tbuckley/cabot-search huggingface dataset:
A Comparison of Verapamil and Propranolol for the Initial Treatment of Hypertension
Authors: Luigi X. Cubeddu
Journal: JAMA (1986)

We compared verapamil and propranolol hydrochloride for monotherapy of hypertension. Verapamil lowered blood pressure (BP) more effectively than propranolol in black and white patients. Verapamil was equally effective in blacks and whites, whereas propranolol was more effective in whites. Heart rate was reduced by 6.0 beats per minute by verapamil, and by 13.6 beats per minute by propranolol. In blacks, verapamil lowered systolic BP 16.9 vs 8.1 mm Hg for propranolol; verapamil reduced diastolic BP 12.8 vs 8.6 mm Hg for propranolol. In whites, verapamil lowered systolic BP 19.0 vs 12.7 mm Hg for propranolol; verapamil reduced diastolic BP 16.7 vs 12.3 mm Hg for propranolol. Increases in systolic BP were observed in 22% and 3.4% of patients receiving propranolol and verapamil, respectively. The PR interval was increased from 163.5 to 174.9 ms for verapamil vs 160.3 to 164.4 ms for propranolol. Constipation (15%) and headaches (10%) were most frequent complaints for verapamil vs fatigue (18%) and dizziness (7%) for propranolol. Changes in blood biochemistry values were of small magnitude. We conclude that verapamil monotherapy is a safe and effective means of achieving BP control in patients with essential hypertension.
Infection and SLE
Authors: A L Hepburn
Journal: Annals of the Rheumatic Diseases (2002)

Soluble TNF receptor treatment does not affect raised TGFβ levels in RAWe read with interest the report by Drynda et al demonstrating that treatment of rheumatoid arthritis (RA) with anti-tumour necrosis factor α (anti-TNFα) induces subtle changes in the cytokine network such as down regulation of the proinflammatory cytokine interleukin 6 (IL6), but does not affect the persistently high plasma levels of transforming growth factor β (TGFβ). 1 Furthermore, they suggest that the latter finding indicates the existence of as yet unknown mechanisms for TGFβ overexpression in RA that may predispose a patient to severe infections and altered tumour defence.Complementary to the observations noted above are our findings using DNA microarray in patients with RA treated with TNF antagonists as compared with patients with RA treated with methotrexate and healthy controls. 2A total of 12 000 genes were analysed (human genome U 95 A Array-Affimetrix) and a variety of gene functions, including apoptosis, transcription factors, cell survival, antigen presentation, cartilage degradation, B and T cell function, intracellular signals, transcription genes, adhesion molecules, inflammatory mediators, clotting factors, HLA class II molecules, oncogenes, cytokine production, and cytokine receptor expression, were altered (up or down regulated) in the group receiving TNF antagonists.Of interest, several proinflammatory cytokine receptors including interferon γ, TNF, IL10, and TGFβ were found to be down regulated.Therefore, pathway signalling of these cytokines including TGFβ may be impaired if their receptors are down regulated.Altered expression of these genes' function, alone or in combination, may have an impact on the predisposition to infection and tumour defence.Such is the case for the induced TNFα inhibitor down regulation in the expression of C9, B and T cell functions, signalling cascade (↓ Jun B), adhesion molecules, heat shock proteins, and antigen presentation, and the predisposition to infection.Likewise, TNF antagonists also regulate the expression of oncogenes, such as Jun B, c-myc, fos and ras, which may have an impact on tumour defence.Therefore, our study with DNA microarray confirms and expands the immunomodulatory functions of TNF antagonists.Data, however, seem to suggest that the increased predisposition to develop infection and altered tumour defence may not be related to increased plasma levels of TGFβ because its receptors are down regulated, but rather to dysregulation of gene expression of other molecules induced by, the TNF antagonists.
Is Atherosclerosis a Disorder of Intramitochondrial Respiration?
Authors: ARTHUR F. WHEREAT
Journal: Annals of Internal Medicine (1970)

Recent interest in the relationship of carbon monoxide to the development of coronary artery disease has implicated disturbances of cellular respiration in the pathogenesis of atherosclerosis. The arterial wall is an active participant in the atherosclerotic process. Arterial fatty acid synthesis takes place in the mitochondria and is regulated by the reduced nicotinamide-adenine dinucleotide to nicotinamide-adenine dinucleotide (NADH/NAD+) ratio. Carbon monoxide and other respiratory inhibitors in our environment cause an abrupt increase in the mitochondrial NADH/NAD+ and consequently greatly stimulate lipid synthesis within the artery. It is suggested that this is the pathogenetic sequence by which carbon monoxide causes increased lipid synthesis and lesion development in the artery.
ABC of Ophthalmology. General medicine and visual side effects.
Authors: P A Gardiner
Journal: BMJ (1979)

Blurring: the major presenting-symptom Many general diseases may affect the eye or present with ocular signs (see list).For example, thyroid disease may present with double vision as the primary complaint, and many of the collagen diseases present primarily with eye signs.Conditions such as Still's disease, spondylitis, and other rheunatoid conditions may be heralded by visual changes caused by -uveitis and choroiditis.Nearly all the ocular conditions mentioned are described by the patient as blurring of vision-if they are mentioned at all.Patients often think .that eye disorders are a natural expectation in the course of a general, disease.Therefore thorough case-history taking should include a specific yroid exophthclmos -reference to vision.Many of these conditions are potentially blinding if hyroid unrecognised and untreated.
Modification of the Fontan Procedure
Authors: Hillel Laks, Abbas Ardehali, Peter W. Grant, Lester Permut, Alon Aharon, Micheal Kuhn, Josephine Isabel-Jones, Alvaro Galindo
Journal: Circulation (1995)

Background A modification of the Fontan procedure with unidirectional cavopulmonary connection is described in which the superior vena cava (SVC) is connected to the left pulmonary artery (PA) and the inferior vena cava (IVC) is connected to the right PA via a lateral tunnel with a snare-controlled, adjustable atrial septal defect (ASD). This allows matching of the SVC and IVC flows with the lung of appropriate size. The obligatory left Glenn shunt provides an adequate arterial oxygen saturation, and the elevation in SVC pressure is well tolerated. The adjustable ASD allows selective decompression of the IVC that maintains cardiac output and reduces fluid accumulation in the serous cavities. Methods and Results Since March 1992, we have performed this procedure in 18 patients. There were 17 children and 1 adult. Median age was 3 years and 9 months (range, 13 months to 36 years). Six patients had been staged with a previous bidirectional Glenn shunt. Preoperative cardiac catheterization revealed a PA pressure of 13±2 mm Hg and a transpulmonary gradient of 5±3 mm Hg. Ventricular function was satisfactory in all patients. At the completion of bypass, the pressures in the SVC and IVC were 16±4 mm Hg and 10±3 mm Hg, respectively ( P &lt;.01). The left atrial pressure was 6.0±3.0 mm Hg and the arterial O 2 saturation on 100% oxygen was 93±3%. There was one death as a result of intractable atrial arrhythmias. The remaining 17 patients had a mean hospital stay of 9.7 days (6 to 18 days). The length of pleural drainage was 7±3 days. The ASD was adjusted in 11 patients before discharge. Oxygen saturation at discharge was 85.4±4%. Nine patients had repeat catheterization. The ASD was completely closed in 6 patients, an average of 2.5 months after surgery (range, 3 weeks to 5 months). After ASD closure, the arterial oxygen saturation was 96±3%, and the SVC and IVC pressures were both 13±3 mm Hg. Conclusions The Fontan procedure with unidirectional cavopulmonary connection and adjustable ASD has several advantages that may reduce mortality and morbidity for the high-risk Fontan candidate.
Myogenic Hyperuricemia
Authors: Ikuo Mineo, Norio Kono, Naoko Hara, Takao Shimizu, Yuya Yamada, Masanori Kawachi, Hiroaki Kiyokawa, Yan Lin Wang, Seiichiro Tarui
Journal: New England Journal of Medicine (1987)

To identify the mechanism of hyperuricemia in glycogen storage diseases (glycogenoses) that affect muscle, we studied the effects of exercise and prolonged rest on purine metabolism in two patients with glycogenosis type III (debrancher deficiency), one patient with type V (muscle phosphorylase deficiency), and one patient with type VII (muscle phosphofructokinase deficiency). All had hyperuricemia except for one patient with glycogenosis type III. Plasma concentrations of ammonia, inosine, and hypoxanthine increased markedly in all the patients after mild leg exercise on a bicycle ergometer. The plasma urate concentrations also increased, but with a delayed response. Urinary excretion of inosine, hypoxanthine, and urate increased greatly after exercise, consistently with the increases in plasma levels. Hypoxanthine and urate concentrations were extremely high in the plasma and urine of the patient with glycogenosis type VII. With bed rest, the plasma hypoxanthine level returned to normal within a few hours, and the plasma urate concentration decreased from 18.6 to 10.6 mg per deciliter (1106 to 630 μmol per liter) within 48 hours. Similarly, the urinary excretion of these purine metabolites was reduced by bed rest. These findings indicate that muscular exertion in patients with glycogenosis types III, V, and VII causes excessive increases in blood ammonia, inosine, and hypoxanthine due to accelerated degradation of muscle purine nucleotides. These purine metabolites subsequently serve as substrates for the synthesis of uric acid, leading to hyperuricemia. (N Engl J Med 1987; 317: 75–80.)
[162] LAMIVUDINE MONOPROPHYLAXIS PREVENTS HBV INFECTION IN RECIPIENTS UNDERGOING LIVE DONOR LIVER TRANSPLANTATION BECAUSE OF NON-HBV RELATED DISEASES, HAVING THEIR GRAFTS FROM CORE-ANTIBODY POSITIVE DONORS
Authors: Z. Karasu, M. Akyildiz, T. Ozacar, F. Yilmaz, U.S. Akarca, G. Ersoz, F. Gunsar, U. Aydin, M. Kilic, T. Ilter
Journal: Journal of Hepatology (2007)
Diurnal Variation in Oral Glucose Tolerance: Blood Sugar and Plasma Insulin Levels Morning, Afternoon, and Evening
Authors: R. J. Jarrett, I. A. Baker, H. Keen, N. W. Oakley
Journal: BMJ (1972)

Twenty-four subjects received three oral glucose tolerance tests, in the morning, afternoon, and evening of separate days. The mean blood sugar levels in the afternoon and evening tests were similar, and they were both significantly higher than those in the morning test. Plasma immunoreactive insulin levels, however, were highest in the morning test. The pattern of insulin levels during the afternoon and evening tests resembled that described as typical of maturity-onset diabetes.
Frequent CALR exon 9 alterations in JAK2 V617F-mutated essential thrombocythemia detected by high-resolution melting analysis
Authors: K-H Lim, Y-C Chang, C Gon-Shen Chen, H-C Lin, W-T Wang, Y-H Chiang, H-I Cheng, N-W Su, J Lin, Y-F Chang, M-C Chang, R-K Hsieh, Y-Y Kuo, W-C Chou
Journal: Blood Cancer Journal (2015)

Essential thrombocythemia (ET) is a clonal hematopoietic stem cell neoplasm and one of the classic BCL-ABL1-negative chronic myeloproliferative neoplasm (MPN), which also includes polycythemia vera and primary myelofibrosis (PMF).1 Recently, two seminal studies discovered a high frequency of somatic calreticulin (CALR) mutations in patients with JAK2/MPL-unmutated ET and PMF.2, 3 The pattern of most CALR mutations in MPN is heterozygous indels in exon 9 causing one-base pair (bp) reading frameshift. CALR mutations have been shown to have important diagnostic and prognostic significance in ET and PMF patients,2, 3, 4 and will likely be incorporated into the World Health Organization (WHO) diagnostic criteria for MPN. In vitro studies on the molecular pathogenesis of CALR mutations in MPN have shown controversial results in regard to the involvement and/or activation of the JAK/STAT signaling pathway,2, 3 and the exact pathogenesis of CALR mutations is not yet completely understood at the present time.5
The Medical Renaissance of the 16th Century
Authors: Guenter B. Risse
Journal: JAMA (1986)

Papers from a conference held at Corpus Christi College, Cambridge University, in September 1983 constitute the core of this most informative work. Under the sponsorship of the Wellcome Trust and the British Academy, a number of prominent historians specializing in 16th-century medicine reviewed a number of key issues, including medical practice, surgery, education, pharmaceutical research, textual analysis, and reform movements. Although the presentations deliberately avoided dealing comprehensively with the entire historical period—the Vesalian and Harveian revolutions were not inluded—the book provides interested readers with a whole range of new information and insights. We learn, for example, from Garcia Ballester about Morisco practitioners in Spain, while Palmer presents a vivid sketch of Venetian apothecaries. Medical teaching and research in Paris and Padua are described by Lonie and Cunningham, respectively. Other contributions focus on the "changing fortunes of a traditional text," the<i>Canon</i>of Avicenna, followed by Berengario da Carpi's anatomic teaching,
Efficacy of a β-adrenergic receptor antagonist, propranolol, in preventing ischaemic ventricular fibrillation: dependence on heart rate and ischaemia duration
Authors: J Aupetit
Journal: Cardiovascular Research (1998)

Objectives: To investigate the prevention of ventricular fibrillation with a β-adrenergic receptor (β-AR) antagonist in anaesthetized, open-chest pigs in a model of ischaemia, intended to reproduce what happens either in anginal attack or in the first hour of infarction. Methods: Ventricular fibrillation threshold (VFT) was determined with trains of diastolic stimuli of 100 ms duration delivered by a subepicardial electrode inserted in the area subjected to ischaemia. Ischaemia was obtained by the complete occlusion of the left anterior descending coronary artery, either near its origin during brief but increasing periods (30, 60, 90, 120, 150, 180, 240, 300 s), or half-way from its origin for a much longer time (more than 60 min). Results: During transient proximal occlusion and isoprenaline infusion (0.25 μg/kg/min), propranolol (50 μg/kg plus 2 μg/kg/min) attenuated both tachycardia and the fall in VFT to 0 mA. The shortening of MAP duration accompanying depolarization of the fibres was concurrently slowed down, and time to fibrillation prolonged (122±15 to 262±14 s, p<0.001). In the absence of isoprenaline infusion, propranolol exerted similar effects, but to a lesser degree, in proportion to heart rate dependent on sympathetic activity. In contrast, it became unable to raise VFT before and during ischaemia, when heart rate was kept constant by pacing. After persistent midportion occlusion, significant differences in VFT were found only at the 5th min, depending on whether heart rate was accelerated by isoprenaline (0.8±0.2 mA), left normal (1.8±0.3 mA) or slowed down by propranolol (1.6±0.3 mA). Later on, especially after 15 and 25 min of ischaemia, VFT, which was below 1.0 mA, did not appear to be influenced by the activation or blockade of β-ARs: spontaneous fibrillations were observed in the same number in this period with or without the administration of propranolol. Beyond 30 min after occlusion, the rise in VFT, subsequent to the first irreversible cell damage, also occurred in the same way. Conclusions: The prevention of ischaemic ventricular fibrillation by a β-AR antagonist, judged from VFT, is easily checked experimentally when ischaemia is only transitory, especially if sympathetic activity is high. The maintenance of VFT at a relatively high level is essentially related to the depressant effect on the sinus rate. The same animal model does not give support to an effective protection in the first hour of infarction. However, the control of heart rate may also be beneficial in these circumstances by attenuating systemic haemodynamic disorders.
Vascular response to hypoxia in humans.
Authors: R Curiel, J Perez-Gonzalez
Journal: Circulation (1980)

activities and sexual intercourse without pain."Cost-containment" arguments do not impress young, formerly active patients faced with those limitations.The cost of medical treatment of coronary atherosclerosis is poorly documented, and comparing the cost of medical therapy with surgical treatment is difficult.Certainly, physicians must be con- scious of the costs of the treatment that they recommend and, when possible, exert influence to control medical costs.However, we believe the most important result of any form of therapy is its effect on the patient and the patient's ability to achieve the goals he deems important in his life.The cost of disability and limitation of lifestyle is borne much more by the individual patient than by the country at large, and decisions regarding therapy of disabling and life- threatening conditions must be made with primary reference to the patient.Our goal in reporting the long-term follow-up of this sur- gical subset is to document the longevity and symptom control 5 years postoperatively.Life is filled with might-have-beens.When our critics state that without operation, "a large number of patients could have been maintained essentially symptom-free" despite the lack of symptom control of their preoperative medical programs, that is speculation.No data are cited to indicate that such widespread relief of symptoms would likely have occurred.What did occur was that two of the 200 surgically treated patients died of cardiac causes in 5 years and 80% of them were asymptomatic.That is fact.
Bacillus Calmette&amp;ndash;Gu&amp;eacute;rin Perfusion Therapy for the Treatment of Transitional Cell Carcinoma in situ of the Upper Urinary Tract
Authors: Norio Nonomura, Yutaka Ono, Masahiro Nozawa, Tatsunari Fukui, Yasunori Harada, Kazuo Nishimura, Natsuki Takaha, Shiro Takahara, Akihiko Okuyama
Journal: European Urology (2000)
Insulin Resistance and Hyperinsulinemia Are Related to Plasma Aldosterone Levels in Hypertensive Patients
Authors: Antonio Perciaccante, Alessandra Fiorentini, Rosita Valente, Angelo Di Stefano, Luigi Tubani
Journal: Diabetes Care (2007)

We read with interest the article by Colussi et al. (1) on the relationship between insulin resistance, hyperinsulinemia, and aldosterone levels in hypertensive patients. The authors observed that the homeostasis model assessment index is correlated with plasma aldosterone. They conclude that in patients with hypertension, this relationship …
Thunderstorm‐asthma and pollen allergy
Authors: G. D'Amato, G. Liccardi, G. Frenguelli
Journal: Allergy (2006)

Thunderstorms have been linked to asthma epidemics, especially during the pollen seasons, and there are descriptions of asthma outbreaks associated with thunderstorms, which occurred in several cities, prevalently in Europe (Birmingham and London in the UK and Napoli in Italy) and Australia (Melbourne and Wagga Wagga). Pollen grains can be carried by thunderstorm at ground level, where pollen rupture would be increased with release of allergenic biological aerosols of paucimicronic size, derived from the cytoplasm and which can penetrate deep into lower airways. In other words, there is evidence that under wet conditions or during thunderstorms, pollen grains may, after rupture by osmotic shock, release into the atmosphere part of their content, including respirable, allergen-carrying cytoplasmic starch granules (0.5-2.5 microm) or other paucimicronic components that can reach lower airways inducing asthma reactions in pollinosis patients. The thunderstorm-asthma outbreaks are characterized, at the beginning of thunderstorms by a rapid increase of visits for asthma in general practitioner or hospital emergency departments. Subjects without asthma symptoms, but affected by seasonal rhinitis can experience an asthma attack. No unusual levels of air pollution were noted at the time of the epidemics, but there was a strong association with high atmospheric concentrations of pollen grains such as grasses or other allergenic plant species. However, subjects affected by pollen allergy should be informed about a possible risk of asthma attack at the beginning of a thunderstorm during pollen season.
Playing the guru
Authors: T. Greenhalgh
Journal: BMJ (1999)

An expert is, by modern definition, a person who comes from a long way away and gives a Powerpoint presentation.

Several months ago I was asked by a group of Italian specialist physicians to speak at their annual bash in Florence. They sent details of the top class hotel and extensive fringe programme, which I carefully scrutinised, and of the conference itself, which I did not. It all seemed like the ultimate free lunch.

My keynote lecture made liberal use of …
Lymphangioma of the Oesophagus Diagnosis and Treatment by Endoscopic Polypectomy
Authors: J. Armengol-Miro, F. Ramentol, J. Salord, M. Puig Costa, A. Palacin, M. Vidal
Journal: Endoscopy (1979)

Finding a lymphangioma in the upper digestive tract is a rather infrequent event. A case of a 64-year-old man is reported. Diagnosis was made in the course of an endoscopic oesophagogastroduodenal examination and tumor excision with a diathermy snare at the same time. Two years after resection there was no sign of recidivation of the tumor.
Retroviral-mediated gene transfer restores IL-12 and IL-23 signaling pathways in T cells from IL-12 receptor β1-deficient patients
Authors: Marita Bosticardo, Iren Witte, Claire Fieschi, Francesco Novelli, Jean-Laurent Casanova, Fabio Candotti
Journal: Molecular Therapy (2004)

<h2>Abstract</h2> Genetic deficiency of human IL-12 receptor β1 chain (IL-12Rβ1) results in increased vulnerability to weakly pathogenic strains of <i>Mycobacteria</i> and <i>Salmonella</i>. This phenotype results from the combined lack of IL-12 and IL-23 signaling as both cytokine receptors share IL-12Rβ1. Such infections can be treated by administration of antibiotics and IFN-γ; however, patients can succumb to infections despite these treatments. Reversion of patients' susceptibility by corrective gene transfer could prevent the infectious episodes, thus providing a beneficial alternative. We therefore evaluated the feasibility of retroviral-mediated gene correction of T cells obtained from patients carrying "null" mutations of IL-12Rβ1. Transduction of the IL-12Rβ1 cDNA restored the expression of IL-12Rβ1 and resulted in the reconstitution of a functional IL-12 signaling pathway, as demonstrated by STAT4 phosphorylation and IFN-γ production. IFN-γ production in response to IL-23 was also corrected after gene transfer. These results indicate that the biological defects of T cells from patients carrying IL-12Rβ1 deficiency can be corrected by gene transfer and form the basis for further development of gene therapy for this disease.