tbuckley/cabot-search huggingface dataset:
Prevention of Gallstones during Weight Reduction
Authors: Nahum Mendez-Sanchez
Journal: Annals of Internal Medicine (1996)

Letters1 March 1996Prevention of Gallstones during Weight ReductionNahum Mendez-Sanchez, MD, MSc, Javier Lizardi-Cervera, MD, and Misael Uribe, MDNahum Mendez-Sanchez, MD, MScNational Institute of Nutrition Salvador Zubiran, Vasco de Quiroga No. 15, Tlalpan 14000, Mexico City, MexicoSearch for more papers by this author, Javier Lizardi-Cervera, MDNational Institute of Nutrition Salvador Zubiran, Vasco de Quiroga No. 15, Tlalpan 14000, Mexico City, MexicoSearch for more papers by this author, and Misael Uribe, MDNational Institute of Nutrition Salvador Zubiran, Vasco de Quiroga No. 15, Tlalpan 14000, Mexico City, MexicoSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-124-5-199603010-00017 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:Shiffman and associates [1] used three different doses [300, 600, and 1200 mg] of UDCA and found 600 mg/d to be highly effective in preventing gallstone formation in patients receiving a very-low-calorie diet. We point out that 1) obesity is the major clinical factor associated with gallstone formation [2]; 2) the risk for developing gallstones in obese persons is three to seven times higher than that in eutrophic persons [3]; and 3) the risk for gallstone formation in patients undergoing rapid weight reduction seems even greater (Table 1). We ask whether these rapid weight-loss programs with very-low-calorie ...References1. Shiffman ML, Kaplan GD, Brinkman-Kaplan V, Vickers FF. Prophylaxis against gallstone formation with ursodeoxycholic acid in patients participating in a very-low-calorie diet program. Ann Intern Med. 1995; 122:899-905. Google Scholar2. Diehl AK. Epidemiology and natural history of gallstone disease. Gastroenterol Clin North Am. 1991; 20:1-19. Google Scholar3. Stampfer MJ, Maclure KM, Colditz GA, Manson JE, Willett WC. Risk of symtomatic gallstone in women with severe obesity. Am J Clin Nutr. 1992; 55:652-8. Google Scholar4. Mendez-Sanchez N, Panduro A, Uribe M, et al. Low dose of ursodeoxycholic acid induces apolipoprotein A-1 gene expression and prolongates cholesterol nucleation time in patients with cholesterol gallstones [Abstract]. Hepatology. 1991; 14:148A. Google Scholar Author, Article, and Disclosure InformationAffiliations: National Institute of Nutrition Salvador Zubiran, Vasco de Quiroga No. 15, Tlalpan 14000, Mexico City, Mexico PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byEpidemiological features of the course of non-tumor mechanical jaundice (comparative clinical and statistical review) 1 March 1996Volume 124, Issue 5Page: 533KeywordsDietFatsNutritionObesityOverweightProphylaxisWeight loss Issue Published: 1 March 1996 Copyright & PermissionsCopyright © 1996 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Analyses of "Cerebrine" and "Medulline."
Authors: J. H. Long
Journal: JAMA (1893)

<h3>To the Editor:</h3> —At a meeting of the Chemical Section of the Chicago Academy of Sciences, held two months ago, Prof. M. Delafontaine of this city, presented some facts regarding tests of the substances known as "cerebrine" and "medulline," and somewhat more in detail than in the note in theJournalof August 26. This work having been criticised in certain quarters, both as regards methods and conclusions, I thought it worth while to make a new examination of the question, avoiding as far as possible sources of error. I accordingly obtained from a well-known Chicago druggist a bottle of each of the two Hammond preparations which I tested, with results agreeing fully with those of Prof. Delafontaine. These tests I considered, however, only as preliminary to more extended ones. For the fuller tests I secured through one of our leading wholesale drug houses four bottles of "cerebrine" and four
Primary Hepatic Lymphoma 1 Year After Resection of Hepatocellular Carcinoma
Authors: Atsushi Nonami, Katsuto Takenaka, Naoki Harada, Kentaro Kono, Kenjiro Kamezaki, Akihiko Numata, Kennosuke Karube, Toshihiro Miyamoto, Koji Nagafuji, Koichi Ohshima, Mine Harada
Journal: Journal of Clinical Oncology (2006)
Reduced Surface Tension Normalizes Static Lung Mechanics in a Rodent Chronic Heart Failure Model
Authors: Dani-Louise Dixon, Carmine G. De Pasquale, Hilde R. De Smet, Sonja Klebe, Sandra Orgeig, Andrew D. Bersten
Journal: American Journal of Respiratory and Critical Care Medicine (2009)

Chronic elevation of pulmonary microvascular pressure in chronic heart failure results in compensatory changes in the lung that reduce alveolar fluid filtration and protect against pulmonary microvascular rupture.To determine whether these compensatory responses may have maladaptive effects on lung function.Six weeks after myocardial infarction (chronic heart failure model) rat lung composition, both gross and histologic; air and saline mechanics; surfactant production; and immunological mediators were examined.An increase in dry lung weight, due to increased insoluble protein, lipid and cellular infiltrate, without pulmonary edema was found. Despite this, both forced impedance and air pressure-volume mechanics were normal. However, there was increased tissue stiffness in the absence of surface tension (saline pressure-volume curve) with a concurrent increase in both surfactant content and alveolar type II cell numbers, suggesting a novel homeostatic phenomenon.These studies suggest a compensatory reduction in pulmonary surface tension that attenuates the effect of lung parenchymal remodeling on lung mechanics, hence work of breathing.
Effect of Intensive Multifactorial Treatment Compared With Routine Care on Aortic Stiffness and Central Blood Pressure Among Individuals With Screen-Detected Type 2 Diabetes
Authors: Nanna B. Johansen, Morten Charles, Dorte Vistisen, Signe S. Rasmussen, Niels Wiinberg, Knut Borch-Johnsen, Torsten Lauritzen, Annelli Sandbæk, Daniel R. Witte
Journal: Diabetes Care (2012)

Diabetes is associated with increased brachial and central blood pressure and aortic stiffness. We examined the effect of intensive multifactorial treatment in general practice on indices of peripheral and central hemodynamics among patients with screen-detected diabetes.As part of a population-based screening and intervention study in general practice, 1,533 Danes aged 40-69 years were clinically diagnosed with screen-detected diabetes. General practitioners were randomized to provide intensive multifactorial treatment or routine care. After a mean follow-up of 6.2 years, an unselected subsample of 456 patients underwent central hemodynamic assessments by applanation tonometry. Central pressure was derived from the radial pulse wave. Aortic stiffness was assessed as carotid-femoral pulse wave velocity (aPWV). The intervention effect on each index of central hemodynamics was analyzed by mixed-effects models adjusted for heart rate, cluster randomization, age, and sex.At screening, median age was 59.2 years (interquartile range 55.2-64.6); 289 patients (63%) were in the intensive treatment group, and 278 patients (61%) were men. Patients in the intensive treatment group had a 0.51 m/s (95% CI -0.96 to -0.05, P = 0.03) lower aPWV compared with routine care. Respective differences for central augmentation index (-0.84% [-2.54 to 0.86]), pulse pressure (0.28 mmHg [-1.75 to 2.32]), and systolic (-1.42 mmHg [-4.47 to 1.64]) and diastolic (-1.79 mmHg [-3.72 to 0.14]) blood pressure were not statistically significant.Intensive multifactorial treatment of screen-detected diabetes during 6 years in general practice has a significant impact on aortic stiffness, whereas the effects on other hemodynamic measures are smaller and not statistically significant.
Abstract 2919: Unexpected role of CRAF in tumor cell mitosis revealed by an allosteric inhibitor
Authors: Ainhoa Mielgo, Eric Murphy, Miller Huang, Laetitia Seguin, Sara Weis, David Cheresh
Journal: Cancer Research (2011)

Abstract RAF kinases regulate fundamental cellular processes such as proliferation and survival and can be mutated or dysregulated in tumors. Although, RAF inhibitors show clinical activity in some cancer patients, recent reports have shown that ATP-competitive RAF inhibitors can enhance the proliferation of RAS driven tumors by promoting B- and CRAF dimerization and phosphorylation of CRAF on serine 338. Recently, we characterized an allosteric inhibitor of RAF that disrupts RAF dimerization, CRAF serine 338 phosphorylation and tumor growth in mice. Here, we report the surprising finding that phospho-S338 CRAF localizes to the mitotic spindle of proliferating tumor cells in vitro and in biopsies from cancer patients. Importantly, treatment of these cells with an allosteric, but not an ATP-competitive inhibitor of RAF, prevents CRAF localization to the mitotic spindle and causes cell cycle arrest at pro-metaphase in a MAPK-independent manner. Mechanistically, phospho-S338 CRAF interacts and co-localizes with active Polo-like kinase 1 (Plk1) at the mitotic spindle of proliferating cells. In fact, allosteric or genetic inhibition of CRAF inhibits Plk1 activity and its accumulation at the kinetochores causing pro-metaphase arrest. These findings define an unexpected role for RAF in mitosis, revealing a novel mechanism for RAF as a therapeutic target in oncology. 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 2919. doi:10.1158/1538-7445.AM2011-2919
Hypertrophic Subaortic Stenosis and Hypercalcemia
Authors: JOHN H. DIXON
Journal: Annals of Internal Medicine (1978)

Letters and Corrections1 April 1978Hypertrophic Subaortic Stenosis and HypercalcemiaJOHN H. DIXON JR., M.D., LAURENCE A. GROSSMAN, M.D.JOHN H. DIXON JR., M.D.Search for more papers by this author, LAURENCE A. GROSSMAN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-88-4-576_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: We read with interest in the January issue the first description of an association between hypercalcemia and idiopathic hypertrophic subaortic stenosis (Ann Intern Med 88:57-58, 1978).We recently evaluated a 64-year-old white woman with presyncope. She was found to have hypertrophic cardiomyopathy both echocardiographically and by cardiac catheterization. Metabolic bone disease was discovered radiographically, and on repeat serum calcium measurement she had values ranging from high normal to mildly elevated range. Serum parathyroid hormone levels were elevated, and surgical exploration of the neck revealed an 8.1-g parathyroid adenoma.This fascinating coexistence should be reported when it is...References1. MCFARLANDSTEFADOUROSABDULLAMCFARLAND KMAD: Hypercalcemia and idiopathic hypertrophic subaortic stenosis. Ann Intern Med 88:57-58, 1978 LinkGoogle Scholar2. EPSTEINHENRYCHESTERROBERTSMARONFERRANSREDWOODMORROW SWCWBVDA: Asymmetric septal hypertrophy. Ann Intern Med 81:650-680, 1974 LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: St. Thomas Hospital Nashville, TN 37202 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByCombined supravalvular aortic stenosis and hypertrophic subaortic stenosis: Coexistence or association?"Association" MisusedA.M. PARFITT, M.D. 1 April 1978Volume 88, Issue 4Page: 576-576KeywordsCalciumCardiac hypertrophyCardiomyopathiesCatheterizationHypercalcemiaMetabolic disordersParathyroid hormoneParathyroid tumorsStenosisSyncope Issue Published: 1 April 1978 PDF DownloadLoading ...
Parathyroid Scintigraphy in Renal Hyperparathyroidism
Authors: David Taïeb, Pablo Ureña-Torres, Paolo Zanotti-Fregonara, Domenico Rubello, Alice Ferretti, Ioline Henter, Jean-François Henry, Francesca Schiavi, Giuseppe Opocher, Johan G. Blickman, Patrick M. Colletti, Elif Hindié
Journal: Clinical Nuclear Medicine (2013)

Secondary hyperparathyroidism (sHPT) is a major complication for patients with end-stage renal disease on long-term hemodialysis or peritoneal dialysis. When the disease is resistant to medical treatment, patients with severe sHPT are typically referred for parathyroidectomy (PTx), which usually improves biological parameters as well as clinical signs and symptoms. Unfortunately, early surgical failure with persistent disease may occur in 5%-10% of patients and recurrence reaches 20%-30% at 5 years. Presently, the use of parathyroid scintigraphy in sHPT is usually limited to the management of surgical failures after initial PTx. This review describes the strengths and limitations of typical (99m)Tc-sestamibi imaging protocols, and highlights the potential benefits of using parathyroid scintigraphy in the initial workup of surgical patients.
Involvement of Tumor Necrosis Factor-α in the Development of T Cell–Dependent Aortitis in Interleukin-1 Receptor Antagonist–Deficient Mice
Authors: Taizo Matsuki, Kikuo Isoda, Reiko Horai, Akiko Nakajima, Yoshifusa Aizawa, Kazuo Suzuki, Fumitaka Ohsuzu, Yoichiro Iwakura
Journal: Circulation (2005)

Background— Interleukin-1 receptor antagonist–deficient (IL-1Ra −/− ) mice on the BALB/c background spontaneously develop inflammatory arthropathy that resembles rheumatoid arthritis in humans. These mice also frequently develop aortitis at the root of the aorta, but the mechanism underlying the development of this disease has not been completely elucidated. Methods and Results— Using IL-1Ra −/− mice (backcrossed 8 generations to the BALB/c background) and wild-type mice, we studied the histopathology and examined the immunologic mechanisms involved in the development of aortic inflammation by cell transplantation experiments. Half of the IL-1Ra −/− mice developed aortitis at the root of the aorta, with massive infiltration of macrophages and monocytes and loss of elastic lamellae in the aortic media. Left ventricular hypertrophy and mild aortic stenosis were also shown by transthoracic echocardiography. Transplantation of T cells from IL-1Ra −/− mice induced aortitis in recipient nu/nu mice. Bone marrow cell transplants from IL-1Ra −/− mice also induced aortitis in irradiated wild-type recipient mice. Furthermore, tumor necrosis factor (TNF)-α deficiency completely suppressed the development of aortitis in IL-1Ra −/− mice, whereas IL-6 deficiency did not affect pathology. Conclusions— These observations suggest that IL-1Ra deficiency in T cells activates them excessively, resulting in the development of aortitis in IL-1Ra −/− mice in a TNF-α–dependent manner.
GW25-e5184 Mitofusin 2 decreases intracellular lipids in macrophages by regulating peroxisome proliferatoractivated receptor-γ
Authors: Chun Liu, Lei Ma, Chao He, Yi Zhang, Xiaowen Liu, Cuiping Qian, Yu Zhang, Wenzhong Peng, Xiaomei Guo
Journal: Journal of the American College of Cardiology (2014)
Erratum: Corrigendum: Aldosterone impairs vascular reactivity by decreasing glucose-6-phosphate dehydrogenase activity
Authors: Jane A Leopold, Aamir Dam, Bradley A Maron, Anne W Scribner, Ronglih Liao, Diane E Handy, Robert C Stanton, Bertram Pitt, Joseph Loscalzo
Journal: Nature Medicine (2009)
Effect of Lead Intoxication on the Postnatal Growth of the Rat Nervous System
Authors: Martin R. Krigman, Edward L. Hogan
Journal: Environmental Health Perspectives (1974)

Lead encephalopathy was induced in developing Long-Evans rats by adding lead carbonate (4% w/w) to the diet of nursing mother immediately after delivery. The morphological and biochemical features of cerebral ontogenesis were studied in 30-day-old rats.By the 30th postnatal day, the overall effect of lead intoxication was retardation of brain growth. The mass of both the cerebral gray and white matter was appreciably reduced in the lead rats without any reduction in cell populations. While the neuronal population was preserved, the growth of neurons was reduced and their maturation retarded. The retarded neuronal growth was characterized by the limited proliferation of processes in the neuropil and by the reduction in the number of synapses per neuron. However, synaptogenesis was neither delayed nor perturbed but reduced by the limited development of neuronal dendritic fields. The myelination was altered and its cerebral content significantly reduced. The effect of lead on myelination was one of hypomyelination. The hypomyelination appears to be primarily related to retarded growth and maturation of the neuron and is not a reflection of a defect in the myelinating glia or a delay in the initiation of myelination.
VERY LATE (5 YEARS) ARTERIAL RESPONSE COMPARISON BETWEEN DURABLE POLYMER SIROLIMUS-ELUTING STENT AND BIODEGRADABLE POLYMER BIOLIMUSA9-ELUTING STENT
Authors: Carlos A. Collet, Jose R. Costa, Daniel Chamié, Amanda Sousa, Rodolfo Staico, Ricardo A. Costa, Dimytri Siqueira, Javier Obregon, Fausto Feres, Alexandre Abizaid, Jose E. Sousa
Journal: Journal of the American College of Cardiology (2011)
Treatment With Insulin Uncovers the Motogenic Capacity of Nitric Oxide in Aortic Smooth Muscle Cells
Authors: Madhulika Dixit, Daming Zhuang, Bogdan Ceacareanu, Aviv Hassid
Journal: Circulation Research (2003)

Contrary to the antimotogenic effect of NO in dedifferentiated vascular smooth muscle cells (VSMCs), we have reported that NO stimulates the motility of differentiated cultured VSMC isolated from adult rats. This process involves upregulation of protein tyrosine phosphatase SHP2, followed by downregulation of RhoA activity. In the present study, we tested the hypothesis that insulin alters the motogenic phenotype of cultured rat aortic smooth muscle cells exposed to NO from inhibition to stimulation of cell motility. We demonstrate for the first time that NO stimulates the motility of VSMCs cultured for several days in the presence but not the absence of insulin. Moreover, we show that NO blocks PDGF-induced cell motility in insulin-naive but not in insulin-treated cells. We also demonstrate that the scaffold adapter protein Gab1, considered a physiological activator of protein tyrosine phosphatase SHP2, increases cell motility in the presence but not the absence of insulin. In cells cultured in the presence of insulin, overexpression of Gab1 mimics, whereas a dominant-negative allele of Gab1 (Gab1YF) blocks, the motility-stimulatory effect of NO. Cotransfection experiments with dominant-negative Gab1 and wild-type SHP2 or wild-type Gab1 and dominant-negative SHP2 indicate that the two proteins work together as a functional unit to induce motility. Because chronic insulin can increase the levels of phosphatidylinositol 3 (PI3) kinase in several models of hyperinsulinemia, we also tested the potential involvement of this enzyme in mechanisms leading to increased cell motility. We found that the motogenic effect of NO, Gab1, and SHP2 was blocked by the selective PI3 kinase inhibitor LY294002, suggesting a requirement of PI3 kinase in mediating motogenesis. These observations may be relevant to molecular mechanisms related to the pathogenesis of vascular disease in hyperinsulinemic diabetes. The full text of this article is available online at http://www.circresaha.org.
The effects of 2-year treatment with the aminobisphosphonate alendronate on bone metabolism, bone histomorphometry, and bone strength in ovariectomized nonhuman primates.
Authors: R Balena, B C Toolan, M Shea, A Markatos, E R Myers, S C Lee, E E Opas, J G Seedor, H Klein, D Frankenfield
Journal: Journal of Clinical Investigation (1993)

This study examined the effect of 2 yr of treatment with the aminobisphosphonate alendronate (ALN) (0.05 or 0.25 mg/kg i.v. ALN every 2 wk) on estrogen deficiency bone loss and bone strength changes in ovariectomized (OVX) baboons (n = 7 per group) and the ALN mode of action at the tissue level. Biochemical markers of bone turnover increased in OVX animals and were maintained by ALN treatment at non-OVX levels (low dose) or below (high dose). 2 yr of treatment produced no cumulative effects on bone turnover markers. Histomorphometry showed a marked increase in cancellous bone remodeling in OVX animals. Activation frequency increased from 0.48 to 0.86 per yr (L5 vertebra), and the osteoid surfaces from 9 to 13.5% (P < 0.05). No changes were observed in eroded and osteoclast surfaces. ALN treatment decreased activation frequency and indices of bone formation to control levels (low dose) or below (high dose), did not change indices of mineralization, and increased bone mineral density (BMD) in the lumbar vertebrae (L2-L4) by 15% at 0.25 mg/kg (P < 0.05), relative to vehicle-treated animals. The mean strength of cancellous bone (L4) increased by 44% (low ALN dose) and 100% (high dose), compared with vehicle. The strength of individual bones correlated with the square of the L2-L4 BMD (r = 0.91, P < 0.0034). In conclusion, ALN treatment reversed the effects of ovariectomy on cancellous bone turnover and increased bone mass and bone strength in baboons.
A New<i>TRPV3</i>Missense Mutation in a Patient With Olmsted Syndrome and Erythromelalgia
Authors: Sabine Duchatelet, Solenn Pruvost, Simon de Veer, Sylvie Fraitag, Patrick Nitschké, Christine Bole-Feysot, Christine Bodemer, Alain Hovnanian
Journal: JAMA Dermatology (2014)

Olmsted syndrome (OS) is a rare keratinizing disorder characterized by excessive epidermal thickening of the palms and soles, with clinical and genetic heterogeneity. Approximately 50 cases have been reported, with the molecular basis described in only 9. Recently, TRPV3 (transient receptor potential vanilloid 3) mutations were identified in autosomal-dominant OS in 7 sporadic cases and 1 familial case, whereas an MBTPS2 (membrane-bound transcription factor protease, site 2) mutation was reported in X-linked recessive OS. We report a new sporadic case of severe, atypical OS and its underlying genetic basis.Our patient is a young girl with severe nonmutilating (palmo)plantar keratoderma without periorificial keratotic plaques associated with intense acute flares of inflammation, itching, burning pain, vasodilatation, and redness of the extremities consistent with erythromelalgia. Whole exome sequencing of patient DNA identified a novel de novo heterozygous missense mutation within TRPV3, p.Leu673Phe, predicted to be damaging.This case study further implicates TRPV3 in OS pathogenesis. In addition, previous reports of OS have not described erythromelalgia as a clinical feature. Its occurrence in our patient could be a chance event, but, if associated with OS, the features of erythromelalgia may expand the phenotypic spectrum of this rare syndrome.
A NOVEL STRATEGY TO REDUCE “OFF-HOURS” DOOR TO BALLOON TIME IN ST ELEVATION MYOCARDIAL INFARCTION
Authors: Syed Tanveer Rab, John S. Douglas, Leeann Bauch, Jane Wilson, Samuel Shartar, Matthew Keadey, Leslie Stigaard, M. Rizwan Khalid, Douglas C. Morris
Journal: Journal of the American College of Cardiology (2010)