides
Journal: JAMA (1965)

IN MEDICAL PRACTICE moderate dehydration is usually diagnosed by observing the turgor of the skin and the fullness of the tongue. Laboratory data have been found to be of little value in determining the presence of dehydration, particularly when the patient first appears for examination in a state of dehydration and with impaired renal function. The physician, after making the diagnosis of dehydration, is often unable to determine the volume of fluid to be replaced since there is little data in the literature<sup>1,2</sup>to guide him. The work of Coller and Maddock<sup>1</sup>has been quoted widely as the basis for the statement that an adult must lose 6% of body weight in water before dehydration is present. The purpose of the present study was to investigate further the amount of fluid that must be lost from the adult human before dehydration becomes apparent on physical examination. Also, an
Total Anomalous Pulmonary Venous Connection
Authors: Anna N. Seale, Hideki Uemura, Steven A. Webber, John Partridge, Michael Roughton, Siew Y. Ho, Karen P. McCarthy, Sheila Jones, Lynda Shaughnessy, Jan Sunnegardh, Katarina Hanseus, Hakan Berggren, Sune Johansson, Michael L. Rigby, Barry R. Keeton, Piers E.F. Daubeney
Journal: Circulation (2010)

Background— Late mortality after repair of total anomalous pulmonary venous connection is frequently associated with pulmonary venous obstruction (PVO). We aimed to describe the morphological spectrum of total anomalous pulmonary venous connection and identify risk factors for death and postoperative PVO. Methods and Results— We conducted a retrospective, international, collaborative, population-based study involving all 19 pediatric cardiac centers in the United Kingdom, Ireland, and Sweden. All infants with total anomalous pulmonary venous connection born between 1998 and 2004 were identified. Cases with functionally univentricular circulations or atrial isomerism were excluded. All available data and imaging were reviewed. Of 422 live-born cases, 205 (48.6%) had supracardiac, 110 (26.1%) had infracardiac, 67 (15.9%) had cardiac, and 37 (8.8%) had mixed connections. There were 2 cases (0.5%) of common pulmonary vein atresia. Some patients had extremely hypoplastic veins or, rarely, discrete stenosis of the individual veins. Sixty (14.2%) had associated cardiac anomalies. Sixteen died before intervention. Three-year survival for surgically treated patients was 85.2% (95% confidence interval 81.3% to 88.4%). Risk factors for death in multivariable analysis comprised earlier age at surgery, hypoplastic/stenotic pulmonary veins, associated complex cardiac lesions, postoperative pulmonary hypertension, and postoperative PVO. Sixty (14.8%) of the 406 patients undergoing total anomalous pulmonary venous connection repair had postoperative PVO that required reintervention. Three-year survival after initial surgery for patients with postoperative PVO was 58.7% (95% confidence interval 46.2% to 69.2%). Risk factors for postoperative PVO comprised preoperative hypoplastic/stenotic pulmonary veins and absence of a common confluence. Conclusions— Preoperative clinical and morphological features are important risk factors for postoperative PVO and survival.
562 HEPATIC INFLOW MODULATION AFTER EXTENDED LIVER RESECTION VIA SHUNT SURGERY
Authors: M. Golriz, A. Edalatpour, M. Hafezi, N. Rezaei, C. Garoussi, J. Arwin, K. Ghazi Moghadam, S. Elsakka, G. Emami, A. Mehrabi
Journal: Journal of Hepatology (2013)
Infection with Parvovirus-like Virus and Aplastic Crisis in Chronic Hemolytic Anemia
Authors: KODURl R. P. RAO
Journal: Annals of Internal Medicine (1983)

From 1980 to 1982 seven adults with chronic hemolytic anemia were admitted to Cook County Hospital, Chicago, with aplastic crisis. Six of these patients had sickle cell anemia, the seventh patient had beta thalassemia intermedia. Virologie studies showed that six patients had acute infection with the human parvovirus-like virus; in the remaining patient the lack of appropriate specimens precluded viral diagnosis. We describe the features of the virus infection and accompanying erythroid aplasia, and discuss the role of parvovirus-like virus as the etiologic agent in the arrest of erythrocyte production.
Improved Outcomes Associated With a Revised Quality Measure for Continuing Perioperative β-Blockade
Authors: Joshua S. Richman, Kamal M. F. Itani, Rhiannon J. Deierhoi, William G. Henderson, Mary T. Hawn
Journal: JAMA Surgery (2014)

The Surgical Care Improvement Project perioperative β-blocker (BB) (SCIP-BB) continuation measure was revised in 2012 to incorporate inpatient BB continuation after discharge from the postanesthesia care unit.To determine whether adherence to the original or revised SCIP-BB measure is associated with decreased adverse events.Retrospective cohort study using national Veterans Affairs patient-level data on adherence to the original SCIP-BB measure and inpatient BB continuation for operations between July 2006 and August 2009.Data for SCIP-BB measure adherence, inpatient BB continuation, and patient and procedure risk variables were used to estimate the associations between adherence to the original and revised SCIP-BB measures and outcomes of major adverse cardiovascular or cerebrovascular events (MACCEs) and their components of cardiovascular events, cerebrovascular events, and 30-day mortality. In addition to unadjusted estimates, propensity score matching and bootstrapping were used to estimate the associations and generate 95% CIs.Major adverse cardiovascular or cerebrovascular events.Of 14,420 nonemergent operations with at least 2 postoperative inpatient days, 13,170 (91.3%) adhered to the original SCIP-BB measure, and 480 (3.3%) experienced a MACCE. Propensity score-matched analyses showed that adherence to the original SCIP-BB measure was not associated with MACCEs (odds ratio [OR], 1.00; 95% CI, 0.66-1.54) but was associated with increased cerebrovascular events (OR, 3.01; 95% CI, 1.00-10.07). Adherence to the revised SCIP-BB measure occurred in 11,597 (80.4%), and in matched analysis adherence was associated with decreased MACCEs (OR, 0.75; 95% CI, 0.57-0.95), cardiovascular events (OR, 0.66; 95% CI, 0.46-0.93), and 30-day mortality (OR, 0.74; 95% CI, 0.53-0.98). Adherence to the revised SCIP-BB measure was not associated with increased cerebrovascular events (OR, 1.22; 95% CI, 0.62-2.38).Adherence to the original SCIP-BB measure was associated with increased cerebrovascular events but not improved cardiovascular event outcomes. β-Blocker continuation consistent with the revised SCIP-BB measure is associated with reduced MACCEs, cardiovascular events, and 30-day mortality. These data provide a cautionary tale of implementing performance measures before they have been rigorously tested. Although the observed associations between adherence to the revised SCIP-BB measure and outcomes are promising, they should be evaluated in the postimplementation period.
Hypertensive Crisis Due to Pargyline and Metaraminol
Authors: A. R. Horler, N. A. Wynne
Journal: BMJ (1965)

Pargyline hydrochloride (N-benzyl-N-methyl-2-propynylamine hydrochloride) is a monoamine-oxidase inhibitor seven to ten times more potent than iproniazid (Glazener et al., 1964, Because of its ability to lower the blood-pressure it is marketed as a hypotensive drug (Eutonyl), and several reports have appeared of its effectiveness (Maronde and Haywood, 1963;Wolf et al., 1963 ;Montuschi and Robinson, 1963).The mechanism of its hypotensive action (B.Mjf.7., 1964b -which may be quite independent of its action as a monoamine-oxidase inhibitor-is not fully understood but appears to resemble that of bretylium, which inhibits the release of noradrenaline at adrenergic nerve endings (Gessa et al., 1963).Because of hypotensive crises reported in patients on treat- ment with monoamine-oxidase inhibitors (Blackwell, 1963;
No Pain, No Gain
Authors: Victor R. Fuchs
Journal: JAMA (1993)

THERE is a widespread belief in the United States that expenditures for health care are too high and growing too rapidly. This belief has stimulated numerous policy proposals for  containment, including such diverse approaches as managed care, managed competition, insurance company regulation, diagnosis related group reimbursement, global budgets, and expenditure caps. The pros and cons of alternative approaches to cost containment have been debated extensively; I have no intention of proposing still another plan. Instead, I shall offer a framework for thinking about cost containment that is applicable to all possible proposals. In developing this framework I will first consider why public policy should pay any special attention to health expenditures. Two popular explanations—share of GNP (gross national product) and effect on global competitiveness—will be examined and rejected; then three valid explanations will be discussed. Finally, I will show why every approach to cost containment requires pain if there
Dimeric Architecture of the Human Bumetanide-Sensitive Na-K-Cl Co-transporter
Authors: Patrick G.J.F. Starremans, Ferry F.J. Kersten, Lambertus P.W.J. van den Heuvel, Nine V.A.M. Knoers, René J.M. Bindels
Journal: Journal of the American Society of Nephrology (2003)

ABSTRACT. The primary mediator of NaCl reabsorption in the renal distal tubule is the human bumetanide-sensitive Na+-K+-2Cl− co-transporter (hNKCC2), located at the apical membrane of the thick ascending limb of Henle's loop. The physiologic importance of this transporter is emphasized by the tubular disorder Bartter syndrome type I, which arises from the functional impairment of hNKCC2 as a result of mutations in the SLC12A1 gene. The aim of the present study was to investigate the oligomeric state of hNKCC2 to understand further its operational mechanism. To this end, hNKCC2 was heterologously expressed in Xenopus laevis oocytes. Chemical cross-linking with dimethyl-3,3-dithio-bis-propionamidate indicated that hNKCC2 subunits can reversibly form high molecular weight complexes. Co-immunoprecipitation of tagged hNKCC2 subunits further substantiated a physical interaction between individual hNKCC2 subunits. The size of the hNKCC2 multimers was determined by sucrose gradient centrifugation, and a preference for dimeric complexes (approximately 320 kD) was demonstrated. Finally, concatemeric constructs consisting of two wild-type subunits or a wild-type and a functionally impaired hNKCC2 subunit (G319R) were expressed in oocytes. Subsequently, the concatemers were functionally characterized, resulting in a significant bumetanide-sensitive 22Na+ uptake of 2.5 ± 0.2 nmol/oocyte per 30 min for the wild-type–wild-type concatemer, which was reduced to 1.3 ± 0.1 nmol/oocyte per 30 min for the wild-type–G319R concatemer. In conclusion, this study suggests that hNKCC2 forms at least functional dimers when expressed in Xenopus laevis oocytes of which the individual subunits transport Na+ independently.
Epstein-Barr Virus and Human Malignancy
Authors: JOHN L. ZIEGLER
Journal: Annals of Internal Medicine (1977)

The association of the Epstein-Barr virus and two human malignancies, Burkitt's lymphoma and nasopharyngeal carcinoma, is reviewed. Seroepidemiologic, virologic, and immunologic evidence is summarized, and several hypotheses regarding a possible etiologic role for the Epstein-Barr virus in these tumors are presented. With our current state of knowledge we cannot conclude that the Epstein-Barr virus is oncogenic in man, nor can we yet ascertain the biological and clinical significance of its association with Burkitt's lymphoma and nasopharyngeal carcinoma.
Oral submucosal fibrosis--a preventable disease.
Authors: V Jayanthi, C S Probert, K S Sher, J F Mayberry
Journal: Gut (1992)

Leading articleOral submucosal fibrosis a preventable disease Oral submucosal fibrosis is a chronic, progressive, and irreversible disease of unknown aetiology.It affects oral, oropharyngeal, and at times oesophageal mucosa.The earliest description of the disease was by Schwartz in 1952,' and the first Indian cases were reported from Bombay2 and Hyderabad.3At the time the condition was thought to be caused by disordered growth ofcollagen.It has drawn greater clinical attention over the past 15 years and the purpose of this review is to reconsider its epidemiology, aetiology, and successful prevention.
Chlorpropamide-induced Hyponatremia: Incidence and Risk Factors
Authors: Takashi Kadowaki, Ryoko Hagura, Hiroshi Kajinuma, Nobusada Kuzuya, Sho Yoshida
Journal: Diabetes Care (1983)

The incidence and risk factors of chlorpropamide-induced hyponatremia were assessed in diabetic outpatients. In 176 chlorpropamide-treated patients, 11 (6.3%) exhibited hyponatremia (serum sodium less than or equal to 129 meq/L) during the mean follow-up period of 7.4 yr. In contrast, only one (0.6%) developed hyponatremia in 162 tolbutamide- or glibenclamide-treated patients (P less than 0.005). Moreover, administration to elderly patients and combination with thiazide diuretics were regarded as significantly potent risk factors for the development of hyponatremia in patients receiving chlorpropamide.
An Unusual Clinical SignMydriasis Associated with Hyperkalemia and Metabolic Acidosis
Authors: LAWRENCE SCHERR
Journal: Annals of Internal Medicine (1962)

Brief Communication1 March 1962An Unusual Clinical SignMydriasis Associated with Hyperkalemia and Metabolic AcidosisLAWRENCE SCHERR, M.D., GLENN D. LUBASH, M.D., ALBERT L. RUBIN, M.D., E. HUGH LUCKEY, M.C., F.A.C.P.LAWRENCE SCHERR, M.D.Search for more papers by this author, GLENN D. LUBASH, M.D.Search for more papers by this author, ALBERT L. RUBIN, M.D.Search for more papers by this author, E. HUGH LUCKEY, M.C., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-56-3-508 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptMuscle paresis or paralysis is infrequently associated with hyperkalemia (1-3). This relationship was noted in the case presented here and was particularly interesting because of associated mydriasis. Treatment of the hyperkalemia resulted in a prompt remission of all muscle signs, including the mydriasis.CASE REPORTA 15-year-old white boy was admitted to a hospital because of uremia secondary to right ureteropelvic obstruction and congenital absence of the left kidney. There was no family history of renal or muscle disease. A right nephrostomy was performed, but the patient's clinical condition continued to deteriorate, and the blood urea nitrogen rose from 30...References1. GROBLILJESTRANDJOHNS DARJ: Potassium movement in normal subjects. Amer. J. Med. 23: 340, 1957. CrossrefMedlineGoogle Scholar2. BULLCARTERLOWE GMABKG: Hyperpotassemic paralysis. Lancet 2: 60, 1953. CrossrefGoogle Scholar3. BEDFORD PD: Acute potassium intoxication. Lancet 2: 268, 1954. CrossrefGoogle Scholar4. SCHWARZCOHENLUBASHRUBIN KBDGDAL: Severe acidosis and hyperpotassemia treated with sodium bicarbonate infusion. Circulation 19: 215, 1959. CrossrefMedlineGoogle Scholar5. GAMSTORPHAUGEHELWEG-LARSENMJONESSAGLID IMHFHV: Adynamia episodica hereditaria. Amer. J. Med. 23: 385, 1957. CrossrefMedlineGoogle Scholar6. WALSH FB: Clinical Neuro-Opthalmalogy, 2d ed., The Williams & Wilkins Co., Baltimore, 1957, p. 144. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: New York, New YorkFrom the Cardiorenal Laboratory, Second (Cornell) Medical Division, Bellevue Hospital, and the Department of Medicine, New York Hospital-Cornell Medical Center.Requests for reprints should be addressed to Lawrence Scherr, M.D., Cardiorenal Laboratory, Second (Cornell) Medical Division, Bellevue Hospital, First Avenue and 26th Street, New York 16, New York. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 March 1962Volume 56, Issue 3Page: 508-510KeywordsElectrocardiographyHospital medicineIngestionKidneysMusclesParalysisPatient advocacyRenal diseasesResearch laboratoriesRespiration Issue Published: 1 March 1962 PDF DownloadLoading ...
Nasal delivery of Japanese cedar pollen Cryj1 by using self-gelling immunostimulatory DNA for effective induction of immune responses in mice
Authors: Yumiko Ishii-Mizuno, Yuka Umeki, Yuki Takahashi, Yukinori Kato, Tetsuji Takabayashi, Shigeharu Fujieda, Yoshinobu Takakura, Makiya Nishikawa
Journal: Journal of Controlled Release (2014)
Abstract IA19: Multiplexing TGFβ in the tumor microenvironment
Authors: Mary Helen Barcellos-Hoff
Journal: Cancer Research (2015)

Abstract The dynamics of TGFβ biology is context dependent. TGFβ is controlled at many levels with a major mechanism in its production as a latent complex from which TGFβ is released extracellularly. TGFβ production and activity is greatly increased in many cancer cells. Tumor microenvironment can also be a significant TGFβ source, particularly bone marrow derived cells (BMDC). TGFβ regulates malignant behaviors and cell phenotype of tumor microenvironment constituents locally and the hematopoietic and immune systems at a distance. We investigated the contribution of TGFβ to the effects of radiotherapy in breast, brain and lung cancer murine models. Our studies show that radiation induces rapid TGFβ activation that can persist for days. Radiation induced TGFβ promotes rapid and effective DNA damage response, mediates tumor microenvironment composition, regulates BMDC recruitment and phenotype, and augments immune evasion. Inhibition of TGFβ during radiotherapy provides significant therapeutic benefit by molecular and microenvironmental mechanisms. TGFβ inhibition during radiotherapy impedes DNA damage recognition, which promotes tumor cell death and thus, tumor growth control. Continued TGFβ inhibition prevents vascular remodeling necessary for tumor regrowth, and blocks BMDC recruitment, which limits an exogenous TGFβ source. Multiplexing these actions with those on tumor immunity suggest potent therapeutic potential of TGFβ inhibition during radiotherapy to eliminate tumor cells and eradicate tumor promoting microenvironments. Citation Format: Mary Helen Barcellos-Hoff. Multiplexing TGFβ in the tumor microenvironment. [abstract]. In: Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; 2014 Feb 26-Mar 1; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2015;75(1 Suppl):Abstract nr IA19. doi:10.1158/1538-7445.CHTME14-IA19
Urolithiasis Due to 2,8-Dihydroxyadenine in an Adult
Authors: M. Henry Gault, H. Anne Simmonds, Walter Snedden, Donald Dow, David N. Churchill, Harold Penney
Journal: New England Journal of Medicine (1981)

CARTIER and Hamet1 described a patient with calculi formed by 2,8-dihydroxyadenine in 1974. Such calculi are positive for uric acid with standard wet chemistry tests.2 The poorly soluble purine 2,8-dihydroxyadenine is excreted in the urine because of a deficiency in the adenine salvage enzyme adenine phosphoribosyltransferase (APRT).1 , 2 The defect is inherited as an autosomal recessive trait1 , 3; the homozygous state is associated with high urinary levels of 2,8-dihydroxyadenine and with crystalluria, calculus formation,4 and potential nephrotoxicity.2 , 5 The condition primarily presents as renal obstructive disease, but some patients have presented with advanced renal failure.2 , 6 Allopurinol therapy appears to be effective.7 Dihydroxyadenine . . .
Impaired conversion of prednisone to prednisolone in patients with liver cirrhosis.
Authors: S Madsbad, B Bjerregaard, J H Henriksen, E Juhl, H Kehlet
Journal: Gut (1980)

Fourteen patients with liver cirrhosis received oral prednisone or prednisolone (0.3 mg per kg) randomised on two consecutive days. Serum prednisone and prednisolone were measured over the following four hours. Mean serum prednisolone concentration after oral prednisone decreased with impaired liver function estimated by galactose elimination capacity (r = 0.64, P less than 0.03). Mean serum prednisolone concentration after oral prednisone in the seven patients with severely impaired liver function was only 53% (P less than 0.05) of that observed in the seven patients with slightly impaired liver function. Conversely, mean serum prednisone concentration after oral prednisone in the patients with severely impaired liver function was 74% higher (P = 0.05) than in patients with slightly impaired liver function. Mean serum prednisolone after oral prednisolone was independent of liver function. As only prednisolone exerts glucocorticoid activity, our results indicate that prednisolone should be preferred to prednisone in the treatment of patients with impaired liver function.
Are Parents of Asthmatic Children Different from Other Parents?
Authors: Elisabeth Christie Askildsen, Reidulf G. Watten, Asbj&oslash;rn O. Faleide
Journal: Psychotherapy and Psychosomatics (1993)

Follow-up results from the Norwegian PRAD study (Psychosocial Risk for Allergic Development) show that parents of children who later developed symptoms of asthma were different from a control group of parents with normal, nonsymp-tomatic children several years preceding the disorder. There were significant within-pair differences in self-reported marital adjustment (DAS – Dyadic Adjustment Scale) for the control group but not for the asthma group. There were no significant between-pair DAS scores for the two groups of parents. The two groups of parents also differed in perceiving how the child had influenced their lives, in description of the childbirth and partially in childcare style. The assumed relationship between parental characteristics and asthma in children is being discussed, and the paper concludes that parents of asthmatic children should be regarded as a risk factor and clinical and therapeutic routines should be developed accordingly.