tbuckley/cabot-search huggingface dataset:
Detrimental sequelae on the hemodynamics of the upper left limb after subclavian flap angioplasty in infancy.
Authors: J A van Son, W N van Asten, H J van Lier, O Daniëls, J G Vincent, S H Skotnicki, L K Lacquet
Journal: Circulation (1990)

The long-term effect of two surgical techniques for repair of coarctation of the aorta in infancy, namely, resection and end-to-end anastomosis (RETE) and subclavian flap angioplasty (SFA) on the blood supply of the upper left limb, was quantified by Doppler spectrum analysis of blood flow velocities in the left brachial artery at rest and during postocclusive reactive hyperemia. Twenty-three patients participated in this study: nine patients after SFA (median age, 8 years), 14 patients after RETE (median age, 8 years), and 10 control subjects (median age, 9.5 years). At rest, a highly significant decrease of blood flow velocities in the left brachial artery was measured in all patients of the SFA group compared with those of the RETE and control groups, as documented by various Doppler spectrum parameters: maximal frequency of advancing curve (p = 0.0001), pulsatility index (p = 0.0005), and resistance index (p = 0.039). During reactive hyperemia, a moderate capacity of physiologic augmentation of blood flow velocities was observed in five patients of the SFA group. This capacity was marginal in two patients with complaints of claudication in the left upper limb during strenuous exercise, which can be related to the number of branches of the left subclavian artery ligated during operation. This study indicates that SFA in infancy may lead to compromised hemodynamics of the upper left limb with potential for symptoms of ischemia during exercise.
443 PROGNOSIS OF SEVERE RECURRENCE OF HCV INFECTION AFTER LIVER TRANSPLANTATION IN A LARGE COHORT OF HIV INFECTED PATIENTS
Authors: T.M. Antonini, A.-M. Roque-Afonso, M. Sebagh, B. Roche, R. Sobesky, C. Guettier, D. Samuel, J.-C. Duclos-Vallée
Journal: Journal of Hepatology (2009)
The Anxiety Disorders
Authors: J. TRIG BROWN
Journal: Annals of Internal Medicine (1984)

Anxiety commonly accompanies serious illness. However, in some patients anxiety is the primary manifestation of illness. Diagnostic criteria for these "primary" anxiety disorders have been redefined in the most recent revision of the American Psychiatric Association's Diagnostic and Statistical Manual. We discuss these new diagnostic categories; review the theoretical basis for the psychodynamic, behavioral, and physiologic manifestations of each of these disorders; and critically examine the treatments offered for each.
Performance of stroke risk scores in older people with atrial fibrillation not taking warfarin: comparative cohort study from BAFTA trial
Authors: F. D. R. Hobbs, A. K. Roalfe, G. Y. H. Lip, K. Fletcher, D. A. Fitzmaurice, J. Mant
Journal: BMJ (2011)

To compare the predictive power of the main existing and recently proposed schemes for stratification of risk of stroke in older patients with atrial fibrillation.Comparative cohort study of eight risk stratification scores.Trial of thromboprophylaxis in stroke, the Birmingham Atrial Fibrillation in the Aged (BAFTA) trial.665 patients aged 75 or over with atrial fibrillation based in the community who were randomised to the BAFTA trial and were not taking warfarin throughout or for part of the study period.Events rates of stroke and thromboembolism.54 (8%) patients had an ischaemic stroke, four (0.6%) had a systemic embolism, and 13 (2%) had a transient ischaemic attack. The distribution of patients classified into the three risk categories (low, moderate, high) was similar across three of the risk stratification scores (revised CHADS(2), NICE, ACC/AHA/ESC), with most patients categorised as high risk (65-69%, n = 460-457) and the remaining classified as moderate risk. The original CHADS(2) (Congestive heart failure, Hypertension, Age ≥ 75 years, Diabetes, previous Stroke) score identified the lowest number as high risk (27%, n = 180). The incremental risk scores of CHADS(2), Rietbrock modified CHADS(2), and CHA(2)DS(2)-VASc (CHA(2)DS(2)-Vascular disease, Age 65-74 years, Sex) failed to show an increase in risk at the upper range of scores. The predictive accuracy was similar across the tested schemes with C statistic ranging from 0.55 (original CHADS(2)) to 0.62 (Rietbrock modified CHADS(2)), with all except the original CHADS(2) predicting better than chance. Bootstrapped paired comparisons provided no evidence of significant differences between the discriminatory ability of the schemes.Based on this single trial population, current risk stratification schemes in older people with atrial fibrillation have only limited ability to predict the risk of stroke. Given the systematic undertreatment of older people with anticoagulation, and the relative safety of warfarin versus aspirin in those aged over 70, there could be a pragmatic rationale for classifying all patients over 75 as "high risk" until better tools are available.
Ahead of the curve
Authors: Fintan R. Steele
Journal: Molecular Therapy (2002)

Clinical research and basic research are, in many ways, very different animals. If one were to "graph" out traditional clinical and basic research studies, there would be an unmistakable bimodal distribution, with relatively little in the middle. Gene therapy, along with other areas of molecular medicine, is changing this traditional distribution. The opposite peaks are beginning to flatten out, and one can even detect the first indications of a bell curve. Plenty of evidence to support this contention can be found throughout this abstract supplement. Interestingly, this "gap-filling" work is performed less by single or a small group of MD/PhD researchers than it is by large collaborative undertakings by teams of basic scientists and clinicians, academicians and industry scientists. Clinical research and basic research are still very different in many ways, but their complimentarity is underlined by many of the things you read here and will hear during the 5th Annual Meeting of the American Society of Gene Therapy. Molecular Therapy is proud to be the official chronicle of this diminishing gap, and is grateful for the trust and support of the Society members in allowing us to continue this work. On behalf of the editorial board and the editorial/production staff in the New York office, I hope you have a great meeting.
Obituary of Hamilton Naki: Obituary was historically inaccurate
Authors: David M Dent
Journal: BMJ (2005)

Junior doctors' shifts and sleep deprivation New on-call rotas do not workEditor-Clearly the editorial by Murray et al on junior doctors' shifts has struck a chord with many, as on-call rotas are something close to many doctors hearts. 1 2 To most it seems the grass is not greener on the other side.Having worked most rotas, be it a traditional one in four, with full weekends, to partial, hybrid, and full shift patterns, I am in a reasonable position to comment on what I think makes a liveable on-call rota.I was under the impression that the European Working Time Directive was set out to improve the health and safety of workers, make working conditions better, but also make life away from work better because doctors would be less tired.The directive scores a "no" against all of these.I find myself more tired at work and at home, less enthusiastic, and less motivated by what is becoming a regular chore.Instead of being on call once a week, I find myself doing an on-call shift two or three times a week (on average), being late home more often than not because fewer juniors are around, and spending less time with my young children.The "old" rota system of a 24 hour oncall, with at least six on a rota, made on-call shifts less frequent, more tolerable, and even enjoyable.It also left plenty of time for training, and so long as there were six or more on rota, it made the annual leave far more flexible and workable.Anaesthetists rarely complained, certainly compared with other specialties' rotas, and everyone knew that however busy, you were always going to go home to a full day off in the morning.Why not listen to those doing the rota, and affected family members, and respect within reason what the workers want to work.
The Effects of Treatment on the Direct Costs of Diabetes
Authors: William H Herman, Richard C Eastman
Journal: Diabetes Care (1998)

Treatment of diabetic complications consumes health care resources. Intensive therapy was shown by the Diabetes Control and Complications Trial (DCCT) to avert complications. Economic analyses and models have been used to evaluate the cost-effectiveness of intensive therapy for people with type 1 and type 2 diabetes. An economic analysis of the DCCT estimated the cost of intensive therapy to be two to three times greater than that of conventional therapy. In contrast, an economic model predicts that intensive therapy, as compared with conventional therapy, could reduce blindness from 34 to 20% or by 41%, end-stage renal disease from 24 to 7% or by 71%, and lower-extremity amputations from 7 to 4% or by 43%. Although intensive therapy is more expensive, when the costs of complications are factored in, it becomes cost-effective for treatment of type 1 diabetes. Similarly, a model to evaluate the cost-effectiveness of intensive therapy for people with type 2 diabetes found that the lifetime costs of general and diabetes-related medical care would be approximately two times greater. However, the reduction in lifetime costs of complications, which would produce substantial reductions in costs of treatment, largely offsets the difference. Intensive therapy for type 1 and type 2 diabetes may be more expensive than conventional therapy, but from an economic perspective, it is comparable in cost to pharmacological therapies for people with hypertension and hypercholesterolemia. From a health system viewpoint, intensive therapy represents a fruitful long-term financial investment.
Immunohistological distribution of the tight junction components ZO-1 and occludin in regenerating human epidermis
Authors: M. Malminen, V. Koivukangas, J. Peltonen, S-L. Karvonen, A. Oikarinen, S. Peltonen
Journal: British Journal of Dermatology (2003)

Summary Background Molecular characterization of tight junction proteins during the past few years has provided novel methods for studying these specialized junctions. Tight junctions have recently been characterized in the granular cell layer of human epidermis, and the role of these junctions in the epidermal barrier is now being re‐evaluated. Objectives To investigate the expression of tight junction components during the re‐epithelialization of suction blisters and the regeneration of the corneal layer after tape stripping. Methods Suction blisters were induced in eight healthy volunteers, and skin biopsies were taken 4 or 6 days afterwards. The restoration of epidermal barrier function was evaluated by measuring water evaporation (WE) from the wound area. Tape stripping was performed on three volunteers to remove the corneal layer. The tissues were immunolabelled using indirect immunofluorescence or the avidin–biotin method. Results Prior to the biopsies, WE from the blister wounds was markedly elevated in comparison with normal skin. In the epidermis surrounding the blister, occludin and ZO‐1 were expressed in the granular cell layer only. In the hyperproliferative zone adjacent to the border of the blister, the expression of ZO‐1 was redistributed into several spinous cell layers, while occludin expression was restricted to the upper epidermis. In the leading edge of migrating keratinocytes, both proteins were expressed exclusively in the most superficial layer of keratinocytes. Double labelling for ZO‐1 and involucrin showed expression of both proteins in the same layers of hyperproliferative keratinocytes, while the expression patterns were clearly different in the migrating keratinocytes. Conclusions Tight junctions of regenerating epidermis may provide a functional barrier prior to regeneration of the corneal layer.
Impaired coronary vasodilator reserve in the immediate postcoronary angioplasty period: Analysis of coronary artery flow velocity indexes and regional cardiac venous efflux
Authors: Morton J. Kern, Ubeydullah Deligonul, Michel Vandormael, Arthur Labovitz, Calapathirao V. Gudipati, Gregory Gabliani, Joseph Bodet, Yogesh Shah, Harold L. Kennedy
Journal: Journal of the American College of Cardiology (1989)
Genetic variants of the T-cell immunoglobin mucin 1 and 3 (TIM1 and TIM3) gene are not associated with asthma in an African American population
Authors: P.S. Gao, R.A. Mathias, B. Plunkett, A. Togias, K.C. Barnes, T.H. Beaty, S.K. Huang
Journal: Journal of Allergy and Clinical Immunology (2005)
Abstract 5702: Oxidative Stress in Patients with Lone Atrial Fibrillation
Authors: Kengo Kusano, Kazufumi Nakamura, Tohru Ohe
Journal: Circulation (2008)

Background: Lone atrial fibrillation (LAF) is a common arrhythmia, but its mechanism and the aggravated factor of arrhythmia are poorly understood. Oxidative stress has been implicated in the pathogenesis of heart failure. We have previously demonstrated that the amount of 4-hydroxy-2-nonenal (HNE) modified protein, which is a major lipid peroxidation product and a cytotoxic aldehyde, causes intracellular Ca2+ overload via reactive oxygen species (ROS) formation in cardiomyocytes and leads to develop arrhythmia. Accordingly we examined the levels of HNE and major histocompatibility complex (MHC) with the disease severity in LAF patients. Method: Atrial and ventricular myocardial samples were obtained from twelve patients (11 men and 1 woman, mean 48±14 years old) by endomyocardial biopsy in 10, autopsy sample in 1 and surgical resection sample in 1. Histological assessments and immunohistochemical analysis for HNE modified protein, MHC class-I and -II antigens (grade 0 to 3) were performed and compared with LAF severity. Results: Histological assessment showed that increased number of interstitial cells (mainly activated T cells) was observed only in the atrium but not in the ventricle. Moderate to severe expression of MHC antigens (grade 2 or 3) was more observed in the atrium than the ventricle (MHC-I: seven in atrium and three in ventricle; MHC-II: ten in atrium and four in ventricle). Atrial myocarditis was detected in 6 out of 11 samples. HNE modified protein was also more observed in the atrium than that in the ventricle. In addition, more severe expression of HNE staining was observed in the samples from persistent/chronic LAF than that in paroxysmal LAF. Conclusion: These data indicates that oxidative stress plays an important role as an aggravating factor in LAF patients.
Packed cell volume, haemoglobin, and oxygen saturation changes in healthy smokers and non-smokers.
Authors: V G Tirlapur, K Gicheru, B M Charalambous, P J Evans, M A Mir
Journal: Thorax (1983)

We have investigated the relationship between cigarette smoking, packed cell volume, haemoglobin concentration, and arterial oxygen saturation (SaO2) in 114 non-smokers, 66 light smokers (1-20 cigarettes a day), and 50 heavy smokers (over 20 cigarettes a day) aged 20-75 years. Packed cell volume was greater in female heavy smokers (p less than 0.001) over 40 years of age and in all female smokers over 60 years (p less than 0.001) than in non-smoking contemporaries. Haemoglobin concentrations were higher in 40-59 year old female heavy smokers (p less than 0.05) and in male and female light (p less than 0.05) and heavy smokers (p less than 0.001) over 60 years of age than in non-smoking contemporaries. SaO2 was lower in 20-39 year old male heavy smokers (p less than 0.02) and female (p less than 0.05) light smokers and also in 40-59 year old male light and heavy smokers (p less than 0.001) and female light smokers (p less than 0.02) than in non-smoking contemporaries. It was also lower in female light (p less than 0.05) and heavy (p less than 0.02) smokers over 60 years, whereas it was higher in male light smokers over 60 (p less than 0.001). Changes in SaO2 were seen at a younger age than changes in haemoglobin concentration and packed cell volume.
Air Pollution and Inflammation (Interleukin-6, C-Reactive Protein, Fibrinogen) in Myocardial Infarction Survivors
Authors: Regina Rückerl, Sonja Greven, Petter Ljungman, Pasi Aalto, Charalambos Antoniades, Tom Bellander, Niklas Berglind, Christina Chrysohoou, Francesco Forastiere, Bénédicte Jacquemin, Stephanie von Klot, Wolfgang Koenig, Helmut Küchenhoff, Timo Lanki, Juha Pekkanen, Carlo A. Perucci, Alexandra Schneider, Jordi Sunyer, Annette Peters
Journal: Environmental Health Perspectives (2007)

Numerous studies have found that ambient air pollution has been associated with cardiovascular disease exacerbation.Given previous findings, we hypothesized that particulate air pollution might induce systemic inflammation in myocardial infarction (MI) survivors, contributing to an increased vulnerability to elevated concentrations of ambient particles.A prospective longitudinal study of 1,003 MI survivors was performed in six European cities between May 2003 and July 2004. We compared repeated measurements of interleukin 6 (IL-6), fibrinogen, and C-reactive protein (CRP) with concurrent levels of air pollution. We collected hourly data on particle number concentrations (PNC), mass concentrations of particulate matter (PM) < 10 microm (PM(10)) and < 2.5 microm (PM(2.5)), gaseous pollutants, and meteorologic data at central monitoring sites in each city. City-specific confounder models were built for each blood marker separately, adjusting for meteorology and time-varying and time-invariant covariates. Data were analyzed with mixed-effects models.Pooled results show an increase in IL-6 when concentrations of PNC were elevated 12-17 hr before blood withdrawal [percent change of geometric mean, 2.7; 95% confidence interval (CI), 1.0-4.6]. Five day cumulative exposure to PM(10) was associated with increased fibrinogen concentrations (percent change of arithmetic mean, 0.6; 95% CI, 0.1-1.1). Results remained stable for smokers, diabetics, and patients with heart failure. No consistent associations were found for CRP.Results indicate an immediate response to PNC on the IL-6 level, possibly leading to the production of acute-phase proteins, as seen in increased fibrinogen levels. This might provide a link between air pollution and adverse cardiac events.
Fat Metabolism and Diabetes: 2003 American Diabetes Association Postgraduate Course
Authors: Zachary T. Bloomgarden
Journal: Diabetes Care (2003)

At the American Diabetes Association Postgraduate Course in New York, New York, on 10 January 2003, David E. Kelley (Pittsburgh, PA) discussed the relationship between fat metabolism and diabetes. Over the past few decades, he noted, the prevalence of obesity has doubled in adults and has quadrupled in teenagers, with more than half of U.S. adults now being overweight or obese. This is a manifestation of a much more longstanding trend. Data from military recruitment records, for example, show that the average weight, adjusted for height, has been increasing over the past 150 years. Sixty-one percent of the prevalence of diabetes can be attributed to obesity. There is a strong correlation between BMI and body fat. One of the correlates of insulin resistance is the blood fatty acid (FA) level. In 1963, Randle (1) initially suggested that FAs compete with glucose for metabolism. Kelley showed that, in a euglycemic clamp, when comparing subjects with and without lipid infusion, the former have marked resistance to muscle glucose uptake, with increased glycolysis and decreased glycogen formation—“precisely the profile we get in type 2 diabetes.”

FA levels are strong predictors of muscle insulin resistance (2). Muscle fat content is increased in obesity and more so in type 2 diabetes. Electron microscopy shows decreased mitochondrial size in muscle from individuals with type 2 diabetes. Fats may not directly mediate insulin resistance, Kelly noted, but FA-derived muscle diacylglycerol (DAG) and fatty acyl CoA lead to increased intramuscular ceramide, which may directly affect muscle glucose uptake and metabolism. FA oxidation is greater and storage is lower in lean than in obese persons, but Kelley described an “inefficient use of fat” in persons with obesity: the normal insulin-induced increase in FA storage is attenuated and fails to improve with weight loss (3). He noted that while muscle …
Coroner overruled: time for reform?
Authors: C Dyer
Journal: BMJ (1987)

As pressure mounts for a change in the way coroners' inquests are conducted more challenges to inquest verdicts are reaching the high court.Last month, quashing the jury's verdict in an inquest described by Mr Justice Peter Pain as "hopelessly flawed," the court recognised "lack of care" as a possible verdict in appropriate cases and clarified the ambit ofthe verdict in cases in which medical care is an issue.'The case concerned a 38 year old epileptic and schizophrenic, Keith Hicks, who was detained in Brixton Prison after an assault on his father while suffering paranoid delusions.On 1 March 1985 he was convicted ofassault, and a hospital order was made by the court, ordering his detention under section 37 of the Mental Health Act 1983, but he died in Brixton Prison on 12 March, the day he was due to be transferred to hospital.The cause of death given on the necropsy report was status epilepticus.The Hicks family was concerned about the quality ofmedical care Keith had received in prison.On 10 January 1985 he had been admitted as an emergency to the Maudsley Hospital.Ten days later he was returned to Brixton, where the treatment started in hospital-phenytoin-was continued.For some days before his death he was unwell.His mother was told that he had had petit mal fits and was not allowed to see him on 6 March.On 7 and 8 March she was again told he was not well.His sister was given the same information on 9, 10, and 11 March.On 11 March he had a grand mal seizure and was put to bed.At necropsy the whole blood phenytoin concentration was 3 mg/l, equivalent to a plasma concentration of 5 mg/l.The question was raised whether that figure indicated that he had not been receiving the proper dose, and the family wanted to know what care he had received between 6 and 12 March.The inquest, at Southwark Coroner's Court, was presided over by a deputy coroner, Dr David Foster.Before the inquest, and again during the proceedings, lawyers for the family asked for Keith's prison medical records and copies of statements by the hospital and prison staff and those who had treated Keith during his stay in prison.Dr Foster refused the request.The coroner called a prison doctor as a witness, believing that he would be able to give evidence about all the treatment Keith had been given in prison and about the contents of the notes that he had brought to court.As it happened, he had not seen Keith after 6 March, though other doctors had.Counsel for the family wanted to find out which other doctors had seen Keith after 5 March so that they might be called as witnesses.He told the coroner: "I do formally apply that this is the crux of the case, to discover what was wrong with this deceased person over the five days before his death, and that we must, if we are to find out, have evidence either in documentary or oral form about why his family were being told that he was so unwell."The application was disallowed, and, though it was put forward several times, it was refused each time.At the end of the evidence counsel applied to address the coroner, London NW1 CLARE DYER, BA, BLS, legal