tbuckley/cabot-search huggingface dataset:
Abstract 3158: Changes In Exracellular Matrix Regulation During Episodes Of Clinical Decompensation In Patients With Systolic Heart Failure
Authors: Andreia Biolo, Mark Fisch, Joshua Balog, Tania Chao, David Denmark, Flora Sam, Henry Ooi, Deborah Siwik, Wilson S Colucci
Journal: Circulation (2007)

Introduction: The extracellular matrix (ECM) plays an active role in myocardial remodeling in heart failure (HF). Episodes of decompensation are associated with increased levels of neurohormones, inflammation and oxidative stress that are known to affect ECM regulation, and may contribute to progression of HF. We hypothesized that HF decompensation is associated with dysregulation of ECM turnover, as reflected by markers of degradation (matrix metalloproteinases [MMPs] and their tissue inhibitors [TIMPs]) and synthesis (pro-collagen N-terminal types I [PINP] and III [PIIINP]). Methods: Blood levels of MMP-2 and -9, TIMP-1, -2 and -4, and PI- and PIIINP were measured in 80 patients in 3 groups: 20 controls without HF, 21 patients with chronic stable systolic HF (no recent admission and no congestion by clinical examination), and 39 patients with acute HF decompensation, in whom measures were done on admission, at discharge, and chronically at least 2 months later. Results: In chronic stable HF, ECM markers were not increased vs. controls. In contrast, in patients with decompensated HF, MMP-2, TIMP-1 and PIIINP levels were increased (vs. stable HF or controls; Table ), while MMP-9, TIMP-2 and -4 or PINP were unchanged. Likewise, following effective therapy and return to clinical compensation (chronically but not at discharge) MMP-2, TIMP-1 and PIIINP levels returned to chronic stable HF levels, whereas MMP-9, TIMP-2 and -4 or PINP remained unchanged. Conclusion: A transient ECM dysregulation occurs during acute episodes of HF decompensation and may contribute to adverse ventricular remodeling. While HF decompensation is associated with certain markers of degradation and synthesis (MMP-2, TIMP-1 and PIIINP), other markers (MMP-9, TIMP-2 and -4 or PINP) are unchanged, suggesting selective pattern of ECM activation. The observation that matrix turnover is increased in decompensated but not stable HF may have implication for the timing of anti-remodeling therapy. ECM markers in controls, stable and decompensated HF
Cognitive Function in Breast Cancer Patients Receiving Adjuvant Chemotherapy
Authors: Christine B. Brezden, Kelly-Anne Phillips, Mohamed Abdolell, Terry Bunston, Ian F. Tannock
Journal: Journal of Clinical Oncology (2000)

PURPOSE: Breast cancer patients receiving chemotherapy have complained of difficulties in their ability to remember, think, and concentrate. This study assessed whether there are differences in cognitive function between breast cancer patients treated with standard-dose adjuvant chemotherapy compared with healthy controls. PATIENTS AND METHODS: The High Sensitivity Cognitive Screen and the Profile of Mood States (POMS) were used to assess cognitive function and mood in a group of 107 women. The women consisted of 31 breast cancer patients receiving adjuvant chemotherapy (group A), 40 breast cancer patients who had completed adjuvant chemotherapy a median of 2 years earlier (group B), and 36 healthy controls (group C). RESULTS: Univariate analysis showed statistically significant differences (P = .009) in overall cognitive function scores between groups A and C, with poorer function in patients receiving adjuvant chemotherapy. These differences remained significant (P = .046) when controlling for age, education level, and menopausal status. More patients had moderate or severe cognitive impairment in groups A and B than in controls (P ≤ .002). There were no significant differences in POMS scores between the groups, suggesting that the differences seen in cognitive scores were unlikely to be because of mood disturbance. CONCLUSION: Cognitive differences were observed in breast cancer patients receiving adjuvant chemotherapy compared with healthy controls. These differences did not seem to be caused by significant differences in mood disturbance between the two groups. If confirmed, these results have substantial implications for informed consent, counseling, and psychosocial support of patients receiving adjuvant chemotherapy for breast cancer.
Differing patterns of methotrexate use for psoriatic disease among dermatologists and rheumatologists
Authors: E.C. Dupuis, V.M. Bhole, J.P. Dutz
Journal: British Journal of Dermatology (2012)

Journal Article Differing patterns of methotrexate use for psoriatic disease among dermatologists and rheumatologists Get access E.C. Dupuis, E.C. Dupuis Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada Search for other works by this author on: Oxford Academic Google Scholar V.M. Bhole, V.M. Bhole Arthritis Research Centre of Canada, Vancouver, BC, Canada Search for other works by this author on: Oxford Academic Google Scholar J.P. Dutz J.P. Dutz Department of Dermatology and Skin Science, Department of Medicine, University of British Columbia, Vancouver, BC, Canada V5Z 4E8 Jan P. Dutz. E‐mail: dutz@interchange.ubc.ca Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 167, Issue 2, 1 August 2012, Pages 448–450, https://doi.org/10.1111/j.1365-2133.2012.10880.x Published: 01 August 2012
Annals Graphic Medicine - Mom's Flock
Authors: Sharon Rosenzweig
Journal: Annals of Internal Medicine (2015)

Web Exclusives4 August 2015Annals Graphic Medicine - Mom's FlockFREESharon Rosenzweig, BFA, MFASharon Rosenzweig, BFA, MFASearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/G14-0003 SectionsAboutVisual AbstractPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Download figure Download PowerPoint Download figure Download PowerPoint Download figure Download PowerPoint Download figure Download PowerPoint Comments0 CommentsSign In to Submit A Comment Author, Article, and Disclosure InformationAffiliations: Disclosures: The author has disclosed no conflicts of interest. Forms can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=G14-0003.Author Information: Sharon Rosenzweig is an investigative cartoonist (thecomictorah.com); e-mail, [email protected]com.Author Contributions: Conception and design: S. Rosenzweig.Analysis and interpretation of the data: S. Rosenzweig.Drafting of the article: S. Rosenzweig.Critical revision for important intellectual content: S. Rosenzweig.Final approval of the article: S. Rosenzweig.Collection and assembly of data: S. Rosenzweig.Written and illustrated by Sharon Rosenzweig, BFA, MFA. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 4 August 2015Volume 163, Issue 3Page: W135-W139KeywordsConflicts of interestDisclosureHealth care ePublished: 4 August 2015 Issue Published: 4 August 2015 Copyright & PermissionsCopyright © 2015 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Granulocyte colony-stimulating factor following peripheral-blood progenitor-cell transplant in non-Hodgkin's lymphoma.
Authors: S Cortelazzo, P Viero, P Bellavita, A Rossi, M Buelli, G M Borleri, S Marziali, R Bassan, B Comotti, A Rambaldi
Journal: Journal of Clinical Oncology (1995)

PURPOSE To compare the hematologic recovery after high-dose chemotherapy and circulating peripheral-blood progenitor-cell (PBPC) transplant between patients who received recombinant human granulocyte colony-stimulating factor (G-CSF) (treated group) and those who did not (control group). PATIENTS AND METHODS From December 1992 through June 1994, two sequential and consecutive cohorts of 20 patients each with histologically proven non-Hodgkin's lymphoma (NHL) received high-dose chemotherapy (carmustine [BCNU], cytarabine [Ara-C], etoposide and melphalan [BEAM]) followed by PBPC transplant. The first 20 patients were treated with G-CSF (5 micrograms/kg/d) after PBPC administration. Since the time of platelet and leukocyte recovery in this group was short (&lt; 15 days), with a narrow standard deviation from the mean value, the last 20 patients were not given G-CSF. Hematologic recovery, number of febrile days, rate of documented infections, number of hospital days, duration of gastrointestinal complications, platelet and RBC transfusions, and antibiotic requirements were compared in the two groups. RESULTS The two groups of patients were comparable according to disease status, histology, stage, bulky disease bone marrow involvement, elevated lactate dehydrogenase (LDH) level, and median number of infused CD34+ cells and colony-forming units granulocyte-macrophage (CFU-GM). The median time to reach 0.5 x 10(9)/L and 1.0 x 10(9)/L neutrophils was 2 days shorter in G-CSF group, but this difference was not statistically significant. The median times to reach 20 x 10(9)/L and 50 x 10(9)/L platelets were, respectively, 10 and 14 days in the G-CSF group and 11 and 16 days in the control group, but again this was not statistically significant. Moreover, when considering clinically relevant end points including the number of documented infections and antibiotic requirements, platelet transfusions, gastrointestinal toxicity, and days of hospitalization, no differences were demonstrated between the two groups. CONCLUSIONS Provided an optimal dose of circulating progenitors is infused, NHL patients transplanted with PBPC do not benefit by the administration of hematopoietic growth factors.
Tumor PIK3CA mutations, lymphocyte infiltration, and recurrence-free survival (RFS) in early breast cancer (BC): Results from the FinHER trial.
Authors: Sherene Loi, Stefan Michiels, Diether Lambrechts, Roberto Salgado, Nicolas Sirtaine, Debora Fumagalli, Bart Claes, Pirkko-Liisa Kellokumpu-Lehtinen, Petri Bono, Vesa V Kataja, Denis Larsimont, Martine J. Piccart-Gebhart, Heikki Joensuu, Christos Sotiriou
Journal: Journal of Clinical Oncology (2012)

507 Background: Tumor PIK3CA mutations (mts) and lymphocyte infiltration (LI) are prognostic in BC, but their importance is unknown in HER2-positive (HER2+) BC treated with adjuvant trastuzumab (T). Methods: The FinHER trial randomized 1010 patients (pts) with pN+ or high-risk pN- BC to 3 cycles of docetaxel (D) or vinorelbine, followed by 3 cycles of FEC. Pts with HER2+ BC were further randomized to 9 weeks of T or no T (n=232). Pts treated with D and T had superior outcome in prior analyses. BC samples were subjected to somatic hotspot mt profiling (Sequenom) and quantification of percentage tumor LI using full-face H&amp;E sections. RFS and interactions with T were explored with Kaplan-Meier and Cox regression analyses. Results: The median FU time was 62 months. 935 (92.6%) and 687 (68.1%) tumors underwent LI and mt analysis, respectively. Correlation of LI assessment between 2 pathologists was 0.78 (p&lt;0.001). 54 mts detected in 13 genes were evaluated. PIK3CA mts (exons 1,2,9,13,18,20) was present in 25.3% (n=174) and ERBB2 mt in 4.5% (n=31) BCs. Only 1 AKT mt was found and none in KRAS, BRAF, NRAS or PTEN. In ER+/HER2-, HER2+ and ER-/HER2- subtypes the prevalence of PIK3CA mts was 30.2%, 19.5% and 9.2%; ERBB2 mt 6.3%, 1.9% and 2.6%, respectively (both p&lt;0.05). Neither PIK3CA nor ERBB2 mts were associated with RFS overall or within BC subgroups. No interaction was found for the benefit with T and presence of PIK3CA mt in HER2+ BC (interaction p=0.17 T vs no T). Increasing LI was associated with favorable RFS in ER-/HER2- BC (continuous score adjusted p=0.032); 3-y RFS was 90% with extensive LI (&gt;30% infiltrated) vs 66% with non-extensive LI (p=0.007). In HER2+ BC, whilst there was no association with prognosis overall, there was a significant interaction with the benefit from T vs. no T and increasing LI (continuous score interaction p=0.042) with 3-yr RFS 96% vs 78% for extensive and non-extensive LI treated with T respectively (p=0.014). Conclusions: We report 3 clinically relevant findings from this large clinical trial dataset: 1) PIK3CA mts were not prognostic; 2) LI is a strong prognostic factor in ER-/HER2- BC and 3) for the first time that extensive LI predicts benefit from adjuvant T.
The role of cyclooxygenas-2 in the protection against apoptosis in vascular endothelial cells induced by cigarette smoking
Authors: Huihui Zeng, Yan Chen, Yanfang Pei
Journal: European Respiratory Journal (2014)

Background: Apoptosis has been demonstrated to be an important upstream event in the pathogenesis of chronic obstructive pulmonary disease (COPD). Cyclooxygenase-2 (COX-2) seems to be biologically relevant in COPD. However, the role of COX-2 in the endothelial apoptosis induced by CSE remains to be elucidated.  Methods:Surgical specimens were obtained from 20 patients with COPD, smoking controls and nonsmoking controls. The apoptotic index and COX-2 protein expression were detected in the lung tissues and HUVECs ( human vascular endothelial cell line) under exposure to varied concentrations of CSE as well as 5.0% CSE for varied durations. Repeatedly, the apoptosis rate and COX-2 expression in HUVECs under 5.0% CSE were examined after exposing to varied concentrations of celecoxib  Results:Significantly increased apoptotic index and expression of COX-2, were found both in the patients with COPD and smoking controls compared with nonsmoking controls. The CSE induced apoptosis in HUVECs are dose-dependent and time-dependent manners. The COX-2 was slightly expressed in the cells after exposing to 5% CSE for 3 and 6 hours, and markedly expressed after the exposure for 9 and 12 hours, but vanished after 24 hours of the exposure. Of interest, with the completely block of the COX-2 expression by celecoxib at 50.0μmol/L, the apoptosis rate was markedly increased again in HUVECsunder exposure to 5.0% CSE.  Conclusion:Endothelialapoptosis and the expression of COX-2 protein were increased in both COPD patients and CSE-induced endothelial cells. Of interest, it seems that the COX-2 probably had a protective role against the endothelial apoptosis induced by cigarette smoking.
A multicenter prospective trial to asses a new real-time polymerase chain reaction for detection of Treponema pallidum, herpes simplex-1/2 and Haemophilus ducreyi in genital, anal and oropharyngeal ulcers
Authors: M. Glatz, N. Juricevic, M. Altwegg, S. Bruisten, P. Komericki, S. Lautenschlager, R. Weber, P.P. Bosshard
Journal: Clinical Microbiology and Infection (2014)

Treponema pallidum, herpes simplex virus types 1 or 2 (HSV-1/2) and Haemophilus ducreyi are sexually transmitted pathogens that can cause genital, anal and oropharyngeal ulcers. Laboratory evaluation of these pathogens in ulcers requires different types of specimens and tests, increasing the risk of improper specimen handling and time lapse until analysis. We sought to develop a new real-time PCR (TP-HD-HSV1/2 PCR) to facilitate the detection of T. pallidum, HSV-1/2 and H. ducreyi in ulcers. The TP-HD-HSV1/2 PCR was tested (i) in a retrospective study on 193 specimens of various clinical origin and (ii) in a prospective study on 36 patients with genital, anal or oropharyngeal ulcers (ClinicalTrials.gov # NCT01688258). The results of the TP-HD-HSV1/2 PCR were compared with standard diagnostic methods (T. pallidum: serology, dark field microscopy; HSV-1/2: PCR; H. ducreyi: cultivation). Sensitivity and specificity of the TP-HD-HSV1/2 PCR for T. pallidum were both 100%, for HSV-1 100% and 98%, and for HSV-2 100% and 98%, respectively. T. pallidum and HSV-1/2 were detected in 53% and 22% of patients in the prospective study; H. ducreyi was not detected. In the prospective study, 5/19 (26%) specimens were true positive for T. pallidum in the TP-HD-HSV1/2 PCR but non-reactive in the VDRL. The TP-HD-HSV1/2 PCR is sensitive and specific for the detection of T. pallidum and HSV-1/2 in routine clinical practice and it appears superior to serology in early T. pallidum infections.
Human MnSOD mRNA and protein expression in transfected mouse MnSOD knockout embryonic fibroblast cell lines: effects of the ala16val polymorphism
Authors: Britt L. McAtee, James D. Yager
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

4597 

The ala16val polymorphism, found in the mitochondrial targeting signal of manganese superoxide dismutase (MnSOD), has been associated with a number of diseases, including breast cancer. MnSOD is an important antioxidant enzyme that functions in the mitochondrial matrix to dismutate superoxide to hydrogen peroxide. A single nucleotide polymorphism causes a change in the amino acid sequence from alanine (ala) to valine (val) at the 16th amino acid and is therefore referred to as the ala16val polymorphism. Previous studies have reported that the polymorphism may cause an increase in import of MnSOD to the mitochondrial matrix in vitro. Altered levels of MnSOD due to the polymorphism are hypothesized to disrupt the oxidative balance in the cell, making the cell more susceptible to oxidative stress. In order to assess the role of this polymorphism in situ, human MnSOD was cloned into the pcDNA3.1/Zeo expression vector with a CMV promoter and stably transfected into mouse embryonic fibroblasts (MEF) developed from the MnSOD knockout mouse. Six cell lines were established, 3 that stably express MnSOD-Ala protein, and 3 that stably express MnSOD-Val. MnSOD enzymatic activity correlated fairly well with MnSOD protein levels determined by Western blot. MnSOD mRNA expression, evaluated by TaqMan™ real-time PCR, was significantly lower in MnSOD-Ala lines versus MnSOD-Val lines (p<0.05). The MnSOD-Ala lines produced significantly more MnSOD protein per unit mRNA than the MnSOD-Val lines (p<0.05). This suggests that the MnSOD-Ala lines are more efficient in their production of MnSOD protein than are MnSOD-Val lines. Studies are in progress to determine if differences in mRNA expression levels are due to human MnSOD DNA copy number and investigation of the effects of more efficient production of MnSOD by the MnSOD-Ala lines on the cellular redox balance is under way. (Supported by NIH grants R01CA94747 and T32ESO7141; MnSOD knockout MEF cells provided by Dr Simon Melov).
Stereotactic radiosurgery: a review and comparison of methods.
Authors: M H Phillips, K J Stelzer, T W Griffin, M R Mayberg, H R Winn
Journal: Journal of Clinical Oncology (1994)

PURPOSE Stereotactic radiosurgery (SRS) is an evolving modality for treating well-circumscribed intracranial lesions. Different physical methods have been developed to deliver highly localized dose distributions accurately. We review the different methods and the documented clinical results to present a coherent view of radiosurgery, and to aid physicians and physicists in the appropriate use of this modality. DESIGN A review of the medical physics and clinical literature was conducted. The physical aspects of the different methods and their impact on treatment were summarized. Results were compiled from those individual clinical series with adequate follow-up data to compare the various modalities with respect to treatment outcome for benign tumors, metastases, and vascular malformations. RESULTS The physical accuracy was comparable between radiosurgical methods. Differences between gamma radiation and linear accelerator methods had little effect on the dose distribution for single isocenter treatments. Charged particle methods could produce better dose localization for large lesions (&gt; 25 cm3) than was possible with photon methods. Clinical results indicate similar lesion control rates between all radiosurgical methods. There was a progressive increase in the median size of treated lesions for gamma radiation, linear accelerator, and charged particle methods. CONCLUSION For small lesions (&lt; 5 cm3), physical dose distributions are similar for the photon methods, but linear accelerator methods offer more flexibility for the treatment of intermediate-sized (5 to 25 cm3) lesions in applying future technical developments. More clinical results are needed before firm conclusions can be drawn on the type of lesions to be treated, and the dose-volume parameters to be used.
Secondary Leukemia or Myelodysplastic Syndrome After Treatment With Epipodophyllotoxins
Authors: Malcolm A. Smith, Lawrence Rubinstein, James R. Anderson, Diane Arthur, Paul J. Catalano, Boris Freidlin, Ruth Heyn, Anita Khayat, Mark Krailo, Vita J. Land, James Miser, Jonathan Shuster, Don Vena
Journal: Journal of Clinical Oncology (1999)

The incidence of secondary leukemia after epipodophyllotoxin treatment and the relationship between epipodophyllotoxin cumulative dose and risk are not well characterized. The Cancer Therapy Evaluation Program (CTEP) of the National Cancer Institute (NCI) has developed a monitoring plan to obtain reliable estimates of the risk of secondary leukemia after epipodophyllotoxin treatment.Twelve NCI-supported cooperative group clinical trials were identified that use epipodophyllotoxins at low (<1.5 g/m2 etoposide), moderate (1.5 to 2.99 g/m2 etoposide), or higher (> or =3.0 g/m2 etoposide) cumulative doses. Cases of secondary leukemia (including treatment-related myelodysplastic syndrome) occurring on these trials have been reported to CTEP, as has duration of follow-up for all patients, thereby allowing calculation of cumulative 6-year incidence rates of secondary leukemia for each etoposide dose group.The calculated cumulative 6-year risks for development of secondary leukemia for the low, moderate, and higher cumulative dose groups were 3.3%, (95% upper confidence bound of 5.9%), 0.7% (95% upper confidence bound of 1.6%), and 2.2%, (95% upper confidence bound of 4.6%), respectively.Within the context of the epipodophyllotoxin cumulative dose range and schedules of administration encompassed by the monitoring plan regimens, and within the context of multiagent chemotherapy regimens that include alkylating agents, doxorubicin, and other agents, factors other than epipodophyllotoxin cumulative dose seem to be of primary importance in determining the risk of secondary leukemia. Data obtained by the CTEP secondary leukemia monitoring plan support the relative safety of using epipodophyllotoxins according to the therapeutic plans outlined in the monitored protocols.
Asthma and COPD in war-related sulfur mustard exposed patients
Authors: Hamidreza Abtahi, Maryamossadat Moinazad Tehrani
Journal: European Respiratory Journal (2014)

Introduction:  There is few data about late respiratory effects of war-related sulfur mustard (SM) inhalation. We evaluated non-bronchiolitis obstructive pulmonary diseases in SM victims of Iran-Iraq war 18-22 years after their SM exposure.   Methods:  A cohort of SM patients of a referral clinic with diagnosis of obstructive pulmonary diseases were evaluated. Comprehensive recording of SM exposure events, demographic characteristics, presenting symptoms and signs, chest X-Ray, inspiratory/expiratory HRCT, baseline and bi-monthly spirometry, and medications was done. The prevalence of asthma and COPD and their association with age on exposure, number of exposures, mask use during exposure and history of smoking was studied.   Results:  In 100 Iranian SM victims (mean age 43.8± 7.6, range 34-75) years, the study was completed. All patients had ocular and dermal symptoms at time of their SM exposure. 43 and 36 out of 100 patients had asthma and COPD respectively. 50% of steroid unresponsive and 70% of steroid responsive COPD patients was less than 45 years old. Asthma prevalence was not different between different age groups. However, asthma accession in the following years in the age group 13-22 years at time of SM exposure is more than older age groups ( P=016). Asthma and COPD prevalence in SM victims were not associated with number of exposures, smoking before or after exposure, and mask use during exposure.   Conclusion:  Some features of asthma and COPD in SM victims were different from typical asthmatic and COPD patients and suggest association between these diseases with mustard gas exposure. Only age at time of the SM exposure was a significant risk factor for having asthma in future in SM victims.