tbuckley/cabot-search huggingface dataset:
Exposure to chemotherapy drugs and adverse health effects in oncology ward of a pulmonary teaching hospital
Authors: Shadi Baniasadi, Maryam Alehashem
Journal: European Respiratory Journal (2014)

Introduction: Occupational exposure to antineoplastic drugs result in various adverse health effects. Very little is known about handling conditions of chemotherapy agents by healthcare workers in Iran.  Aims: To monitor the adverse effects associated with occupational exposure to antineoplastic drugs and identify the factors that increase the exposure.  Methods: A cross sectional study was conducted during six weeks in oncology ward of a pulmonary teaching hospital. Everyday a toxicologist visited the ward and collected data on three handling activities: preparation of chemotherapy agents, drug administration and patient contact, and cleaning and safety box replacement. In addition, adverse effects during work in oncology ward were asked.  Results: During 77 preparation times, a total amount of 449.296 gram of chemotherapy drugs was prepared. 98.70% of preparations; 62.13% of administrations and patient contacts; 54.16% of hood cleanings, and 10% of safety box replacements were done by using personal protective equipment. Skin reactions (26.79%) were the most frequent adverse effects reported by health care workers. Central nervous system (24.40%), respiratory (23.40%), vision (18.48%), gastrointestinal (6.9%) reactions also reported during the study period. Handling time of antineoplastic drugs was associated with the time of symptom appearance. Laboratory tests and spirometery results were normal.  Conclusions: Due to inadequate protective equipment, hospital workers were exposed to antineoplastic drugs and showed acute adverse effects. Establishment of safety regulations and training of health care workers in order to prevention of exposure to chemotherapy drugs are needed.
Fat Metaplasia and Backfill Are Key Intermediaries in the Development of Sacroiliac Joint Ankylosis in Patients With Ankylosing Spondylitis
Authors: Walter P. Maksymowych, Stephanie Wichuk, Praveena Chiowchanwisawakit, Robert G. Lambert, Susanne J. Pedersen
Journal: Arthritis & Rheumatology (2014)

Fat metaplasia in bone marrow on T1-weighted magnetic resonance imaging (MRI) scans may develop after resolution of inflammation in patients with ankylosing spondylitis (AS) and may predict new bone formation in the spine. Similar tissue, termed backfill, may also fill areas of excavated bone in the sacroiliac (SI) joints and may reflect resolution of inflammation and tissue repair at sites of erosions. The purpose of this study was to test our hypothesis that SI joint ankylosis develops following repair of erosions and that tissue characterized by fat metaplasia is a key intermediary step in this pathway.We used the Spondyloarthritis Research Consortium of Canada (SPARCC) SI structural lesion score (SSS) method to assess fat metaplasia, erosions, backfill, and ankylosis on MRIs of the SI joints in 147 patients with AS monitored for 2 years. Univariate and multivariate regression analyses focused first on identifying significant MRI predictors of new backfill and fat metaplasia. We then assessed the role of backfill and fat metaplasia in the development of new ankylosis. All analyses were adjusted for demographic features, treatment, and baseline and 2-year change in SSS values for parameters of inflammation and MRI structural lesions.Resolution of inflammation and reduction of erosions were each independently associated with the development of new backfill and fat metaplasia at 2 years on multivariate analyses. Multivariate regression analysis that included demographic features, baseline and 2-year change in parameters of inflammation and MRI structural lesion showed that reduction in erosions (P = 0.0005) and increase in fat metaplasia (P = 0.002) at 2 years was each independently associated with the development of new ankylosis.Our data support a disease model whereby ankylosis develops following repair of erosions, and fat metaplasia and backfill are key intermediary steps in this pathway.
Abstract 1587: Impact of Universal Medical Coverage on Medical Care and Outcomes in Low Income Patients Hospitalised for Acute Myocardial Infarction: An Analysis From the French National Health Insurance Database
Authors: Anke Neumann, Nicolas Danchin, Philippe Tuppin, Alain Weill, Philippe Ricordeau, Christine De Peretti, Hubert Allemand
Journal: Circulation (2009)

Background and aim: France offers a universal medical coverage insurance (CMUC) to persons <60 years of age with income <600 euros/month. We investigated whether CMUC permitted low income patients ...
Invasive group A streptococcal infections in adults, France (2006–2010)
Authors: C. Plainvert, A. Doloy, J. Loubinoux, A. Lepoutre, G. Collobert, G. Touak, P. Trieu-Cuot, A. Bouvet, C. Poyart
Journal: Clinical Microbiology and Infection (2011)
Abstract 8987: Prostacyclin Reduction Upregulates Tissue Factor and Predisposes COX-2 Knockout Mice to Thrombosis
Authors: Silvia S Barbieri, Sara Gianellini, Patriza Amadio, Elena Zacchi, Louise R Howe, Babette B Weksler, Luciana Mussoni, Elena Tremoli
Journal: Circulation (2011)

Selective inhibitors of cyclooxygenase-2 (COX-2) increase the risk of myocardial infarction and athero-thrombotic events, but the mechanisms responsible for these effects are not fully understood. To assess the role of COX-2 in arterial thrombosis, a well-studied model of ferric chloride-induced carotid artery injury was applied to COX-2 knockout (COX-2KO) mice and data were compared with those obtained in wild-type (WT) mice. We found that thrombus formation was significantly greater in COX-2-null compared to WT mice. We then explored the role of platelets in this model. Platelets isolated from blood of COX-2KO mice showed enhanced aggregation responses to collagen and ADP together with greater thromboxane production than WT platelets. Interestingly, cyclooxygenase-1 and thromboxane synthase protein levels were similar in both animal groups. In cross-transfusion experiments, we found that platelets from COX-2KO mice behaved similarly to WT platelets in terms of in vivo thrombus formation. Importantly, we observed that the activity of tissue factor (TF), initiator of blood coagulation, was elevated both in concentrated microparticles derived from plasma and in leukocytes or in the carotid arteries of COX-2KO mice. Furthermore, the arterial wall of COX-2KO mice expressed higher levels of TF mRNA compared to WT animals, and these levels correlated with both reduced prostacyclin synthase mRNA levels and decreased prostacyclin production. In addition, treatment with CA10441, a prostacyclin receptor (IP) antagonist, increased TF activity in WT mice. Conversely, carbaprostacyclin, a stable IP agonist, reduced TF activity in COX-2KO mice. Overall, these findings reveal for the first time that the propensity to thrombosis observed in association with COX-2 inhibition is consequent to the impairment in the generation of prostacyclin by vascular endothelium, which in turn results in increased TF expression and activity.
Abstract 16623: Elevated Depressive Symptoms Help Predict Major Adverse Cardiovascular Outcomes Irrespective of History of Depression
Authors: Pankaj Manocha, Danny J Eapen, Riyaz S Patel, Hatem A Kassem, Ravi A Nanjundappa, Nima Ghasemzadeh, Amit J Shah, Aymen Samman Tahaan, Muhammad Hammadah, Pratik M Pimple, Kaustub Dabhadkar, Michael M Halista, Naureen Farook, Revanth S Yendamuri, Mohamed Khayata, Youssef O Garcia-Bengochea, Emir Veledar, Laurence Sperling, Charles L Raison, Arshed A Quyyumi, Viola Vaccarino
Journal: Circulation (2012)

Background: Although a clinical diagnosis of depression has been associated with worse long term outcome in patients with cardiovascular disease (CVD), whether patients who have elevated depressive...
Glucosyltransferase activity of<i>Clostridium difficile</i>Toxin B is essential for disease pathogenesis
Authors: Zhiyong Yang, Yongrong Zhang, Tuxiong Huang, Hanping Feng
Journal: Gut Microbes (2015)

Clostridium difficile TcdB harbors a glucosyltransferase that targets host Rho GTPases. However, the role of the enzyme activity in the induction of host intestinal disease has not been demonstrated. In this study, we established a mouse acute intestinal disease model by cecum injection of wild type and glucosyltransferase-deficient TcdB and a chronic model by delivering toxin intraluminally via engineered surrogate host Bacillus megaterium. We demonstrated, for the first time, that the glucosyltransferase activity of TcdB is essential for inducing disease symptoms and intestinal pathological responses that resemble human disease, highlighting the importance of targeting toxin glucosyltransferase activity for future therapy.
Representations of Taste Modality in the Drosophila Brain
Authors: David T. Harris, Benjamin R. Kallman, Brendan C. Mullaney, Kristin Scott
Journal: Neuron (2015)

Gustatory receptors and peripheral taste cells have been identified in flies and mammals, revealing that sensory cells are tuned to taste modality across species. How taste modalities are processed in higher brain centers to guide feeding decisions is unresolved. Here, we developed a large-scale calcium-imaging approach coupled with cell labeling to examine how different taste modalities are processed in the fly brain. These studies reveal that sweet, bitter, and water sensory cells activate different cell populations throughout the subesophageal zone, with most cells responding to a single taste modality. Pathways for sweet and bitter tastes are segregated from sensory input to motor output, and this segregation is maintained in higher brain areas, including regions implicated in learning and neuromodulation. Our work reveals independent processing of appetitive and aversive tastes, suggesting that flies and mammals use a similar coding strategy to ensure innate responses to salient compounds.
Laparoscopic peritoneal lavage or sigmoidectomy for perforated diverticulitis with purulent peritonitis: a multicentre, parallel-group, randomised, open-label trial
Authors: Sandra Vennix, Gijsbert D Musters, Irene M Mulder, Hilko A Swank, Esther C Consten, Eric H Belgers, Anna A van Geloven, Michael F Gerhards, Marc J Govaert, Wilhelmina M van Grevenstein, Anton G Hoofwijk, Philip M Kruyt, Simon W Nienhuijs, Marja A Boermeester, Jefrey Vermeulen, Susan van Dieren, Johan F Lange, Willem A Bemelman
Journal: The Lancet (2015)
Abstract 13293: Safety of Same-Day Discharge After Implantable Cardioverter Defibrillator or Permanent Pacemaker Implant: A Single-Center Experience
Authors: Atul Bhatia, Imran Sheikh, Jeffrey Lurie, John Hare, Indrajit Choudhuri, Mohamed Djelmami-Hani, Mortada M. Eyman, Jasbir Sra
Journal: Circulation (2011)

Objective: HRS/EHRA Consensus recommends that follow-up post-device implant must be individualized to device and patient-related factors. Also, postimplant monitoring within 24 hours should include...
Abstract 11004: The NCDR Bleeding Risk Calculator Predicts Mortality
Authors: Sameer J Khandhar, Helen E Vlachos, Suresh Mulukutla, Sun Scolieri, Catalin Toma, Saleem Ahmed, Joon S Lee, John T Schindler, Conrad A Smith, Faith Selzer, Maria M Brooks, Oscar C Marroquin
Journal: Circulation (2013)

INTRO: Bleeding after percutaneous coronary intervention (PCI) is associated with adverse outcomes. The National Cardiovascular Data Registry (NCDR) developed and validated a bleeding risk score ba...
Abstract 4831: The A2B Adenosine Receptor Contributes to Post-Infarction Heart Failure
Authors: Jason E Maas, Milka Koupenova, Katya Ravid, John A Auchampach
Journal: Circulation (2008)

Recent studies have been directed at understanding the role of the A 2B receptor in regulating cardioprotection, coronary blood flow, fibroblast function, and inflammation. Unlike the other adenosine receptor subtypes, the A 2B receptor is emerging as a promoter of inflammation in chronic diseases such as asthma and conditions associated with tissue fibrosis. In this study, we used A 2B receptor gene “knock-out” (A 2B −/− ) mice to test the role of the A 2B receptor in infarction-induced heart failure and cardiac remodeling. A 2B −/− mice or wild-type (WT) littermates were subjected to permanent ligation of the left coronary artery or sham surgery. Cardiac morphology and function were assessed at 4 and 8 weeks after surgery by echocardiography. At the end of the study, systemic arterial and left ventricular pressures were obtained, after which the hearts were removed and histologically assessed for infarct size and fibrosis. WT hearts experienced significant left ventricular dilation and reduced systolic (fractional area shortening, myocardial performance index, and +dP/dt max ) and diastolic (end-diastolic pressure [EDP] elevated from 3.2 ± 0.8 mmHg in sham mice to 8.8 ± 1.5 mmHg in infarcted mice and tau was prolonged from 11.6 ± 1.7 ms to 22.3 ± 2.0 ms) function at 8 weeks after coronary artery ligation. Compared to WT mice, there were no significant differences in measures of post-infarction systolic function in A 2B −/− mice. However, EDP and tau were significantly improved (2.5 ± 1.5 mmHg and 17 ± 1.4 ms, respectively) and were not worsened compared to sham-operated A 2B −/− mice (2.7 ± 2.1 mmHg and 14.5 ± 1.8 ms, respectively). Moreover, interstitial fibrosis was elevated in the non-infarcted myocardium of WT mice subjected to coronary ligation, but not in A 2B −/− mice. Importantly, infarct size (WT = 39 ± 2% of the left ventricle; A 2B −/− = 43 ± 3%) and systemic blood pressure were not significantly different between WT and A 2B −/− mice. The data suggest that absence of the A 2B receptor results in preservation of diastolic function and decreased development of reactive fibrosis following myocardial infarction. These findings support the concept that adenosine signaling via the A 2B receptor contributes to post-infarction heart failure and adverse cardiac remodeling. This research has received full or partial funding support from the American Heart Association, AHA National Center.
Abstract 3465: Fkbp12.6 Overexpression in Mouse Cardiac Myocytes Offers Minor Protection Against Pressure Overload-Induced Cardiac Remodeling and Failure
Authors: Laurent Vinet, Mylène Pezet, Miresta Prévilon, Barnabas Gellen, Celine Dachez, Patricia Rouet-Benzineb, Jean-Jacques Mercadier
Journal: Circulation (2008)

Alterations in RyR2 function is a hallmark of heart failure (HF). Decreased FKBP12.6 binding to RyR2 has been put forward to explain the diastolic SR Ca 2+ leakage observed in this condition. Previous work in the mouse has shown that cardiac FKBP12.6 overexpression protects against the development of myocardial infarction-induced heart failure. We tested the hypothesis that cardiac FKBP12.6 overexpression protects against transverse aortic constriction (TAC)-induced cardiac remodeling and failure. We used a mouse model of conditional cardiac-specific FKBP12.6 overexpression. Ten weeks after TAC, male transgenic mice (TG) and their wild-type controls (WT) underwent heart catheterization. Hemodynamic and gravimetric data are shown in the table . Ventricular expression of the hypertrophic gene program and calcium handling proteins were assessed by real-time PCR and Western blot, respectively. Ten weeks after TAC, the mortality rate was 23% in WT and 13% in TG (14/60 vs 5/39, ns). The percentage of mice with HF, estimated on the presence of pulmonary oedema, was 42% in WT-TAC and 32% in TG-TAC (15/36 vs 7/22, ns). BNP mRNA level increased 2.8 fold in WT-TAC (p&lt;0.01 vs WT-Shams) and 2.4 fold in TG-TAC (p&lt;0.01 vs TG-Shams). α-skeletal actin mRNA level increased 4.3 fold in WT-TAC (p&lt;0.001 vs WT-Shams) and 3.8 fold in TG-TAC (p&lt;0.001 vs TG-Shams). β-MHC/α-MHC mRNA ratio increased 2.8 fold in WT-TAC (p&lt;0.01 vs WT-Shams) and 4.3 fold in TG-TAC (p&lt;0.05 vs TG-Shams). RyR2 protein level decreased by 58% in WT-TAC and 41% in TG-TAC (p&lt;0.01 and p&lt;0.05 vs sham-operated mice, respectively). SERCA2a protein level decreased by 29% in WT-TAC and 16% in TG-TAC (p&lt;0.01 and p&lt;0.05 vs sham-operated mice, respectively). No statistical difference was found between TG-TAC and WT-TAC for any of these parameters. Conclusion: Cardiac FKBP 12.6 overexpression offers weak protection if any against TAC-induced cardiac remodeling and failure in the mouse.
Influence of hospital and clinician workload on survival from colorectal cancer: cohort study Commentary: How experienced should a colorectal surgeon be?
Authors: F Kee, R H Wilson, C Harper, C C Patterson, K McCallion, R F Houston, R J Moorehead, J M Sloan, B J Rowlands, R. Shields
Journal: BMJ (1999)

<b>Objective</b>: To determine whether clinician or hospital caseload affects mortality from colorectal cancer. <b>Design</b>: Cohort study of cases ascertained between 1990 and 1994 by a region-wide colorectal cancer register. <b>Outcome measures</b>: Mortality within a median follow up period of 54 months after diagnosis. <b>Results</b>: Of the 3217 new patients registered over the period, 1512 (48%) died before 31 December 1996. Strong predictors of survival both in a logistic regression (fixed follow up) and in a Cox9s proportional hazards model (variable follow up) were Duke9s stage, the degree of tumour differentiation, whether the liver was deemed clear of cancer by the surgeon at operation, and the type of intervention (elective or emergency and curative or palliative intent). In a multilevel model, surgeon9s caseload had no significant effect on mortality at 2 years. Hospital workload, however, had a significant impact on survival. The odds ratio for death within 2 years for cases managed in a hospital with a caseload of between 33 and 46 cases per year, 47 and 54 cases per year, and 55 cases per year (compared to one with ≤23 cases per year) were respectively 1.48 (95% confidence interval 1.03 to 2.13), 1.52 (1.08 to 2.13), and 1.18 (0.83 to 1.68). <b>Conclusions</b>: There was no detectable caseload effect for surgeons managing colorectal cancer, but survival of patients treated in hospitals with caseloads above 33 cases per year was slightly worse than for those treated in hospitals with fewer caseloads. Imprecise measurement of clinician specific “events rates” and the lack of routinely collected case mix data present major challenges for clinical audit and governance in the years ahead.
Endothelial dysfunction and systemic inflammation in different COPD phenotypes
Authors: Andrea Vukić Dugac, Marko Jakopović, Sanja Popović-Grle, Blaženka Barišić, Sonja Badovinac, Miroslav Samaržija, Alen Ružić
Journal: European Respiratory Journal (2014)

Background: Endothelial dysfunction is a possible link between increased cardiovascular mortality and systemic inflammation in patients with COPD. Previous studies suggest an association between acute exacerbation of COPD and deterioration of endothelial function, but so far systematic studies of endothelial dysfunction in two phenotypically distinct groups of COPD patients has not been done.  Aim: The aim of this study was to investigate whether there are differences in endothelial function and systemic inflammation between the two groups of COPD patients: „frequent exacerbator“ and „infrequent exacerbator“.  Methods: 117 patients were enrolled. COPD patients were divided into two groups according to the criteria of frequency of acute exacerbation: 41 „frequent exacerbator“ and 41 „infrequent exacerbator“. The control group consists of 35 healthy smokers. In all three groups were determined vWF as a marker of endothelial dysfunction and CRP and fibrinogen as markers of systemic inflammation.  Results: We found an increase of all markers of endothelial function and sistemic inflammation in the „frequent exacerbator“ group compared to the “infrequent exacerbator“ group and compared to the healthy control group ( vWF 181.0 vrs 157.5 vrs 132.1, CRP 5.6 vrs 2.7 vrs 1.7, fibrinogen 4.8 vrs 4.1 vrs 3.7). The differences found were statistically significant in all cases (p  Conclusion: Between the two phenotypic groups of COPD patients, there is a difference in the degree of endothelial dysfunction and systemic inflammation.
Outcome of Adolescents and Young Adults Versus Patients&gt;30 Years with Ewing Sarcoma Family Tumors (Eft): Update on a Retrospective Single-Center Experience
Authors: W. Lamm, G. Amann, M. Bojic, T. Brodowicz, K. Dieckmann, P. Funovics, W. Klepetko, I. Nöbauer, S. Schur, W. Köstler
Journal: Annals of Oncology (2014)
The basophil surface marker CD203c identifies Aspergillus species sensitization in patients with cystic fibrosis
Authors: Bojana Mirković, Gillian M. Lavelle, Ahmed Abdul Azim, Kristine Helma, Fatma S. Gargoum, Kevin Molloy, Yael Gernez, Katie Dunne, Julie Renwick, Philip Murphy, Richard B. Moss, Catherine M. Greene, Cedric Gunaratnam, Sanjay H. Chotirmall, Noel G. McElvaney
Journal: Journal of Allergy and Clinical Immunology (2015)
Fortnightly review: Management of abnormal bleeding in women receiving hormone replacement therapy
Authors: C P Spencer, A J Cooper, M I Whitehead
Journal: BMJ (1997)

Hormone replacement therapy relieves climacteric symptoms and reduces the risk of cardiovascular disease and osteoporosis. Less than 10% of postmenopausal women, however, have ever taken hormone replacement therapy.1 Studies report a high degree of non-compliance, with about 70% of women stopping hormone replacement therapy after a year.2 One of the main reasons for non-compliance is vaginal bleeding, which occurs in 30-80% of women who stop treatment.3 4

Postmenopausal women who still have a uterus are given progestogens to protect the endometrium.5 6 Table 1 shows the types and doses of oral progestogens in current use. Progestogens can be administered sequentially for at least 10-12 days of each 28 day treatment cycle or calendar month. Sequential regimens are prescribed to perimenopausal and early postmenopausal women with intermittent and unpredictable ovarian function. About 85% of women receiving such sequential progestogen will experience withdrawal bleeding towards the end of, or immediately after, the progestogen phase (when the progestogen is added). Most women taking sequential therapy continue to bleed each month for as long as hormone replacement therapy is prescribed; a minority (often older women) develop amenorrhoea.

View this table:

Table 1 
Progestogens in current use with hormone replacement therapy



To overcome the re-establishment of vaginal bleeding, progestogens are increasingly being administered continuously in combination with the oestrogen. The aim is to achieve amenorrhoea by rendering the endometrium atrophic.7 It is hoped that women who have been postmenopausal for many years and are used to not bleeding regularly will accept continuous combined therapies more readily than sequential ones. In some women additional factors may need to be considered: there are no data to show that continuous combined hormone replacement therapy reduces the risk of heart disease, so that sequential regimens are advised in women with cardiovascular risk factors such as a family history, hypertension, …
Evidence of a Graft Versus Lymphoma (gvl) Effect in a Case of Aggressive Non-hodgkins-lymphoma (nhl)
Authors: André Bosly, P. Staquet, J. Collignon, Linda Dhondt, Bernard Chatelain, B. Deprijck, G. Alsteens, Jean-Marie Scheiff, Chantal Doyen, C. Gisselbrecht, F. Reyes
Journal: Blood (1994)
Treatment should be tailored for each patient
Authors: K. Wolff, A. Hay, D. Raistrick
Journal: BMJ (1995)

EDITOR,—Michael Farrell and colleagues note that for successful maintenance treatment of people dependent on opiates high doses of methadone are needed, and they recommend a dose of 70-120 mg a day.1 High doses are essential for people with chronic dependence, particularly long term injecting misusers, who may use more than one drug, but it is doubtful whether extended treatment with high doses is suitable for people who smoke heroin and who meet the criteria for substitute prescribing. When heroin is smoked or inhaled (rather than injected) the equivalent …