tbuckley/cabot-search huggingface dataset:
Subpulmonary obstruction in congenitally corrected transposition of the great arteries due to ventricular membranous septal aneurysms.
Authors: E Krongrad, K Ellis, C N Steeg, F O Bowman, J R Malm, W M Gersony
Journal: Circulation (1976)

The clinical, hemodynamic, and angiographic observations, as well as the surgical approach used for repair in three patients with congenitally corrected transposition of the great arteries and ventricular membranous septal aneurysms, are presented. In two of the three patients the membranous septal aneurysm caused subpulmonary obstruction, with 94 and 125 mm Hg systolic gradients. In each patient the aneurysm was demonstrated by angiocardiography, which also showed differences in size and shape with cardiac systole and diastole. Review of the previously described reports indicates that patients with congenitally corrected transposition often display various forms of pulmonary outflow obstruction and when a ventricular membranous septal aneurysm exists, a significant subpulmonary obstruction is present in most patients. The unique anatomic relationship between the pulmonary artery and a ventricular membranous septal aneurysm in patients with transposition of the great arteries with and without atrioventricular discordance explains why subpulmonary obstruction sometimes develops.
Abstract 5579: Selenomethionine does not protect against testosterone plus 17 beta-estradiol-induced prostate carcinogenesis and prostatic oxidative stress in NBL rats
Authors: Nur Ozten, Michael J. Schlicht, Maarten C. Bosland
Journal: Cancer Research (2011)

Abstract Previous studies with selenium and/or vitamin E in prostate carcinogenesis animal models have been negative, but these models may not involve oxidative stress mechanisms. Selenium and vitamin E have been the subject of one of the largest trials ever conducted, SELECT, which was discontinued because there was no difference between the study arms and there were side effects, including an increased chance of developing diabetes mellitus with the use of selenium. We previously found that selenomethionine supplementation did not prevent prostate cancer in NBL rats treated with testosterone plus 17 beta-estradiol (T+E2), a model that does involve sex-hormone induced oxidative stress mechanisms and prostatic inflammation; this result was fully predictive of the outcome of the SELECT trial. Based on the outcomes of SELECT and our NBL rat study, we hypothesized that selenium has no protective effect against T+E2-induced prostate cancer development because it does not protect against oxidative stress. In the present study, we examined the potential of selenomethionine to modulate prostatic oxidative stress and induction of dysplasia and inflammation in the T+E2-treated NBL rat. Nbl/Crl rats were treated for 16 weeks with T+E2 by Silastic implants and were fed a natural ingredient control diet (NIH-07) with or with L-selenomethionine at a concentration of 1.5 or 3.0 mg/kg (as selenium). These diets were initiated one week post hormone implantation. T+E2 significantly increased immunohistochemical staining for 8-hydroxy-deoxyguanosine (8-OHdG) in prostatic ducts, and in the lateral and dorsal prostate which are the main sites of T+E2-induced inflammation and preneoplasia after 16 weeks of hormone treatment, and in the seminal vesicles. However, selenomethionine did not reduce these effects and did not, by itself, change 8OHdG staining. There was a lobe-specific differential response and modulation of antioxidant enzymes. Glutathione peroxidase activity and protein expression level of manganese superoxide dismutase were induced by T+E2, which effects were counteracted by selenomethionine in the dorsolateral prostate, which is the main site of T+E2-induced inflammation and preneoplasia occurring after 16 weeks of hormone treatment. However, selenomethionine did not influence the induction by T+E2 of marked inflammation and dysplasia in the lateral prostate. These findings partially explain the negative outcome of our previous NBL rat study and is consistent with the negative results of the SELECT trial. (Supported in part by Grant No. CA104334) Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 5579. doi:10.1158/1538-7445.AM2011-5579
An unusual case of calf pain
Authors: N. Cassar, B. Dunjic, K. Cassar
Journal: BMJ (2010)

Thank you for your interest in spreading the word about The BMJ.NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address. Username * Your Email * Send To * You are going to email the following An unusual case of calf pain Your Personal Message CAPTCHA This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
p53-Dependent and p53-Independent Activation of Autophagy by ARF
Authors: Wassim M. Abida, Wei Gu
Journal: Cancer Research (2008)

The ARF tumor suppressor is a crucial component of the cellular response to hyperproliferative signals, including oncogene activation, and functions by inducing a p53-dependent cell growth arrest and apoptosis program. It has recently been reported that the ARF mRNA can produce a smARF isoform that lacks the NH(2)-terminal region required for p53 activation. Overexpression of this isoform can induce autophagy, a cellular process characterized by the formation of cytoplasmic vesicles and the digestion of cellular content, independently of p53. However, the level of this isoform is extremely low in cells, and it remains unclear whether the predominant form of ARF, the full-length protein, is able to activate autophagy. Here, we show that full-length ARF can induce autophagy in 293T cells where p53 is inactivated by viral proteins, and, notably, expression of the NH(2)-terminal region alone, which is required for nucleolar localization, is sufficient for autophagy activation, independently of p53. Given the reported ability of p53 to induce autophagy, we also investigated the role of p53 in ARF-mediated autophagy induction. We found that full-length ARF expression induces p53 activation and promotes autophagy in a p53-positive cell line, and that ARF-mediated autophagy can be abrogated, at least in part, by RNAi-mediated knockdown of p53 in this cellular context. Thus, our findings modify the current view regarding the mechanism of autophagy induction by ARF and suggest an important role for autophagy in tumor suppression via full-length ARF in both p53-dependent and p53-independent manners, depending on cellular context.
Plasma elastase levels and the development of the adult respiratory distress syndrome.
Authors: S C Donnelly, I MacGregor, A Zamani, M W Gordon, C E Robertson, D J Steedman, K Little, C Haslett
Journal: American Journal of Respiratory and Critical Care Medicine (1995)

Inflammatory cells, particularly neutrophil granulocytes, have been implicated in the pathogenesis of the adult respiratory distress syndrome (ARDS). In this study, we investigated whether a relationship exists between neutrophil elastase in the plasma of multiple-trauma patients on initial hospital presentation and the subsequent development of lung injury and ARDS. Sixty-one multiple-trauma patients were enrolled prospectively. Neutrophil elastase was measured by a specific radioimmunoassay, and analysis was performed by nonparametric statistical methods. A highly significantly elevated plasma elastase level was found in patients who progressed to ARDS (median 217 ng/ml, range 127 to 480) (n = 8) compared with those who did not (median 117 ng/ml, range 21.4 to 685) (n = 53) (p = 0.009). Significant correlation was found between initial elastase values and subsequent requirement for mechanical ventilation (p = 0.01), lowest arterial oxygen saturation/oxygen supplementation recorded (p = 0.003), and organ failure score (p = 0.006). This study shows that within minutes of the initiating trauma event, there is evidence of enhanced neutrophil degranulation as manifested by elevated levels of immunoreactive neutrophil elastase in the peripheral blood. The level of this enzyme correlates with the degree of subsequent lung injury and ARDS. These findings reinforce the importance of neutrophils and their secretory products in early ARDS disease pathogenesis.
Osteoporosis in Hemochromatosis: Iron Excess, Gonadal Deficiency, or Other Factors?
Authors: Terrence Diamond
Journal: Annals of Internal Medicine (1989)

Study Objective: To define the prevalence, severity, type and pathogenesis of osteopenia in idiopathic hemochromatosis. Design: Prospective study conducted over 18 months. Setting: Tertiary care center. Subjects: Twenty-two men with idiopathic hemochromatosis and 20 age-matched controls. There were 5 hypogonadal patients, 9 eugonadal nonvenesected patients, and 8 eugonadal venesected patients. Measurements and Main Results: All patients and controls were evaluated by spinal radiography, spinal and fore-arm bone mineral density estimations, dynamic skeletal histomorphometry, and serum biochemistry. Ten patients (45%; 95% CI, 24% to 68%) had osteoporosis as defined by spinal and forearm bone density measurements. Trabecular bone volumes were significantly reduced in the patients (the difference in means between patients and age-matched controls was 3.9%; CI, 1.3% to 6.7%). No patient had osteomalacia. Hypogonadal men had lower bone mass measurements than eugonadal men (radial bone density: beta coefficient = -20. 5; CI, -29.2 to -11.8; trabecular bone volume: beta coefficient = -7. 1; CI, -10.8 to -3.3). Osteoid and osteoblastic surfaces and bone formation rates were significantly greater in the eugonadal venesected compared with the eugonadal nonvenesected persons (P < 0.05 for all measurements). Conclusions: A significant decrease in bone density is seen in idiopathic hemochromatosis, particularly when hypogonadism is present. Low serum free-testosterone concentrations rather than the calciotrophic hormones determine bone mass in this condition.
Kidney stones and hypertension: population based study of an independent clinical association.
Authors: F P Cappuccio, P Strazzullo, M Mancini
Journal: BMJ (1990)

OBJECTIVE--To test the hypothesis that kidney stone disease is more frequent among hypertensive men when the effect of possible confounders is allowed for. DESIGN--Cross sectional study of a sample of the male working population conducted as part of the 10 year follow up of a nationwide survey of the prevalence of cardiovascular risk factors. SETTING--The Olivetti factory in Pozzuoli, a suburban area of Naples. POPULATION--688 Male workers (87.9% of the male workforce) aged 21-68. INTERVENTIONS--Anthropometric and blood pressure measurements, blood tests, and administration of a detailed questionnaire aimed at detecting a history of urolithiasis. MAIN OUTCOME MEASURES--Prevalence of a history of urolithiasis among normotensive and untreated and treated hypertensive men adjusted for the possible confounding effects of age, body mass index, renal function, and serum urate and total calcium concentrations. RESULTS--Of the 688 participants 509 were normotensive. Of the remainder, 118 had untreated and 61 treated hypertension. The overall prevalence of a history of urolithiasis was 16.3% (112/688). The relative risk of hypertensive subjects having a history of kidney stones was twice that of the normotensive group (odds ratio 2.11; 95% confidence interval 1.17 to 3.81), the risk being higher when only treated hypertensives were considered (odds ratio 3.16; 95% confidence interval 1.75 to 5.71). The prevalence of a history of urolithiasis was 13.4% (68/509) in the normotensive subjects, 20.3% (24/118) in the untreated hypertensives, and 32.8% (20/61) in the treated hypertensives (p less than 0.001). The age adjusted relative risk in treated hypertensive men was higher than that in the normotensive group (Mantel-Haenszel pooled estimate of odds ratio 2.63; 95% confidence interval 2.23 to 3.10). CONCLUSION--An independent clinical association exists between the occurrence of urolithiasis and hypertension. The increased urinary calcium excretion commonly detected in hypertension may be the pathogenetic link.
Hospital Noise — Levels and Potential Health Hazards
Authors: Stephen A. Falk, Nancy F. Woods
Journal: New England Journal of Medicine (1973)

Abstract Hospital noise levels were measured in infant incubators, recovery room and two rooms of an acute-care unit. Sources of the noise were noted, and 24-hour measurements were made. The average noise levels were as follows: 57.7 dB(A) and 74.5 dB (linear) for the incubators; 65.6 dB(A) and 80.0 dB (linear) at patients' heads; 57.2 dB(A) and 69.8 dB (linear) for the recovery room; and for the acute care unit 60.1 dB(A) and 73.3dB (linear) for room 1 and 55.8 dB(A)and 68.1 dB (linear) for room 2. In the recovery room and acute-care unit noise levels were correlated with number of hospital staff. On the basis of present knowledge of the physiologic effects of noise, these noise levels probably stimulate the hypophyseal-adrenocortical axis of patients, exceed the noise threshold for peripheral vasoconstriction, pose a threat to hearing in patients receiving aminoglycosidic antibiotics and are incompatible with sleep. (N Engl J Med 289:774–781, 1973)
Gelatinous Degeneration of the Bone Marrow Mimicking Osseous Metastasis on 18F-FDG PET/CT
Authors: Ari Chong, Ho-Chun Song, Jong-Ryool Oh, Jung-Min Ha, Jung-Joon Min, Hee-Seung Bom, Yoo-Duk Choi, Ji Shin Lee
Journal: Clinical Nuclear Medicine (2012)

Gelatinous degeneration of the bone marrow is rare, and its pathogenesis is unknown. A 61-year-old man with rectal cancer, who was treated successfully with surgery and chemotherapy 1 year ago, underwent 18F-FDG PET/CT for restaging, which showed a focal hot spot in the left scapula mimicking osseous metastasis. Excision bone biopsy revealed gelatinous degeneration of the bone marrow.
EU offers incentives to firms to produce medicines for children
Authors: Rory Watson
Journal: BMJ (2006)

Pharmaceutical companies are being encouraged to develop medicines specifically for children, under European Union legislation approved this week.

The new rules, which are expected to come into force early next year, will reward firms that produce new paediatric drugs by giving them a six month extension to their patents. Manufacturers of orphan medicines for children will enjoy an extra two years of market exclusivity on top of the 10 years already in operation for adult drugs.

Francoise Grossetete, the French Conservative MEP who steered the legislation through the European Parliament, said that it would …
Long-term Follow-up of Surgically Treated Thyrotoxic Patients
Authors: A. D. McNeill, J. A. Thomson
Journal: BMJ (1968)

Review of 123 patients whose thyroidectomy for thyrotoxicosis had been performed more than five years previously showed that there were no deaths attributable to surgery, while one hundred patients (81.3%) had been rendered euthyroid. Varying degrees of hyperthyroidism had occurred in 15 (12.2%), and six of these were first diagnosed at follow-up. Hypothyroidism was present in eight (6.5%). Long-term complications of operation were found in 20 patients—subjective voice disturbance in 13, unsightly scars in 4, and hypoparathyroidism in 3.
The Influence of the General Medical Council on Education
Authors: A. P. Thomson
Journal: BMJ (1958)

influence of a strong president.Fortunately for the subsequent developmnents of the Council's activities, such a presi- dent was found in Sir Donald MacAlister, whose term of office (1904-31), by far the longest of any President, must be accounted that which has had the greatest influence on the Council's history.Nobody to-day would claim that the Council is our " Medical Parliament."By the press and the public it is chiefly regarded as " our High Court."But that it has become a model of organization for other professions and other countries is sufficient tribute to its success in achieving two aims which the framers of the 1858 Act may have regarded as incompatible-the serving of the public interest and the advancement of the medical profession.Many other books and articles, apart from those mentioned in the References, have also been consulted, but I am especially in- debted for help and advice to Mr.
THE PSYCHONEUROTIC FACTOR IN THE IRRITABLE HEART OF SOLDIERS
Authors: B. S. OPPENHEIMER
Journal: JAMA (1918)

In 1871, Da Costa published his observations On the Irritable Heart as seen among soldiers invalided for this malady during the Civil War. During the present war this condition has again become prominent and names such as disordered action of the heart (D. A. H.), effort syndrome, debility and neuro-circulatory asthenia are employed to describe the affection. The group includes all cases which present a well defined syndrome in which certain nervous and circulatory symptoms are associated with increased susceptibility to fatigue and in which no definite pathologic condition can be found to which to ascribe the clinical symptoms. The underlying pathogenic process is still unknown; and when we speak of the psychoneurotic factor in the irritable heart of soldiers, we do not imply an immediate causal relationship between the two, or that the symptoms of the two originate in the same way, but rather that possibly both groups may
Human Serum IgE against Two Major Allergens from Cow Hair and Dander: Determination of Affinity and Quantity of Antigen‐Specific IgE
Authors: P. Prahl, E. Nexø
Journal: Allergy (1982)

The quantity and quality of antigen-specific IgE against purified major allergens from cow hair and dander was measured by a double-antibody radioimmunoassay. In serum from patients with allergic asthma to cow the affinity constant varied from 1 to 150 X 10(9) l/mol and the number of antibody combining sites from 0.01 to 0.4 X 10-9 mol/l serum for each antigen.
Candidate Biomarker Discovery for Angiogenesis by Automatic Integration of Orbitrap MS1 Spectral- and X!Tandem MS2 Sequencing Information
Authors: Mark K. Titulaer
Journal: Genomics Proteomics & Bioinformatics (2013)

Abstract Candidate protein biomarker discovery by full automatic integration of Orbitrap full MS1 spectral peptide profiling and X!Tandem MS2 peptide sequencing is investigated by analyzing mass spectra from brain tumor samples using Peptrix. Potential protein candidate biomarkers found for angiogenesis are compared with those previously reported in the literature and obtained from previous Fourier transform ion cyclotron resonance (FT-ICR) peptide profiling. Lower mass accuracy of peptide masses measured by Orbitrap compared to those measured by FT-ICR is compensated by the larger number of detected masses separated by liquid chromatography (LC), which can be directly linked to protein identifications. The number of peptide sequences divided by the number of unique sequences is 9248/6911 ≈ 1.3. Peptide sequences appear 1.3 times redundant per up-regulated protein on average in the peptide profile matrix, and do not seem always up-regulated due to tailing in LC retention time (40%), modifications (40%) and mass determination errors (20%). Significantly up-regulated proteins found by integration of X!Tandem are described in the literature as tumor markers and some are linked to angiogenesis. New potential biomarkers are found, but need to be validated independently. Eventually more proteins could be found by actively involving MS2 sequence information in the creation of the MS1 peptide profile matrix.
Suppression of autophagy during liver regeneration impairs energy charge and hepatocyte senescence in mice
Authors: Takeo Toshima, Ken Shirabe, Takasuke Fukuhara, Toru Ikegami, Tomoharu Yoshizumi, Yuji Soejima, Tetsuo Ikeda, Shinji Okano, Yoshihiko Maehara
Journal: Hepatology (2014)

Autophagy is a homeostatic mechanism that regulates protein and organelle turnover and uses the amino acids from degraded proteins to produce adenosine 5′-triphosphate (ATP). We investigated the activity of autophagy-associated pathways in liver regeneration after partial hepatectomy (PHx) in liver-specific autophagy-related gene 5 (Atg5) knockout (KO) mice. Liver regeneration was severely impaired by 70% PHx, with a reduction in postoperative mitosis, but a compensating increase in hepatocyte size. PHx induced intracellular adenosine triphosphate and β-oxidation reduction as well as injured cellular mitochondria. Furthermore, PHx in Atg5 KO mice enhanced hepatic accumulation of p62 and ubiquitinated proteins. These results indicated that reorganization of intracellular proteins and organelles during autophagy was impaired in the regenerating liver of these mice. Up-regulation of p21 was associated with hepatocyte senescence, senescence-associated β-galactosidase expression, irreversible growth arrest, and secretion of senescence-associated molecules, including interleukin (IL)-6 and IL-8. Conclusion : These findings indicate that autophagy plays a critical role in liver regeneration and in the preservation of cellular quality, preventing hepatocytes from becoming fully senescent and hypertrophic. (Hepatology 2014;60:290–300)
Restricted Randomization in Randomized Controlled Trials-Reply
Authors: Douglas G. Altman
Journal: JAMA (1995)

<h3>In Reply.</h3> —We thank Drs ter Riet and Kessels for attempting to explain the similar sample sizes we found in treatment and control groups. Unfortunately, their suggestion of widespread use of a form of restricted randomization does not shed any new light on our findings. In our original article, we stated, "The strong tendency for the comparison groups to be of equal or similar sizes may be explained by unreported use of (1) restriction, usually blocking...." That explanation includes the model postulated by ter Riet and Kessels, which is just one of many different forms of restriction. Ter Riet and Kessels observe that our "model does not reflect randomized trial conduct in practice." Indeed, that just restates our main argument. The authors of the 96 reports stated or (more usually) implied use of simple, unrestricted randomization. Thereby, they, not we, specified the form of the model used. Furthermore, our approach
Coping With Violence Epidemic
Authors: Teri Randall
Journal: JAMA (1990)

WITHIN the last decade, injury and death from violence have become one of the most critical health problems this country faces. Many epidemiologists, stepping into what has traditionally been the domain of the criminal justice system, now claim that violence-prevention strategies might be found through public health perspectives and practices. "It's a direction in which public health has to move or it's going to be avoiding one of the most significant health problems," predicts Linda Saltzman, PhD, behavioral scientist-criminologist for the CDC's intentional injuries section, which originated as the violence epidemiology branch in 1983. Homicide has climbed the ranks to become the 11th leading cause of death in the United States, a rise attributed to both increased homicide rates and the elimination or treatment of certain infectious and chronic diseases. Among 15- to 24-year-olds, homicide ranks as the third leading cause of death. And among black males aged 15 to