tbuckley/cabot-search huggingface dataset:
Association of melanoma with glioblastoma multiforme
Authors: A. S. Desai, S. A. Grossman
Journal: Journal of Clinical Oncology (2008)

2082 Background: There are few well-established risk factors for the development of primary brain tumors. We conducted a descriptive, retrospective chart review, with the goal of identifying other systemic malignancies, including melanomas, which develop in adult patients with glioblastoma multiforme (GBM). We hypothesized an increased association of melanomas with GBM based on anecdotal observations. Methods: We queried the Johns Hopkins Cancer Registry to create a database of all patients with pathologically confirmed GBM diagnosed or treated at Johns Hopkins Hospital from June 1, 2000 to June 1, 2007. We performed a comprehensive review of the electronic medical record of these patients to describe personal history of prior or concomitant cancers, excluding non-melanomatous skin cancers. Multiple diagnoses in a single individual were recorded independently. We excluded individuals less than 18 years of age and those people with missing cancer history. We compared these data to historical controls based on publicly available Surveillance, Epidemiology, and End Results (SEER 17) data. Results: 510 records were assessed, with 12 excluded because of age less than 18, and 43 excluded because of absence of cancer history. From the remaining 455 individuals, representing 290 men and 165 women, we described 53 cancer diagnoses. Only 5 individuals contributed more than one cancer to this total number. The most commonly represented prior or concomitant malignancies were breast (n=6), melanoma (7), colorectal (8), and prostate (12). Expected counts for these cancers, based on SEER complete prevalence statistics, are respectively 5, 1, 2, and 6. Conclusions: In this preliminary retrospective analysis of a large GBM population, melanomas appear over-represented disproportionate to breast or prostate cancer. There has been previous suggestion of a possible association between gastrointestinal cancers and primary brain tumors, as in Turcot's syndrome. As melanomas and gliomas share common potential pathophysiologic pathways and responsiveness to temozolomide, these results may provoke further analysis to characterize a population at higher risk for development of these aggressive malignancies. No significant financial relationships to disclose.
Epidemiologic analysis of the laboratory-confirmed cases of influenza A(H1N1)v in Colombia
Authors: M Á Castro-Jiménez, J O Castillo-Pabón, G J Rey-Benito, P A Pulido-Domínguez, J Barbosa-Ramírez, D A Velandia-Rodriguez, E S Angulo-Martínez, None on behalf of the Virology Group and
Journal: Eurosurveillance (2009)

From 2 May to 16 July 2009, a total of 183 laboratory-confirmed cases of influenza A(H1N1)v were reported in Colombia, 117 (63.9%) of these had travelled outside the country. Hospital admission was necessary in 26 (14.21%) cases and seven patients died (fatality-case ratio: 3.8%). The infection affected younger age-groups and the symptoms most frequently reported were cough, fever and sore throat. Our findings are consistent with recent reports from other countries.
Scimitar Sign in a Patient With an Atrial Septal Defect
Authors: Sarinya Puwanant, Monravee Tumkosit, Surapun Sitthisook, Wacin Buddhari, Voravut Rungpradubvong, Smonporn Boonyaratavej
Journal: Journal of the American College of Cardiology (2009)
Abstract 13311: Cardiac SIRT1 Deficiency Sensitizes Myocardium to Ischemia and Reperfusion Injury
Authors: Jinli Wang, Yina Ma, Wanqing Sun, George Techiryan, Yanqing Wang, Ji Li
Journal: Circulation (2014)

Introduction: A “longevity” gene, sirtuin 1 (SIRT1) is a conserved NAD + -dependent protein deacetylase that regulates life span extension. We have reported that SIRT1 is down-regulated in the aged heart which shows larger infarct size and deteriorative heart function during ischemia and reperfusion (I/R) compared with that of young heart. Hypothesis: Cardiac specific SIRT1 deficiency could increase the sensitivity of heart to ischemic insults caused by ischemia and reperfusion. Methods: Male SIRT1 flox/flox mice and tamoxifen-inducible, cardiac-specific SIRT1 KO mice were subjected to I/R, which were induced by occluding the left anterior descending coronary (LAD) and subsequent releasing it. Langendorff-perfused heart model was used to monitor the heart function during I/R. Results: Adult cardiac-specific SIRT1 KO demonstrated significant cardiac hypertrophy, fibrosis and macrophage infiltration under normal physiological conditions versus the SIRT1 flox/flox hearts by immunohistochemical staining (all p&lt;0.05). The cardiac functions measured by the pressure-volume loop remained normal in SIRT1 KO mice as compared with SIRT1 flox/flox mice under physiological conditions. The ex vivo heart perfusion results showed that the heart rate-left ventricular developed pressure product in SIRT1 KO hearts was decreased by 30% versus the SIRT1 flox/flox hearts (p&lt;0.05), and the infarct size of SIRT1 KO hearts was 1.7-fold larger than that of SIRT1 flox/flox hearts (p&lt;0.05). The immunoblotting data demonstrated that SIRT1 KO hearts had impaired responsive activation of AMP-activated protein kinase (AMPK) signaling during I/R versus the SIRT1 flox/flox hearts. Furthermore, real-time qRT-PCR showed that cardiac SIRT1 KO resulted in up-regulation of pro-inflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin-1 β and growth differentiation factor15 (GDF15), as well as a heart failure marker ANP (atrial natriuretic peptide) versus SIRT1 flox/flox hearts during I/R. Conclusions: SIRT1 plays a vital role in regulation of myocardial infarction, heart function and inflammation induced by I/R in the heart. SIRT1 specific agonists may have therapeutic potential for treatment of ischemic heart disease.
Abstract 12532: Left Ventricular Diastolic Dysfunction and Exercise Intolerance in Type 2 Diabetes Patients With Endothelial Dysfunction
Authors: Tadafuni Sugimoto, Kaoru Dohi, Katsuya Onishi, Masahide Horiguchi, Takeshi Takamura, Tetsuya Seko, Atsunobu Kasai, Masaaki Ito
Journal: Circulation (2014)

Introduction: Endothelial dysfunction plays a central role in the pathogenesis of diabetic vascular disease. Hypothesis: Although resultant left ventricular diastolic dysfunction is hypothesized to reduce exercise capacity, limited data exist on the relation between endothelial function, left ventricular diastolic function and exercise capacity in patients with type 2 diabetes. Methods: We recruited 231 subjects with type 2 diabetes, a preserved ejection fraction, a negative stress test and a sodium-restricted diet. All subjects underwent a brachial artery flow-mediated dilation (FMD) measurement, a transthoracic echocardiography and a standard submaximal Bruce protocol treadmill exercise test during the hospitalization period for diabetes education program. Results: Impaired FMD (%FMD 8) were found in 193 subjects (84%) and 174 subjects (75%), respectively, of which 11 (5%) had diastolic dysfunction (E/E’ &gt;15). Mean E/E’ by quartile (Q) were: Q1 6.9, Q2 8.9, Q3 10.4, and Q4 14.0. E/E’ was inversely correlated with %FMD (2.9 ± 4.3%, r = -0.19, p = 0.003) and exercise duration (460 ± 150 sec, r = -0.30, p &lt;0.001). Compared with subjects in Q4, those in Q1, Q2 and Q3 had longer exercise duration (Q1 500 ± 150 sec, Q2 510 ± 140 sec, Q3 460 ± 140 sec and Q4 390 ± 140 sec, p &lt;0.001). After adjustment for potential confounders including age, gender, smoking, body mass index, medication for hypertension, diabetes duration of more than 5 years, HbA1c and systolic blood pressure, %FMD and exercise duration were significantly associated with E/E’ (β = -0.17 and -0.18, p = 0.006 and 0.014) in all subjects. Conclusions: Diabetes patients with impaired endothelial function have impaired left ventricular diastolic function potentially leading to exercise intolerance.
Abstract 19298: Heterozygosity for ABCC6 R1141X Does Not Associate with Risk of Ischemic Vascular Disease in 67,000 Individuals Including 14,000 Ischemic Events
Authors: Louise S Hornstrup, Ruth Frikke-Schmidt, Christiane L Haase, Borge G Nordestgaard, Peer Grande, Henrik Sillesen, Anne Tybjaerg-Hansen
Journal: Circulation (2010)
Assessing the Value of Intensive Care
Authors: Ian J. Barbash, Jeremy M. Kahn
Journal: JAMA (2015)

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
Mycobacterial Cell Wall-DNA Complex (MCC) for the treatment of carcinoma <i>in situ</i> of the bladder: Non-clinical and clinical phase I-II results
Authors: A. Morales, F. Hollande, N. Mottet, J. Ryan, N. Phillips, M. Filion, I. Voccia, M.-É. Fréchette, M. Rivière
Journal: Journal of Clinical Oncology (2005)

4587 Background: We report on MCC preclinical activity and the results from 2 clinical trials in patients with carcinoma in situ of the bladder (CIS). Methods: Immune stimulatory and anti-cancer activities of MCC were determined; toxicology profile following intravesical and intravenous administration was characterized. Clinical efficacy and safety were evaluated in two trials where 128 patients with CIS associated or not with papillary tumors (<T2) received MCC (4 or 8 mg). Patients received 6 weekly intravesical instillations and a maintenance treatment of up to 10 months. Safety was evaluated by adverse events (AEs); complete response (CR) was defined as negative biopsy, cystoscopy and cytology. Results: Apoptosis and inhibition of proliferation were shown in vitro in bladder cancer ATCC cell lines and in human bladder tumour cells in primary culture. Immuno-stimulation was seen in human PBMC. In toxicology studies MCC was non toxic intravenously at a human equivalent dose up to 4.32 mg/kg. In 2 clinical studies MCC was well tolerated by all patients with 20–37% drug related AEs and less than 1% drug-related SAEs. The CR rates were 63%, 49% and 41% at weeks 12, 24 and 60 for the phase I study. For the phase II study, the CR rates at weeks 12, 26, months 12 and 18 in the ITT population were 27%, 27%, 32% and 23% at a dose of 4 mg and 46%, 46%, 64% and 73% at a dose of 8 mg. Increases in urinary cytokines and apoptosis markers were observed in the majority of patients. Conclusions: Pre-clinical and clinical data demonstrated anticancer activity of MCC, clinical efficacy and an excellent safety profile. MCC is different from and has a different mechanism of action than BCG, the standard treatment for CIS. A multicenter phase 3 trial is being set up to confirm the efficacy and safety of MCC at a dose of 8 mg. No significant financial relationships to disclose.
Abstract 17963: Potential Mechanistic Insights on Genomic Myocardial Infarction Variants
Authors: Riyaz S Patel, Shaoyong Su, Ayushi Ahuja, Ian J Neeland, Salman Sher, John Douglas, Michael Mcdaniel, A Maziar Zafari, Viola Vaccarino, Arshed A Quyyumi
Journal: Circulation (2010)

Background: The mechanistic basis of 9 novel myocardial infarction (MI) risk variants discovered through GWAS is still undefined. We hypothesized that these loci act at different stages in the athe...
Genetic variability and occupational chronic obstructive pulmonary disease in subjects exposed to different environmental factors
Authors: Lioubov Shpagina, Mikhail Voevoda, Olga Kotova, Vladimir Maksimov, Ilya Shpagin, Pavel Orlov, Oksana Gerasimenko
Journal: European Respiratory Journal (2014)

Background. Chronic obstructive pulmonary disease (COPD) is a severe lung disease with high prevalence and mortality, caused by noxious particles including occupational dusts and fumes. Genetic features of COPD due to different occupational factors are not enough studied.  Objective is to investigate the association of single nucleotide polymorphisms (SNPs) rs 1800470 transforming growing factor β1 (TGF β1) gene, rs 1828591 hedgehog interacting protein (HHIP) gene, rs 4129267 interleukin 6 receptor (IL-6R) gene, rs 1051730 nicotinic acetylcholine receptor 3 (CHRNA 3) gene with COPD in subjects who exposed to different occupational risk factors.  Methods. Fifty two COPD subjects exposed to dusts and 30 exposed to aromatic series hydrocarbons fume enrolled. Control group – 105 healthy donors. Associations were modeled using logistic regression.  Results. SNP rs 1828591 was associated with COPD both in subjects exposed to dusts and in those exposed to chemicals. In the group exposed to dusts, for genotypes AA and AG OR = 2.22, 95 % CI = 1.01–4.91 and OR = 2.05, 95 % CI = 1.03 – 4.06, respectively. In the group exposed to chemicals, for genotype AG OR = 0.17, 95 % CI = 0.04 – 0.70, for genotype GG OR = 5.10, 95 % CI = 1.15 – 17.12. SNP rs 1800470 was associated with COPD in subjects exposed to dusts only. For genotypes AA and AG OR = 0.34, 95 % CI = 0.15 – 0.72 and OR = 0.4, 95 % CI = 0.2 – 0.8, respectively. SNPs rs 4129267 and rs 1051730 was not associated with occupational COPD.  Conclusions. Occupational COPD due to dusts is associated with SNP rs1800470 and SNP rs1828591. Occupational COPD due to chemicals is associated with SNP rs1828591.
Preventing sex offences: the Dunkelfeld project
Authors: B. Hillier, P. Murphy
Journal: BMJ (2015)

Ho and Rampling highlight the ongoing debate regarding sex offenders.1 2 The situation is not as simple as sex offenders being perpetrators who should be punished, as they have often been victims themselves. Moreover, mental disorder is not uncommon in this group, and there may be a genetic component.3 4

Forensic services …
Abstract 5317: Preclinical evaluation of IQS019, a novel BCR kinase inhibitor, in in vitro and in vivo models of non-Hodgkin lymphoma
Authors: Patricia Balsas, Jocabed Roldan, Laura Jimenez, Vanina Rodriguez, Raimon Puig de la Bellacasa, Jordi Teixido, Alba Matas-Cespedes, Alexandra Moros, Antonio Martinez, Elias Campo, Jose I Borrell, Patricia Perez-Galan, Dolors Colomer, Gael Roue
Journal: Cancer Research (2015)

Abstract Constitutive activation of B-cell receptor (BCR) signaling is a hallmark of several B-cell non-Hodgkin lymphoma (B-NHL), including diffuse large B-cell lymphoma (DLBCL), mantle cell lymphoma (MCL), follicular lymphoma (FL) and chronic lymphocytic leukemia (CLL). Despite the promising clinical activity of the first BCR kinase inhibitors in some of these entities, the design of new compounds is warranted to improve the survival of B-NHL patients who are poorly responsive, and/or who eventually develop resistance to current BCR-targeting therapies. In this context, we recently described the synthesis of IQS019, a 4-aminopyrido[2,3-d]pyrimidine with improved inhibition pattern against the three BCR-related kinases Lyn, Syk and Btk, when compared to reference BCR kinase inhibitors. Here, by assessing the activity of IQS019 in a panel of 21 human cell lines and 17 primary samples representative of the main B-NHL subtypes, we show that doses of IQS019 in the micromolar range allowed to a rapid and dose-dependent de-phosphorylation of both constitutive and Ig-activated Syk, Lyn and Btk in CLL, MCL, FL and DLBCL cell lines and CLL primary cultures. IQS019 treatment impairs cell proliferation and CXCL12-dependent cell migration, and leads to the induction of caspase-dependent apoptosis. Of interest, in CLL primary cells, these effects were independently of IGVH mutational status. In xenotransplant mouse models of MCL and FL, daily dosing of 2 mg/kg IQS019 for two weeks demonstrated to be safe for the animals and allowed to a 50-60% reduction in tumor outgrowth and glucose uptake, together with a 52% decrease in cell infiltration into the spleen (p &amp;lt; 0.05). These effects were accompanied by a significant (p &amp;lt; 0.05) downregulation of p-Syk, p-Lyn and p-Btk, and consequent mitotic arrest and induction of apoptosis in human malignant B cells. Altogether, these results define the BCR kinase inhibitor IQS019 as a potential candidate in antitumor therapy against a variety of B-NHL subtypes with aberrant activation of BCR pathway. Citation Format: Patricia Balsas, Jocabed Roldan, Laura Jimenez, Vanina Rodriguez, Raimon Puig de la Bellacasa, Jordi Teixido, Alba Matas-Cespedes, Alexandra Moros, Antonio Martinez, Elias Campo, Jose I Borrell, Patricia Perez-Galan, Dolors Colomer, Gael Roue. Preclinical evaluation of IQS019, a novel BCR kinase inhibitor, in in vitro and in vivo models of non-Hodgkin lymphoma. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 5317. doi:10.1158/1538-7445.AM2015-5317
FTIR characterization of the secondary structure of proteins encapsulated within PLGA microspheres1An article of related interest has been published by Yang et al. in J. Pharm. Sci., 88(2), Feb. 1999, accepted Nov. 1998.1
Authors: Karen Fu, Kai Griebenow, Lisa Hsieh, Alexander M Klibanov, None Robert Langer
Journal: Journal of Controlled Release (1999)
Hepatitis C and G Virus Infection and Liver Dysfunction After Allogeneic Bone Marrow Transplantation: Results From a Prospective Study
Authors: Elena Rodriguez-Iñigo, José-Francisco Tomás, Valle Gómez-Garcı́a de Soria, Javier Bartolomé, Inmaculada Pinilla, Marı́a-José Amaro, Vicente Carreño, José-Marı́a Fernández-Rañada
Journal: Blood (1997)
Multiparameter flow cytometry for the identification of the Waldenström’s clone in IgM-MGUS and Waldenström’s Macroglobulinemia: new criteria for differential diagnosis and risk stratification
Authors: B Paiva, M C Montes, R García-Sanz, E M Ocio, J Alonso, N de las Heras, F Escalante, R Cuello, A G de Coca, J Galende, J Hernández, M Sierra, A Martin, E Pardal, A Bárez, J Alonso, L Suarez, T J González-López, J J Perez, A Orfao, M-B Vidríales, J F San Miguel
Journal: Leukemia (2013)
Abstract 20251: A Novel Role for Brown Adipose Tissue in Cardioprotection
Authors: Robrecht Thoonen, Laura Ernande, Allyson Hindle, Juan Cheng, Wei Chao, Kenneth D Bloch, Emmanuel S Buys, Marielle Scherrer-Crosbie
Journal: Circulation (2014)

Introduction: Brown adipose tissue (BAT), upon activation by natriuretic peptides and catecholamines, converts the energy of free fatty acids and glucose oxidation into heat (thermogenesis) through uncoupling protein 1 (UCP1). BAT activation has also been reported to increase triglyceride uptake and improve insulin resistance in obesity. Hypothesis: We hypothesized that activated BAT limits myocardial injury and remodeling in a catecholamine-induced cardiomyopathy model. Methods: Isoproterenol (ISO, 60 mg/kg/day) or saline were infused in wild type (WT, n=12) and UCP1-deficient (UCP1-/-, n=11) mice for 14 days using an osmotic minipump. Plasma cardiac troponin I levels (cTnI) were measured after 3 days of treatment. Echocardiograms were performed before and after treatment for 14 days. BAT and LV were harvested for RNA and histology. The experiments were repeated in mice that had undergone prior BAT transplantation (WT to WT n=8; WT to UCP1-/- n=7; UCP1-/- to UCP1-/- n=6). Results: At baseline LV size, mass and ejection fraction (LVEF) were similar in WT and UCP1-/- mice, cTnI was undetectable. Gene expression in BAT of UCP1-/- mice revealed decreased lipid metabolism and oxidative phosphorylation. After 3 days of ISO treatment plasma cTnI was markedly increased in UCP1-/- mice compared to WT (Table). After 14 days of ISO infusion UCP1-/- mice developed greater LV hypertrophy and fibrosis than WT mice (Table). Transplantation of UCP1-/- BAT to UCP1-/- or WT mice did not decrease isoproterenol-induced cTnI release, however, transplantation of WT BAT to UCP1-/- mice reversed the increased cTnI and adverse remodeling. Conclusions: UCP1-deficiency causes BAT dysfunction, and increases cardiomyocyte injury and adverse LV remodeling in a mouse model of catecholamine-induced cardiomyopathy. Cardiomyocyte injury and adverse LV remodeling are rescued by transplantation of functional BAT in to UCP1-/- mice, suggesting that functional BAT is cardioprotective.
Double-blind comparison of sertraline, imipramine, and placebo in the treatment of dysthymia: psychosocial outcomes
Authors: J H Kocsis, S Zisook, J Davidson, R Shelton, K Yonkers, D J Hellerstein, J Rosenbaum, U Halbreich
Journal: American Journal of Psychiatry (1997)

Objective: The purpose of this study was to determine the effects of antidepressant pharmacotherapy on mood symptoms and psychosocial outcomes in dysthymia.Method: In a multicenter, double-blind, parallel-group trial, 416 patients with a diagnosis of early-onset primary dysthymia (DSM-III-R) of at least 5 years' duration without concurrent major depression were randomly assigned to 12 weeks of acute-phase therapy with sertraline, imipramine, or placebo.The psychosocial outcome measures used in the study were the Global Assessment of Functioning Scale, the Social Adjustment Scale, the Longitudinal Interval Follow-up Evaluation psychosocial ratings, and the Quality of Life Enjoyment and Satisfaction Questionnaire.Results: Sertraline and imipramine were significantly better than placebo in improving psychosocial outcomes as measured by the first three instruments.The Quality of Life Enjoyment and Satisfaction Questionnaire scores demonstrated significant improvements from baseline, and both active treatments produced significantly greater improvements than placebo.Significantly fewer patients discontinued sertraline (6.0%) than discontinued imipramine (18.4%) because of adverse events.Conclusions: Pharmacotherapy is an effective treatment for dysthymia in terms of psychosocial functioning as well as depressive symptoms, even when the dysthymia is long-standing.