tbuckley/cabot-search huggingface dataset:
Risk of diagnosis of ovarian cancer after raised serum CA 125 concentration: a prospective cohort study
Authors: I. J Jacobs, S. Skates, A. P. Davies, R. P Woolas, A. Jeyerajah, P. Weidemann, K. Sibley, D. H Oram
Journal: BMJ (1996)

<h3>Abstract</h3> <b>Objective</b>: To determine the risk of invasive epithelial ovarian cancer and fallopian tube cancer associated with a raised concentration of the tumour marker CA 125 in asymptomatic postmenopausal women. <b>Design</b>: Serum CA 125 concentration was measured annually in study participants for one to four years. Participants with a concentration &gt;/=30 U/ml were recalled for abdominal ultrasonography. Follow up was by annual postal questionnaire. <b>Setting</b>: General practice, occupational health departments, ovarian cancer screening unit in a teaching hospital. <b>Subjects</b>: 22 000 volunteers, all postmenopausal women &gt;/=45 years of age; recruited between 1 June 1986 and 1 May 1990. <b>Intervention</b>: Surgical investigation if the ultrasound examination was abnormal. <b>Main outcome measures</b>: Cumulative and relative risk of developing an index cancer (invasive epithelial cancer of the ovary or fallopian tube) after a specified CA 125 result. <b>Results</b>: 49 index cancers developed in the study population during a mean follow up of 6.76 years. The overall cumulative risk of developing an index cancer was 0.0022 for the entire study population and was lower for women with a serum CA 125 concentration &lt;30 U/ml (cumulative risk 0.0012) but was appreciably increased for women with a concentration &gt;/=30 U/ml (0.030) and &gt;100 U/ml (0.149). Compared with the entire study population the relative risk of developing an index cancer within one year and five years was increased 35.9-fold (95% confidence interval 18.3 to 70.4) and 14.3-fold (8.5 to 24.3) respectively after a serum CA 125 concentration &gt;/=30 U/ml and 204.8-fold (79.0 to 530.7) and 74.5-fold (31.1 to 178.3) respectively after a concentration &gt;/=100 U/ml. <b>Conclusion</b>: CA 125 is a powerful index of risk of ovarian and fallopian tube cancer in asymptomatic postmenopausal women. <h3>Key messages</h3> This study shows that raised serum CA 125 concentration is a powerful index of risk of ovarian cancer in asymptomatic postmenopausal women The risk in the year after a serum CA 125 concentration &gt;/=100 U/ml is similar to the lifetime risk to women in high risk families The importance of a raised serum CA 125 concentration in relation to risk of other cancers is not yet known The role of CA 125 as a component of a screening strategy for ovarian cancer is under investigation, but the impact on mortality is not known
Desmoplastic Fibroma of Bone
Authors: David C. Dahlin, Norman W. Hoover
Journal: JAMA (1964)

FIVE EXAMPLES of this distinctive lesion of bone were described by Jaffe<sup>1</sup>in 1958. Whitesides and Ackerman<sup>2</sup>documented three cases in 1960, and Sheer and Kuhlman<sup>3</sup>reported an additional case in 1963. Thorough review of more than 3,000 pathologically verified bone tumors in the files of the Mayo Clinic has disclosed only two tumors of this type. The rarity of this recently recognized lesion prompted us to report the following cases. <h3>Report of Cases</h3><h3>Case 1.—</h3> A 21-year-old woman registered at the Mayo Clinic on Nov 30, 1911. Four years previously she had "sprained" her right ankle. Three years later she was kicked on this ankle; since then it had been painful and at times swollen. No roentgenographic report is available, but on Dec 8, 1911, a fibrous tumor was excised from within the os calcis and the site was cauterized. The lesion recurred and required another
A young man becomes short of breath and yellow
Authors: K. Sambasivan, E. Osman
Journal: BMJ (2011)

A previously well 48 year old man presented with a two week history of worsening shortness of breath, leg swelling, and “yellowing of his skin.” His medical history included excessive alcohol intake (65 units/week) and carpal tunnel syndrome, and he was taking no regular medication. On inspection he was tachypnoeic (respiratory rate 30 breaths/min), tachycardic (heart rate 102 beats/min), and jaundiced. His blood pressure was 98/60 mm Hg. Cardiovascular examination showed a raised jugular venous pressure (visible at the earlobe), a pansystolic murmur at the left sternal edge, and bilateral pedal oedema. Both respiratory and abdominal examinations were unremarkable, and resting electrocardiography showed a sinus tachycardia.

Blood tests on admission showed deranged liver function (alanine aminotransferase 332 U/L, aspartate aminotransferase 80 U/L, bilirubin 37 µmol/L, international normalised ratio 1.6) and a red cell macrocytosis (mean cell volume 98 fL). Chest radiography showed an enlarged heart shadow with a globular outline. An ultrasound of the abdomen showed the liver to be normal in size, shape, and echo texture. The common bile duct was not dilated.

Blood tests three days later showed a rapid deterioration in liver function (alanine aminotransferase 938 U/L, aspartate aminotransferase 846 U/L, bilirubin 53 µmol/L, and international normalised ratio 1.9). Hepatitis serology, tissue autoantibodies, ferritin, and caeruloplasmin were normal. Abdominal ultrasound was repeated and showed 18 cm hepatomegaly (with normal texture and reflectivity of the liver), with distension of the inferior vena cava and hepatic veins.



### 1 What is the diagnosis?

#### Short answer

Congestive cardiac failure.

#### Long answer

This …
TREATMENT OF PERNICIOUS ANEMIA BY A SPECIAL DIET
Authors: GEORGE R. MINOT
Journal: JAMA (1926)

This paper concerns the treatment in a series of forty-five  of pernicious anemia in which the patients were given a special form of  While the problem of diet in the treatment of pernicious anemia is by no means new, in our opinion its possible importance has not heretofore been generally recognized. In 1863, seven years after the publication of Addison's second, but best known, description of the disease now called pernicious anemia, Habershon1wrote concerning this condition: Many patients at an early stage completely recover under the influence of bracing air and a nutrient and stimulating diet. Other early investigators of the disease, as Biermer2in 1872, and Pepper,3in 1875, appreciated the desirability of prescribing easily digested foods as a form of medication, but no greater emphasis was placed on the value of  Osler,4however, in 1885, mentioned that cases [of pernicious
Pulmonary toxicology of silica, coal and asbestos.
Authors: A G Heppleston
Journal: Environmental Health Perspectives (1984)

Mineral particles are customarily inhaled as mixtures, though one component may predominate and determine the response. Although the lesions often possess a characteristic structure, according to the main type of particle deposited, morphology affords little indication of pathogenesis. Being a major element in the evolution of dust lesions, macrophage behavior has been examined extensively in vitro after treatment with mineral particles, attention being directed to membrane and biochemical changes; however, no clear lead to the origin of the lesions has emerged. Pulmonary fibrosis, as one of the ultimate consequences of dust accumulation, required a direct in vitro approach in which the products of the macrophage-particle interaction were utilized to provoke collagen formation by fibroblasts in a two-phase system. By this means, silica and asbestos stimulated connective tissue formation and application of the technique to coal dusts appears promising. Coal workers may develop a peculiar type of emphysema in relation to lesions whose fibrous content is comparatively small. Type II alveolar epithelium is also stimulated by inhaled particles and lipid accumulation follows. Alveolar lipidosis interferes with the fibrotic response by preventing contact between macrophage and particles. This phenomenon may account in part for anomalies, apparent in coal workers, between epidemiological findings and dust composition. Carcinogenesis is a well-recognized feature of asbestos exposure, but, as with fibrosis, risk prediction on the basis of in vitro tests of cytotoxicity is premature and may not be valid.
Bed sharing, smoking, and alcohol in the sudden infant death syndrome. New Zealand Cot Death Study Group.
Authors: R Scragg, E A Mitchell, B J Taylor, A W Stewart, R P Ford, J M Thompson, E M Allen, D M Becroft
Journal: BMJ (1993)

OBJECTIVES--To investigate why sharing the bed with an infant is a not consistent risk factor for the sudden infant death syndrome in ethnic subgroups in New Zealand and to see if the risk of sudden infant death associated with this practice is related to other factors, particularly maternal smoking and alcohol consumption. DESIGN--Nationwide case-control study. SETTING--Region of New Zealand with 78% of all births during 1987-90. SUBJECTS--Home interviews were completed with parents of 393 (81.0% of total) infants who died from the sudden infant death syndrome in the postneonatal age group, and 1592 (88.4% of total) controls who were a representative sample of all hospital births in the study region. RESULTS--Maternal smoking interacted with infant bed sharing on the risk of sudden infant death. Compared with infants not exposed to either risk factor, the relative risk for infants of mothers who smoked was 3.94 (95% confidence interval 2.47 to 6.27) for bed sharing in the last two weeks and 4.55 (2.63 to 7.88) for bed sharing in the last sleep, after other confounders were controlled for. The results for infants of non-smoking mothers were inconsistent with the relative risk being significantly increased for usual bed sharing in the last two weeks (1.73; 1.11 to 2.70) but not for bed sharing in the last sleep (0.98; 0.44 to 2.18). Neither maternal alcohol consumption nor the thermal resistance of the infant9s clothing and bedding interacted with bed sharing to increase the risk of sudden infant death, and alcohol was not a risk factor by itself. CONCLUSION--Infant bed sharing is associated with a significantly raised risk of the sudden infant death syndrome, particularly among infants of mothers who smoke. The interaction between maternal smoking and bed sharing suggests that a mechanism involving passive smoking, rather than the previously proposed mechanisms of overlaying and hyperthermia, increases the risk of sudden infant death from bed sharing.
Doctor in the booth
Authors: James Owen Drife
Journal: BMJ (2007)

It's five years since we've been in the recording studios, but little has changed. Some gizmos have been updated and the photo of the producer as a member of a long-haired pop group has gone, replaced by a picture of his contemporaries, the Beatles. Still, the elderly sofa and scattered musical instruments are comfortably familiar.

Can it really be more than three decades since our first show in the Edinburgh Fringe? This time we've decided to break with tradition and learn …
Sleep related vehicle accidents
Authors: J A Horne, L A Reyner
Journal: BMJ (1995)

To assess the incidence, time of day, and driver morbidity associated with vehicle accidents where the most likely cause was the driver falling asleep at the wheel.Two surveys were undertaken, in southwest England and the midlands, by using police databases or on the spot interviews.Drivers involved in 679 sleep related vehicle accidents.Of all vehicle accidents to which the police were summoned, sleep related vehicle accidents comprised 16% on major roads in southwest England, and over 20% on midland motorways. During the 24 hour period there were three major peaks: at around 0200, 0600, and 1600. About half these drivers were men under 30 years; few such accidents involved women.Sleep related vehicle accidents are largely dependent on the time of day and account for a considerable proportion of vehicle accidents, especially those on motorways and other monotonous roads. As there are no norms for the United Kingdom on road use by age and sex for time of day with which to compare these data, we cannot determine what the hourly exposure v risk factors are for these subgroups. The findings are in close agreement with those from other countries.
Asphyxia with Nitrogen
Authors: M. A. Weller
Journal: BMJ (1959)

Asphyxia with NitrogenA case of asphyxia with almost pure nitrogen under pressure is reported because of its rarity and because cases of -a similar nature are likely to become more frequent as "free" diving with self-contained underwater-breathing apparatus (S.C.U.B.A.) becomes an increasingly popular pastime. CASE REPoRT
Inhaled p38α Mitogen-activated Protein Kinase Antisense Oligonucleotide Attenuates Asthma in Mice
Authors: Wei Duan, Jasmine H. P. Chan, Kelly McKay, Jeffrey R. Crosby, Hui Hwa Choo, Bernard P. Leung, James G. Karras, W. S. Fred Wong
Journal: American Journal of Respiratory and Critical Care Medicine (2004)

The p38 mitogen-activated protein kinase (MAPK) plays a critical role in the activation of inflammatory cells. Therefore, we investigated the antiinflammatory effects of a respirable p38alpha MAPK antisense oligonucleotide (p38alpha-ASO) in a mouse asthma model. A potent and selective p38alpha-ASO was characterized in vitro. Inhalation of aerosolized p38alpha-ASO using an aerosol chamber dosing system produced measurable lung deposition of ASO and significant reduction of ovalbumin (OVA-)-induced increases in total cells, eosinophils, and interleukin 4 (IL-4), IL-5, and IL-13 levels in bronchoalveolar lavage fluid, and dose-dependent inhibition of airway hyperresponsiveness in allergen-challenged mice. Furthermore, inhaled p38alpha-ASO markedly inhibited OVA-induced lung tissue eosinophilia and airway mucus hypersecretion. Quantitative polymerase chain reaction analysis of bronchoalveolar lavage fluid cells and peribronchial lymph node cells showed that p38alpha-ASO significantly reduced p38alpha MAPK mRNA expression. Nose-only aerosol exposure of mice verified the p38alpha-ASO-induced inhibition of OVA-induced pulmonary eosinophilia, mucus hypersecretion, and airway hyperresponsiveness. None of the effects of the p38alpha-ASO were produced by a six-base mismatched control oligonucleotide. These findings demonstrate antisense pharmacodynamic activity in the airways after aerosol delivery and suggest that a p38alpha MAPK ASO approach may have therapeutic potential for asthma and other inflammatory lung diseases.
Behavioral Risk Factors and Coronary Heart Disease
Authors: David Jenkins, Stephen J. Zyzanski
Journal: Psychotherapy and Psychosomatics (1980)

After a historical review, three clusters of social psychological variables are discussed: (1) socioeconomic factors and social disorganization; (2) sustained, intensely disturbing emotions, and (3) behavioral risk factors characterized by the hard-driving, type A coronary-prone behavior pattern. Empirical evidence from the bulk of research on various aspects of these risk factors suggests that the three clusters have a significant bearing on the pathogenesis of coronary heart disease. Reduction of behavioral risk factors should concentrate on three interventions: (1) reducing the type A pattern; (2) treating emotional drain and exhaustion, and (3) treating sustained episodes of interpersonal conflict.
Abstract 2457: Laminin receptor cross-talk stimulates receptor internalization and migration of human prostate cancer cells
Authors: Todd A. Anderson, Jaime MC Gard, Isis C. Sroka, Stephanie R. Strautman, Colm Morrissey, Beatrice S. Knudsen, Anne E. Cress
Journal: Cancer Research (2012)

Abstract Integrin cell adhesion receptors are internalized and recycled to the plasma membrane during cellular migration. The laminin binding A3B1 and A6B1 integrin receptors are differentially expressed on prostate tumor cells in Gleason grades 3-5 as detected in biopsy and prostatectomy specimens. The A6 integrin exists as a full length form or as a pro-metastatic variant, A6pB1, a receptor form missing the extracellular laminin binding domain via the action of the serine protease, uPA. The objective of this study is to determine whether internalization of the A6 integrin occurs in human bone metastatic lesions and whether cross-talk between the laminin receptors A6B1, A6pB1 and A3B1 modifies their respective internalization rates. In a tissue microarray of 185 metastatic prostate cancers from 45 patients, approximately 70% of bone metastases expressed A6B1 on tumor plasma membrane and/or within the cytoplasm. The A6 and A6p integrins in DU145 cells are constitutively internalized with a biological half life of approximately 30 minutes as compared to 60 minutes for A3 or 20 minutes for the unrelated transferrin receptor. Increasing production of A6pB1 by supplying exogenous uPA stimulated A3 internalization. Conversely, blockage of A6pB1 production using an A6 specific antibody (J8H) decreased A3 internalization. Targeted depletion of the A3 integrin increased DU145 cell migration that was dependent upon A6 integrin as detected by antibody blocking experiments using J8H (A6 specific) and AIIB2 (B1 specific). Analysis of transcriptomic data from prostate cancer xenografts, revealed three different candidate receptor recycling genes that significantly correlated with the loss of membrane and increase in cytoplasmic expression. Taken together, these data indicate that cross-talk between A6B1 and A3B1 modifies their internalization rates and prostate tumor cell migration. This suggests that successful therapeutic targeting of metastasizing prostate cancer cells may depend upon coordinated targeting of both receptors and the recycling machinery. Current work is to determine the involvement of candidate recycling genes in the biological control of laminin binding integrins in human prostate cancer. (Supported in part by NIH grants P30CA023074, 1RO1 CA159406 and the TACMASS core service of the University of Arizona Cancer Center). Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2457. doi:1538-7445.AM2012-2457
Prophylactic thrombolysis by thrombin-activated latent prourokinase targeted to PECAM-1 in the pulmonary vasculature
Authors: Bi-Sen Ding, Nankang Hong, Juan-Carlos Murciano, Kumkum Ganguly, Claudia Gottstein, Melpo Christofidou-Solomidou, Steven M. Albelda, Aron B. Fisher, Douglas B. Cines, Vladimir R. Muzykantov
Journal: Blood (2007)
Abstract 4505: Preparation and anti-tumor growth of polyethylene glycol-poly lactic acid block copolymers sorafenib nanoparticles.
Authors: Jianmin Qin
Journal: Cancer Research (2013)

Abstract BACKGROUND&amp;AIMS: In vitro and in vivo studies have showed that sorafenib can inhibit the growth of liver cancer cells and solid tumor. However, poor water solubility, short half-life, high side-effect limit its clinical application in malignant tumor treatment. In this study, we report on the preparation of sorafenib nanoparticles by nanotechnology, and to observe the anti-hepatocarcinoma effect and in vivo metabolism of sorafenib nanoparticles. Methods:Polyethylene glycol-poly lactic acid block copolymers were synthesized with ring-opening polymerization technique as drug carrier material. Polyethylene glycol-poly lactic acid block copolymers sorafenib nanoparticles were prepared with nanometer precipitation method. The particle diameter and surface potential of sorafenib nanoparticles were determined by nanometer particle size and zeta otentiometer(Nano-ZS ZEN3600, Malvern). Drug-loading rate and entrapment rate were determined by ultraviolet spectrophotometer. In vitro slow release of sorafenib nanoparticles was determined by extracorporeal dialysis. The effect of sorafenib nanoparticles on H22 liver cancer cells proliferation was determined with CCK8 reagent in vitro culture .In vivo pharmacokinetics of sorafenib nanoparticles was analysed with DAS2.1.1 software. Results:Sorafenib nanoparticles were round, particle diameter was 127.3±2.0 nm, Zeta potential was -3.35±0.42 mV, drug-loading rate was 6.78%, entrapment rate was 98.21%. In vitro accumulative release rate of sorafenib nanoparticles at 24h, 48h, 72h, 96h were respectively 50.9073%, 56.2395%, 60.2561%, 63.2843%. The inhibitive effect of sorafenib nanoparticles on H22 liver cancer cells proliferation was more enhanced than that of sorafenib at the same drug concentration(F=74.988,P&amp;lt;0.05), The inhibitive effect of sorafenib nanoparticles on H22 liver cancer cells proliferation enhanced at the increase of sorafenib concentration. The in vivo metabolism time of sorafenib in sorafenib nanoparticles group was longer than that of sorafenib group (SNP t1/2, 13.95h vs S t1/2, 9.67h; t=2.618, P&amp;lt;0.05). Conclusion:Sorafenib nanoparticles can significantly inhibit the cells proliferation of liver cancer, and prolong in vivo metabolism of srafenib. The preparation of sorafenib nanoparticles has established good theoretical basis to further study in vivo anti-tumor effect and mechanism of sorafenib nanoparticles . Citation Format: Jianmin Qin. Preparation and anti-tumor growth of polyethylene glycol-poly lactic acid block copolymers sorafenib nanoparticles. [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 4505. doi:10.1158/1538-7445.AM2013-4505
Protection from lethal septic peritonitis by neutralizing the biological function of interleukin 27
Authors: Stefan Wirtz, Ingrid Tubbe, Peter R. Galle, Hans J. Schild, Mark Birkenbach, Richard S. Blumberg, Markus F. Neurath
Journal: The Journal of Experimental Medicine (2006)

The immune response to bacterial infections must be tightly controlled to guarantee pathogen elimination while preventing tissue damage by uncontrolled inflammation. Here, we demonstrate a key role of interleukin (IL)-27 in regulating this critical balance. IL-27 was rapidly induced during murine experimental peritonitis induced by cecal ligation and puncture (CLP). Furthermore, mice deficient for the EBI3 subunit of IL-27 were resistant to CLP-induced septic peritonitis as compared with wild-type controls, and this effect could be suppressed by injection of recombinant single-chain IL-27. EBI3−/− mice displayed significantly enhanced neutrophil migration and oxidative burst capacity during CLP, resulting in enhanced bacterial clearance and local control of infection. Subsequent studies demonstrated that IL-27 directly suppresses endotoxin-induced production of reactive oxygen intermediates by isolated primary granulocytes and macrophages. Finally, in vivo blockade of IL-27 function using a newly designed soluble IL-27 receptor fusion protein led to significantly increased survival after CLP as compared with control-treated mice. Collectively, these data identify IL-27 as a key negative regulator of innate immune cell function in septic peritonitis. Furthermore, in vivo blockade of IL-27 is a novel potential therapeutic target for treatment of sepsis.