tbuckley/cabot-search huggingface dataset:
Bird fancier's disease.
Authors: D Davies
Journal: BMJ (1983)

laboration with the Royal College of Radiologists.5This refreshingly clear and concise report emphasises the vital part that nuclear medicine now plays in good medical practice and recommends that facilities should be made available in all district general hospitals if optimal medical care is to be available uniformly throughout the country.Facilities should be centralised under a properly trained clinician, who should have spent two years' training in a recognised department, says the report.It considers he should give about half his time to the specialty and be either a general physician, who could encompass the whole range of nuclear medicine techniques, or a radiologist, who would supervise nuclear medicine imaging and who would be well placed to integrate this with both old and the newer radiological methods and with ultrasound.In both instances help from non-medical scientists would be needed, not necessarily all on site.The intercollegiate report also gives sensible advice on training and accreditation of the clinician and-thank goodness-considers that no new examination is needed in nuclear medicine.Financial restraints will make all this difficult to implement, as they have done for a decade, but nevertheless the report points out (and several precise financial details are given) that the cost of these services is comparable with conventional radiological techniques and considerably cheaper than others,
Can I take a space flight? Considerations for doctors
Authors: S. M. Grenon, J. Saary, G. Gray, J. M. Vanderploeg, M. Hughes-Fulford
Journal: BMJ (2012)

S Marlene Grenon, assistant professor of surgery12, Joan Saary, assistant professor3, consultant 4, Gary Gray, senior consultant flight surgeon5, James M Vanderploeg, associate professor6, chief medical officer 7, Millie Hughes-Fulford, professor89Division of Vascular and Endovascular Surgery, University of California, San Francisco, CA 94121, USADepartment of Surgery, San Francisco Veterans Affairs Medical Center, San Francisco, USADepartment of Occupational Medicine, University of Toronto, Toronto, CanadaCanadian Forces Environmental Medicine Establishment, Toronto, CanadaCanadian Space Agency, Montreal, CanadaAerospace Medicine Program, Department of Preventive Medicine and Community Health, University of Texas Medical Branch, Galveston, USAVirgin Galactic, New Mexico, USAHughes-Fulford Laboratory, Veterans Affairs Medical Center, San Francisco, USADepartment of Medicine, University of California, San Francisco, USACorrespondence to: S M Grenon marlene.grenon{at}ucsfmedctr.orgAccepted 6 November 2012
Effects of flecainide and quinidine on human atrial action potentials. Role of rate-dependence and comparison with guinea pig, rabbit, and dog tissues.
Authors: Z G Wang, L C Pelletier, M Talajic, S Nattel
Journal: Circulation (1990)

Flecainide and other class IC antiarrhythmic drugs are effective in the prevention and termination of atrial fibrillation, but the mechanism of this action is unknown. To gain insights into potential cellular mechanisms, we evaluated the response of human atrial action potentials to equimolar therapeutic concentrations of flecainide and quinidine and compared this response to that of guinea pig, rabbit, and dog atria. Both compounds reduced Vmax more as activation rate increased, but flecainide was more potent than quinidine and had slower kinetics. The rate-dependence of Vmax reduction was similar for all species, but human tissue was more sensitive to the drugs tested. In contrast to changes in Vmax, drug-induced alterations in action potential duration showed opposite rate-dependence for the two drugs. Quinidine increased action potential duration to 95% repolarization (APD95) in human atria by 33 +/- 7% (mean +/- SD) at a cycle length of 1,000 msec, but this effect was reduced as cycle length decreased, to 12 +/- 4% (p less than 0.001) at a cycle length of 300 msec. Flecainide increased APD95 (by 6 +/- 3%) much less than quinidine at a cycle length of 1,000 msec, but its effect was increased by faster pacing, to 27 +/- 12% at a cycle length of 300 msec and 35 +/- 8% (p less than 0.001) at the shortest 1:1 cycle length. The rate-dependent response of APD to drugs was qualitatively similar but quantitatively different among species. Human tissue showed the greatest frequency-dependent drug effects on repolarization, followed by tissue from dogs and rabbits. Guinea pig atria showed the least (and statistically nonsignificant) rate-dependence of drug effect on APD. Drug-induced changes in refractoriness paralleled those in APD. We conclude that: 1) flecainide and quinidine both increase APD in human atrial tissue but with opposite rate-dependence, 2) the effects of flecainide to increase atrial APD and refractoriness are enhanced by the rapid rates typical of atrial fibrillation, and 3) animal tissues may differ importantly from human in both their sensitivity and rate-dependent response to antiarrhythmic drugs. The salutary response of atrial fibrillation to flecainide may be due to enhancement of drug action by the rapid atrial activation rates characteristic of this arrhythmia.
Ras-Driven Transcriptome Analysis Identifies Aurora Kinase A as a Potential Malignant Peripheral Nerve Sheath Tumor Therapeutic Target
Authors: Ami V. Patel, David Eaves, Walter J. Jessen, Tilat A. Rizvi, Jeffrey A. Ecsedy, Mark G. Qian, Bruce J. Aronow, John P. Perentesis, Eduard Serra, Timothy P. Cripe, Shyra J. Miller, Nancy Ratner
Journal: Clinical Cancer Research (2012)

Patients with neurofibromatosis type 1 (NF1) develop malignant peripheral nerve sheath tumors (MPNST), which are often inoperable and do not respond well to current chemotherapies or radiation. The goal of this study was to use comprehensive gene expression analysis to identify novel therapeutic targets.Nerve Schwann cells and/or their precursors are the tumorigenic cell types in MPNST because of the loss of the NF1 gene, which encodes the RasGAP protein neurofibromin. Therefore, we created a transgenic mouse model, CNP-HRas12V, expressing constitutively active HRas in Schwann cells and defined a Ras-induced gene expression signature to drive a Bayesian factor regression model analysis of differentially expressed genes in mouse and human neurofibromas and MPNSTs. We tested functional significance of Aurora kinase overexpression in MPNST in vitro and in vivo using Aurora kinase short hairpin RNAs (shRNA) and compounds that inhibit Aurora kinase.We identified 2,000 genes with probability of linkage to nerve Ras signaling of which 339 were significantly differentially expressed in mouse and human NF1-related tumor samples relative to normal nerves, including Aurora kinase A (AURKA). AURKA was dramatically overexpressed and genomically amplified in MPNSTs but not neurofibromas. Aurora kinase shRNAs and Aurora kinase inhibitors blocked MPNST cell growth in vitro. Furthermore, an AURKA selective inhibitor, MLN8237, stabilized tumor volume and significantly increased survival of mice with MPNST xenografts.Integrative cross-species transcriptome analyses combined with preclinical testing has provided an effective method for identifying candidates for molecular-targeted therapeutics. Blocking Aurora kinases may be a viable treatment platform for MPNST.
Incidence of Snakebite in Wilderness Rescue
Authors: Kenneth V. Iserson
Journal: JAMA (1988)

<h3>To the Editor.—</h3> Snakebites are a common fear among the lay population. This is especially true in the desert environment of southern Arizona, where there are 11 different species of rattlesnake.<sup>1</sup>Between 1985 and 1987, more than 380 individuals in this region have been seen at medical facilities with crotalid bites— all by rattlesnakes.<sup>2</sup>Eight of nine fatalities from snakebite in Arizona between 1969 and 1984 occurred in this area.<sup>3</sup> It has been suggested that patients with unfavorable interactions with snakes (bites) frequently contribute to the situation, usually by overtly disturbing these timid creatures.<sup>4,5</sup>Those bitten by crotalids are most often purposely handling the snakes, mentally incompetent to judge the danger of the situation—usually due to drugs or a young age—or inappropriately protected by clothing from the environment.<sup>3,6</sup> For the past 30 years, volunteers of the Southern Arizona Rescue Association have been traversing, on foot,
Mucosal factors inducing neutrophil movement in ulcerative colitis: the role of interleukin 8 and leukotriene B4.
Authors: A T Cole, B J Pilkington, J McLaughlan, C Smith, M Balsitis, C J Hawkey
Journal: Gut (1996)

The movement of neutrophils into the colonic mucosa in ulcerative colitis is induced by chemokines including interleukin 8 (IL8) and leukotriene B4 (LTB4).To compare the ability of mucosa from ulcerative colitis patients and controls to stimulate neutrophil movement, to define the contribution of LTB4 to this, and to define the relative biological importance of LTB4 and IL8.Resected mucosa was obtained from seven control patients and 10 patients with ulcerative colitis.Mucosal homogenate supernatants were used to stimulate isolated neutrophils and the effect assessed by the neutrophil shape change response. Responses were inhibited with either the LTB4 receptor antagonist SC41930- or neutralising anti-IL8 antibody. LTB4 was extracted and assayed by RIA.Homogenate supernatants from inflamed mucosa were more bioactive (median 1.2 mg/ml-1 induced 50% response) than those from uninflamed mucosa (4.25 mg/ml-1 induced 50% response; difference 2.8 mg/ml-1 (96.5% CI 0.5 to 6.1, p < 0.05). Maximal inhibition by SC41930 of the response was significantly greater in inflamed mucosa (54% median) than in uninflamed mucosa (34%). This inhibition correlated with the level of immunoreactive LTB4 (r = 0.78). Anti-IL8 reduced bioactivity of homogenate supernatants from inflamed mucosa (at 1:10 dilution) by 11.4% (IQR 1.2 to 51.8, p = 0.021) whereas SC41930 reduced it by 54.8% (35.6 to 77.5, p = 0.008).Inflamed colonic mucosa releases more neutrophil movement inducing bioactivity than uninflamed mucosa, and has greater LTB4 dependent activity. It yields both IL8 and LTB4 dependent activity but greater LTB4 dependent activity.
Cognitive Therapy for the Prevention of Suicide Attempts
Authors: Gregory K. Brown, Thomas Ten Have, Gregg R. Henriques, Sharon X. Xie, Judd E. Hollander, Aaron T. Beck
Journal: JAMA (2005)

ContextSuicide attempts constitute a major risk factor for completed suicide, yet few interventions specifically designed to prevent suicide attempts have been evaluated.ObjectiveTo determine the effectiveness of a 10-session cognitive therapy intervention designed to prevent repeat suicide attempts in adults who recently attempted suicide.Design, Setting, and ParticipantsRandomized controlled trial of adults (N = 120) who attempted suicide and were evaluated at a hospital emergency department within 48 hours of the attempt. Potential participants (N = 350) were consecutively recruited from October 1999 to September 2002; 66 refused to participate and 164 were ineligible. Participants were followed up for 18 months.InterventionCognitive therapy or enhanced usual care with tracking and referral services.Main Outcome MeasuresIncidence of repeat suicide attempts and number of days until a repeat suicide attempt. Suicide ideation (dichotomized), hopelessness, and depression severity at 1, 3, 6, 12, and 18 months.ResultsFrom baseline to the 18-month assessment, 13 participants (24.1%) in the cognitive therapy group and 23 participants (41.6%) in the usual care group made at least 1 subsequent suicide attempt (asymptotic z score, 1.97; P = .049). Using the Kaplan-Meier method, the estimated 18-month reattempt-free probability in the cognitive therapy group was 0.76 (95% confidence interval [CI], 0.62-0.85) and in the usual care group was 0.58 (95% CI, 0.44-0.70). Participants in the cognitive therapy group had a significantly lower reattempt rate (Wald χ21 = 3.9; P = .049) and were 50% less likely to reattempt suicide than participants in the usual care group (hazard ratio, 0.51; 95% CI, 0.26-0.997). The severity of self-reported depression was significantly lower for the cognitive therapy group than for the usual care group at 6 months (P= .02), 12 months (P = .009), and 18 months (P = .046). The cognitive therapy group reported significantly less hopelessness than the usual care group at 6 months (P = .045). There were no significant differences between groups based on rates of suicide ideation at any assessment point.ConclusionCognitive therapy was effective in preventing suicide attempts for adults who recently attempted suicide.
Abstract 89: Osteopontin-c and osteopontin-b splicing isoforms activate prostate cancer progression features
Authors: Tatiana M. Tilli, Kivvi Duarte De Mello, Maria Theresa Accioly, Paulo Antonio Faria, Etel Rp Gimba
Journal: Cancer Research (2012)

Abstract Osteopontin (OPN) is one of the proteins overexpressed in prostate cancer (PCa) and is involved in tumorigenesis and metastasis. Alternative splicing of the OPN gene generates three protein splicing isoforms (OPN-SI), designated as OPNa, OPNb and OPNc, which have demonstrated specific roles in different tumor models. However, the roles of each of these isoforms have not been previously characterized in PCa. Our previous study reported that OPN-SI were overexpressed in PCa tissues, strongly associated with PCa occurrence and with tumor cell differentiation. Besides, OPNc was the most upregulated variant. We have also demonstrated that OPNc splicing isoform can contribute for PCa diagnosis and prognosis. Based on these results, the present study aimed to evaluate the putative roles of OPN-SI in PCa biology using in vitro and in vivo functional assays. PC-3 was stably transfected with expression vectors containing OPNa, OPNb and OPNc, as well as empty vector control. PC-3 cells overexpressing each construct were analyzed for in vivo tumor growth and in relation to different aspects mimicking tumor progression, such as cell proliferation, migration, invasion and soft agar colony formation. OPNc and OPNb overexpressing cells significantly activated enhanced xenograft tumor growth and PC-3 proliferation, migration, invasion, and soft agar colony formation, as well as the expression of several cancer related genes. Additionally, we have also shown that some of the OPNc and OPNb-dependent pro-tumorigenic roles are mediated by PI3K/Akt signaling pathway. Inhibition of this pathway by using LY294002 specifically inhibited tumor progression features evoked by OPNc and OPNb overexpression. According to our data, OPNc and OPNb roles on favoring different aspects of PCa progression suggest that these isoforms contribute to the physiopathology of prostate cancer progression and tumorigenesis. Altogether, the data open possibilities of new therapeutic approaches for prostate cancer that selectively downregulate OPNc and OPNb, altering its properties favoring prostate tumor progression. 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 89. doi:1538-7445.AM2012-89
Racial Inequalities in the Use of Procedures for Ischemic Heart Disease
Authors: David Hodges
Journal: JAMA (1989)

<h3>To the Editor. —</h3> We commend the study by Drs Wenneker and Epstein<sup>1</sup>entitled "Racial Inequalities in the Use of Procedures for Patients With Ischemic Heart Disease in Massachusetts" in the January 13 issue of<i>JAMA</i>. However, both the authors and the subsequent media coverage obscured the most important point: the most likely reason for these inequalities is that physicians value black lives less than white lives. We are physician-researchers. We recognize that in scientific studies, the cause of a finding is rarely established beyond a shadow of a doubt. We also recognize the need to consider alternative hypotheses, usually in decreasing order of likelihood, that would explain the observed effect. The authors stress the hypothesis that black patients are less likely to accept surgery and other technological interventions when offered. They refer to this as a "cultural difference." This comes dangerously close to blaming the victim. The cultural
Lymphomatoid granulomatosis--a condition with affinities to Wegener's granulomatosis and lymphoma.
Authors: A R Gibbs
Journal: Thorax (1977)

A case of lymphomatoid granulomatosis of the lung is described in which the presenting features were a skin eruption and peripheral neuropathy. The onset of the pulmonary symptoms of breathlessness and productive cough was delayed nine months but, when apparent, the extent of the radiological changes contrasted with the mildness of the symptoms and the triviality of the physical signs. Biopsy of the affected lung revealed a mixed lymphocytic, plasma cell, and histiocytic infiltrate following a perivascular distribution. This combination of clinical and pathological findings is in every detail that of lymphomatoid granulomatosis as recently identified by Liebow et al. (1972). Additional, previously undescribed, and unexplained findings in this case were persistent hypercalciuria and the presence in three axillary lymph nodes of subcapsular groups of cells resembling those of a benign naevus. This is the first case described in the British literature, and it is important that more cases be reported in order that the prevalence, prognosis, and aetiology of the condition should be further established.
Protective effects of fibronectin in galactosamine-induced liver failure in rats
Authors: Takashi Moriyama, Hiromu Aoyama, Shin Ohnishi, Michio Imawari
Journal: Hepatology (1986)

The effects of supplementation with fibronectin on liver damage and survival in rats with galactosamine-induced liver failure were studied. In rats with acute liver failure induced by a low dose of galactosamine, supplementation with purified plasma fibronectin at 3 hr after the administration of galactosamine provided significant increase of plasma fibronectin levels and augmentation of reticuloendothelial system function at 4 hr, significantly higher plasma fibronectin levels and significant protection of liver damage with shorter prothrombin times, lower AST and less histological damage at 48 hr as compared to control animals. Plasma fibronectin levels were inversely correlated with both plasma prothrombin times and AST. Fibronectin supplementation at 6 hr also resulted in the significant decrease of liver damage at 48 hr as evaluated histologically. When rats with liver failure, induced by a high dose of galactosamine, were supplemented with fibronectin at 3 hr, the survival rate was significantly higher than that of control rats. The results indicate that fibronectin supplementation in the early stages of acute liver failure could reduce liver damage and improve the survival of rats with galactosamine-induced liver failure.
Circulating CD34+ progenitor cell frequency is associated with clinical and genetic factors
Authors: Kenneth S. Cohen, Susan Cheng, Martin G. Larson, L. Adrienne Cupples, Elizabeth L. McCabe, Ying A. Wang, Julius S. Ngwa, Roderick P. Martin, Rachael J. Klein, Basma Hashmi, Yin Ge, Christopher J. O'Donnell, Ramachandran S. Vasan, Stanley Y. Shaw, Thomas J. Wang
Journal: Blood (2013)
Morphological Constitution and Smoking
Authors: Joseph L. Fleiss
Journal: JAMA (1965)

<h3>To the Editor:—</h3> I must take issue with the conclusion reached by Livson and Stewart in their study of the association between body build and cigarette smoking (<b>192</b>:806 [June 7] 1965), and with the spirit of the editorial on this subject in the same issue (p 907). An attempt was made to replicate a study involving Harvard undergraduates in whom it was found that smokers were generally larger and heavier than nonsmokers. While the differences on a number of dimensions were statistically significant in the Harvard study, no differences attained significance in Livson and Stewart's study. The authors and the editorial suggest that this "discrepancy" may have resulted from differences on demographic variables, impurity of samples, etc, but they all ignored the fact that Livson and Stewart studied only 97 males, compared with a sample size of 697, exactly seven times greater, in the Harvard study. Even fairly large
Response to comments in: Statin use is associated with reduced incidence and progression of knee osteoarthritis in the Rotterdam study by Clockaerts<i>et al</i>
Authors: Daniel L Riddle, George Moxley, Levent Dumenci
Journal: Annals of the Rheumatic Diseases (2013)

We thank Clockaerts et al for their thoughtful commentary on our paper and will address a number of their comments. They expressed concern regarding lack of verification of our data related to statin use, duration of use and dosage, and indicated these data were based on self-report. While we acknowledged in our paper1 that we did not have dosage data, the verification was that participants brought their medications with them during yearly follow-up visits and we were able to confirm that statins were prescribed for these patients. This approach was not as valid as a pill count but, in our view, is more rigorous than self-report.

Clockaerts et al accounted for duration of statin use by examining effects for those with 1–119 days, 120–364 days and 365 days or greater of statin use at 50% or more of the recommended daily dosage. Our approach was to use the yearly follow-up visit prescription data indicating 0, 1, 2, 3 or 4 years of statin use to examine the effects on changes in …
Cooperative study on the value of long term anticoagulation in patients with stroke and non-rheumatic atrial fibrillation
Authors: J Lodder, M S Dennis, L Van Raak, L N Jones, C P Warlow
Journal: BMJ (1988)

The benefits of long term anticoagulant treatment of patients with non-rheumatic atrial fibrillation and cerebral infarction were studied by comparing two series of patients with stroke from centres with different policies on anticoagulant treatment. The long term prognosis of 50 patients from the Oxfordshire community stroke project, who did not receive anticoagulants, was compared with that of 70 similar patients from Maastricht, who were treated with anticoagulants. After a mean follow up of 27 months there was no significant difference in either the rate of survival or the rate of recurrent stroke between the two groups. These data suggest that any benefit of anticoagulation is modest. A large randomised trial is planned to establish whether long term anticoagulant treatment is of value and, if so, to what extent.