tbuckley/cabot-search huggingface dataset:
The impact of implementing a COPD care bundle on the delivery of care to patients admitted with an acute exacerbation of COPD
Authors: Sarah Davies, Stuart Packham, Sarah Dyer, Michelle Davies, Linzi Johnstone, Siara Lloyd
Journal: European Respiratory Journal (2013)

Aim: To study the impact of implementing a COPD care bundle on the management of patients admitted with an acute exacerbation of COPD.  Method. COPD care bundles have been proposed as a method of improving outcomes of patients admitted with COPD. The bundle used in our unit consists of six evidence-based interventions implemented prior to discharge for all patients admitted with COPD (Hopkinson N et al  Thorax.  2012. 67(1): 90–92), (1) review by specialist nurse/respiratory team (RN), (2) offer smoking cessation (SC), (3) refer for pulmonary rehabilitation (PR), (4)give written information and self-management booklet (SM), (5) demonstrate satisfactory use of inhaler (IN), (6) follow-up appointment with a specialist (FU). Data was collected prospectively from 1st June to 31st December 2012 and compared with data from previous audits to assess whether improvements in care had occurred.  Results. 42 patients (48% male) were included in the study period, mean age 71 years, 26% current smokers years compared to mean age 72 years (50% male), 33% smokers prior to bundle.100% saw the respiratory team compared to 67% prior to the bundle, 91% were offered SC, 66% PR, increased by 55%, 45% SM, 86% IN and 83% FU. Median stay 6 days and 30 day readmission rate was 21% compared to 8 days and 25% prior to the bundle. 90 day mortality prior was 12% and 25% prior to bundle use. During telephone follow up 12% of patients had intervention targeted at admission avoidance.  Conclusion. Implementation of a structured care bundle for patients admitted with exacerbations of COPD resulted in improved healthcare delivery, less utilization of healthcare resources and improved morbidity.
Early Administration of Reteplase Plus Abciximab vs Abciximab Alone in Patients With Acute Myocardial Infarction Referred for Percutaneous Coronary Intervention&lt;SUBTITLE&gt;A Randomized Controlled Trial&lt;/SUBTITLE&gt;
Authors: Adnan Kastrati
Journal: JAMA (2004)

IN HOSPITALS WITH CATHETERIZAtion facilities, primary percutaneous coronary interventions (PCIs) are better than thrombolysis in patients with ST-segment elevation acute myocardial infarction (MI). 1 Specifically designed randomized trials have also shown that patients with acute MI presenting at hospitals without catheterization facilities benefit more from PCI performed after transfer to centers with catheterization laboratories than from on-site thrombolysis. 2-
Regulation of the MicroRNA Processor DGCR8 by the Tumor Suppressor ING1
Authors: Daniel Gómez-Cabello, Sergio Callejas, Alberto Benguría, Alberto Moreno, Javier Alonso, Ignacio Palmero
Journal: Cancer Research (2010)

The ING family of tumor suppressor proteins controls several cellular functions relevant to antitumor protection, such as cell cycle control, apoptosis, senescence, or migration. ING proteins are functionally linked to the p53 pathway, and they participate in transcriptional control via the recognition of histone marks and recruitment of protein complexes with chromatin-modifying activity to specific promoters. Here, we have investigated the global effect of ING1 in gene regulation through genome-wide analysis of expression profiles in primary embryonic fibroblasts deficient for the Ing1 locus. We find that Ing1 has a predominant role as transcriptional repressor in this setting, affecting the expression of genes involved in a variety of cellular functions. Within the subset of genes showing differential expression, we have identified DGCR8, a protein involved in the early steps of microRNA biogenesis. We show that ING1 binds to the DGCR8 promoter and controls its transcription through chromatin regulation. We also find that ING1 and DGCR8 can cooperate in restraining proliferation. In summary, this study reveals a novel connection between ING1 and a regulator of microRNA biogenesis and identifies new links between tumor suppressor proteins and the microRNA machinery.
Disappearance of bradykinin in the renal circulation of dogs. Effects of kininase inhibition.
Authors: A Nasjletti, J Colina-Chourio, J C McGiff
Journal: Circulation Research (1975)

In chloralose-anesthetized dogs, we investigated the disappearance of bradykinin on passage across the renal circulation. The peptide was infused into a renal artery at various doses (5-200 ng/kg min-1); renal blood flow and the concentration of kinins in renal venous blood were then determined and the percent survival of bradykinin on passage through the kidney calculated. Bradykinin caused a dose-related increase in renal blood flow, urine flow, sodium excretion, and kinin content of renal venous blood. Intravenous administration of BPP9alpha (300 mug/kg), a peptide kininase II inhibitor, potentiated the renal vasodilator, diuretic, and natriuretic actions of bradykinin and augmented the survival of the kinin on passage through the kidney from 12.72 +/- 1.64% in control dogs to 53.92 +/- 7.48% (P less than 0.001). Furthermore, the values of peptide survival were positively correlated with the increases in renal blood flow (r = 0.92, P less than 0.01), urine flow (r = 0.75, P less than 0.01), and sodium excretion (r = 0.68, P less than 0.01) produced by bradykinin. In addition, BPP9alpha by itself increased renal blood flow (16%, P less than 0.01), urine flow (115%, P less than 0.005), and sodium excretion (167%, P less than 0.02). Similarly, the concentration of kinin in renal venous blood and the excretion of urinary kinins rose from 0.11 +/- 0.03 ng/ml and 4.1 +/- 1.1 ng/min to 0.24 +/- 0.05 ng/ml (P less than 0.005) and 38.5 +/- 12.2 ng/min (P less than 0.02). These studies suggest that kinins generated intrarenally play a role in the regulation of renal blood flow and salt-water excretion and that variations in the capacity of the kidney to inactivate kinins may be a determinant of the intrarenal activity of the kallikrein-kinin system.
Recurrence of Breast Cancer in Elderly Women
Authors: Diego Serraino, Massimiliano Berretta, Umberto Tirelli
Journal: Journal of Clinical Oncology (2013)

TO THE EDITOR: In their article, Partridge et al concluded that “age was not strongly associated with risk of early recurrence or prediction of benefit from trastuzumab therapy.” In our opinion, such conclusive statement is weakly supported by the data shown in tables. In both the observation and the trastuzumab groups, the authors do not provide detailed data on the age distribution of studied women. This lack of information is, in our opinion, of particular importance with regard to the women aged over 40 years. With a reported median age of 52 years, 670/671 older women in the observation group and 669 older women in the trastuzumab group should be aged 53 years or older. There seems to be enough statistical power to expand the older than 40 years group in the Cox model (eg, 41 to 59, 60-69, 70 years or older) for comparison with women aged 40 years or younger (ie, 357 in the observation group and 365 in the trastuzumab group). We would be interested in seeing whether the findings reported by Partrdige et al will be homogenous across age strata in older women.
Reflections of a Medical Editor
Authors: A. G. Signy
Journal: BMJ (1963)

Looking back to 1946, when it was first suggested that the Association of Clinical Pathologists should launch its own journal, I am left wondering why we thought it so necessary at that moment.The association was not quite 20 years old, was not yet expanding into its post- war boom, and the National Health Service, which was to play such a great part in the development of clinical pathology in this country, was only just being introduced by Act of Parliament.Could it possibly have been that the sponsors of the new journal felt that pathologists at that time did not have enough reading material ?Was it possibly because the existing journals were so heavily oversubscribed that pathologists found difficulty in getting their papers accepted and published ?Was it perhaps to be a " status symbol" for the association itself ?Or was it really, as the council of the day was persuaded to accept, that with the increasing pressure on the four main disciplines in clinical pathology it was becoming essential to provide a platform on which some unification of those disciplines could be maintained and encouraged ?Objectives Until now, therefore, we have tried to maintain the Journal of Clinical Pathology as a general journal in clinical pathology, carefuly allocating approximately one-quarter of the available space to each main subject.Although the objective of the editorial board remains the same, as each discipline becomes more specialized we shall find fewer general practitioners in clinical pathology and more of our readers will be turning to their own specialized periodicals.I have therefore been examining the needs of pathologists as writers and readers with a view to making tentative proposals for the future of the journal, and I have been especially concerned with its place in the general medical literature of the day.Inevitably I have been drawn into the whole question of scientific, and particularly medical, literature, and though I shall make generalizations I shall attempt to particularize where possible for pathology.I have asked myself a number of questions, to some of which I found no answer.(1) Why do we as an association of clinical pathologists need to maintain a journal, and should we go on doing so ? (2)Why do so many people wish to write for medical journals, and why do they wish to see their papers published in the Journal of Clinical Pathology ? (3)Why do other subscribers take our journal ? (4)What other journals of pathology do pathologists read ?(5) If the journal is to continue, should it maintain its present form ?If not, what changes are possible, or can we offer any suggestions for easing the burden of the pathologist as a reader as well as a writer ?
Prospective study on the FDG–PET/CT predictive and prognostic values in patients treated with neoadjuvant chemoradiation therapy and radical surgery for locally advanced rectal cancer
Authors: A.A. Martoni, F. Di Fabio, C. Pinto, P. Castellucci, S. Pini, C. Ceccarelli, D. Cuicchi, B. Iacopino, P. Di Tullio, S. Giaquinta, L. Tardio, R. Lombardi, S. Fanti, B. Cola
Journal: Annals of Oncology (2010)
Vascular endothelial cell-derived endothelin-1 mediates vascular inflammation and neointima formation following blood flow cessation
Authors: Dyah W. Anggrahini, Noriaki Emoto, Kazuhiko Nakayama, Bambang Widyantoro, Suko Adiarto, Naoko Iwasa, Hidemi Nonaka, Yoshiyuki Rikitake, Yaz Y. Kisanuki, Masashi Yanagisawa, Ken-ichi Hirata
Journal: Cardiovascular Research (2009)

Although endothelin-1 (ET-1) has been suggested to contribute to the pathogenesis of neointima formation and atherosclerosis, the individual roles of ET-1 derived from certain cell types in this disease remain unclear. In this study, we determined the role of vascular endothelial ET-1 on vascular inflammation and neointima formation using vascular endothelial ET-1-knockout [ET-1f/f; Tie2-Cre (+)] mice. Intimal hyperplasia was induced by complete ligation of the left carotid artery in 12-week-old male ET-1f/f;Tie2-Cre (+) mice (n = 35) and the wild-type (WT) littermates (n = 34). Following this intervention, neointima formation was reduced in ET-1f/f;Tie2-Cre (+) mice compared with the WT mice, independent of the difference in blood pressure. This reduction was associated with a decrease in inflammatory cell recruitment to the vessel wall, which was accompanied by reduced expression levels of endothelial adhesion molecules as well as chemokines and a decrease in vascular smooth muscle cell proliferation. The results of our study provide direct evidence for the role of vascular endothelial ET-1 in mediating vascular inflammation and neointima formation following vascular injury in addition to promoting vasoconstriction and cell proliferation. Furthermore, this study suggests a strategy for the efficient design of ET receptor antagonists with targeted inhibition of ET-1 signalling in vascular endothelial cells.
Cytokine-mediated deployment of SDF-1 induces revascularization through recruitment of CXCR4+ hemangiocytes
Authors: David K Jin, Koji Shido, Hans-Georg Kopp, Isabelle Petit, Sergey V Shmelkov, Lauren M Young, Andrea T Hooper, Hideki Amano, Scott T Avecilla, Beate Heissig, Koichi Hattori, Fan Zhang, Daniel J Hicklin, Yan Wu, Zhenping Zhu, Ashley Dunn, Hassan Salari, Zena Werb, Neil R Hackett, Ronald G Crystal, David Lyden, Shahin Rafii
Journal: Nature Medicine (2006)
Epigenetic reactivation of estrogen receptor-α (ERα) by genistein enhances hormonal therapy sensitivity in ERα-negative breast cancer
Authors: Yuanyuan Li, Syed M Meeran, Shweta N Patel, Huaping Chen, Tabitha M Hardy, Trygve O Tollefsbol
Journal: Molecular Cancer (2013)

Estrogen receptor-α (ERα)-negative breast cancer is clinically aggressive and normally does not respond to conventional estrogen target-directed therapies. The soybean isoflavone, genistein (GE), has been shown to prevent and inhibit breast cancer and recent studies have suggested that GE can enhance the anticancer capacity of an estrogen antagonist, tamoxifen (TAM), especially in ERα-positive breast cancer cells. However, the role of GE in ERα-negative breast cancer remains unknown.We have evaluated the in vitro and in vivo epigenetic effects of GE on ERα reactivation by using MTT assay, real-time reverse transcription-polymerase chain reaction (RT-PCR) assay, western-blot assay, immunoprecipitation (ChIP) assay, immunohistochemistry and epigenetic enzymatic activity analysis. Preclinical mouse models including xenograft and spontaneous breast cancer mouse models were used to test the efficacy of GE in vivo.We found that GE can reactivate ERα expression and this effect was synergistically enhanced when combined with a histone deacetylase (HDAC) inhibitor, trichostatin A (TSA), in ERα-negative MDA-MB-231 breast cancer cells. GE treatment also re-sensitized ERα-dependent cellular responses to activator 17β-estradiol (E2) and antagonist TAM. Further studies revealed that GE can lead to remodeling of the chromatin structure in the ERα promoter thereby contributing to ERα reactivation. Consistently, dietary GE significantly prevented cancer development and reduced the growth of ERα-negative mouse breast tumors. Dietary GE further enhanced TAM-induced anti-cancer efficacy due at least in part to epigenetic ERα reactivation.Our studies suggest that soybean genistein can epigenetically restore ERα expression, which in turn increases TAM-dependent anti-estrogen therapeutic sensitivity in vitro and in vivo. The results from our studies reveal a novel therapeutic combination approach using bioactive soybean product and anti-hormone therapy in refractory ERα-negative breast cancer which will provide more effective options in breast cancer therapy.
Poly(ADP-ribose) polymerase-2 depletion reduces doxorubicin-induced damage through SIRT1 induction
Authors: Magdolna Szántó, Ibolya Rutkai, Csaba Hegedűs, Ágnes Czikora, Máté Rózsahegyi, Borbála Kiss, László Virág, Pál Gergely, Attila Tóth, Péter Bai
Journal: Cardiovascular Research (2011)

Doxorubicin (DOX) is widely used in cytostatic treatments, although it may cause cardiovascular dysfunction as a side effect. DOX treatment leads to enhanced free radical production that in turn causes DNA strand breakage culminating in poly(ADP-ribose) polymerase (PARP) activation and mitochondrial and cellular dysfunction. DNA nicks can activate numerous enzymes, such as PARP-2. Depletion of PARP-2 has been shown to result in a protective phenotype against free radical-mediated diseases, suggesting similar properties in the case of DOX-induced vascular damage.PARP-2(+/+) and PARP-2(-/-) mice and aortic smooth muscle (MOVAS) cells were treated with DOX (25 mg/kg or 3 μM, respectively). Aortas were harvested 2-day post-treatment while MOVAS cells were treated with DOX for 7 hours. Aortas from PARP-2(-/-) mice displayed partial protection against DOX toxicity, and the protection depended on the conservation of smooth muscle but not on the conservation of endothelial function. DOX treatment evoked free radical production, DNA breakage and PARP activation. Importantly, depletion of PARP-2 did not quench any of these phenomena, suggesting an alternative mechanism. Depletion of PARP-2 prevented DOX-induced mitochondrial dysfunction through SIRT1 activation. Genetic deletion of PARP-2 resulted in the induction of the SIRT1 promoter and consequently increased SIRT1 expression both in aortas and in MOVAS cells. SIRT1 activation enhanced mitochondrial biogenesis, which provided protection against DOX-induced mitochondrial damage.Our data identify PARP-2 as a mediator of DOX toxicity by regulating vascular SIRT1 activity and mitochondrial biogenesis. Moreover, to the best of our knowledge, this is the first report of SIRT1 as a protective factor in the vasculature upon oxidative stress.
Margaret McCartney: The power of patients’ stories
Authors: Margaret McCartney
Journal: BMJ (2015)

Stories in medicine are often rich in fascination and inspiration.We tell stories to each other all the time: which patients we saw, which ones we visited-and who we have only just realised is related to whom.Stories create sense out of disparate happenings, melding understandings of why things happen and who is affected when they do.
Severe asthma and ARDS triggered by acute short-term exposure to commonly used cleaning detergents
Authors: C.E. Mapp, V. Pozzato, V Pavoni, G Gritti
Journal: European Respiratory Journal (2000)

This report presents a case of severe asthmatic attack and adult respiratory distress syndrome, which occurred in an asthmatic subject following acute short-term exposure to commonly used cleaning detergents. Premorbid lung conditions, i.e. asthma and airway hyperresponsiveness, might have been risk factors for illness severity but not for persistent complaints. This case report indicates that nonindustrial exposures due to household product misuse, especially to mixing cleaning agents, may cause adult respiratory distress syndrome and not only irritant-induced asthma.
Role of Palliative Care in Adolescent and Young Adult Oncology
Authors: Simon Wein, Shlomit Pery, Alona Zer
Journal: Journal of Clinical Oncology (2010)

Adolescents and young adults (AYAs) with cancer are a heterogeneous group. Nevertheless, there are sufficient unifying characteristics to form a distinct clinical entity. Management of this special group requires a broad-based interdisciplinary clinical team, which should include palliative care (PC), psychology, social work, oncology, and nursing representatives. The function of PC is to provide impeccable pain and other symptom control and to coordinate care as the disease progresses. Features unique to AYAs with cancer include the psychosocial developmental phases, a young person facing death, grief, and bereavement. Pharmacologic and medical interventions by PC in AYAs are broadly similar to adults. Developing trust and being flexible are key skills that PC must use with AYAs. There is a paucity of high-quality controlled studies in the PC literature in general and AYA-PC in particular. Therefore, the methodology of this article is largely based on the narrative and clinical experience. The experience is based on clinicians' work with AYAs with cancer in Israel and Australia. Clinical lessons will be drawn by comparing and contrasting the cultures. Nevertheless, most PC clinical interventions, both pharmacologic and psychosocial, are derived from literature where there is a good evidence base. Future development of PC within AYAs should be coordinated at a national level via appropriate palliative and oncology professional organizations.
Nucleolar localization of RPS19 protein in normal cells and mislocalization due to mutations in the nucleolar localization signals in 2 Diamond-Blackfan anemia patients: potential insights into pathophysiology
Authors: Lydie Da Costa, Gil Tchernia, Philippe Gascard, Annie Lo, Joerg Meerpohl, Charlotte Niemeyer, Joel-Anne Chasis, Jason Fixler, Narla Mohandas
Journal: Blood (2003)
John David Baum Queenie Muriel Francis Adams Sinnadorai Bala Ian Hamilton Barclay Samuel Lovell Davidson Kenneth Hollinrake Peter Anthony Layard Horsfall Henry Lach William Tennant McClatchey John Charlton Moor
Authors: T. Chambers, M C S Cannell, K. Bala, S. Barclay, R. W Logan, A W Bullen, E R Williams, E. Waldman, F. Sorrell, T. Freeman, B. Evans
Journal: BMJ (1999)
An assessment of the haemodynamic alterations in acute myocardial infarction using the systolic time intervals
Authors: E. D. Bennett, C. S. Smithen, E. Sowton
Journal: Thorax (1971)

Systolic time intervals were measured in 24 patients with acute myocardial infarction and compared to normal values predicted for heart rate and sex. Pulmonary artery pressures were measured in 18 patients and cardiac outputs using the Fick technique in 10 patients. In all patients the QS2 interval (total electromechanical systole) was short during the acute episode. This shortening in the QS2 interval was due primarily to a reduction in left ventricular ejection time (r=0·71; P&lt;0·001) with no change in the pre-ejection period. The mean deviation from normal of the QS2 interval was 27 ± 3·6 msec in patients with an uncomplicated clinical course and 52 ± 4·7 msec in patients with a complicated course, the difference being significant at the 1% level. Those patients with the highest pulmonary artery diastolic pressure tended to have the shortest QS2 intervals (r=−0·58; P&lt;0·01). There was no relationship between stroke volume and the deviations in the QS2 and left ventricular ejection time intervals from normal. The implication of these findings is discussed.
Assessment of caesarean section and inguinal hernia repair as proxy indicators of total number of surgeries
Authors: Anders Wold Bjerring, Marius E Lier, Siri M Roed, Pia F Vestby, Birger H Endreseth, Øyvind Salvesen, Johan von Schreeb, Arne Wibe, T B Kamara, Haakon A Bolkan
Journal: The Lancet (2015)
Adherence to American Diabetes Association Standards of Care by Rural Health Care Providers
Authors: Patricia Coon, Karen Zulkowski
Journal: Diabetes Care (2002)

OBJECTIVE—To determine whether rural health care providers are compliant with American Diabetes Association (ADA) clinical practice guidelines for glycemic, blood pressure, lipid management, and preventative services. RESEARCH DESIGN AND METHODS—This study was performed using a retrospective chart review of 399 patients 45 years of age and older, with a definitive diagnosis of diabetes seen for primary diabetes care at four rural health facilities in Montana between 1 January 1999 and 1 August 2000. RESULTS—Glycemic testing was adequate (85%), and glycemic control (HbA1c 7.43 ± 1.7%) was above the national average. Comorbid conditions of hypertension and dyslipidemia were not as well managed. Mean systolic blood pressure (SBP) was 139 ± 18.8 mmHg and LDL was 119 ± 33 mg/dl. Of 399 patients, 11 were considered as needing no additional treatment based on ADA guidelines of an HbA1c level &amp;lt;7%, a BP &amp;lt;130/85 mmHg, and a LDL level &amp;lt;100 mg/dl. Monofilament testing and dilated eye examinations were poorly documented, as were immunizations. There were few referrals for diabetic education. CONCLUSIONS—Rural health care practitioners are not adequately following the ADA standards for comprehensive management of their patients with diabetes. Glycemic testing is being ordered, but HbA1c values indicate that patients do not have their diabetes under optimal control. The comorbid conditions of hypertension and dyslipidemia are not optimally managed according to the ADA guidelines.