tbuckley/cabot-search huggingface dataset:
Clinical Decision Support Systems and Advanced Diagnostic Imaging
Authors: Timothy Wayne Cook, Luciana Tricai Cavalini
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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Prevention or Modification of Epileptogenesis after Brain Insults: Experimental Approaches and Translational Research
Authors: Wolfgang Löscher, Claudia Brandt
Journal: Pharmacological Reviews (2010)

Diverse brain insults, including traumatic brain injury, stroke, infections, tumors, neurodegenerative diseases, and prolonged acute symptomatic seizures, such as complex febrile seizures or status epilepticus (SE), can induce "epileptogenesis," a process by which normal brain tissue is transformed into tissue capable of generating spontaneous recurrent seizures. Furthermore, epileptogenesis operates in cryptogenic causes of epilepsy. In view of the accumulating information about cellular and molecular mechanisms of epileptogenesis, it should be possible to intervene in this process before the onset of seizures and thereby either prevent the development of epilepsy in patients at risk or increase the potential for better long-term outcome, which constitutes a major clinical need. For identifying pharmacological interventions that prevent, interrupt or reverse the epileptogenic process in people at risk, two groups of animal models, kindling and SE-induced recurrent seizures, have been recommended as potentially useful tools. Furthermore, genetic rodent models of epileptogenesis are increasingly used in assessing antiepileptogenic treatments. Two approaches have been used in these different model categories: screening of clinically established antiepileptic drugs (AEDs) for antiepileptogenic or disease-modifying potential, and targeting the key causal mechanisms that underlie epileptogenesis. The first approach indicated that among various AEDs, topiramate, levetiracetam, carisbamate, and valproate may be the most promising. On the basis of these experimental findings, two ongoing clinical trials will address the antiepileptogenic potential of topiramate and levetiracetam in patients with traumatic brain injury, hopefully translating laboratory discoveries into successful therapies. The second approach has highlighted neurodegeneration, inflammation and up-regulation of immune responses, and neuronal hyperexcitability as potential targets for antiepileptogenesis or disease modification. This article reviews these areas of progress and discusses the challenges associated with discovery of antiepileptogenic therapies.
Analyses of TET2 mutations in post-myeloproliferative neoplasm acute myeloid leukemias
Authors: L Couronné, E Lippert, J Andrieux, O Kosmider, I Radford-Weiss, D Penther, N Dastugue, F Mugneret, M Lafage, N Gachard, N Nadal, O A Bernard, F Nguyen-Khac
Journal: Leukemia (2009)
Responses against islet antigens in NOD mice are prevented by tolerance to proinsulin but not IGRP
Authors: Balasubramanian Krishnamurthy, Nadine L. Dudek, Mark D. McKenzie, Anthony W. Purcell, Andrew G. Brooks, Shane Gellert, Peter G. Colman, Leonard C. Harrison, Andrew M. Lew, Helen E. Thomas, Thomas W.H. Kay
Journal: Journal of Clinical Investigation (2006)

Type 1 diabetes (T1D) is characterized by immune responses against several autoantigens expressed in pancreatic β cells. T cells specific for proinsulin and islet-specific glucose-6-phosphatase catalytic subunit–related protein (IGRP) can induce T1D in NOD mice. However, whether immune responses to multiple autoantigens are caused by spreading from one to another or whether they develop independently of each other is unknown. As cytotoxic T cells specific for IGRP were not detected in transgenic NOD mice tolerant to proinsulin, we determined that immune responses against proinsulin are necessary for IGRP-specific T cells to develop. On the other hand, transgenic overexpression of IGRP resulted in loss of intra-islet IGRP-specific T cells but did not protect NOD mice from insulitis or T1D, providing direct evidence that the response against IGRP is downstream of the response to proinsulin. Our results suggest that pathogenic proinsulin-specific immunity in NOD mice subsequently spreads to other antigens such as IGRP.
IMAGING VALUATION MODELS IN HUMAN CHOICE
Authors: P. Read Montague, Brooks King-Casas, Jonathan D. Cohen
Journal: Annual Review of Neuroscience (2006)

To make a decision, a system must assign value to each of its available choices. In the human brain, one approach to studying valuation has used rewarding stimuli to map out brain responses by varying the dimension or importance of the rewards. However, theoretical models have taught us that value computations are complex, and so reward probes alone can give only partial information about neural responses related to valuation. In recent years, computationally principled models of value learning have been used in conjunction with noninvasive neuroimaging to tease out neural valuation responses related to reward-learning and decision-making. We restrict our review to the role of these models in a new generation of experiments that seeks to build on a now-large body of diverse reward-related brain responses. We show that the models and the measurements based on them point the way forward in two important directions: the valuation of time and the valuation of fictive experience.
Microfluidic Models of Vascular Functions
Authors: Keith H.K. Wong, Juliana M. Chan, Roger D. Kamm, Joe Tien
Journal: Annual Review of Biomedical Engineering (2012)

In vitro studies of vascular physiology have traditionally relied on cultures of endothelial cells, smooth muscle cells, and pericytes grown on centimeter-scale plates, filters, and flow chambers. The introduction of microfluidic tools has revolutionized the study of vascular physiology by allowing researchers to create physiologically relevant culture models, at the same time greatly reducing the consumption of expensive reagents. By taking advantage of the small dimensions and laminar flow inherent in microfluidic systems, recent studies have created in vitro models that reproduce many features of the in vivo vascular microenvironment with fine spatial and temporal resolution. In this review, we highlight the advantages of microfluidics in four areas: the investigation of hemodynamics on a capillary length scale, the modulation of fluid streams over vascular cells, angiogenesis induced by the exposure of vascular cells to well-defined gradients in growth factors or pressure, and the growth of microvascular networks in biomaterials. Such unique capabilities at the microscale are rapidly advancing the understanding of microcirculatory dynamics, shear responses, and angiogenesis in health and disease as well as the ability to create in vivo-like blood vessels in vitro.
The activating effect of IFN-γ on monocytes/macrophages is regulated by the LIF–trophoblast–IL-10 axis via Stat1 inhibition and Stat3 activation
Authors: Angham Dallagi, Julie Girouard, Jovane Hamelin-Morrissette, Rachel Dadzie, Laetitia Laurent, Cathy Vaillancourt, Julie Lafond, Christian Carrier, Carlos Reyes-Moreno
Journal: Cellular and Molecular Immunology (2014)
Paclitaxel plus Bevacizumab versus Paclitaxel Alone for Metastatic Breast Cancer
Authors: Kathy Miller, Molin Wang, Julie Gralow, Maura Dickler, Melody Cobleigh, Edith A. Perez, Tamara Shenkier, David Cella, Nancy E. Davidson
Journal: New England Journal of Medicine (2007)

In an open-label, randomized, phase 3 trial, we compared the efficacy and safety of paclitaxel with that of paclitaxel plus bevacizumab, a monoclonal antibody against vascular endothelial growth factor, as initial treatment for metastatic breast cancer.
Reply to S.S. Agarwala et al
Authors: Dimitrios Pectasides, Urania Dafni, Helen Gogas
Journal: Journal of Clinical Oncology (2009)

In the letter by Agarwala et al, two main concerns are raised regarding the design of the noninferiority study by Pectasides et al. 1 They refer to the noninferiority margin used and the interferon alfa-2b dose used.These points according to Agarwala et al are mentioned in the article but not given the appropriate weight.In our opinion they are.The noninferiority margin as clearly stated in the article is based "on the hypothesis that the 1-month induction regimen (arm A) would be considered as efficacious as the conventional regimen (arm B) if the relapse rate at 3 years from study entry was no more than 15% higher in arm A compared with arm B." This margin was chosen in 1997 by the protocol team as the maximum difference that would allow us to consider arm A noninferior to arm B. The final interpretation of noninferiority obviously depends on the size of the noninferiority margin, the observed 3-year relapse rates that are virtually identical in the two groups and the estimated 95% CI upper limit of the difference on this basis of 9% to 10%.In the final conclusion of the article, it is emphasized that "this study does not rule out the possibility of smaller differences between arms A and B." In short, we have presented the results with caveats regarding all of the points repeated here by Agarwala et al.On the second point, the result of European Organisation for the Research and Treatment of Cancer trial 18952, 2 published in 2005, that the 10 ϫ 10 6 U administered subcutaneously for 1 year as maintenance therapy is no different from observation, is consistent with this noninferiority study.No claim of comparison of either of the two regimens in Pectasides et al to the Eastern Cooperative Oncology Group (ECOG) standard dosages is made.As we mention in our concluding statement the ECOG 1697 trial is posed to answer the question of efficacy for the high-dose interferon portion of the standard ECOG high-dose interferon regimen.
EGFR regulation by microRNA in lung cancer: correlation with clinical response and survival to gefitinib and EGFR expression in cell lines
Authors: G.J. Weiss, L.T. Bemis, E. Nakajima, M. Sugita, D.K. Birks, W.A. Robinson, M. Varella-Garcia, P.A. Bunn, J. Haney, B.A. Helfrich, H. Kato, F.R. Hirsch, W.A. Franklin
Journal: Annals of Oncology (2008)
Comparison of the long-term outcome for patients with rheumatoid arthritis with persistent moderate disease activity or disease remission during the first year after diagnosis: data from the ESPOIR cohort
Authors: B Combe, I Logeart, M C Belkacemi, S Dadoun, T Schaeverbeke, J P Daurès, M Dougados
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Objective</h3> To investigate if patients with early RA with persistent moderate disease activity during the first year after diagnosis have a worse 3–5 year outcome than those who achieve sustained clinical remission within the first year, in a daily life setting. <h3>Methods</h3> The ESPOIR cohort included patients with early arthritis of &lt;6 months' duration. Treatment was the standard of care. We had 5-year follow-up data for 573 patients. This study compared patients who had persistent moderate disease activity (Disease Activity Score in 28 joints (DAS28)&gt;3.2 and ≤5.1) at both the 6- and 12-month visits, with those who were in sustained DAS28 remission. The primary outcome was radiographic progression at the 36-month visit. Secondary endpoints were clinical remission (DAS28 score, Simplified Disease Activity Index, ACR/EULAR criteria), Health Assessment Questionnaire-Disability Index (HAQ-DI) and number of missed workdays at months 36 and 60. A Fisher exact test was used to compare categorical variables, and the Kruskal–Wallis test for quantitative variables. Logistic regression analysis was used to determine predictors of outcome. <h3>Results</h3> Patients were aged 48.1±12.5 years and their duration of symptoms was 103.2±52.1 days. Mean baseline DAS28 was 5.1±1.3. Persistent moderate disease activity (107 patients) rather than sustained remission (155 patients) during the first year was associated with increased radiographic disease progression at 3 years (OR=1.99 (95% CI 1.01 to 3.79)), increased HAQ-DI at 3 and 5 years (5.23 (2.81 to 9.73) and 4.10 (2.16 to 7.80), respectively), a 7–11 times smaller chance of achieving clinical remission and a five times greater number of missed workdays. <h3>Conclusions</h3> Patients with early RA with persistent moderate disease activity during the first year had a worse outcome than patients who achieved sustained clinical remission. Persistent moderate disease activity affects long-term structure, remission rate and functional and work disability. Such patients may benefit from intensive treatment.
Intradermal CpG-B Activates Both Plasmacytoid and Myeloid Dendritic Cells in the Sentinel Lymph Node of Melanoma Patients
Authors: Barbara G. Molenkamp, Paul A.M. van Leeuwen, Sybren Meijer, Berbel J.R. Sluijter, Pepijn G.J.T.B. Wijnands, Arnold Baars, Alfons J.M. van den Eertwegh, Rik J. Scheper, Tanja D. de Gruijl
Journal: Clinical Cancer Research (2007)

Abstract Purpose: A decrease in the frequency and activation state of dendritic cells in the sentinel lymph node (SLN) has been observed in early stages of melanoma development. This may hinder the generation of effective antitumor T-cell responses and increase the likelihood of metastatic spread. Immunopotentiation of the melanoma SLN may therefore be a valuable adjuvant treatment option. One way to achieve this is through the use of bacterially derived unmethylated cytosine-phosphate-guanine (CpG) DNA sequences that bind Toll-like receptor 9 and activate plasmacytoid dendritic cells (PDC). CpG-activated PDC, in turn, release IFNα and may thus boost T-cell and natural killer cell responses as well as activate conventional myeloid dendritic cells (MDC). Experimental Design: We studied the effects of preoperative local administration of the CpG B-type oligodeoxynucleotide (ODN) PF-3512676 (formerly known as CPG 7909) on dendritic cell and T-cell subsets in the SLN of 23 stage I to III melanoma patients, randomized to receive intradermal injections of either PF-3512676 or saline (NaCl 0.9%). Results: PF-3512676 administration resulted in bulkier SLN, higher yields of isolated SLN leukocytes, and activation of BDCA-2+CD123+ PDC as well as of CD1a+ MDC. In addition, PF-3512676 administration was associated with the presence of a newly identified CD11chiCD123+CD83+TRAIL+ mature SLN-MDC subset, an increased release of a variety of inflammatory cytokines, and lower frequencies of CD4+CD25hiCTLA-4+FoxP3+ regulatory T cells in the SLN. Conclusions: These findings point to the possible utility of the conditioning of SLN by PF-3512676 as an adjuvant immunotherapeutic modality for early-stage melanoma.
Effect of rare variants in ADRB2 on risk of severe exacerbations and symptom control during longacting β agonist treatment in a multiethnic asthma population: a genetic study
Authors: Victor E Ortega, Gregory A Hawkins, Wendy C Moore, Annette T Hastie, Elizabeth J Ampleford, William W Busse, Mario Castro, Domingo Chardon, Serpil C Erzurum, Elliot Israel, Federico Montealegre, Sally E Wenzel, Stephen P Peters, Deborah A Meyers, Eugene R Bleecker
Journal: The Lancet Respiratory Medicine (2014)
Sclerosing therapy and eccentric training in flexor carpi radialis tendinopathy in a tennis player
Authors: Karsten Knobloch, Marcus Spies, Kay H Busch, Peter M Vogt
Journal: British Journal of Sports Medicine (2007)

Tendinopathy of the flexor carpi ulnaris tendon is a rare entity. Recent research revealed the role of a neurovascular ingrowth at the point of pain in various tendinopathic locations, such as at the Achilles and patellar tendon, in plantar fasciitis as well as in supraspinatus and tennis elbow tendinopathy. However, beyond the elbow no such neovascularisation has been reported to date.We present a 35-year old tennis player suffering tremendous pain (visual analogue scale (VAS) rating of 9/10) at the flexor carpi ulnaris tendon with adjacent calcification in close proximity to the pisiform bone. The patient was assessed with power Doppler and laser Doppler quantification of neovascularisation at the point of pain.Power Doppler and laser Doppler quantification of neovascularisation at the point of pain identified higher capillary blood flow at three points over the painful vs the non-painful tendon (146/240/232rU vs 93/74/70rU at the non-affected side). Sclerosing therapy using polidocanol under power and laser Doppler guidance was initiated, with immediate decrease of capillary blood flow by 25% with resolution of the neovascularisation in power Doppler. Immediately following sclerosing, the patient's reported pain level on the VAS was reduced from 9/10 to 4/10. Following a short period of rest, eccentric training of the forearm muscle was initiated over 12 weeks with functional complete recovery and complete resolution of wrist pain.Sclerosing therapy using polidocanol under power- and laser-Doppler guidance can decrease capillary blood flow by 25% with resolution of the neovascularisation. Subsequent eccentric training of the forearm muscle over 12 weeks can result in complete resolution of wrist pain.
Executive function and language deficits associated with aggressive-sadistic personality
Authors: Anthony C. Ruocco, Steven M. Platek
Journal: Behavioral and Brain Sciences (2006)

Aggressive-sadistic personality disorder (SPD) involves derivation of pleasure from another's physical or emotional suffering, or from control and domination of others. Findings from a head-injured sample indicate that SPD traits are associated with neuropsychological deficits in executive function and language, suggesting difficulties in frontal-lobe-mediated self-regulation of aggressive and emotional impulses. Implications for rehabilitation of aggressive offenders are discussed.
A Novel Angiogenic Role for Prostaglandin F2α-FP Receptor Interaction in Human Endometrial Adenocarcinomas
Authors: Kurt J. Sales, Tammy List, Sheila C. Boddy, Alistair R.W. Williams, Richard A. Anderson, Zvi Naor, Henry N. Jabbour
Journal: Cancer Research (2005)

Abstract Prostaglandins have been implicated in several neovascular diseases. In the present study, we found elevated FP receptor and vascular endothelial growth factor (VEGF) expression colocalized in glandular epithelial and vascular cells lining the blood vessels in endometrial adenocarcinomas. We investigated the signaling pathways activated by the FP receptor and their role in modulating VEGF expression in endometrial adenocarcinoma (Ishikawa) cells. Ishikawa cells were stably transfected with FP receptor cDNA in the sense or antisense orientations. Treatment of Ishikawa cells with prostaglandin F2α (PGF2α) rapidly induced transphosphorylation of the epidermal growth factor receptor (EGFR) and phosphorylation of extracellular signal-regulated kinase (ERK) 1/2 via the FP receptor. Activation of EGFR-Ras-mitogen-activated protein kinase/ERK kinase (MEK) signaling via the FP receptor resulted in an increase in VEGF promoter activity, expression of VEGF mRNA, and secretion of VEGF protein. These effects of PGF2α on the FP receptor could be abolished by treatment of cells with a specific FP receptor antagonist, chemical inhibitors of c-Src, matrix metalloproteinase, and EGFR kinase or by inactivation of signaling with dominant-negative mutant isoforms of EGFR, Ras, or MEK or with small inhibitory RNA oligonucleotides targeted against the EGFR. Finally, we confirmed that PGF2α could potentiate angiogenesis in endometrial adenocarcinoma explants by transactivation of the EGFR and induction of VEGF mRNA expression.
Hepatic surgeons are like the child who rescued dying fishes
Authors: Tian Yang, Wan Yee Lau, Han Zhang, Meng‐Chao Wu, Feng Shen
Journal: Hepatology (2015)

Potential conflict of interest: Nothing to report. To the Editor: Let us first share with you a story. Under a scorching sun, numerous fish were stranded on the beach after a receding tide, waiting to die. A child picked these fish up one by one and threw them back into the sea. An old man asked the child, "There are so many of them, who cares for one or two fish?" The child did not stop his work and replied, "Look, this one cares, and that one cares too." We, hepatic surgeons, are like this child. We are aware that we are unable to cure all our patients with hepatocellular carcinoma (HCC), but we never stop to give a chance of cure to them by surgery. Although the current European and American guidelines for HCC do not recommend hepatic resection for patients with intermediate or advanced HCCs, with Child B liver function, or concurrent portal hypertension, many hepatic surgeons around the world still operate on such patients on a selective basis provided the perioperative mortality and morbidity rates are estimated to be low.1 In real life, a significant proportion of these patients would also choose surgical resection because of the potential cure despite a high tumor recurrence rate after resection. In the latest editorial of hepatology,4 Dr. Bruix, one of the originators of the Barcelona Clinic Liver Cancer system, admitted surgical outcomes in "suboptimal" candidates based on the current guidelines for HCC appear to be better than with other treatments or no treatment. This conclusion was based on an international multicenter study by Roayaie et al.,1 which reported a 5‐year overall survival rate of >30% in the suboptimal group. This group of patients accounted for nearly 70% of all the patients who underwent hepatic resection during the study period. These figures tell us that currently there are many hepatic surgeons who do not follow the guidelines for HCC. Are these surgeons irresponsible? Or have patients been misled by these surgeons to make a wrong decision? In Table 1 of the editorial4 the authors listed all the factors to consider in the selection of treatment for HCC. In our opinion, what was really missing was the factor of a patient's own choice. Patients should be given the right to make the ultimate decision for the treatment, after the pros and cons of the different feasible treatment modalities have been adequately explained by their clinicians. We can switch our roles as clinicians with our patients and answer the following question: if we become those unfortunate fish who got stranded on the beach one day, would anyone of us like to be the fortunate fish which were rescued by the child? In conclusion, the role of hepatic resection and the patient's decision should also be considered in the current guidelines for HCC. Most hepatic surgeons will continue to carry out liver resection in selected patients who are not recommended by the current guidelines to receive surgery because "This one cares, and that one cares too."