tbuckley/cabot-search huggingface dataset:
Total serum bilirubin levels are not related to the severity of COPD
Authors: Frits M.E. Franssen, Martijn A. Spruit, Lucie G.M. Fransen, Emiel F.M. Wouters
Journal: European Respiratory Journal (2011)

Introduction:  It was recently reported that lower serum total bilirubin (tBLN) levels are associated with higher incidence of COPD and all-cause mortality, after adjustment for other risk factors, including smoking [1]. Aim of this study was to investigate whether serum total bilirubin levels are related to the degree of airflow limitation and other determinants of severity of COPD.   Methods:  Data were extracted from the records of 1239 patients with COPD (58% males, age 64±10y, FEV 1  46±19%, BMI 25.4±5.3kg/m 2 ) referred for pulmonary rehabilitation. Serum tBLN >22μmol/L was an exclusion criterium. Lung function (FEV 1 , diffusion capacity (DL CO )), arterial blood gases, body composition and six-minute walking distance (6MWD) were measured as part of integrated assessment of health status.   Results:  tBLN levels were comparable in all GOLD stages. In male patients tBLN levels were 12.0±4.2μmol/L (GOLD 1), 12.1±4.0μmol/L (GOLD 2), 12.7±3.7μmol/L (GOLD 3) and 11.8±3.8μmol/L (GOLD 4), while levels were 10.8±3.7μmol/L (GOLD 1), 10.6±4.0μmol/L (GOLD 2), 10.2±3.6μmol/L (GOLD 3) and 10.6±3.8μmol/L (GOLD 4) in female patients (all p 1 , arterial p a O 2 , BMI, number of pack years or 6MWD. A statistically significant but weak bivariate correlation was observed between tBLN and arterial p a CO 2  (r =-0.084, p CO  (r=-0.070, p   Discussion:  Serum total bilirubin levels are neither related to the degree of airflow limitation nor to other variables of disease severity in patients with COPD. Further research is needed clarify a possible contribution of low tBLN levels to the development of COPD.   Reference:   1Horsfall LJ, Serum bilirubin and risk of respiratory disease and death, JAMA 2011.
Allogeneic bone marrow transplantation for low-grade lymphoma.
Authors: Koen Van Besien, Kathleen A. Sobocinski, Philip A. Rowlings, Sandra C. Murphy, James O. Armitage, Michael R. Bishop, Ok Kyong Chaekal, Robert Peter Gale, John P. Klein, Hillard M. Lazarus, Philip L. McCarthy, John M.M. Raemaekers, Josy Reiffers, Gordon L. Phillips, Anton V.M.B. Schattenberg, Leo F. Verdonck, Julie M. Vose, Mary M. Horowitz
Journal: Blood (1998)
Abstract 1833: De novo <i>EGFR</i> T790M mutation in lung cancer patients harboring sensitive <i>EGFR</i> mutations
Authors: Youngjoo Lee, Geon Kook Lee, Yeon-Su Lee, Wenji Zhang
Journal: Cancer Research (2014)

Abstract Background EGFR T790M mutation drives acquired drug resistance to EGFR tyrosine kinase inhibitors (EGFR-TKI) in EGFR-mutant lung cancer. However, it was reported that this mutation may exist before drug exposure. This study aimed to evaluate whether the clinical outcomes are affected by the proportion of preexisting T790M mutations within a tumor. Methods We collected pretreatment tissues from 124 advanced non-small cell lung cancer patients with sensitizing EGFR mutations that were detected by direct sequencing. Genotyping for EGFR T790M was further performed using matrix-assisted laser desorption/ionization-time of flight/mass spectrometry. T790M-positive patients were divided to two subgroups according to T790M mutant signal frequency. Results The T790M mutation was found in 31 (25.0%) patients. The T790M mutation frequency at which the risk of progression to EGFR-TKI begins to increase was estimated to be 2.0%. The patients with T790M-positive tumor had shorter time to progression (TTP) after EGFR-TKI (median 6.3 months vs. 11.5 months; P &amp;lt; 0.001) and overall survival (OS) (median 16.1 months vs. 26.5 months; P = 0.065) than those with T790M-negative tumor. Among the T790M-positive patients, the patients with high T790M frequency (n= 9) had shorter TTP (median 2.4 months vs. 6.7 months; P = 0.009) and OS (median 9.1 months vs. 18.7 months; P = 0.018) than those with low T790M frequency (n= 22). Conclusions Preexisting EGFR T790M mutation was noted in 25% of patients with EGFR-mutant lung cancer. Patients with high T790M mutation frequency had worse clinical outcomes to EGFR-TKI than patients with low T790M mutation frequency. Citation Format: Youngjoo Lee, Geon Kook Lee, Yeon-Su Lee, Wenji Zhang. De novo EGFR T790M mutation in lung cancer patients harboring sensitive EGFR mutations. [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 1833. doi:10.1158/1538-7445.AM2014-1833
Abstract 1880: Pathologic response pattern of breast cancer after neoadjuvant chemotherapy: its correlation with molecular subtypes
Authors: In-Hye Song, Hee Jin Lee, Gyungyub Gong
Journal: Cancer Research (2014)

Abstract Background: Several ways to assess pathologic response of breast cancer after neoadjuvant chemotherapy (NAC) are currently used, including Miller-Payne system and residual cancer burden. However, the relationship between pathologic response pattern and molecular subtype of breast cancer is unclear. Methods: We investigated the pathologic response pattern of breast cancer after NAC in each molecular subtype. Female breast cancer patients who received NAC and subsequent breast operation were retrospectively analyzed. The NAC regimen used for breast cancer was primarily anthracycline and taxane-based, depending on the axillary lymph node involvement. We evaluated the molecular subtypes by immunohistochemistry, pretreatment tumor sizes by MRI, absolute invasive tumor cellularities in pretreatment biopsy and operation specimens, pathologic complete response (pCR) rates, posttreatment pathologic tumor sizes, overall residual tumor cellularities, and grades for Miller-Payne system. Results: A total of 119 patients (age: 45.2 ± 9.5 yr) were enrolled. Sixty-six cases were hormone receptor positive (ER or PR positive), 18 cases were HER2 positive (ER and PR negative), and 35 cases were triple negative. There were no significant differences in pretreatment tumor size by MRI and absolute cellularity in biopsy between three groups. After NAC, hormone receptor positive tumors showed the lowest pCR rate (18.2 %) while triple negative tumors showed the highest pCR rate (45.7 %, p=0.013). In patients with residual carcinoma, hormone receptor positive tumors showed the largest ypT size (p=0.016), the least reduction of tumor size (p=0.001), and the least absolute invasive tumor cellularity (p=0.006). Overall residual tumor cellularity and Miller-Payne grade were not significantly different between three groups (p=0.4 and p=0.703, respectively). Conclusion: These results suggest that each molecular subtype of breast cancer shows characteristic pathologic response patterns following NAC. Citation Format: In-Hye Song, Hee Jin Lee, Gyungyub Gong. Pathologic response pattern of breast cancer after neoadjuvant chemotherapy: its correlation with molecular subtypes. [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 1880. doi:10.1158/1538-7445.AM2014-1880
741. VSV-G Pseudotyped, MLV-Based, Semi-Replication-Competent Retroviruses for Cancer Gene Therapy
Authors: Jian Qiao, Jesus Moreno, Michael Forshaw, Rosa M. Diaz, Richard G. Vile
Journal: Molecular Therapy (2004)

Retroviral vectors have been widely used as gene delivery vehicles for cancer gene therapy. However, insufficient levels of gene delivery with replication defective vectors have severely limited their efficacy for clinical protocols using direct in vivo delivery. Therefore, we have investigated the potential of developing replication-competent and semi-replication competent retroviruses for cancer gene therapy. Given recent adverse events in patients receiving replication defective vectors for modification of cells ex vivo, inclusion of multiple safety features are clearly necessary if such a vector is to pursued for in vivo delivery.
Sustainability, the Environment and Urbanization, by Ed Cedric Pugh
Authors: P. Garner
Journal: BMJ (1997)

Ed Cedric Pugh Earthscan, £16.95, pp 250 ISBN 1 85383 357 6

Cities in many developing countries have been growing since the 1960s at a remarkable rate, and now over 430 million poor people live in them. The impact on the environment is immense. A city of 100 000 people consumes 200 tonnes of food and generates 385 tonnes of garbage and human waste a day, so it is not surprising that city planners and inhabitants alike are concerned with services and meeting basic living requirements.

Ironically, city growth is part of industrial development. Cities are huge economic machines, …
Abstract 15873: Adverse Cardiac and Pulmonary Vascular Change in Patients With Subclinical and Clinical Copd
Authors: Jie Cao, Kathy Halloran, Joshua Cheng, Michael Passick, Nora Ngai
Journal: Circulation (2014)

Background:  COPD is associated with altered right ventricular (RV) and pulmonary vascular function. However, little is known about such change in patients with subclinical COPD.   Methods:  Thirty nine volunteers were recruited prospectively to undergo echocardiography, MRI and pulmonary function test (PFT). COPD was defined as FEV1/FVC 75% with no smoking history (N=9). Cardiac function was assessed by cine MRI. All subjects underwent first pass lung perfusion using a partial Fourier saturation recovery SSFP technique. The absolute lung perfusion was calculated using dynamic contrast signal in the pulmonary artery as input and that in the lungs. Total lung blood volume was the function of mean blood transit time and cardiac output in main pulmonary artery (PA).   Results:  Average FEV1/FVC was 84±6%, 73±3% and 50±15% for normal, subclinical and clinical COPD groups, respectively (p   Conclusions:  Our findings suggest that the decline of cardiovascular function precedes the full development of COPD. Future research on pulmonary and cardiovascular change in patients with subclinical COPD is warranted.
Danazol and Cholestatic Hepatitis
Authors: BOUE FRANÇOIS
Journal: Annals of Internal Medicine (1986)

Letters and Corrections1 July 1986Danazol and Cholestatic HepatitisBOUE FRANÇOIS, M.D., BENOIT COFFIN, M.D., JEAN-FRANÇOIS DELFRAISSY, M.D.BOUE FRANÇOIS, M.D., BENOIT COFFIN, M.D., JEAN-FRANÇOIS DELFRAISSY, M.D.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-105-1-139_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Danazol, used since 1971 for treatment of pelvic endometriosis, cystic disease of the breast, and hereditary angioneurotic edema, has recently been reported to be effective in idiopathic thrombocytopenic purpura (1). Because danazol is a C17 alkylated anabolic steroid, hepatic dysfunction and jaundice might be expected. We report a case of cholestatic hepatitis apparently induced by danazol.A 73-year-old woman was referred with idiopathic thrombocytopenic purpura responding to prednisone. Treatment was stopped 6 months later with a good result. A moderate relapse occurred 1 year afterwards, and prednisone therapy was restarted. Because of iatrogenic Cushing's syndrome, prednisone was...References1. AHNHARRINGTONSIMONMYLVAGANAMPALLSO YWSRRA. Danazol for the treatment of idiopathic thrombocytopenic purpura. N Engl J Med. 1983;308:1396-9. CrossrefMedlineGoogle Scholar2. MADANESFARBER AM. Danazol. Ann Intern Med. 1982;96:625-30. LinkGoogle Scholar3. PEARSONZIMMERMAN KH. Danazol and liver damage. Lancet. 1980;1:645-6. CrossrefMedlineGoogle Scholar4. NESHERDOLLBERGZIMRAN GLA. Hepatosplenic peliosis after danazol and glycocorticoids for ITP. N Engl J Med. 1985;312:242. CrossrefMedlineGoogle Scholar5. BUAMAH P. An apparent danazol-induced primary hepatocellular carcinoma: case report. J Surg Oncol. 1985;28:114-6. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: HOPITAL ANTOINE BECLERE 92141 Clamart France PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byDrugs and ToxinsUsing Chemical-Induced Gene Expression in Cultured Human Cells to Predict Chemical ToxicityHepatic injury due to drugs, herbal compounds, chemicals and toxinsDanazolDanazol‐induced hepatocellular carcinomaHepatotoxityDanazol-induced hepatocellular adenoma9 Drug-induced cholestasis 1 July 1986Volume 105, Issue 1Page: 139-140KeywordsEdemaGenetic diseasesHepatitisHepatitis AIdiopathic thrombocytopenic purpura ePublished: 1 December 2008 Issue Published: 1 July 1986 PDF downloadLoading ...
Abstract 13673: Aging Impairs Cardiac Akt Activity Leading to Myocardial Sarcopenia
Authors: Yasuko K Bando, Morihko Aoyama, Haruya Kawase, Akio Monji, Cheng Xiangwu, Masafumi Kuzuya, Toyoaki Murohara
Journal: Circulation (2014)

Introduction: Aging causes skeletal muscle atrophy (i.e. sarcopenia). In heart, aging is also known to cause cardiac dysfunction such as diastolic dysfunction; however, the impact of aging on myocardial cell growth remains uncertain. Hypothesis: Because of the pivotal role of protein kinase Akt in cellular aging and growth of cardiomyocytes, we hypothesized whether #1 aging may impairs cardiac Akt activation leading to myocardial atrophy in aged heart and #2 regular exercise may enhance cardiac Akt activity, leading to augmentation of cardiomyocyte growth that results in reversal of the aging-mediated cardiac atrophy. Methods: [cohort-1]: Male genetically senescence-accelerated [(SAM; senescence-accelerated prone (P10)] and senescence-resistant counterpart (R1) were allocated to EX [60-min running by treadmill/day for 6 months] and EX-free control (CON). [cohort-2] Male aged (40 w/o) and young (14 w/o) C57BL6 mice were subjected to the EX (agedC57EX and agedC57CON). Results: At baseline, cardiac geometry of R1 revealed normal, whereas P10 exhibited LV wall thinning and diastolic dysfunction. Systolic function of both P10 and R1 was preserved. After EX, body and heart weight (HW/BW) of R1 were increased (BW; +6.7% and HW; +3.5% versus R1CON); however, EX had no influence on HW/BW of P10. EX promoted LV hypertrophy in R1EX with concomitant increase in cardiac capillary density through activation of Akt/eNOS pathway, which was absent in P10EX. EX had no influence on systolic function of R1EX, however, EX promoted systolic dysfunction in P10EX [EF(%) 68.9±1.5 for P10EX versus 74.3±1.2 for P10CON] with attenuation of phosphorylated Akt and phospholamban levels in myocardium. In youngC57EX, EX promoted myocardial hypertrophy with augmentation of cardiac Akt/mTOR/S6K axis, which was diminished in agedC57EX. Age- and gender-matched Akt knockout mice exhibited lack of the EX-induced cardiac hypertrophy. Conclusions: Aging promotes cardiac sarcopenia in mice, in which Akt plays an essential role. EX-induced adaptive cardiac hypertrophy requires Akt activation and aging heart lacks the EX-induced Akt activation.
A phase 1 study of the selective cyclin dependent kinase inhibitor P276-00 in patients with advanced refractory neoplasms
Authors: H. Hirte, D. Raghunadharao, T. Baetz, S. Hotte, S. Rajappa, A. Iacobucci, S. Sharma, H. Parikh, S. Kulkarni, S. Patil, S. Gaston
Journal: Cancer Research (2007)

4368    Introduction:  In human cancers, genetic and epigenetic events result in over-expression of cyclins or absence or diminished levels of Cdk inhibitors, which provides tumor cells with selective growth advantage. These observations have prompted the development of pharmacological Cdk inhibitors that could potentially produce anti-tumor effect. P276-00 is a selective Cdk4-D1 and Cdk1-B inhibitor obtained by modifications of compounds derived from a synthetic library. This study was designed to determine the maximum tolerated dose (MTD), toxicity profile, pharmacokinetics, and antitumour activity of P276-00 given intravenously to patients with advanced refractory solid tumours.   Patients and Methods:  P276-00 was administered in escalating doses to cohorts of eligible patients (pts), starting with a dose of 9 mg/m 2  as a 30 minute iv infusion day 1 to 5, and day 8 to 12, q 3 weekly. To date 22 pts have been entered on the study (cohort 1 - 4 pts at 9 mg/m 2 , cohort 2 - 4 pts at 12.6 mg/m 2 , cohort 3 - 6 pts at 17.6 mg/m 2 , cohort 4 - 8 pts at 24.6 mg/m 2 ) with PS 0-2, and mean age of 56 years. Pharmacokinetic profiles were obtained on cycle 1 days 1 and 5. Where possible, skin biopsies were obtained immediately prior to starting study treatment and on day 21 of cycle 2 and will be analyzed for Ki67, cleaved caspase 3, phospho-Rb, cyclin D1 and cdk4, and microarray.   Results:  To date dose limiting toxicity has occurred in one pt. Grade 3 fatigue occurred in 1 pt at 17.6 mg/m 2 . The most common drug-related adverse events, all of which were grade 1 or 2, were fatigue, nausea, hypotension, sweating, and dry mouth. No Grade 3 biochemical toxicities have been reported so far. There have been no responses noted to date. 4 pts have stable disease after 2 cycles which has been confirmed in 1 pt after 4 cycles. Pharmacokinetic results: The C max , t 1/2 , and AUC 0-∞  on day 1 were as follows: 9 mg/m 2 - 315 ng/mL, 6.6 hr, 883 ng.h/mL; 12.6 mg/m 2 - 402 ng/mL, 5.5 hr, 848 ng.h/mL; 17.6 mg/m 2 - 589 ng/mL, 5.3 hr, 1289 ng.h/mL; 24.6 mg/m 2 - 621 ng/mL, 5.6 hr, 1286 ng.h/mL. Skin biopsies will be analyzed once all matching pairs of samples have been collected from patients on study.   Conclusions:  P276-00 is well tolerated, but grade 3 fatigue has been noted in 1 pt at 17.6 mg/m 2  dose level. We have observed confirmed stable disease in one patient. PK results indicate that at 9 mg/m 2 ,12.6 mg/m 2 , 17.6 mg/m 2  and 24.6 mg/m 2  we are able to cross the cdk4 enzyme IC 50  approximately 10, 13, 19 and 20 times and cross the anti-proliferative IC 50  1.1 , 1.4, 2.1 and 2.2 times respectively. Accrual continues at the 34.4 mg/m 2  dose level.
A Host of Novel Agents for Treating Psoriasis, Psoriatic Arthritis Stir Interest
Authors: Lynne Lamberg
Journal: JAMA (2003)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Abstract 12498: Management and Outcomes of Cardiac Tamponade during Atrial Fibrillation Ablation in the Presence of Therapeutic Anticoagulation with Warfarin
Authors: Rakesh Latchamsetty, Sandeep Gautam, Deepak Bhakta, Roy John, Laurence Epstein, John Miller, Gregory Michaud, Hakan Oral, Fred Morady, Krit Jongnarangsin
Journal: Circulation (2010)

Background: Cardiac tamponade (CT) is an important complication associated with catheter ablation of atrial fibrillation (AF). The incidence of CT has been reported to be unchanged when ablation is...
Follow-up Surveillance After Endovascular Aneurysm Repair
Authors: Andrew W. Hoel, Andres Schanzer
Journal: JAMA Surgery (2015)

In disease surveillance, a tension exists between adequate detection of disease progression and the risk for overdiagnosis and unnecessary use of resources.The goal of imaging surveillance after endovascular aneurysm repair (EVAR) can be stated simply: early detection of asymptomatic problems to avoid potentially severe consequences (ie, post-EVAR aneurysm rupture).Existing guidelines for surveillance after EVAR 1 are based largely on expert opinion, and high-quality evidence to inform the ideal post-EVAR surveillance regimen does not exist.In a well-executed and provocative study, Garg and colleagues 2 explore this gap in our understanding of the ideal post-EVAR surveillance regimen.Using a retrospective evaluation of Medicare claims data, they evaluated post-EVAR adverse events based on whether or not patients received post-EVAR surveillance imaging that adheres to existing guidelines.As the authors have previously demonstrated, 3 approximately half of Medicare patients do not have post-EVAR surveillance that adheres to existing guidelines.In the present study, the authors demonstrate that patients with incomplete surveillance had lower rates of reintervention, allcause mortality, and aneurysm-related events, including rupture.These findings appear to be at odds with the concept that rigorous follow-up improves long-term patient outcomes.However, for a number of reasons, we believe that concluding from this work that less frequent surveillance will result in equivalent outcomes is inaccurate.First, complex aor-