tbuckley/cabot-search huggingface dataset:
Abstract 51: Seasonal Variation in Out-of-Hospital Cardiac Arrest
Authors: Awani Deshmukh, Nileshkumar J Patel, Abhishek Deshmukh, Neil Patel, Achint Patel, Christopher Desimone, Shantanu Solanki, Avirup Guha, Grishma Dhaduk, Sadip Pant, Sohilkumar Manvar, Shilpkumar Arora, Nilay Patel, Vinaykumar Panchal, Badal Thakkar, Apurva O Badheka, Marcin Kowalski, Hakan Paydak, Khaled Al Khasawneh, Manish Joshi
Journal: Circulation (2014)

Introduction: Heart Disease and Stroke Statistics_2014 Update suggests more than 424,000 people suffer out of hospital cardiac arrest (OHCA) in the United States. Hypothesis: We assessed seasonal variation in OHCA from a large national hospitalisation database in the past decade. Methods: The Nationwide Inpatient Sample database was used to estimate the annual number of hospitalisations with from 2000-2011. Identification of out of hospital cardiac arrest related hospitalisations was based on the designation of the International Classification of Diseases (9th Edition) Clinical Modification (ICD-9-CM) diagnosis code 427.5 (OHCA) as the principal discharge diagnosis. The frequency of hospitalisation for each month cumulative over 11 years was calculated and divided by number of days in that month to obtain the mean hospitalisations per day for each month. All calculations were carried out using the weighted estimates approximating nationwide population estimates. Results: An estimated 93,209 hospitalisations with primary diagnosis of OHCA occurred in the United States from the beginning of the calendar year 2000 to the end of the calendar year 2011. The number of hospitalisations per day in each month is shown in Figure 1.The number of hospitalisation was maximum in the winter months and minimum in summer months. Specifically, the mean number of hospitalisation each day (averaged over 11 years) was least in August (242). There was a rising trend from August to January. The average number of hospitalisation was highest in January (310); thereafter, the hospitalisation rate dropped to a nadir in August. There was however no seasonal pattern in inhospital mortality. Conclusions: We identified for the first time in United States an impressive pattern of seasonal variation in hospitalisations for OHCA. Further efforts must be made to identify triggers and methods to prevent OHCA and reduce its burden on health care system.
Effects of Selective Matrix Metalloproteinase Inhibitor (PG-116800) to Prevent Ventricular Remodeling After Myocardial Infarction
Authors: Michael P. Hudson, Paul W. Armstrong, Witold Ruzyllo, Jose Brum, Lisa Cusmano, Piotr Krzeski, Robert Lyon, Miguel Quinones, Pierre Theroux, Diana Sydlowski, Henry E. Kim, Mario J. Garcia, Wael A. Jaber, W. Douglas Weaver
Journal: Journal of the American College of Cardiology (2006)
Abstract 3516: The mitochondrial sirtuin SIRT3 promotes survival of human melanoma cells <i>in vitro</i>
Authors: Jasmine George, Minakshi Nihal, Chandra K. Singh, Weixiong Zhong, Nihal Ahmad
Journal: Cancer Research (2014)

Abstract Melanoma, a potentially lethal form of skin cancer, is the fifth most common type of new cancer diagnosis in American men and the sixth most common type in American women. Alarmingly, the annual incidence of melanoma among whites has increased steadily (&amp;gt;60% over the past 30 years). Despite new developments in therapy, the overall survival of patients with advance-stage melanoma has not significantly improved. Therefore, concerted mechanism-based efforts are needed for prevention, diagnosis and treatment of this deadly neoplasm. A better understanding of molecular mechanisms contributing to melanoma development and progression can be useful in crafting new strategies for melanoma management. We are studying the role of sirtuin family of proteins in melanoma development and progression. Mammalian sirtuins (SIRT 1-7) are nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylases, which have been shown to regulate metabolism, stress responses, and longevity, in model organisms. The role of sirtuins in cancer is fairly complex with dichotomous functions (tumor promoter versus tumor suppressor) depending on cell contexts. SIRT3 is a mitochondrial deacetylase that has been shown to be important in maintaining cellular metabolism by regulating mitochondrial functions. We have previously shown that SIRT3 was overexpressed in human melanoma cells and tissues and its inhibition resulted in an antiproliferative response in human melanoma cells (In: AACR Annual Meeting: Proceedings; 2013 April 6-April 10, Washington, DC; Abstract # 13-LB-9391). In this study, we found that short hairpin RNA (shRNA)-mediated knockdown of SIRT3 in SK-MEL-28 melanoma cells resulted in 1) G1-phase arrest of cell cycle, 2) induction of senescence as assessed by increase in senescence-associated β-galactosidase (SA-β-gal) activity, 3) senescence associated hetrochromatin formation (SAHF), 4) decrease in cell migration, and 5) increase in protein levels of p53, phospho-p53 (Ser15), p21Waf1, pRb and p16INK4a. Further, a stable exogenous overexpression of SIRT3 resulted in an increase in cell growth and clonogenic survival in Hs 294T melanoma cells. Based on our data we suggest that SIRT3 could be a contributing factor in melanoma survival. However, further extensive in-vitro and in- vivo studies are needed to ascertain the functional significance of SIRT3 in melanoma development and progression. Citation Format: Jasmine George, Minakshi Nihal, Chandra K. Singh, Weixiong Zhong, Nihal Ahmad. The mitochondrial sirtuin SIRT3 promotes survival of human melanoma cells in vitro. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3516. doi:10.1158/1538-7445.AM2014-3516
In vitro and in vivo anticancer efficacy of silibinin against human pancreatic cancer BxPC-3 and PANC-1 cells
Authors: Dhanya Nambiar, Vandana Prajapati, Rajesh Agarwal, Rana P. Singh
Journal: Cancer Research (2005)

Silibinin suppresses the growth of many cancers; however, its efficacy against pancreatic cancer has not been evaluated in established preclinical models. Here, we investigated in vitro and in vivo effects of sil- ibinin against lower and advanced stages of human pancreatic carcinoma cells. Silibinin (25-100 lM) treatment for 24-72 h caused a dose- and time-dependent cell growth inhibition of 27-77% (P < 0.05- 0.001) in BxPC-3 cells, and 22-45% (P < 0.01-0.001) in PANC-1 cells. Silibinin showed a strong dose- dependent G1 arrest in BxPC-3 cells (upto 72% versus 45% in control; P < 0.001), but a moderate response in advanced PANC-1 cells. Cell death observed in cell growth assay, was accompanied by up to 3-fold increase (P < 0.001) in apoptosis in BxPC-3 cells, and showed only slight effect on PANC-1 cells. Dietary feeding of silibinin (0.5%, w/w in AIN-93M diet for 7 weeks) inhibited BxPC-3 and PANC-1 tumor xeno- grafts growth in nude mice without any apparent change in body weight gain and diet consumption. Tumor volume and weight were decreased by 47% and 34% (P 6 0.001) in BxPC-3 xenograft, respectively. PANC-1 xenograft showed slower growth kinetics and silibinin decreased tumor volume by 34% (P < 0.001) by 7 weeks. Another 4 weeks of silibinin treatment to PANC-1 xenograft showed 28% and 33% decrease in tumor volume and weight, respectively. Silibinin-fed group of BxPC-3 tumors showed decreased cell proliferation and angiogenesis and an increased apoptosis, however, considerable inhibi- tory effect was observed only for angiogenesis in PANC-1 tumors. Overall, these findings show both in vitro as well as in vivo anticancer efficacy of silibinin against pancreatic cancer that could involve inhi- bition of cell proliferation, cell cycle arrest, apoptosis induction and/or decrease in tumor angiogenesis. 2012 Elsevier Ireland Ltd. All rights reserved.
Fortification of flour with folic acid
Authors: E. Reynolds
Journal: BMJ (2002)

# Fortification has several potential risks {#article-title-2} EDITOR—Wharton and Booth recommend caution and carrying out a field trial before a policy of fortifying flour with folic acid is implemented, but both they and the Department of Health's report understate the potential risks of the policy to the nervous system.1 In people with vitamin B-12 deficiency, giving folic acid does much more than mask any anaemia. The response of pernicious anaemia to folic acid is usually suboptimal and temporary and often followed by relapse. The vitamin precipitates not only neurological complications, sometimes after some initial temporary improvement, but also anaemia, although not necessarily to the same degree or in the same time scale. 2 3 Can these problems with usually pharmacological doses of folic acid (1-50 mg daily) be avoided with minimum food fortification? The only evidence I know of is a review of 38 patients with vitamin B-12 deficiency treated with ![Graphic][1]</img>1 mg folic acid, 30% of whom showed a significant haematological … [1]: /embed/inline-graphic-1.gif
Effects of Oral Contraceptives and Pregnancy on Melanomas
Authors: A B Lerner, J J Nordlund, J M Kirkwood
Journal: New England Journal of Medicine (1979)

The action of estrogens testosterone and progesterone and the role of pregnancy in primary or metastatic melanoma are not clear.  There is no evidence that steroidal hormones or pregnancy participate in the conversion of a benign pigmental lesion into a melanoma or the acceleration of metastases from a primary melanoma.  Shiu et al. found that pregnancy had an adverse effect on women who already had metastases.  Nevertheless there are reports of four women whose melanomas either began or metastasized after they were placed on estrogens or progesterone (or both) for symptoms of menopause or for birth control.  Moreover Sadoff et al. reported on two men who had melanoma after taking stilbestrol for prostatic cancer.  We wish to report on three additional patients.  A 13-year-old girl had a Grade III superficial spreading melanoma removed from her back.  There was no further evidence of the melanoma until eight months after she started taking an anovulatory drug at 19 years of age.  She later had metastatic lesions.  Another woman had a nevus of Ota present from birth.  Two years after she started using oral contraceptives a melanoma developed in the nevus.  Both patients died from metastases.  The third patient a 31-year-old woman with a congenital interscapular nevus noted enlargement ulceration and bleeding of the nevus during the last trimester of pregnancy.  After delivery the lesion regressed and remained quiescent for two years.  Now she has regional metastases.  Lopez et al. recently suggested that estrogens accelerate the growth of melanomas in mice.  Physicians should report on patients who later show melanomas and those who already have melanomas if their clinical courses change after taking estrogens androgens or progesterone of if they become pregnant.  Until more data are available women who have been operated on for removal of primary melanomas should avoid taking anovulatory agents.  (FULL-TEXT)
Combined CT Coronary Angiography and Stress Myocardial Perfusion Imaging for Hemodynamically Significant Stenoses in Patients With Suspected Coronary Artery Disease
Authors: Brian S. Ko, James D. Cameron, Michael Leung, Ian T. Meredith, Darryl P. Leong, Paul R. Antonis, Marcus Crossett, John Troupis, Richard Harper, Yuvaraj Malaiapan, Sujith K. Seneviratne
Journal: JACC. Cardiovascular imaging (2012)
SIRT1, SIRT2, SIRT6 and P21 gene expression in the lungs of mice chronically exposed to ambient particulate matter
Authors: Thais Mauad, Gabriel Ribeiro, Mariana Veras, Natália Costa, Ana Shimada, Adair Alemany, Thais Mendes, Paulo Saldiva, Sandra Farsky
Journal: European Respiratory Journal (2014)

Introduction:   The genes of the sirtuin family are involved in the regulation of oxidative stress, cell survival and metabolism. The cyclin-dependent kinase inhibitor P21 is a regulator of the cell cycle and can modulate cellular senescence. The expression the members of the P21 and sirtuins can be influenced by environmental changes, such as air pollution.   Objective:   To evaluate the gene expression of sirtuins (SIRT1, SIRT2, SIRT6) and P21in the lungs of mice exposed to particulate matter.   Materials and Methods:   Ten C57 BL/6 mice, age 07 weeks (weight +/- 25g), were divided in 2 groups: were exposed to paticulate matter (PM 2,5 ) (1200 ug/m 3  per day)or filtered air (control), using the Harvard Ambient Particle Concentrator, during 30 days. After the end of the exposure period, the animals were euthanized and lung samples collected for PCR analysis.   Result:   The group exposed to PM 2,5  showed increased gene expression of SIRT2 (p = 0.0001) and SIRT6 (p = 0.001), without difference in SIRT1 gene expression. The expression of P21 (p = 0.001) was also increased in the exposed group.   Conclusion:   Increased levels of expression of SIRT2, SIRT6 and P21 genes could be an attempt to modulate the harmful stimuli caused by air pollution. Our data suggest a possible adaptive lung response on cell cycle regulation and protection to damage DNA in response to ambient air pollution.
Isolated Noncompaction of the Myocardium
Authors: Bernd van der Loo, Rolf Jenni
Journal: Circulation (2003)

Isolated Noncompaction of the MyocardiumTo the Editor:McCrohon and colleagues 1 present a case of isolated ventricular noncompaction (IVNC) diagnosed by magnetic resonance (MR) imaging.They suggest that MR may improve the detection rates of IVNC as, in their case, the diagnosis would have been missed if only echocardiography had been used.Cardiac ultrasound, previously performed in their case, had shown no significant abnormalities.It is correct that this disease is not widely known, and, as a consequence of ignorance, its diagnosis is frequently missed.To facilitate its diagnosis, we have recently established 4 clear-cut echocardiographic diagnostic criteria, 2 namely: (1) absence of coexisting cardiac abnormalities; (2) a 2-layered structure of the left ventricular wall, with the end systolic ratio of noncompacted to compacted layer Ͼ2; (3) finding this structure predominantly in the apical and mid-ventricular areas; and (4) blood flow directly from the ventricular cavity into the deep intertrabecular recesses as assessed by Doppler echocardiography.This study 2 clearly demonstrated that IVNC can be accurately diagnosed by echocardiography, as we validated our results against pathological-anatomical preparations.Although MR imaging may also be helpful, no diagnostic criteria have yet been proposed. 3Furthermore, as is the case for echocardiography, MR imaging also necessitates experienced operators.The MR images of the present case show multiple intertrabecular recesses.We are surprised that a skilled echocardiographer would miss the diagnosis in ultrasound, particularly if he had previous experience of such conditions.Furthermore, the corresponding left ventricular angiogram might have given an additional hint, as this has been demonstrated to be indicative in another previously published report. 4e conclude that echocardiography currently remains the gold standard for the diagnosis of IVNC, at least when performed by experienced investigators.
Recombinant tissue-type plasminogen activator and immediate angioplasty in acute myocardial infarction. One-year follow-up. The European Cooperative Study Group.
Authors: A E Arnold, M L Simoons, F Van de Werf, D P de Bono, J Lubsen, J G Tijssen, P W Serruys, M Verstraete
Journal: Circulation (1992)

BACKGROUND The European Cooperative Study Group conducted two randomized trials in patients with suspected myocardial infarction to assess the effect of 100 mg single-chain recombinant tissue-type plasminogen activator (rt-PA, alteplase) on enzymatic infarct size, left ventricular function, morbidity and mortality relative to placebo (alteplase/placebo trial) and to assess the effect of immediate percutaneous transluminal coronary angioplasty (PTCA) in addition to alteplase (alteplase/PTCA trial). One-year follow-up results are reported. METHODS AND RESULTS In the alteplase/placebo trial, 721 patients with chest pain of less than 5 hours and extensive ST-segment elevation were allocated at random to 100 mg alteplase or placebo (double-blind) over 3 hours. In the alteplase/PTCA trial, 367 similar patients received alteplase and subsequently were allocated at random to immediate coronary angiography and angioplasty of the infarct-related vessel or control. All patients received aspirin and intravenous heparin. In the alteplase/placebo trial, mortality during the first year was reduced by 36% with alteplase (from 9.3% to 5.6%; difference, -3.7%; 95% confidence interval, -7.5% to 0.2%). Revascularization was performed more frequently after alteplase, and more patients in the alteplase group were in New York Heart Association functional class I or II. Reinfarction tended to occur more frequently after alteplase than after placebo. In the alteplase/PTCA trial, reinfarction was less common after immediate PTCA, and revascularization procedures were less frequent. However, this benefit was offset by a high rate of immediate reocclusion and early recurrent ischemia and by higher mortality at 1 year (9.3% versus 5.4%; difference, 3.9%; 95% confidence interval, -1.5% to 9.2%) in the invasive group. In a multivariate analysis of 1,043 hospital survivors, mortality after discharge was related to coronary anatomy, left ventricular function, age, and previous infarction but not to initial treatment allocation. Reinfarction after hospital discharge tended to be more common after alteplase and related to coronary anatomy. CONCLUSIONS Benefit from treatment with alteplase, heparin, and aspirin is not diminished at 1 year. Routine immediate PTCA does not confer additional benefit. Prognosis after hospital discharge mainly is determined by coronary anatomy and residual left ventricular function and is unrelated to initial treatment assignment.
Book: Partners of the Heart
Authors: A. K Banerjee
Journal: BMJ (1999)

Vivien Thomas University of Pennsylvania Press, £13.95, pp 245 ISBN 0 8122 1634 2 ——————— Rating: ![Graphic][1]</img>![Graphic][2]</img>![Graphic][3]</img> Multidisciplinary team working is the employment benchmark in the health service this decade. This applies not only in the provision of clinical services, but also in the prosecution of surgical research. However, the concept is not new. Many of the great surgical research laboratories of the past had fruitful collaboration between expert technicians and clinician scientists. In no department was this relationship better illustrated than at the Johns Hopkins Medical School. This autobiography by Vivien Thomas, who ultimately became supervisor at the Surgical Research Laboratory of the renowned Professor Alfred Blalock, essentially concerns this relationship. However, at a different level, the place of … [1]: /embed/inline-graphic-1.gif [2]: /embed/inline-graphic-2.gif [3]: /embed/inline-graphic-3.gif
Abstract 1988: Non-culprit Coronary Plaque Morphology in Patients WIth Acute Myocardial Infarction : An Optical Coherence Tomography Study in Vivo
Authors: Kenichi Fujii, Motomaru Masutani, Takahiro Okumura, Daizo Kawasaki, Takafumi Akagami, Tsuyoshi Sakoda, Tohru Masuyama, Mitsumasa Ohyanagi
Journal: Circulation (2007)

Background: In vivo imaging studies in patients with acute myocardial infarction (AMI) have demonstrated important lesions at sites other than the culprit. However, it is not well assessed whether non-culprit plaques in the non-infarct-related artery have similar markers of plaque instability compared to non-culprit plaques in the infarct-related artery. The aim of this study is to investigate the morphologic features of the non-culprit plaque in infarct-related artery in comparison with that in non-infarct-related artery for AMI patients using optical coherence tomography (OCT) in vivo. Methods: OCT examinations were attempted prospectively using motorized pullback in all 3 major coronary arteries (at least 2/3 segment of each artery) for 34 AMI patients. In 34 patients, 118 focal plaques were identified (3.5 plaques per patient). Qualitative OCT analyses for each focal atherosclerotic plaque were performed using the previously validated criteria. TCFA was defined as a plaque with lipid content in a quadrant and the thinnest part of a fibrous cap measuring &lt;65 μm. A plaque rupture contained a cavity that communicated with the lumen with an overlying residual fibrous cap fragment. A thrombus was defined as an irregular mass protruding into the lumen. Non-culprit plaques were divided into two groups according to their location: plaques in infarct-related artery (n=35) and plaques in non-infarct-related artery (n=83). Results: Non-culprit TCFA, plaque rupture, and thrombus were observed in 50 lesions of 26 patients (76%), 14 lesions of 11 patients (34%), and 27 lesions of 15 patients (44%), respectively. OCT analyses are shown in the Table . Conclusions: The morphology of non-culprit plaques in AMI patients is similar whether these plaques occur in the infarct-related artery or the non-infarct-related artery. This suggests that plaque destabilization is a systemic phenomenon rather than a local, artery-specific process. OCT Analyses
Standardization and Quality of Endoscopy Text Reports in Ulcerative Colitis
Authors: T de Lange, B A Moum, J K Tholfsen, S Larsen, L Aabakken
Journal: Endoscopy (2003)

Background and Study Aims: The text report is the primary tool for documenting endoscopic findings but there is no consensus on the content and structure of these reports. Therefore, at four Norwegian hospitals, the content of endoscopy reports concerning ulcerative colitis was assessed. Quality indices for the medical history of active ulcerative colitis and endoscopic signs of inflammation were determined, as well as technical items in the report. The effect of structured compared with free-text reporting was evaluated. Materials and Methods: Endoscopy reports in 445 cases of ulcerative colitis were retrieved. Two of the hospitals used a semi-structured computerized documentation system, and two hospitals used transcription-based free-text reports.
No association between vitamin D and atopy, asthma, lung function or atopic dermatitis: a prospective study in adults
Authors: B. H. Thuesen, N. G. Heede, L. Tang, T. Skaaby, J. P. Thyssen, N. Friedrich, A. Linneberg
Journal: Allergy (2015)

Studies suggest that vitamin D may be involved in the pathogenesis of allergic disorders, asthma and decreased lung function. However, results are inconsistent and only few prospective studies have examined adults. The purpose of this study was to investigate the association of serum 25-hydroxy vitamin D (s25(OH)D) with atopy, atopic dermatitis (AD), asthma, wheezing and impaired lung function in a prospective study of Danish adults. A random sample of 3471 persons was examined in 2006-2008. Of these, 2308 were re-examined 5 years later. s25(OH)D and specific IgE against four common inhalant allergens were measured by standard procedures. Wheezing, asthma and AD were assessed from questionnaires and lung function was measured by spirometry. We found no statistically significant associations between s25(OH)D and prevalence or incidence of atopy, AD, asthma or wheezing. Associations with lung function were inconsistent. We conclude that vitamin D status does not influence these conditions in adults.