tbuckley/cabot-search huggingface dataset:
Seizures Apparently Triggered by Video Games
Authors: Paul C. Helfgott
Journal: JAMA (1983)

To the Editor.—  We would like to add another case to the report of Dahlquist et al (1983;249:776) regarding video game-precipitated epilepsy.  Report of a Case.—  An 8-year-old boy traveled overnight with his family to a mountain resort, obtaining little sleep. After skiing for several hours, the patient separated from his family and began playing an arcade video game, where he suffered an unobserved fall. He was unresponsive for several minutes but gradually awoke and regained orientation. He did not recall falling.  He was admitted to a local hospital, where, while sleeping in the early morning, he was observed to have a brief generalized convulsion. He was discharged receiving phenobarbital. An EEG obtained several weeks later demonstrated frequent spontaneous bursts of left focal polyspike and slow wave activity.  The patient's first year of life was remarkable for a probable near-sudden infant death syndrome, from which he was resuscitated by his
Depressed in vivo myocardial reactivity to dobutamine in streptozotocin diabetic rats: influence of exercise training
Authors: B. A HELLER, D. J PAULSON, S. J KOPP, D. G PEACE, J. P TOW
Journal: Cardiovascular Research (1988)

To assess the effects of chronic diabetes on in vivo myocardial reactivity to beta1 adrenergic receptor stimulation and to evaluate the therapeutic effect of exercise training in preventing the cardiac abnormalities induced by diabetes four groups of rats were studied: sedentary control, trained control, sedentary diabetic, and trained diabetic. Trained rats were adapted to treadmill running before the induction of diabetes with streptozotocin 55 mg·kg−1 iv. The duration, speed, and grade of exercise were then progressively increased during eight weeks of training until the rats could run for 90 min at 18 m/min, 5% grade. A training effect was confirmed by an increase in plantaris muscle cytochrome oxidase activity. In vivo cardiac contractile performance was assessed by intracardiac catheterisation. Heart rate, left intraventricular peak systolic pressure, and positive and negative dP/dt were measured under basal conditions and after the intravenous administration of dobutamine 10−10 to 5 × 10−7 mol·kg−1 body weight. Under basal conditions, there were no differences among the four groups in left intraventricular peak systolic pressure, positive dP/dt, and heart rate, but negative dP/dt was lower in both diabetic groups. The response to dobutamine of the sedentary diabetic group, as reflected in the measured cardiodynamic variables, was significantly attenuated compared with that of the sedentary control group. Exercise training tended to improve cardiac function towards the level detected in the sedentary controls; however, the differences between sedentary and trained diabetic groups were not statistically significant. Exercise training also did not significantly alter the response of the control group to dobutamine. These findings suggest that myocardial reactivity to betai adrenergic stimulation is impaired in diabetic rats. Exercise training at the intensity used failed significantly to improve this condition.
Short-term changes in magnetic resonance imaging and disease activity in response to infliximab
Authors: H M Bonel, C Boller, B Saar, S Tanner, S Srivastav, P M Villiger
Journal: Annals of the Rheumatic Diseases (2009)

To characterise and quantify short-term changes in local inflammation using magnetic resonance imaging (MRI), and to correlate the findings with clinical disease activity in response to infliximab in patients with spondyloarthritis.28 consecutive patients with established spondyloarthritis under successful long-term treatment with infliximab underwent MRI immediately before and one week after re-administration of the TNF blocker. C-reactive protein and the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) were assessed at both time points. The MRI protocol included coronal and sagittal turbo-short T1 inversion recovery (STIR) images as well as contrast-enhanced sagittal T1-weighted, fat-suppressed images. Images were assessed in independent sessions using the ASspiMRI-a score, the signal-difference-to-noise ratios (SDNR) and volumetry to assess oedematous and inflamed tissues.BASDAI values were expectedly low at study entry (3.3, SD 2.3). One week after administration of infliximab, 46% of patients reached a BASDAI 20, 39% a BASDAI 50. Kappa values for qualitative assessments and all measurements were excellent (range between 0.83 and 1.0) The ASspiMRI-a dropped most in the thoracic (3.3 points), less in the lumbar (1.21 points) and least in the cervical spine (0.38 points). The decrease of the ASspiMRI-a, the SDNR and the inflamed volumes in response to infliximab re-treatment was significant (p<0.01). The BASDAI showed a weak correlation with the ASspiMRI-a (r = 0.41).MRI proves to be a valid method to assess and quantify short-term effects of therapy in spondyloarthritis. Comparison between MRI and BASDAI changes show that the BASDAI may underestimate local inflammation. It suggests an explanation for the structural disease progression despite clinical remission.
Anti-TNF antibody treatment improves glucocorticoid induced insulin-like growth factor 1 (IGF1) resistance without influencing myoglobin and IGF1 binding proteins 1 and 3
Authors: Piercarlo Sarzi-Puttini, Fabiola Atzeni, Jürgen Schölmerich, Maurizio Cutolo, Rainer H Straub
Journal: Annals of the Rheumatic Diseases (2005)

<b>Background:</b> Insulin-like growth factor 1 (IGF1) is an important determinant of muscle mass because it promotes growth and suppresses protein degradation. IGF1 is decreased in rheumatoid arthritis and juvenile idiopathic arthritis because its synthesis is inhibited by inflammation. In parallel, glucocorticoids induce IGF1 resistance and add to muscle degradation. <b>Objective:</b> To investigate the influence of anti-tumour necrosis factor antibody treatment (anti-TNF) with adalimumab on levels of myoglobin (degradation marker) and IGF1 in patients with rheumatoid arthritis with and without prednisolone treatment. <b>Methods:</b> Subcutaneous adalimumab was given to 32 patients with longstanding rheumatoid arthritis (16 with and 16 without prednisolone) in a longitudinal study. IGF1, IGF1 binding protein 1 (IGFBP-1), IGFBP-3, and myoglobin were measured by enzyme linked immunosorbent assay. <b>Results:</b> Rheumatoid patients had normal serum myoglobin. Patients on prednisolone had higher myoglobin than patients not receiving prednisolone, indicating increased muscle degradation. On treatment with anti-TNF, myoglobin levels did not change in either patient group. Serum IGF1 was increased in patients with <i>v</i> without prednisolone, indicating IGF1 resistance (mean (SEM): 221 (23) <i>v</i> 122 (14) μg/l, p&lt;0.001). Adalimumab treatment decreased the raised IGF1 levels in patients with prednisolone, so that after 12 weeks of treatment they reached the level of patients without prednisolone. Serum IGFBP-1 and IGFBP-3 did not differ in the two groups, and anti-TNF did not change these concentrations. <b>Conclusions:</b> Anti-TNF antibody treatment over 12 weeks improved glucocorticoid induced IGF1 resistance without influencing myoglobin and IGF1 binding proteins. Thus, in rheumatoid patients on glucocorticoids with generally decreased muscle mass anti-TNF treatment with adalimumab has favourable effects.
The Mystery of the Eosinophil
Authors: H. M. S. Turner
Journal: BMJ (1948)

been oedema, diarrhoea, or vomiting.No other drugs had been given and the patient's conduct prior to the commencement of treatment in hospital had been normal.i The patient was now a pleasant and co-operative individual who was rather vague about what had been happening to him during the days when his behaviour was abnormal.He scarcely ever touched alcohol because of his disability and had no previous history of mental aberration.
Social Risk or Genetic Liability for Psychosis? A Study of Children Born in Sweden and Reared by Adoptive Parents
Authors: Susanne Wicks, Anders Hjern, Christina Dalman
Journal: American Journal of Psychiatry (2010)

Recent studies suggest a role for social factors during childhood in the later development of schizophrenia. Since social conditions in childhood are closely related to parental psychiatric illness, there is a need to disentangle how genes and social environmental factors interact.A total of 13,163 children born in Sweden between 1955 and 1984 and reared in Swedish adoptive families were linked to the National Patient Register until 2006 regarding admissions for non-affective psychoses, including schizophrenia. Hazard ratios for nonaffective psychoses were estimated in relation to three indicators of socioeconomic position in childhood (household data of the rearing family obtained via linkage to the National Censuses of 1960-1985) and in relation to indicator of genetic liability (biological parental inpatient care for psychosis). In addition, the total Swedish-born population was investigated.Increased risks for nonaffective psychosis were found among adoptees (without biological parental history of psychosis) reared in families with disadvantaged socioeconomic position, which consisted of adoptive parental unemployment (hazard ratio=2.0), single-parent household (hazard ratio=1.2), and living in apartments (hazard ratio=1.3). The risk was also increased among persons with genetic liability for psychosis alone (hazard ratio=4.7). Among those exposed to both genetic liability and a disadvantaged socioeconomic situation in childhood, the risk was considerably higher (hazard ratio=15.0, 10.3, and 5.7 for parental unemployment, single-parent household, and apartment living, respectively). Analyses in the larger population supported these results.The results indicate that children reared in families with a disadvantaged socioeconomic position have an increased risk for psychosis. There was also some support for an interaction effect, suggesting that social disadvantage increases this risk more in children with genetic liability for psychosis.
Comparative effectiveness of the tumour diagnostics, CA 19-9, CA 125 and carcinoembryonic antigen in patients with diseases of the digestive system.
Authors: K Sakamoto, Y Haga, R Yoshimura, H Egami, Y Yokoyama, M Akagi
Journal: Gut (1987)

Serum concentrations of CA 19-9, CA 125 and carcinoembryonic antigen (CEA) in 145 patients with gastrointestinal carcinomas and 89 with non-neoplastic diseases were determined to compare the clinical usefulness of these tumour markers. Significantly fewer positive cases were obtained with serum CA 19-9 (9%) and CA 125 (8%) tests than the CEA test (22%) (both p less than 0.05) in patients with benign diseases, while comparable sensitivities were achieved with the CA 19-9 (44%) test, the CA 125 (41%) test and the CEA test (47%) in those with a carcinoma. High incidences of raised concentrations of serum CA 19-9 and CA 125 were observed in case of cancer of the pancreas (CA 19-9: 87%, CA 125: 67%) and biliary tract (CA 19-9: 63%, CA 125: 48%). Combined tests of CA 19-9 and CA 125 revealed increments in the sensitivity (61%) and provided a higher specificity (87%) than that of the single CEA test (78%). These combined tests were most useful for a differential diagnosis of pancreatic carcinoma (97% positive) and biliary tract carcinoma (74%) from chronic pancreatitis (4%) and cholelithiasis (0%), respectively. Studies on the relations of clinical staging and serum concentrations of CA 19-9 and CA 125 revealed significant rises in cases of disseminated carcinoma. These results clearly show that serum CA 19-9 and CA 125 tests are most pertinent for diagnosing advanced carcinomas of organs in the digestive system.
Preliminary Results of Radiation Therapy Oncology Group 97-03: A Randomized Phase II Trial of Concurrent Radiation and Chemotherapy for Advanced Squamous Cell Carcinomas of the Head and Neck
Authors: A.S. Garden, J. Harris, E.E. Vokes, A.A. Forastiere, J.A. Ridge, C. Jones, E.M. Horwitz, B.S. Glisson, L. Nabell, J.S. Cooper, W. Demas, E. Gore
Journal: Journal of Clinical Oncology (2004)

To define further the role of concurrent chemoradiotherapy for patients with advanced squamous carcinoma of the head and neck.The Radiation Therapy Oncology Group developed this three-arm randomized phase II trial. Patients with stage III or IV squamous carcinoma of the oral cavity, oropharynx, or hypopharynx were eligible. Each of three arms proposed a radiation schedule of 70 Gy in 35 fractions. Patients on arm 1 were to receive cisplatin 10 mg/m(2) daily and fluorouracil (FU) 400 mg/m(2) continuous infusion (CI) daily for the final 10 days of treatment. Treatment on arm 2 consisted of hydroxyurea 1 g every 12 hours and FU 800 mg/m(2)/d CI delivered with each fraction of radiation. Arm 3 patients were to receive weekly paclitaxel 30 mg/m(2) and cisplatin 20 mg/m(2). Patients randomly assigned to arms 1 and 3 were to receive their treatments every week; patients on arm 2 were to receive their therapy every other week.Between 1997 and 1999, 241 patients were entered onto study; 231 were analyzable. Ninety-two percent, 79%, and 83% of patients on arms 1, 2, and 3, respectively, were able to complete their radiation as planned or with an acceptable variation. Fewer than 10% of patients had unacceptable deviations or incomplete chemotherapy in the three arms. Estimated 2-year disease-free and overall survival rates were 38.2% and 57.4% for arm 1, 48.6% and 69.4% for arm 2, and 51.3% and 66.6% for arm 3.We have demonstrated that three different approaches of concurrent multiagent chemotherapy and radiation were feasible and could be delivered to patients in a multi-institutional setting with high compliance rates.
Photodynamic therapy for dysplastic Barrett's oesophagus: a prospective, double blind, randomised, placebo controlled trial
Authors: R Ackroyd
Journal: Gut (2000)

<h3>BACKGROUND AND AIMS</h3> Photodynamic therapy (PDT) is a treatment in which cell damage is achieved by the action of light on a photosensitising agent. We have assessed the potential use of PDT in the ablation of Barrett9s oesophagus. <h3>METHODS</h3> Thirty six patients with dysplastic Barrett9s oesophagus receiving acid suppression medication with omeprazole were randomised to receive oral 5-aminolaevulinic acid (ALA) 30 mg/kg or placebo, followed four hours later by laser endoscopy. Follow up endoscopy was performed at one, six, 12, and 24 months. <h3>RESULTS</h3> Of 18 patients in the ALA group, a response was seen in 16 (median decrease in area in the treated region 30%; range 0–60%). In the placebo group, a decrease in area of 10% was observed in two patients with no change in 16 (median 0%; range 0–10%; treatment <i>v</i>placebo, p&lt;0.001). No dysplasia was seen in the columnar epithelium within the treatment area of any patient in the PDT group. However, in the placebo group, persistent low grade dysplasia was found in 12 patients (p&lt;0.001). There were no short or long term major side effects. The effects of treatment were maintained for up to 24 months. <h3>CONCLUSIONS</h3> This is the first randomised controlled trial of PDT for Barrett9s oesophagus. It demonstrates that ALA induced PDT can provide safe and effective ablation of low grade dysplastic epithelium.
Telomerase activity distinguishes between neuroblastomas with poor prognosis
Authors: C. Poremba, H. Willenbring, B. Hero, H. Christiansen, K.-L. Schäfer, C. Brinkschmidt, H. Jürgens, W. Böcker, B. Dockhorn-Dworniczak
Journal: Annals of Oncology (1999)
Renal Insufficiency and Heart Failure
Authors: Finlay A. McAlister, Justin Ezekowitz, Marcello Tonelli, Paul W. Armstrong
Journal: Circulation (2004)

The prevalence, prognostic import, and impact of renal insufficiency on the benefits of ACE inhibitors and beta-blockers in community-dwelling patients with heart failure are uncertain.We analyzed data from a prospective cohort of 754 patients with heart failure who had ejection fraction, serum creatinine, and weight measured at baseline. Median age was 69 years, and 43% had an ejection fraction > or =35%. By the Cockcroft-Gault equation, 118 patients (16%) had creatinine clearances < or =30 mL/min and 301 (40%) had creatinine clearances between 30 and 59 mL/min. During follow-up (median 926 days), 385 patients (37%) died. Even after adjustment for all other prognostic factors, survival was significantly associated with renal function (P=0.002) in patients with either systolic or diastolic dysfunction; patients exhibited a 1% increase in mortality for each 1-mL/min decrease in creatinine clearance. The associations with 1-year mortality reductions were similar for ACE inhibitors (OR 0.46 [95% CI 0.26 to 0.82] versus OR 0.28 [95% CI 0.11 to 0.70]) and beta-blockers (OR 0.40 [95% CI 0.23 to 0.70] versus OR 0.41 [95% CI 0.19 to 0.85]) in patients with creatinine clearances <60 mL/min versus > or =60 mL/min, although these drugs were used less frequently in patients with renal insufficiency.Renal insufficiency is more prevalent in patients with heart failure than previously reported and is an independent prognostic factor in diastolic and systolic dysfunction. ACE inhibitors and beta-blockers were associated with similar reductions in mortality in patients with and without renal insufficiency.
TPMT in the treatment of Crohn's disease with azathioprine
Authors: L Lennard
Journal: Gut (2002)

Azathioprine induced profound myelosuppression linked to TPMT deficiency has now been documented in many patient groups, including those with Crohn9s disease. At the start of azathioprine or mercaptopurine therapy, measurement of TPMT activity has a role in identifying the 1 in 300 patients who are at risk of severe myelosuppression when treated with standard thiopurine dosages. During the initial months of azathioprine therapy a knowledge of TPMT status warns of early bone marrow toxicity. In patients established on azathioprine these is no clear evidence to suggest that TPMT is predictive of clinical response or drug toxicity, indicating a role for TPMT in the prediction of early events rather than long term control. In patients with Crohn9s disease on long term azathioprine therapy, it is clear that myelosuppression, particularly leucopenia, is caused by other factors in addition to variable TPMT activity and therefore monitoring of blood cell counts throughout treatment is essential.
Abnormal iron metabolism in fibroblasts from a patient with the neurodegenerative disease hereditary ferritinopathy
Authors: Ana G Barbeito, Thierry Levade, Marie B Delisle, Bernardino Ghetti, Ruben Vidal
Journal: Molecular Neurodegeneration (2010)

Abstract Background Nucleotide duplications in exon 4 of the ferritin light polypeptide (FTL) gene cause the autosomal dominant neurodegenerative disease neuroferritinopathy or hereditary ferritinopathy (HF). Pathologic examination of patients with HF has shown abnormal ferritin and iron accumulation in neurons and glia in the central nervous system (CNS) as well as in cells of other organ systems, including skin fibroblasts. To gain some understanding on the molecular basis of HF, we characterized iron metabolism in primary cultures of human skin fibroblasts from an individual with the FTL c.497_498dupTC mutation. Results Compared to normal controls, HF fibroblasts showed abnormal iron metabolism consisting of increased levels of ferritin polypeptides, divalent metal transporter 1, basal iron content and reactive oxygen species, and decreased levels of transferrin receptor-1 and IRE-IRP binding activity. Conclusions Our data indicates that HF fibroblasts replicate the abnormal iron metabolism observed in the CNS of patients with HF. We propose that HF fibroblasts are a unique cellular model in which to study the role of abnormal iron metabolism in the pathogenesis of HF without artifacts derived from over-expression or lack of endogenous translational regulatory elements.
Patterns of GI disease in adulthood associated with mutations in the CFTR gene
Authors: M. Wilschanski, P. R Durie
Journal: Gut (2007)

There has been tremendous growth in the population of adults with cystic fibrosis (CF). This demographic change has created the need for special clinics to care for adults with CF and has resulted in an awakening of interest in CF among physicians caring for adults. The protean and varied manifestations of CF disease in multiple organs call for expanded knowledge of the condition among physicians in a wide variety of subspecialties, including, but not limited to, pulmonary medicine, gastroenterology, hepatology, clinical nutrition, endocrinology, infectious diseases, rheumatology and andrology. This review will focus on disease pathobiology of the gastrointestinal and hepatic manifestations of CF disease which the internist is likely to encounter.

We will first examine the clinical manifestations of CF disease that are directly associated with loss of function of the cystic fibrosis transmembrane regulator (CFTR) protein and then summarise those which are secondary. We will elaborate the challenges of establishing or excluding a CF diagnosis in patients who present de novo in adulthood, with particular attention to conditions with CF-like phenotypes that are associated with an increased frequency of mutations in the CFTR gene. Finally, we will briefly discuss emerging knowledge of the potential contribution of mutations in the CFTR gene to other complex genetic conditions.

Over the past three decades the most striking result of advances in the care of patients with CF has been the dramatic improvement in survival. Whereas median survival in the United States was only 16 years in 1970, it has risen to over 32 years in 2005. For patients born in the 1990s median survival is predicted to exceed 40 years.1 Of patients born in the United Kingdom in 1980, 82% were alive at age 20, whereas for children born in 1990, 96.5% are alive at age 15 (fig 1).2 As …
Pepsin 1 secretion in chronic peptic ulceration.
Authors: V Walker, W H Taylor
Journal: Gut (1980)

In patients with peptic ulceration, both vagal stimulation by insulin hypoglycaemia and stimulation by pentagastrin cause pepsin 1 to be secreted into gastric juice. There is a secretory threshold for pepsin 1, below which only pepsins 3 and 5 are secreted. Pepsin 1 accounts for an increasing proportion of the total peptic activity/ml of gastric juice as the total activity increases. Higher concentrations of pepsin 1 in the basal gastric secretion occurred significantly more frequently in patients with duodenal ulcer than with gastric ulcer. In these patients there may be an increased 9background9 secretory drive.