tbuckley/cabot-search huggingface dataset:
Abstract 18641: An m-Health Application of Daily Text Messages to Address Forgetfulness as Contributor to Non-adherence to Medications Post-myocardial Infarction
Authors: Avinash Pandey, Niteesh Choudhry
Journal: Circulation (2015)

Introduction: Forgetfulness has been consistently identified as a contributor to non-adherence to medications. In post myocardial infarction (MI) patients, up to 50% of patients may remain non-adherent to medication at one year. Text message reminders to patients’ cell phones could be a cost-effective method to reduce medication non-adherence. Hypothesis: It was hypothesized that daily text message reminders would improve adherence to medications in post-MI patients. Methods: This was a single center, randomized trial of text message system conducted in a cardiac rehabilitation facility. Patients post-MI on a once daily regimen of aspirin, a beta-blocker, an angiotensin converting enzyme inhibitor or angiotensin receptor blocker and a statin were recruited. Participants were randomized to usual care or to receive daily text messages at the prescribed timings indicating which medication that should be taken at each time. We performed pre-specified subgroup analysis in the elderly (age ≥ 65 years) and those with less education (grade 12 or less). Results: In a two month recruitment period, ninety patients were screened and thirty-four were randomized, 36% of which were female, and with an average age of 64 years. No significant baseline differences between intervention and controls patients were identified. In the control group, adherence fell from 92% after month 1 to 70% at month 12. In the intervention group, adherence dropped from 98% after month 1 to 90% at month 12 (p&lt;0.0001 for difference between intervention and control at month 12). In all evaluated subgroups, text message reminders consistently improved adherence to medications. Reminders appeared to particularly effective in subgroups with lower baseline adherence such as the elderly and those with less education. In interviews, forgetfulness was identified as a leading cause of their non-adherence to medications. Conclusions: In post-MI patients, this study demonstrates significant improvement in adherence to medications with an automated, daily text message reminder system over one year of follow-up. Simple and scalable systems such as this text message reminder system may improve adherence to evidence-based therapies in this high risk population by addressing forgetfulness.
Timing of Continuous Renal Replacement Therapy
Authors: Leano Violo, Marianna De Francesco
Journal: JAMA Surgery (2017)

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 Surgery HomeNew OnlineCurrent IssueFor Authors Podcast 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) 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 Surgery journal
Activation of inflammatory cells during asthma exacerbations is initiated prior to their migration to the lung
Authors: A. C. Jones, J. Bizzintino, S. Khoo, K. Rueter, I. A. Laing, J. Goldblatt, P. N. Le Soeuf, P. D. Sly, D. H. Strickland, A. Bosco, P. G. Holt
Journal: Allergy (2017)
Early impact of 13-valent pneumococcal conjugate vaccine on pneumococcal meningitis—Burkina Faso, 2014–2015
Authors: Dinanibè Kambiré, Heidi M. Soeters, Rasmata Ouédraogo-Traoré, Isaïe Medah, Lassana Sangaré, Issaka Yaméogo, Guetawendé Sawadogo, Abdoul-Salam Ouédraogo, Soumeya Ouangraoua, Lesley McGee, Velusamy Srinivasan, Flavien Aké, Malika Congo-Ouédraogo, Absatou Ky Ba, Cynthia G. Whitney, Ryan T. Novak, Chris Van Beneden
Journal: Journal of Infection (2017)
Beyond neonatal imitation: Aerodigestive stereotypies, speech development, and social interaction in the extended perinatal period
Authors: Nazim Keven, Kathleen A. Akins
Journal: Behavioral and Brain Sciences (2017)

Abstract In our target article, we argued that the positive results of neonatal imitation are likely to be by-products of normal aerodigestive development. Our hypothesis elicited various responses on the role of social interaction in infancy, the methodological issues about imitation experiments, and the relation between the aerodigestive theory and the development of speech. Here we respond to the commentaries.
Association of basal marker expression with outcome and trastuzumab resistance in HER2-positive breast cancer.
Authors: Alice P. Chung, Michael Phillip Choi, Shikha Bose, Xiao Zhang, Marian Varda, Xiaojiang Cui, Armando Giuliano
Journal: Journal of Clinical Oncology (2014)

608 Background: Herceptin resistance is a significant challenge in the treatment of Her2-positive (Her2+) breast cancer. A subset of Her2+ breast cancers are known to express basal genes (basal Her2). We investigated the effect of basal gene expression on cell viability and Herceptin response in Her2+ breast cancer cell lines and on prognosis in patients with Her2+ breast cancer who received Herceptin. Methods: We selected 4 cell lines to represent basal Her2 (HCC1569, HCC1954) and non-basal Her2 (BT474, SKBR3) breast cancer based on their basal gene signature in microarray analysis, and treated each with vehicle, Herceptin (H), Paclitaxel (P), and H + P. Cell viability was assessed by MTT assays. Her2 pathway suppression was compared between groups using immunoblotting with anti-Her2, p-AKT, p-ERK antibodies. Expression of CK5/6, CK14, and EGFR was evaluated after immunohistochemical staining in paraffin-embedded tissue of 88 patients with Stage 1-3 Her2+ breast cancer treated with chemotherapy and Herceptin. Groups with and without basal gene expression were compared with respect to clinicopathologic parameters and survival. Results: All cell lines expressed similar levels of Her2. Both H and P alone inhibited proliferation of non-basal cell lines, and H + P had an additive cytotoxic effect. Basal cells were resistant to H, P inhibited proliferation, but H + P had no additive cytotoxic effect on cell growth in basal cells. Immunoblotting showed a significant decrease in p-Akt levels after treatment with H or H + P in non-basal cells but not in basal cells. No alterations were observed in p-ERK levels in the 4 cell lines when treated with H and H + P. Of the Her2+ patients, 33/88 (37.5%) expressed at least one basal gene. Basal Her2 tumors were associated with higher grade (p=0.04) and more ER/PR-negativity (p<0.01). CK14 expression correlated with worse overall survival by log-rank test (p=0.02), while EGFR showed a similar trend (p=0.06). Conclusions: Basal Her2 cell lines are resistant to Herceptin. This resistance is associated with Herceptin refractory PI3K/Akt activity. CK14 expression is predictive of worse prognosis in Her2+ breast cancer patients treated with Herceptin.
Arachidonic acid metabolism in the Min mouse intestine: colon tumor lipoxygenase activity and effects of green tea polyphenols
Authors: Mathilde G. Lepage, Michael Wargovich, Theresa J. Smith
Journal: Cancer Research (2005)

752   12-Lipoxygenase (12-LOX) catalyzes the transformation of arachidonic acid into 12-hydroxyeicosatetraenoic acid (12-HETE). 12-LOX and its product 12-HETE have been implicated in cancer development and are a potential target for cancer chemoprevention. In our effort to study the effects of green tea polyphenols (GTPP) on arachidonic acid metabolism in the Min mouse, we investigated cyclooxygenase (COX) and lipoxygenase (LOX) activity in the microsomal and cytosolic fractions of the Min colon (stripped of all visible polyps) and Min colon polyps (MCT). COX was the major pathway for arachidonic acid metabolism in the colon with PGE 2  being the major metabolite. Inhibition studies with NS398, a selective COX-2 inhibitor, suggested that COX-2 was responsible for 30% of the activity. On the other hand, PGE 2  formation was not detectable in MCT. A metabolite that was only detectable in the MCT fractions coeluted with 12-HETE/8-HETE standards suggesting 12-LOX and/or 8-LOX activity. The majority of this activity was located in the microsomal fraction. The general LOX inhibitor nordihydroguaiaretic acid (25 μM) completely inhibited activity in the microsomal and cytosolic MCT fractions. Baicalein (5 μM), a selective 12-LOX inhibitor completely inhibited the cytosolic 12-LOX (c12-LOX) activity and reduced the microsomal 12-LOX (m12-LOX) activity by 75%, thereby suggesting 12-LOX activity. However, the microsomal and cytosolic fractions reacted differently to the presence of glutathione. Glutathione (1mM) increased m12-LOX activity by 2-fold while c12-LOX activity was completely inhibited. The 2 fractions also differed in their response to the presence of GTPPs. Epicatechin-3-gallate (ECG) and epigallocatechin-3-gallate (EGCG) were the most effective GTPPs at inhibiting both enzymes. IC 50  values for m12-LOX were 5 μM and 8 μM while IC 50  values for c12-LOX were 10 μM and 40 μM for ECG and EGCG, respectively. Moreover, EGCG had a complex effect on the c12-LOX. Low concentrations of EGCG increased c12-LOX activity reaching a maximum when EGCG was present at a concentration of 5 μM after which a dose dependent inhibition was observed. The above differences between the c12-LOX and m12-LOX suggest that 2 functionally distinct forms of 12-LOX may be present in the colon tumor tissue. The results of this study demonstrate the presence of 12-LOX activity in colon polyps resulting in a shift in arachidonic acid metabolism from the COX pathway in the ‘tumor free’ colon to the 12-LOX pathway in the colon tumors and inhibition of this activity by GTPP suggests that green tea may exert it chemopreventive effects through inhibition of 12-LOX. This study was supported by NIH grant CA096694.
Search Images and Extrapolation Risk
Authors: Bruce M. Rothschild
Journal: JAMA Internal Medicine (2017)

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 Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast 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) 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 Internal Medicine journal
Final results of a phase II, double blind, placebo controlled, randomized trial of preoperative chemotherapy +/- gefitinib with biomarker evaluation in operable breast cancer
Authors: Guarneri, A Frassoldati, G Ficarra, G Jovic, F Puglisi, A Michelotti, C Boni, N Battelli, A Santoro, P. Conte
Journal: Annals of Oncology (2006)
Abstract 15861: Adherence to the 2012 Canadian Lipid Screening Guidelines in Primary Prevention Patients: The CANHEART Study
Authors: Jack V Tu, Anna Chu, Sharon Johnston, Cynthia A Jackevicius, Laura C Maclagan, Arlene S Bierman, William Hogg, Peter C Austin, Karen Tu, Jacob A Udell, Clare L Atzema, Peter P Liu, Mostafa Alabousi, Jane J Park, Dennis T Ko
Journal: Circulation (2016)

Background:  The 2012 Canadian Cardiovascular Society’s (CCS) lipid guidelines recommend universal lipid testing of males aged ≥40 and females ≥50 every 3 to 5 years and selective testing in high-risk patients aged    Methods:  We conducted an analysis of lipid testing and results in 9.4 million primary prevention patients aged 20 to 105, as of January 2008, from Ontario, Canada in the Cardiovascular Health in Ambulatory Care Research Team (CANHEART) ‘big data’ cohort (www.canheart.ca) created through the linkage of multiple population-health databases. This cohort was followed for 5 years up to December 2012 to determine rates of lipid testing by sex and 10-year age bands. We also examined the frequency of elevated low-density lipoprotein (LDL) levels (>3.5 mmol/L or 135 mg/dL) in non-statin users and those without a history of hyperlipidemia. At LDLs above this level, consideration of statin therapy is recommended in those at intermediate cardiovascular risk in Canada.   Results:  Overall, 69.2% of males and 74.1% of females aged 20 to 105 with no past history of cardiovascular disease had lipid testing over the 5-year time period. Rates of testing were highest (>80%) amongst males and females 50 to 79 years, but only 75% of males aged 40 to 49 received testing (Figure). Approximately half of Canadians aged  3.5 mmol/L. The frequency of elevated LDL was greatest in males aged 40 to 49 and females aged 60 to 69, and was lowest in those aged 20 to 29 and aged 80 and over.   Conclusions:  High rates of lipid testing in Canadians aged 50 to 79 are in concordance with Canadian lipid guidelines. The optimal lipid testing strategy in younger adults and the very elderly remains to be determined.
Antidepressant Outcomes Predicted by Genetic Variation in Corticotropin-Releasing Hormone Binding Protein
Authors: Chloe P. O’Connell, Andrea N. Goldstein-Piekarski, Charles B. Nemeroff, Alan F. Schatzberg, Charles Debattista, Tania Carrillo-Roa, Elisabeth B. Binder, Boadie W. Dunlop, W. Edward Craighead, Helen S. Mayberg, Leanne M. Williams
Journal: American Journal of Psychiatry (2017)

Genetic variation within the hypothalamic-pituitary-adrenal (HPA) axis has been linked to risk for depression and antidepressant response. However, these associations have yet to produce clinical gains that inform treatment decisions. The authors investigated whether variation within HPA axis genes predicts antidepressant outcomes within two large clinical trials.The test sample comprised 636 patients from the International Study to Predict Optimized Treatment in Depression (iSPOT-D) who completed baseline and 8-week follow-up visits and for whom complete genotyping data were available. The authors tested the relationship between genotype at 16 candidate HPA axis single-nucleotide polymorphisms (SNPs) and treatment outcomes for three commonly used antidepressants (escitalopram, sertraline, and extended-release venlafaxine), using multivariable linear and logistic regression with Bonferroni correction. Response and remission were defined using the Hamilton Depression Rating Scale. Findings were then validated using the Predictors of Remission in Depression to Individual and Combined Treatments (PReDICT) study of outcome predictors in treatment-naive patients with major depression.The authors found that the rs28365143 variant within the corticotropin-releasing hormone binding protein (CRHBP) gene predicted antidepressant outcomes for remission, response, and symptom change. Patients homozygous for the G allele of rs28365143 had greater remission rates, response rates, and symptom reductions. These effects were specific to drug class. Patients homozygous for the G allele responded significantly better to the selective serotonin reuptake inhibitors escitalopram and sertraline than did A allele carriers. In contrast, rs28365143 genotype was not associated with treatment outcomes for the serotonin norepinephrine reuptake inhibitor venlafaxine. When patients were stratified by race, the overall effect of genotype on treatment response remained. In the validation sample, the GG genotype was again associated with favorable antidepressant outcomes, with comparable effect sizes.These findings suggest that a specific CRHBP SNP, rs28365143, may have a role in predicting which patients will improve with antidepressants and which type of antidepressant may be most effective. The results add to the foundational knowledge needed to advance a precision approach to personalized antidepressant choices.
Abstract B28: Identification of breast cancer metastasis promoting genes by next generation sequencing
Authors: Karol Szczepanek, Kent Hunter
Journal: Cancer Research (2016)

Abstract Breast cancer is a leading cause of cancer-related mortality of women in the United States. The majority of cancer deaths are due to metastases rather than the primary tumor, therefore a better understanding of the mechanisms that lead to metastatic disease is critical to reducing breast cancer-related mortality. A majority of cancer cells that leave the primary tumor are either removed by the immune system or fail to survive in distant organs. However, some cancer cells acquire molecular features that allow them to survive and proliferate in secondary sites, such as lung, liver, brain, and bone. In order to design highly efficient anti-metastatic therapies, it is crucial to address metastasis-specific mechanisms of growth and survival. One of the major hurdles to developing these therapies is the genotypic and phenotypic heterogeneity between primary tumors and metastases, as well as between individual metastases. The goal of this project is to characterize the transcriptomic landscape of breast cancer metastases using Next Generation Sequencing (NGS) tools in order to identify potential genes that drive (metastasis promoters) or inhibit (metastasis suppressors) the metastatic outgrowth in distant organs. Therefore, RNA sequencing was performed on breast cancer primary tumors and matching lung metastases from two different mouse models: Polyomavirus Middle-T antigen (PyMT) transgenic mice, a model of spontaneous and highly aggressive breast cancer, as well as from mouse mammary cancer cells orthotopically injected into FVB mice. RNA sequencing using the NGS platform revealed genes that were highly expressed in metastases compared to primary tumors. Interestingly, overlapping the RNA-seq datasets from these two distinct models revealed a shared subset of upregulated genes, strongly suggesting that these genes are likely to be common metastatic outgrowth promoters. To validate these candidate genes, we are currently developing a CRISPR sgRNA library for orthotopic transplant experiments. The genes displaying in vivo effects on metastatic outgrowth in the lungs will be further explored for the development of targeted anti-metastatic therapies. Citation Format: Karol Szczepanek, Kent Hunter. Identification of breast cancer metastasis promoting genes by next generation sequencing. [abstract]. In: Proceedings of the AACR Special Conference on Tumor Metastasis; 2015 Nov 30-Dec 3; Austin, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(7 Suppl):Abstract nr B28.
Impaired path integration in mice with disrupted grid cell firing
Authors: Mariana Gil, Mihai Ancau, Magdalene I. Schlesiger, Angela Neitz, Kevin Allen, Rodrigo J. De Marco, Hannah Monyer
Journal: Nature Neuroscience (2017)

Path integration (PI) is a highly conserved, self-motion-based navigation strategy. Since the discovery of grid cells in the medial entorhinal cortex, neurophysiological data and computational models have suggested that these neurons serve PI. However, more direct empirical evidence supporting this hypothesis has been missing due to a lack of selective manipulations of grid cell activity and suitable behavioral assessments. Here we report that selective disruption of grid cell activity in mice can be achieved by removing NMDA glutamate receptors from the retro-hippocampal region and that disrupted grid cell firing accounts for impaired PI performance. Notably, the genetic manipulation did not affect the activity of other spatially selective cells in the medial entorhinal cortex and the hippocampus. By directly linking grid cell activity to PI, these results contribute to a better understanding of how grid cells support navigation and spatial memory. Grid cell activity may subserve path integration, but a direct link is lacking. The authors selectively disrupt retro-hippocampal region grid cell activity and show that disrupted grid cell firing impairs performance in a path integration task.
Diagnostic modalities for nonalcoholic fatty liver disease, nonalcoholic steatohepatitis, and associated fibrosis
Authors: Zobair M. Younossi, Rohit Loomba, Quentin M. Anstee, Mary E. Rinella, Elisabetta Bugianesi, Giulio Marchesini, Brent A. Neuschwander‐Tetri, Lawrence Serfaty, Francesco Negro, Stephen H. Caldwell, Vlad Ratziu, Kathleen E. Corey, Scott L. Friedman, Manal F. Abdelmalek, Stephen A. Harrison, Arun J. Sanyal, Joel E. Lavine, Philippe Mathurin, Michael R. Charlton, Zachary D. Goodman, Naga P. Chalasani, Kris V. Kowdley, Jacob George, Keith Lindor
Journal: Hepatology (2017)

Nonalcoholic fatty liver disease (NAFLD) is a spectrum comprised of isolated steatosis, nonalcoholic steatohepatitis (NASH), advanced fibrosis, and cirrhosis. The majority of NAFLD subjects do not have NASH and do not carry a significant risk for liver-related adverse outcomes (cirrhosis and mortality). Globally, the prevalence of NAFLD is approximately 25%. In Asia, a gradient of high to low prevalence rates is noted from urban to rural areas. Given the prevalence of NAFLD, the clinical and economic burden of NAFLD and NASH can be substantial. With increasing recognition of NASH as an important liver disease, the diagnosis of NASH still requires a liver biopsy that is suboptimal. Although liver biopsy is the most accurate modality to diagnose and stage the severity of NASH, this method suffers from being invasive, costly, associated with potential complications, and plagued with interobserver variability of individual pathological features. A number of noninvasive modalities to diagnose NASH and stage liver fibrosis are being developed. These modalities include predictive models (NAFLD fibrosis score) and serum biomarkers such as enhanced liver fibrosis (ELF). Other tests are based on radiological techniques, such as transient elastography (TE) or magnetic resonance elastography (MRE), which are used to estimate liver stiffness as a potential surrogate of hepatic fibrosis. Although a dynamic field of research, most of these diagnostic modalities have area under the curve ranging between 0.76 and 0.90%, with MRE having the best predictive performance. In summary, developing safe and easily accessible noninvasive modalities to accurately diagnose and monitor NASH and associated fibrosis is of utmost importance in clinical practice and clinical research. These tests are not only important to risk stratify subjects at the greatest risk for progressive liver disease, but also to serve as appropriate surrogate endpoints for therapeutic clinical trials of NASH. (Hepatology 2018;68:349-360).