tbuckley/cabot-search huggingface dataset:
Abstract 654: The effect of lung cancer screening awareness on smoking behavior among U.S. adults
Authors: Dianne N. Thompson, Richard A. Barrett, Anand Deonarine, Carla D. Williams, Debra White-Coleman, Alicia Thomas, Sara Horton, Amanda J. Cross, Adeyinka O. Laiyemo
Journal: Cancer Research (2012)

Abstract Background: Emphasizing the risk of lung cancer can encourage smoking cessation, but use of spiral low-dose CT scans reduced lung cancer mortality in a recent randomized screening trial. It is unknown if awareness of lung cancer screening will influence smoking behavior. Aim: To evaluate the awareness of lung cancer screening and to determine if awareness of lung cancer screening affects smoking cessation-related behavior among current smokers. Methods: We identified 7,282 adult respondents who answered questions concerning their smoking-related behavior in the 2007 Health Information National Trends Survey (HINTS). We used logistic regression models to evaluate the association of smoking status with awareness of lung cancer screening and we also investigated the association of lung cancer screening awareness with smoking cessation behaviors among current smokers. Results: The mean age of responders was 54.1 years and 61.2% were females. There were 3,813 (52.4%) never smokers; 2,222 (30.5%) former smokers; and 1,247 (17.2%) current smokers. Overall, 2,183 (30.6%) of respondents had heard of a lung cancer screening test (29.6% never smokers, 33.4% former smokers, and 28.5% current smokers; P value = 0.002). Chest X-ray (64.4%) and CT scan (5.7%) were among the screening tests that they have heard of. Among current smokers, awareness of lung cancer screening had no effect on smoking cessation behavior after adjusting for age, sex, race, education, income and marital status (Table). Conclusion: Awareness of lung cancer screening tests did not affect smoking cessation behavior of current smokers. However, smoking cessation should be recommended for all current smokers and those with a history of smoking should be informed about lung cancer screening with CT scan. 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 654. doi:1538-7445.AM2012-654
Imatinib Mesylate — The New Gold Standard for Treatment of Chronic Myeloid Leukemia
Authors: Karl Peggs, Stephen Mackinnon
Journal: New England Journal of Medicine (2003)

Chronic myeloid leukemia (CML) is a clonal stem-cell disorder in which the reciprocal translocation t(9;22) generates two novel fusion genes: BCR-ABL on the derivative 22q– (Philadelphia) chromosome, and ABL-BCR on chromosome 9q+. The ABL gene product is a protein tyrosine kinase, and the fusion protein BCR-ABL has constitutive kinase activity that deregulates signal transduction pathways, causing abnormal cell cycling, inhibition of apoptosis, and increased proliferation of cells. The natural course of the disease is usually characterized by three sequential phases (the chronic, accelerated, and blast-crisis phases), during which there is progressively more resistance to therapy.Interferon alfa therapy extends survival . . .
Insights into the pathogenesis of alcoholic liver necrosis and fibrosis: Status report
Authors: Hidekazu Tsukamoto, Karl Gaal, Samuel W. French
Journal: Hepatology (1990)

The use of the Tsukamoto-French rat model of alcoholic liver disease facilitated pathological, physiological, biochemical and cell biological experiments that examined the validity of some of the existing hypotheses for pathogenesis of alcoholic liver necrosis and fibrosis. Results obtained to date strongly support the contribution of centrilobular hypoxia as a pathogenetic mechanism of alcoholic liver necrosis. The enhanced hepatic lipid peroxidation was not evident at the early stage of ethanol-induced liver necrosis but could be demonstrated at the late stage when the liver damage progressed to liver fibrosis. This suggests that the lipid peroxidation may not be an important mechanism of alcoholic liver necrosis but may be an initiation factor for liver fibrogenesis as recently proposed by others (88). The high-fat diet appears to have promoting effects on both induction of alcoholic liver necrosis and stimulation of liver fibrogenesis. The former may be related to the induction of MEOS by the high-fat diet and consequent centrilobular hypoxia caused by inadequately compensated hepatic overuse of oxygen. The latter can be mediated through sensitization of Ito cells by a high-fat diet. We propose that Kupffer cell-derived TGF beta is, at least in part, responsible for some of phenotypical changes of Ito cells associated with their activation. Our model provides maximal experimental control and induces the discrete stages of alcoholic liver injury that can be reproduced with its pathological evolution telescoped into a short time. Because of these features, replication of the experimental conditions in different laboratories is possible so that results can be validly compared through precise standardization of the experimental protocols. This model requires some training in implantation and maintenance of the gastric catheter. However, the training can be easily attained by anyone who has experience in animal surgery. Another requirement is the initial fund to acquire infusion devices and metabolism cages. Once this equipment is purchased, however, the maintenance cost is low. Even if the initial expenses are included, the cost per animal is relatively inexpensive when compared with the cost involved in the use of larger animals such as baboons or pigs. Since administration of diet and ethanol (or isocaloric glucose solution) is precisely controlled by infusion pumps, this system makes unnecessary the measurement of diet consumption that has to be done daily for each animal with other methods.(ABSTRACT TRUNCATED AT 250 WORDS)
The Millennium Development Goals: a cross-sectoral analysis and principles for goal setting after 2015
Authors: Jeff Waage, Rukmini Banerji, Oona Campbell, Ephraim Chirwa, Guy Collender, Veerle Dieltiens, Andrew Dorward, Peter Godfrey-Faussett, Piya Hanvoravongchai, Geeta Kingdon, Angela Little, Anne Mills, Kim Mulholland, Alwyn Mwinga, Amy North, Walaiporn Patcharanarumol, Colin Poulton, Viroj Tangcharoensathien, Elaine Unterhalter
Journal: The Lancet (2010)
Vascular Oxidant Stress Enhances Progression and Angiogenesis of Experimental Atheroma
Authors: Jaikirshan J. Khatri, Chad Johnson, Richard Magid, Susan M. Lessner, Karine M. Laude, Sergey I. Dikalov, David G. Harrison, Hak-Joon Sung, Yuan Rong, Zorina S. Galis
Journal: Circulation (2004)

Background— Although multiple pathological processes have been associated with oxidative stress, the causative relation between oxidative stress and arterial lesion progression remains unclear. Methods and Results— To test the effect of creating arterial wall oxidative stress, we compared progression of mouse carotid lesions induced by flow cessation in the wild-type (WT) versus transgenic mice (Tg p22vsmc ), in which overexpression of p22phox, a critical component of NAD(P)H oxidase was targeted to smooth muscle cell (SMC). Compared with WT mice, arterial lesions grew significantly larger in Tg p22vsmc ( P &lt;0.001) and demonstrated elevated hydrogen peroxide (H 2 O 2 ) and vascular endothelial growth factor (VEGF) levels at all time points examined ( P &lt;0.001, n=4 animals per time point), probably related to increased expression of hypoxia inducible factor (HIF)-1α via SMC oxidative stress in the Tg p22vsmc arteries, both basally (203±12% versus WT, P &lt;0.001, n=3) and after lesion formation. Interestingly, Tg p22vsmc lesions were complicated by extensive neointimal angiogenesis. In vitro experiments confirmed SMCs isolated from Tg p22vsmc to be the source for increased H 2 O 2 , VEGF, and HIF-1α and their capacity to induce angiogenic cord-like structures when cocultured with endothelial cells. The antioxidant ebselen inhibited SMC activities in vitro and intralesion angiogenesis and lesion progression in vivo. Conclusions— We have demonstrated a novel pathway by which oxidative stress can trigger in vivo an angiogenic switch associated with experimental plaque progression and angiogenesis. This pathway may be related to human atheroma progression and destabilization through intraplaque hemorrhage.
King's Fund report on improving the quality of care in general practice
Authors: R. Baker
Journal: BMJ (2011)

Commissioning consortiums need to use professional leadership to improve care

International comparative studies show that strong primary care can be the foundation for efficient healthcare systems.1 In England, almost all the population is registered with general practitioners who work with multidisciplinary primary healthcare teams that provide a wide range of services. Care is largely free, and general practitioners act as gatekeepers into most specialist care. The system is therefore often seen as an exemplar of how primary care can enable good health outcomes to be achieved at reasonable cost.

Yet the English health system is embarking on major and controversial reorganisation, with general practice at the centre of the changes.2 The general practitioner commissioning groups now being established as part of the reforms will have a duty to help the NHS Commissioning Board in continuously improving the quality of general practice. With enviable prescience, two years ago the King’s Fund commissioned an inquiry to review the quality of general practice in England and make recommendations on how general practice can be supported to improve quality.3 The report is published this week, and it should be studied carefully by all those leading commissioning consortiums.

Chaired …
S129 The natural history of bronchial pre-invasive disease
Authors: JM Brown, G Hardavella, B Carroll, M Falzon, N Navani, PJ George, SM Janes
Journal: Thorax (2013)

<h3>Background</h3> Bronchial pre-invasive lesions represent the earliest stages of the stepwise progression of squamous carcinogenesis, they predominantly affect the large airways and are readily detectable using autofluoresence bronchoscopy (AFB) however very little is known about the natural history of these lesions and no randomised data exists to determine whether intervention before progression to invasion improves outcome. <h3>Methods</h3> A total of 94 patients with bronchial dysplasia were enrolled into an on-going surveillance cohort at University College London Hospital running prospectively since 1999. Lesions were biopsied longitudinally and kept under regular surveillance with AFB and low dose annual CT scanning until resolution or progression to invasive disease occurred. Retrospective analysis of lesional destiny was undertaken to determine the proportions of progressive vs. regressive lesions that occur in low grade dysplasia (LGD- squamous metaplasia, mild and moderate dysplasia) vs. high grade dysplasia (HGD- severe dysplasia (SD) and carcinoma-in-situ). A lesion was considered to have progressed/ regressed if it crossed between groups (LGD, HGD, invasive cancer). <h3>Results</h3> A total of 117 separate lesions that were biopsied on more than one occasion were identified of which 61 were HGD and 56 LGD. Of the low grade lesions 54/56 (96%) regressed or remained static, 1 (2%) progressed to CIS and 1 (2%) to invasive carcinoma both of these lesions progressed from moderate dysplasia. Of the high grade lesions there were 13 SD and 48 CIS, overall 35/61 (57%) of HGD progressed to invasive cancer 9/61 (15%) regressed and 17/61 (28%) remained static. There was a trend toward higher progression to cancer (62% vs 56%) and lower rates of regression (8% vs. 17%) for SD versus CIS in the HGD cohort although the numbers are too small to be statistically significant (see fig. 1). In the HGD group median time to invasion was 9.5 months (range 3–49), static lesions were documented to have remained as such for a median of 17 months (range 4–60). <h3>Conclusions</h3> In our cohort we see very few lesions following the traditional stepwise progression and LGD remains relatively indolent. There is a significant proportion of HGD that progresses to invasive cancer and further studies are required to test the role of endobronchial intervention to prevent progression and to determine the most efficacious modality of treatment.
THE ROLE OF LYMPHOCYTES IN THE SENSITIZATION OF RATS TO RENAL HOMOGRAFTS
Authors: S. Strober, J. L. Gowans
Journal: The Journal of Experimental Medicine (1965)

In order to study the role of blood-borne small lymphocytes in the sensitization of rats to renal homografts 2 techniques for the perfusion of isolated rat kidneys were employed: (a) the in vitro perfusion of kidneys with thoracic duct cells suspended in either an artificial medium or in blood; the perfusates were then injected into rats syngeneic with the lymphocyte donors; (b) the in vivo perfusion of kidneys with blood issuing from the femoral artery and returning to the femoral vein of living rats. The degree of sensitization conferred on the recipients by the perfusates was assessed by applying a skin homograft from the kidney donor and scoring the epithelial necrosis at 6 days. The in vitro experiments indicated that parental strain thoracic duct cells, which had passed through an F1 hybrid kidney could confer upon a parental rat sensitivity to an F1 skin graft. Several perfusions with radioactively labelled lymphocytes showed that the injected cells migrated to the lymph nodes and spleen of the recipients Labelled large pyroninophilic cells were occasionally seen in the spleen and lymph nodes of recipients, and it was suggested that these had arisen from the injected cells. Although the in vitro perfusions with blood indicated that renal homografts might sensitize their hosts within 1 hour, the in vivo perfusions suggested that about 5 to 12 hours were required. The more rapid sensitization in vitro was possibly due to the more frequent opportunity for contact between lymphocytes and kidney vascular endothelium which was afforded by the conditions in vitro.
Diverticulum of the Female Urethra
Authors: J. H. N. Ferris
Journal: BMJ (1965)

Listeriosis-Barber and Okubadejo MWIt loULEvidence that maternal infection with Listeria may be a cause of abortion has come from several other sources.Gray et al. (1955) produced abortions in pregnant does by intraocular infection with Listeria.They also showed that pregnancy appears to predispose to infection with Listeria, since after oral challenge of pregnant rabbits the bacteria could be isolated from the vagina, but this was not the case with non-pregnant animals.Further evidence in humans has come from Seeliger (1958), who found that 16% of the mothers who gave birth to infants infected with Listeria had a history of previous abortions or stillborn infants.Rost et al. (1958) found that many women with a history of abortion had a high circulating antibody titre to Listeria monocytogenes and also that after antibiotic treatment the women gave birth to healthy full-term infants.These findings and those of other investigators are discussed by Gray (1960), who points out that further studies using a satisfactory isolation technique (see McBride and Girard, 1960) might indicate a high incidence of Listeria in the human genital tract.The single negative study in Britain (Macnaughton, 1962) of 78 women with threatened or incomplete abortion is not necessarily conclusive, since the technique of isolation differed in certain respects from that of Rappaport et al. (1960). SummaryA bacteriologically proved case of listeriosis in both mother and prematurely born infant is recorded for the first time in Britain.A review of the literature indicates that in some parts of the world not only is neonatal listeriosis relatively common but genital listeriosis may be a significant cause of repeated abortion.Since Listeria monocWogenes is both difficult to obtain in primary culture and easily confused with a skin-contaminating diphtheroid, it is suggested that the low incidence of infection in Britain may be at least partly due to failure to recognize the condition.
Lung Volume Reference Values for Women and Men 65 to 85 Years of Age
Authors: Francisco Garcia-Rio, Ali Dorgham, José M. Pino, Carlos Villasante, Cristina Garcia-Quero, Rodolfo Alvarez-Sala
Journal: American Journal of Respiratory and Critical Care Medicine (2009)

Rationale: In elderly subjects, static lung volumes are interpreted using prediction equations derived from primarily younger adult populations.Objectives: To provide reference equations for static lung volumes for European adults 65 to 85 years of age and to compare the predicted values of this sample with those from other studies including middle-aged adults. We compare the lung volumes by plethysmography and helium dilution in elderly subjects.Methods: Reference equations were derived from a randomly selected sample from the general population of 321 healthy never-smoker subjects 65 to 85 years of age. Spirometry and lung volume determinations by plethysmography and multibreath helium equilibration method were performed following the American Thoracic Society/European Respiratory Society recommendations. Reference values and lower and upper limits of normal were derived using a piecewise polynomial model.Measurements and Main Results: Plethysmography provided higher values than the dilutional method for all lung volumes, with wide limits of agreement. In addition to height, our reference equations confirm the age- and body size dependence of lung volumes in older subjects. Practically all the estimations performed by extrapolating reference equations of middle-aged adults overpredicted the true lung volumes of our healthy elderly volunteers. Middle-aged reference equations classify subjects as being below the total lung capacity lower limit of normal between 17.9 and 62.5% of the women and between 12.5 and 42.2% of the men of the current study.Conclusions: These results underscore the importance of using prediction equations appropriate to the origin, age, and height characteristics of the subjects being studied.
Lower risk of atopic dermatitis among infants born extremely preterm compared with higher gestational age
Authors: S. Barbarot, C. Gras-Leguen, H. Colas, E. Garrot, D. Darmaun, B. Larroque, J.C. Roze, P.Y. Ancel
Journal: British Journal of Dermatology (2013)

It is not yet known whether the risk of developing atopic dermatitis (AD) is influenced by preterm birth. Moreover, AD risk has not been assessed in a large sample of extremely preterm infants (< 29 weeks' gestation).To determine whether the risk of AD is influenced by preterm birth.We investigated the relationship between gestational age (GA) and AD using data from two independent population-based cohorts, including a total of 2329 preterm infants, of whom 479 were born extremely preterm.There was a lower percentage of children with AD in the extremely preterm group compared with those born at a greater GA (Epipage cohort, 2-year outcome: 13·3% for 24-28 weeks, 17·6% for 29-32 weeks, 21·8% for 33-34 weeks, P = 0·02; LIFT cohort, 5-year outcome: 11% for 24-28 weeks, 21·5% for 29-32 weeks, 19·6% for 33-34 weeks, P = 0·11). After adjusting for confounding variables, a lower GA (< 29 weeks) was significantly associated with decreased risk of AD in the Epipage cohort [adjusted odds ratio (aOR) 0·57, 95% confidence interval (CI) 0·37-0·87; P = 0·009] and the LIFT cohort (aOR 0·41, 95% CI 0·18-0·90; P = 0·03).Very low GA (< 29 weeks) was associated with a lower risk of AD compared with higher GA (29-34 weeks) and full-term birth.
Diverticular disease of the colon: a deficiency disease of Western civilization.
Authors: N S Painter, D P Burkitt
Journal: BMJ (1971)

We present a hypothesis as to the cause of diverticulosis coli which is consistent with its geographical distribution, its recent emergence as a medical problem, and its changing incidence.Diverticulosis appears to be a deficiency disease caused by the refining of carbohydrates which entails the removal of vegetable fibre from the diet.Consequently we consider it to be prevent- able.Diverticulitis first became a clinical problem at the turn of the century, and the term "diverticulosis" first appeared in 1914.As recently as 1916 the disease was not important enough to merit a mention in textbooks.'Though the present incidence of diverticulosis is unknown it is certainly endemic in our aged citizens.This dramatic increase in incidence occurred in only 70 years and cannot possibly be explained on a genetic basis.This change might be due to observer error and be apparent rather than real, but we believe that their writings show that the clinicians of the last century were just as capable as those of today of recognizing diverti- culitis.We believe that there is another possibility-namely, that the colon's environment has changed and that diverticula are caused by the diet of so-called "civilized" countries.Historical Impact of Diverticular Disease on Medicine DIVERTICULA AS A CURIOSITY The term "divertikel" was used by Fleischman in 1815.2Gross in 1845,3 Cruveilhier in 1849,4 Rokitansky in 1849,5 Haberschon in 1857,6 and Klebs in 18697 realized that diverti- cula were acquired and thought they were caused by consti- pation.The danger of diverticula as sites of infection and perforation was pointed out by Cruveithier;4 in 1859 Sidney Jones described vesicocolic fistula due to diverticulitis.8Harrison Cripps in 1888 collected 63 enterovesical fistulae but believed that they were caused by ingested foreign bodies.'He emphasized that they were usually the result of "inflammatory mischief" and not of cancer, but he blamed only diverticulitis in the case of Jones.Virchow in 1853 described perisigmoiditis,l" while Loomis in 1870 recorded peritonitis resulting from diverticulitis."1Since this complication was still regarded as a surgical curiosity 30
THE MODERN TREATMENT OF DIABETES MELLITUS: An Abstract of Three Lectures delivered at the London Hospital
Authors: O. Leyton
Journal: BMJ (1917)

A FEw weeks ago the followiing dialogue imiight lhave been lheard in the staff loomii of tlhe London Hospital:Surgical Colleague: T see that you are lecturing oni the modern treatment of diabetes; nloxw.teil me, are you goinlg to tell us anythinlg whichi I was not taught as a student?
Illness related deception: social or psychiatric problem?
Authors: C. Bass, P. W Halligan
Journal: Journal of the Royal Society of Medicine (2007)

In this paper we question the validity of factitious disorder as a meaningful psychiatric diagnosis. When the diagnosis is used there is often the assumption that the person engaging in the ‘deception’ is not lying in the traditional sense of being deliberately misleading. Moreover, little is known about the aetiology or psychopathology underlying factitious disorder, and the legitimacy of deception as a mental disorder has been questioned. It is argued that while illness deception may be more common that hitherto assumed, factitious disorder as a distinct type of psychiatric disorder is conceptually flawed, diagnostically impractical and clinically unhelpful and should be dropped from existing nosologies.