tbuckley/cabot-search huggingface dataset:
Abstract 2222: Synergistic effects of NAT2 and GSTT1 null polymorphism in lung cancer: a study from North India
Authors: Rajni Kant Shukla, Surya Kant, Sandeep Bhattacharya, Balraj K. Mittal
Journal: Cancer Research (2014)

Abstract Purpose: Polymorphism in carcinogen detoxification enzymes, NAT2 and GSTT1, has been suggested as susceptibility factor for DNA damage and lung cancer. However, little information is available on DNA adduct burden in lung tissue and polymorphisms in NAT2 and GSTs gene. We investigated the independent and combined effect of metabolic gene polymorphisms NAT2 and GSTs in lung cancer north India patients. Aim: Present study was conducted to examine: 1) whether GSTT1 Null and NAT2 genotypes have combined risk factors for Lung cancer, 2) To study possible association of tobacco smoking with NAT2 and GSTT1 null genotype of these patients. Materials and Methods: This case control study was undertaken over a period of 19 months and included 100 Lung cancer patients and 145 controls. The GSTT1 Null and NAT2 genotypes were identified by PCR-RFLP method in peripheral blood DNA samples. Genotypes frequencies and the association of the genotypes among patients and controls group were assessed by X2 test and Binary Logistic regression. Results: The NAT2 slow acetylator genotype frequency of slow or fast acetylator genotypes was not significant in lung cancer patients alone (OR = 1.18, 95% CI: 0.69 - 2.03, p value = 0.583).when we combined GSTT1Null/NAT2 slow, then we found no significant association (OR = 0.85, 95% CI: 0.47 - 1.54, p value = 0.610) between case and controls. While on comparing data with smoker as well non-smoker NAT2 polymorphism have no association but GSTT1 null have significant association (P=0.004) in smoker patients. Conclusion: These data demonstrate that there have no combined affect GSTT1 Null NAT2 slow acetylator genotype did not associated with the risk of developing lung cancer in North Indian population when compared with controls. Note: This abstract was not presented at the meeting. Citation Format: Rajni Kant Shukla, Surya Kant, Sandeep Bhattacharya, Balraj K. Mittal. Synergistic effects of NAT2 and GSTT1 null polymorphism in lung cancer: a study from North India. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2222. doi:10.1158/1538-7445.AM2014-2222
Autoantibodies in simple atrophic gastritis
Authors: N. F. Coghill, D. Doniach, I. M. Roitt, D. L. Mollin, A. W. Williams
Journal: Gut (1965)

The authors have examined a group of 47 patients who had been found to have chronic gastritis, in nine superficial and in 38 atrophic.Patients with pernicious anaemia were excluded and in only two was there a doubtful family history of pernicious anaemia.A relatively high incidence of autoantibodies to the parietal cells of the stomach was found.In no case, however, were there antibodies to intrinsic factor, though these were detected in nearly 60% of patients with pernicious anaemia.Interesting correlations were found between the parietal cell antibodies and such factors as the degree of loss of parietal cells, the severity of the gastric secretory defect, and the presence of thyroid antibodies.Recent work has shown that the majority of adult patients with Addisonian pernicious anaemia have autoantibodies in their blood reacting specifically with the parietal cells of the gastric mucosa (Irvine, Davies, Delamore, and Williams, 1962; Taylor, Roitt, Doniach, Couchman, and Shapland, 1962; Markson and Moore, 1962b).Autoantibodies against gastric intrinsic factor itself have been demonstrated in the blood of 40% of patients with pernicious anaemia by a test in vivo (Taylor, 1959a; Schwartz, 1960), and by an electrophoretic retention method in vitro (Jeffries, Hoskins, and Sleisenger, 1962; Taylor et al., 1962).Recently new methods in vitro for the detection of antibodies to intrinsic factor have been introduced by Abels, Bouma, Jansz, Woldring, Bakker, and Nieweg (1963) and Ardeman and Chanarin (1963).The latter reported finding such antibodies in 57 % of a group of patients with pernicious anaemia and this has been confirmed by Roitt, Doniach, and Shapland (1964).That there may be a connexion between gastritis and thyroiditis is suggested by the finding of pernicious anaemia and hypothyroidism (atrophic thyroiditis) in the same patient, first described by Charcot in 1881 (Tudhope and Wilson, 1960, 1962;
Anxiety During MRI
Authors: Stefan A. Persili
Journal: JAMA (1994)

<h3>To the Editor.</h3> —The article by Mr Mélendez and Dr McCrank<sup>1</sup>provides an excellent review of anxiety-related reactions associated with magnetic resonance imaging (MRI) examinations. However, missing from their review were some relevant articles<sup>2-4</sup>that we came across in preparing our own ongoing study on anxiety-induced artifacts in MRI. Two of these studies<sup>2,3</sup>were probably not known to the authors because they were published in European journals: one in German and the other in Italian (both, however, have English abstracts). We would especially like to draw your readers' attention to the study by Oberstein et al.<sup>2</sup>With 21 633 subjects, it is by far the largest study so far published in this field. The results of this detailed study reveal two main obstacles that reduce the value of MRI routine examinations. First, an impaired tolerance to the investigation occurred in an average of 12% of cases
Inhibition of c-Jun-N-terminal-Kinase Sensitizes Tumor Cells to CD95-Induced Apoptosis and Induces G2/M Cell Cycle Arrest
Authors: Christian Kuntzen, Nilüfer Sonuc, Enrico N. De Toni, Christine Opelz, Simon R. Mucha, Alexander L. Gerbes, Sören T. Eichhorst
Journal: Cancer Research (2005)

Loss of susceptibility to apoptosis signals is a crucial step in carcinogenesis. Therefore, sensitization of tumor cells to apoptosis is a promising therapeutic strategy. c-Jun-N-terminal-kinases (JNK) have been implicated in stress-induced apoptosis, but may also contribute to survival signaling. Here we show that CD95-induced apoptosis is augmented by the JNK inhibitor SP600125 and small interfering RNA directed against JNK1/2. SP600125 potently inhibited methyl methane sulfonate-induced phosphorylation of c-Jun, but had minimal effect on apoptosis alone. In contrast, it strongly enhanced CD95-mediated apoptosis in six of eight tumor cell lines and led to a G2/M phase arrest in all cell lines. SP600125 enhanced cleavage of caspase 3 and caspase 8, the most upstream caspase in the CD95 pathway. JNK inhibition up-regulates p53 and its target genes p21Cip1/Waf1 and CD95. However, although HCT116 p53-/- cells and p21+/+ cells were less sensitive to CD95 stimulation than their p53+/+ and p21-/- counterparts, p53 and p21 were not involved in the JNK-mediated effect. JunD, which was described to be protective in tumor necrosis factor-induced apoptosis, was not regulated by JNK inhibition on the protein level. When transcription was blocked by actinomycin D, JNK inhibition still enhanced apoptosis to a comparable extent. We conclude that JNK inhibition has antitumor activity by inducing growth arrest and enhancing CD95-mediated apoptosis by a transcription-independent mechanism.
D3-04: MAP4/OP18 mRNA expression predicts progression in patients treated with vinorelbine plus carbolpatin in advanced lung cancer patients in a multicenter trial
Authors: Antonio Galan, Sonia del Barco, Miguel Mendez, Gaspar Esquerdo, Pablo Cerezuela, Marisol G. Huarriz, Eva Bandres, Ana B. Paules, Javier Gayo, Jesús Garcia-Foncillas
Journal: Journal of Thoracic Oncology (2007)
A Controlled Trial of an Educational Program to Prevent Low Back Injuries
Authors: Lawren H. Daltroy, Maura D. Iversen, Martin G. Larson, Robert Lew, Elizabeth Wright, James Ryan, Craig Zwerling, Anne H. Fossel, Matthew H. Liang
Journal: New England Journal of Medicine (1997)

Low back injuries are common and costly, accounting for 15 to 25 percent of injuries covered by workers' compensation and 30 to 40 percent of the payments made under that program. The high costs of injury, the lack of effective treatment, and the evidence that there are behavioral risk factors have led to widespread use of employee education programs that teach safe lifting and handling. The effectiveness of those programs, however, has received little rigorous evaluation.
Self-Reported Cardiovascular Disease and the Risk of Lung Cancer, the HUNT Study
Authors: Peter Hatlen, Arnulf Langhammer, Sven Magnus Carlsen, Øyvind Salvesen, Tore Amundsen
Journal: Journal of Thoracic Oncology (2014)

Inflammation is involved in development of lung cancer and cardiovascular disease (CVD), and we hypothesize that self-reported CVD is an independent risk factor for lung cancer.Data from the Nord-Trøndelag Health Study (1984-2008) linked to the Norwegian Cancer and Death Cause Registry were analyzed stratified by smoking status. In total, 97,087 persons (1,634,967 person years) were included (never smokers 567,575 person years, former smokers 295,685 person years, current smokers 444,922 person years, and unknown 326,785 person years) and followed for an average of 15 years. The proportional hazard model was applied to estimate the hazard ratio (HR) with a 95% confidence interval (CI) for self-reported CVD on lung cancer incidence rate adjusted for age, sex, body mass index, burden of tobacco smoking and chronic cough with phlegm.1080 cases of lung cancer (1.1%) occurred. A total of 5981 (6.9%) participants had at baseline or developed during follow-up self-reported CVD. After adjusting for confounders, self-reported CVD was an independent risk factor for the development of lung cancer in former (HR [95% CI] 1.74 [1.11-2.73]) and current smokers (HR [95% CI] 1.38 [1.04-1.83]), but not in never smokers (HR [95% CI] 0.87 [0.34-2.23]).Self-reported CVD was independently associated with increased occurrence of lung cancer in former and current smokers. CVD may be a novel risk factor for lung cancer screening.
TRANSMISSION AND BEHAVIOR OF TYPHOID POISON AS OBSERVED IN COUNTRY PRACTICE.
Authors: LEWIS N. DAVIS
Journal: JAMA (1892)

By a vast majority of the observers who would seem best calculated to know the facts, typhoid fever is now thought to be due to the invasion of the blood by a specific microörganism, known as the germ of Eberth, or the bacillus typhosus. The same observers believe that water is the principal, in fact, almost the only, medium that operates in the transmission of this infectious germ from its focus development, outside of the human body, to the subject of enteric fever. The germs or their spores are said to be eliminated from the typhoid patient, with the alvine discharges in a totally passive state. They increase rapidly in number and soon develop virulence and activity, under the favorable conditions afforded by filth, heat and moisture. Water is supposed to be a favorable habitat for typhoid germs1. These microbes may find ready access to the surface water by a
Myocardial infarction in Carlisle in 1783.
Authors: W P Honeyman
Journal: BMJ (1982)

GPs in communities most affected by redun- dancies, nevertheless, the system of medical care survives intact.The wisdom of those who understood that service, free at the point of care, was the most important principle of medical care is never more evident than when another system without that guiding principle is subjected to similar stresses.I do not know which of my patients is delaying coming to see me because he is out of work.I am sure there are many who daily weigh their own long-term health and that of their family against immediate needs of transportation, housing, and food.Nearly every community- based physician in the US acknowledges this choice for patients.It is also a choice which in a Western and industrialised country in the late twentieth century should never need exist if the medical care system were indeed a humane one.
Row rumbles on over suitability of top Indian doctor for WMA president
Authors: P. Pulla
Journal: BMJ (2015)

A row has erupted among prominent Indian doctors about the suitability of Ketan Desai, a former president of the Medical Council of India, as president of the World Medical Association, a position he is due to take up in October 2016.

The disagreement centres around charges brought against Desai in 2010 by India’s Central Bureau of Investigation, which accused him of having sought a bribe from a private medical college that was seeking approval from the council when he was president.1 Desai denies the charges.

Desai was originally declared president elect of the WMA in 2009 and was due to take up the post in October 2010. But he failed to attend the association’s annual meeting and was not appointed.2 After Desai was arrested on the bribery charges in April 2010, the council was disbanded by the government before being reconstituted in November 2013. Meanwhile, Desai’s licence to practise medicine, which was suspended in 2010, was …
Need for beta-blockade in hypertension reduced with long-term minoxidil.
Authors: H R Brunner, P Jaeger, R K Ferguson, E Jequier, G Turini, H Gavras
Journal: BMJ (1978)

Sequential changes in plasma renin activity and urinary aldosterone and noradrenaline were assessed in eight patients with severe hypertension after minoxidil had been added to their treatment. Doses of 2.5--27.5 (mean 12.5) mg/day reduced the mean blood pressure from 166/113 +/-6/2 mm Hg to 124/88+/-4/2 mm Hg in one week. Plasma renin activity and urinary aldosterone and noradrenaline increased twofold to threefold initially but returned to baseline values within two to three weeks and remained unchanged during a mean follow-up of 5.1 months. Beta-blocking drugs were then withdrawn slowly in six patients without adverse effects, though blood pressure and heart rate increased in three patients, who required minimal doses of beta-blockers. Plasma renin activity and urinary aldosterone and noradrenaline did not change significantly after beta-blockade had been stopped. We conclude that the need for beta-blockade is greatly reduced with long-term minoxidil treatment and that it may be unnecessary in some patients.
Medic Alert in Emporiatrics
Authors: George M. Wheatley
Journal: JAMA (1983)

<h3>To the Editor.—</h3> I would like to add an item to Dr Jonathan Mann's helpful review of procedures and practices to protect the health of the international traveler (1983;249:24). This is to remind physicians of an important service for the international traveler, namely, the Medic Alert Emergency Medical Identification System. Patients planning a trip abroad should know of this means of protection and help in an emergency. The distinctive Medic Alert metal disk, worn on the wrist or about the neck, the wallet card, and the around-the-clock telephone answering service to give access to the member's medical file provide three levels of emergency service. With more than two million members and 16 worldwide affiliates, Medic Alert has more than 25 years of experience assisting travelers in medical emergencies. Physicians who suggest Medic Alert membership to patients planning international travel are offering them a valuable means of health protection. At $15
STUDIES ON THE RELATIONSHIP OF THE SEX HORMONES TO INFECTION
Authors: Douglas H. Sprunt, Sara McDearman, James Raper
Journal: The Journal of Experimental Medicine (1938)

The essential findings of these experiments may be summarized as follows: The estrogenic hormone after being given for 1 week slows up the spread of India ink but allows it to reach and exceed a normal spread after 24 hours. After injections of the estrogenic hormone for 3 weeks the spread of India ink is much less than in the control animals. The resistance of the rabbit to vaccinia is increased if the rabbit has been castrated and then given the estrogenic hormone for a period of 3 weeks before being vaccinated. At the present time nothing can be said about the action of the gonadotropic hormone on India ink, as the experiments did not agree.
Digoxin Immune Fab Therapy for Digoxin Toxicity
Authors: Scott D. Phillips
Journal: Annals of Internal Medicine (1994)

Letters1 February 1994Digoxin Immune Fab Therapy for Digoxin ToxicityScott D. Phillips, MDScott D. Phillips, MDRocky Mountain Poison Center; University of Colorado Health Sciences Center; Denver, CO 80204Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-120-3-199402010-00014 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:The interesting observational study by Ujhelyi and colleagues [1] showing “rebound” toxicity after the use of digoxin immune Fab fragments raised some important concerns. The clinical features of acute and chronic digitalis toxicity differ substantially. Pharmacologically, it would have been better to separate the two groups. The timing of the last doses of digoxin before blood sampling is unclear, as is the possible effect of ingesting other drugs. Further, the serum creatinine levels in the 14 patients ranged widely from normal to markedly abnormal; thus, creatinine clearances should have been compared in the group with chronic digitalis ...References1. Ujhelyi MR, Robert S, Cummings DM, Colucci RD, Green PJ, Sailstad J, et al. Influence of digoxin immune Fab therapy and renal dysfunction on the disposition of total and free digoxin. Ann Intern Med. 1993; 119:273-7. Google Scholar2. Graves SW, Brown B, Valdes R Jr. An endogenous digoxin-like substance in patients with renal impairment. Ann Intern Med. 1983; 99:604-8. Google Scholar3. Craver JL, Valdes R Jr. Anomalous serum digoxin concentration in uremia. Ann Intern Med. 1983; 98:483-4. Google Scholar4. Karboski JA, Godley PJ, Frohna PA, Horton MW, Reitmeyer WJ. Marked digoxin-like immunoreactive factor interference with an enzyme immunoassay. Drug Intell Clin Pharm. 1988; 22:703-5. Google Scholar5. Morris RG, Frewin DB, Saccoia NC, Goldsworthy WL, Jeffries WS, McPhee AJ. Interference from digoxin-like immunoreactive substance(s) in commercial digoxin kit assay methods. Eur J Clin Pharmacol. 1990; 39:359-63. Google Scholar Author, Article, and Disclosure InformationAffiliations: Rocky Mountain Poison Center; University of Colorado Health Sciences Center; Denver, CO 80204 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByHemodialysis 1 February 1994Volume 120, Issue 3Page: 247KeywordsBloodCreatinineDrugsIntoxicationObservational studiesRenal failureToxicity Issue Published: 1 February 1994 CopyrightCopyright © 1994 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
Assisted suicide: sheer cliff or clinical reality?
Authors: S. A. King
Journal: JAMA (1994)

To the Editor.  —Quill 1 appears to be sincere in his efforts to promote a rational debate on the issue of physician-assisted death. However, his arguments are undermined by his ignoring and misrepresenting information that contradicts his views.  In his discussion of the importance of proper pain management for terminally ill patients, he notes that Experts who can provide formal or informal consultation in pain control and in palliative care are available in most major cities and extensive literature is available. He fails to cite the studies and reports that indicate that many physicians neither are aware of nor use these resources in managing the pain of terminally ill patients. 2,3 In fact, the literature has demonstrated that physicians, including those directly involved in the care of patients with cancer, are often poorly trained in pain assessment and management. 4 Yet Quill continues to ignore this extremely important point and
Kwashiorkor in African Children in Durban
Authors: J. Scragg, C. Rubidge
Journal: BMJ (1960)

of possible tuberculous infection than a contrast series: and that it approaches that of a group of patients suffering from pulmonary tuberculosis.Bass and Vader (1957), in Eindhoven, collected a series of 128 patients with sarcoidosis, the diagnosis being made on clinical grounds mainly, biopsy evidence being positive in 16.Contact with active tuberculosis, often with longer intervals than two years, within and without the family totalled 23 (18%), to which they added contact with inactive tuberculosis in 17 (13%X,) and with cattle in 6 (5%), giving them a total of 36% with tuberculous contacts; both latter groups were inaccessible in our patient questionary retrospective survey.It seems that their higher incidence may be partly due to different means of selection of the patients, different definition of contact history, and the advantages of a full radiological survey of the possible contacts.These significant findings clearly bear upon the problem of the part which tuberculous infection may play in the genesis of sarcoidosis.They suggest that contact with tuberculosis may well be a substantial rather than a minor cause; for, if the contact history is a mere coincidence, it is difficult to explain why it should differ from that of the contrast group.This evidence of a relationship between tuberculous infection and the onset of sarcoidosis raises many further problems.It may, for instance, well be that the role of infection with M. tutbercuiilosis is catalytic for an immune process of a highly specific type.Evidence for altered immune reactions in patients with active sarcoidosis has been recorded by Greenwood et al. (1958).The familial aspects of tuberculosis in this series of patients with sarcoidosis lends support to this in that there seems to be some evidence of inherited resistance to tuberculosis.There are five families in this series with sarcoidosis.The relationship is close in all of them, and yet in only one of these families is another relative known to have tuberculosis, and there the contact was not recent.Although this is a small experience it does suggest that there may well be an immune process which is determined genetically.There seems to be a place for a longer survey of the contacts of patients with tuberculosis, particularly where the population is compact and stable. SummaryThree series of patients, with tuberculosis, sarcoidosis, and asthma or bronchitis, have been investigated for contact with tuberculosis, and this has been correlatedwith the onset of the disease in the first two series.Similar incidence of recent contact was found in the series with sarcoidosis (12% of 210) and with tuberculosis (160/, of 315), contrasting with the control group (2% of 214).The relationship of this to the aetiology of sarcoidosis is discussed.I thank Dr.Howard Nicholson, of the Brompton Hospital, and Dr. Bruce Pearson, of King's College Hospital, and the staffs in their various clinics from which these series were drawn, especially Dr.
Cancer care urgently needs a real reform engine
Authors: Nick Bosanquet, Karol Sikora
Journal: Journal of the Royal Society of Medicine (2009)

The 2007 Cancer Reform Strategy (CRS)1 is a bold plan for improving cancer services in the UK. There is much that is positive about it – but can it be achieved in practice? Here we provide a reality check of achieving its goals in the changing NHS landscape. Ageing populations, the increasing incidence and prevalence of cancer, technological acceleration in drug and radiation therapy, and an informed, demanding clientele provide considerable challenges.2 The CRS document sets some very clear positive directions – but will there be the drive and funding required to really make it happen? The strategy outlines a model of care building on the 15-year-old hub and spoke model first proposed by the Expert Advisory Group on Cancer in 19933 and amplified in the NHS Cancer Plan of 20004. It creates a much broader framework incorporating prevention, screening, access to care and survivorship. What are the changes needed to ensure this happens?