tbuckley/cabot-search huggingface dataset:
Use of Colony-Stimulating Factors With Chemotherapy: Opportunities for Cost Savings and Improved Outcomes
Authors: A. L. Potosky, J. L. Malin, B. Kim, E. A. Chrischilles, S. B. Makgoeng, N. Howlader, J. C. Weeks
Journal: JNCI Journal of the National Cancer Institute (2011)

Myeloid colony-stimulating factors (CSFs) decrease the risk of febrile neutropenia (FN) from high-risk chemotherapy regimens administered to patients at 20% or greater risk of FN, but little is known about their use in clinical practice. We evaluated CSF use in a multiregional population-based cohort of lung and colorectal cancer patients (N = 1849). Only 17% (95% confidence interval [CI] = 8% to 26%) patients treated with high-risk chemotherapy regimens received CSFs, compared with 18% (95% CI = 16% to 20%) and 10% (95% CI = 8% to 12%) of patients treated with intermediate- (10%-20% risk of FN) and low-risk (<10% risk of FN) chemotherapy regimens, respectively. Using a generalized estimating equation model, we found that enrollment in a health maintenance organization (HMO) was strongly associated with a lower adjusted odds of discretionary CSF use, compared with non-HMO patients (odds ratio = 0.44, 95% CI = 0.32 to 0.60, P < .001). All statistical tests were two-sided. Overall, 96% (95% CI = 93% to 98%) of CSFs were administered in scenarios where CSF therapy is not recommended by evidence-based guidelines. This finding suggests that policies to decrease CSF use in patients at lower or intermediate risk of FN may yield substantial cost savings without compromising patient outcomes.
Studying ischemic preconditioning in isolated cardiomyocyte models
Authors: R DIAZ, G WILSON
Journal: Cardiovascular Research (2006)

Isolated cardiomyocytes, obtained by enzymatic digestion of whole hearts, have multiple advantages, most related to their accessibility to microscopic visualization, beyond the obvious elimination of other cell types that exist in the heart. Conversely, they cannot reproduce the mechanical disruption of reperfusion hypercontracture or the vascular phenomena of leukocyte plugging and compression from interstitial edema and contracture that can lead to the no-reflow phenomenon. Nevertheless, ischemic preconditioning has been consistently demonstrated to be a potent protective mechanism in freshly isolated and cultured cardiomyocytes across multiple species, indicating that much of the innate protection of ischemic preconditioning resides in cardiomyocytes. Centrifuging freshly isolated cardiomyocytes into a pellet with only a thin layer of supernatant covered by oil has proven to be an excellent model of simulated ischemia. In culture, cardiomyocytes may be exposed to severe hypoxia only or to various protocols for simulated ischemia in which an acid/lactate-rich, hyperkalemic extracellular environment with substrate deprivation (lacking glucose) is typically added. Reperfusion is simulated by well-oxygenated media of normal ionic composition. Cardiomyocyte injury has been usually evaluated by cell membrane permeability to dyes, often under hypo-osmotic conditions (osmotic fragility) or enzyme release. A survey of the use of cardiomyocyte models to study preconditioning is presented with the emphasis on examples of the innovative measurements, increasingly involving molecular techniques, that point to an increasing future role for these models in preconditioning research and, more generally, in the mechanistic study of myocardial ischemia/reperfusion.
Sweat pores on fingertips
Authors: J. L. Rees
Journal: British Journal of Dermatology (1988)

Journal Article Sweat pores on fingertips Get access J. L. Rees J. L. Rees University Department of Dermatology, Royal Victoria Infirmary, Newcastle upon Tyne, U.K. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 118, Issue 4, 1 April 1988, Pages 584–585, https://doi.org/10.1111/j.1365-2133.1988.tb02474.x Published: 01 April 1988
RISK FACTORS FOR RUNNING RELATED INJURIES IN NOVICE RUNNERS PARTICIPATING IN A 6-WEEK RUNNING PROGRAM
Authors: B Kluitenberg, H van der Worp
Journal: British Journal of Sports Medicine (2014)

Background Running is a sport practiced by many individuals. The positive health effects as a result of running are well known. On the other side, between 17 and 79% of the runners sustain an injury each year. Several studies examined potential risk factors for injuries, however, due to the often underpowered studies it is not possible to reveal the complex mechanism leading to a running related injury yet. Objective To examine the incidence of running related injuries and its determinants in novice runners. Design Prospective cohort study. Participants Novice runners participating in a “Start to Run” course were eligible for inclusion. 1075 novice runners were included in the study and were followed during the six week running program. Risk factor assessment Before the start of the running course, all runners completed a baseline questionnaire concerning personal characteristics and sports and injury history. During the running program training information was monitored with a digital weekly running log. This running log was used to obtain running exposure and register running related injuries. Main outcome measures A running related injury. Results During the running course 181 running related injuries were registered in 120 participants, which represents an incidence of 11.2%. The data on predisposing variables on injury development was not analyzed yet, but will be available at the conference April 2014. Conclusion During a six-week running course for novice runners, 11.2% of the participants will sustain at least one running related injury.
Systemic Delivery of Microencapsulated 3-Bromopyruvate for the Therapy of Pancreatic Cancer
Authors: Julius Chapiro, Surojit Sur, Lynn Jeanette Savic, Shanmugasundaram Ganapathy-Kanniappan, Juvenal Reyes, Rafael Duran, Sivarajan Chettiar Thiruganasambandam, Cassandra Rae Moats, MingDe Lin, Weibo Luo, Phuoc T. Tran, Joseph M. Herman, Gregg L. Semenza, Andrew J. Ewald, Bert Vogelstein, Jean-François Geschwind
Journal: Clinical Cancer Research (2014)

This study characterized the therapeutic efficacy of a systemically administered formulation of 3-bromopyruvate (3-BrPA), microencapsulated in a complex with β-cyclodextrin (β-CD), using an orthotopic xenograft mouse model of pancreatic ductal adenocarcinoma (PDAC).The presence of the β-CD-3-BrPA complex was confirmed using nuclear magnetic resonance spectroscopy. Monolayer as well as three-dimensional organotypic cell culture was used to determine the half-maximal inhibitory concentrations (IC50) of β-CD-3-BrPA, free 3-BrPA, β-CD (control), and gemcitabine in MiaPaCa-2 and Suit-2 cell lines, both in normoxia and hypoxia. Phase-contrast microscopy, bioluminescence imaging (BLI), as well as zymography and Matrigel assays were used to characterize the effects of the drug in vitro. An orthotopic lucMiaPaCa-2 xenograft tumor model was used to investigate the in vivo efficacy.β-CD-3-BrPA and free 3-BrPA demonstrated an almost identical IC50 profile in both PDAC cell lines with higher sensitivity in hypoxia. Using the Matrigel invasion assay as well as zymography, 3-BrPA showed anti-invasive effects in sublethal drug concentrations. In vivo, animals treated with β-CD-3-BrPA demonstrated minimal or no tumor progression as evident by the BLI signal as opposed to animals treated with gemcitabine or the β-CD (60-fold and 140-fold signal increase, respectively). In contrast to animals treated with free 3-BrPA, no lethal toxicity was observed for β-CD-3-BrPA.The microencapsulation of 3-BrPA represents a promising step towards achieving the goal of systemically deliverable antiglycolytic tumor therapy. The strong anticancer effects of β-CD-3-BrPA combined with its favorable toxicity profile suggest that clinical trials, particularly in patients with PDAC, should be considered.
Phase I Trial of Gefitinib in Combination With Radiation or Chemoradiation for Patients With Locally Advanced Squamous Cell Head and Neck Cancer
Authors: Changhu Chen, Madeleine Kane, John Song, John Campana, Adam Raben, Kenneth Hu, Louis Harrison, Harry Quon, Janet Dancey, Anna Baron, Sherif Said, S. Gail Eckhardt, David Raben
Journal: Journal of Clinical Oncology (2007)

Purpose To establish the safety and toxicity profile of daily gefitinib with radiation alone or with concurrent chemoradiotherapy in previously untreated patients with locally advanced squamous cell head and neck cancer (LAHNC). Patients and Methods Patients with intermediate-stage LAHNC were treated with concomitant boost radiation (RT) alone with escalating doses of daily gefitinib (250 or 500 mg; cohort I). Once a safety profile was determined with RT alone, patients with high-risk disease were then treated with daily gefitinib (250 or 500 mg), weekly cisplatin (CDDP; 30 mg/m 2 ), and once-daily RT (cohort II). Patients also received post-RT gefitinib at 250 mg daily for a period of up to 2 years. Results Twenty-three patients were enrolled and assessable for toxicity. No dose-limiting toxicities (DLTs) were observed in patients treated in cohort I at either 250 or 500 mg of gefitinib daily with concomitant boost RT to 72 Gy. In patients receiving chemoradiotherapy and gefitinib (cohort II), DLTs included one grade 4 diarrhea and one grade 4 neutropenic fever. Fifteen patients started maintenance gefitinib, and eight (53%) experienced grade 1 to 2 acne-like skin rash and diarrhea, but no grade 3 or 4 toxicity occurred. Conclusion Gefitinib (250 or 500 mg daily) was well tolerated with concomitant boost RT or concurrent chemoradiotherapy with weekly CDDP. Protracted administration of gefitinib for up to 2 years at 250 mg daily was also tolerated well.
Adjuvant low-dose interferon α2a with or without dacarbazine compared with surgery alone: a prospective-randomized phase III DeCOG trial in melanoma patients with regional lymph node metastasis
Authors: C. Garbe, P. Radny, R. Linse, R. Dummer, R. Gutzmer, J. Ulrich, R. Stadler, M. Weichenthal, T.K. Eigentler, U. Ellwanger, A. Hauschild
Journal: Annals of Oncology (2008)
Acute Muscle Wasting Among Critically Ill Patients
Authors: Andrew G. Day
Journal: JAMA (2014)

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
Stroke incidence in rural and urban Tanzania: a prospective, community-based study
Authors: Richard Walker, David Whiting, Nigel Unwin, Ferdinand Mugusi, Mark Swai, Eric Aris, Ahmed Jusabani, Gregory Kabadi, William K Gray, Mary Lewanga, George Alberti
Journal: The Lancet Neurology (2010)

There are no methodologically rigorous studies of the incidence of stroke in sub-Saharan Africa. We aimed to provide reliable data on the incidence of stroke in rural and urban Tanzania.The Tanzania Stroke Incidence Project (TSIP) recorded stroke incidence in two well defined demographic surveillance sites (DSS) over a 3-year period from June, 2003. The Hai DSS (population 159,814) is rural and the Dar-es-Salaam DSS (population 56,517) is urban. Patients with stroke were identified by use of a system of community-based investigators and liaison with local hospital and medical centre staff. Patients who died from stroke before recruitment into the TSIP were identified via verbal autopsy, which was done on all those who died within the study areas.There were 636 strokes during the 3-year period (453 in Hai and 183 in Dar-es-Salaam). Overall crude yearly stroke incidence rates were 94.5 per 100,000 (95% CI 76.0-115.0) in Hai and 107.9 per 100,000 (88.1-129.8) in Dar-es-Salaam. When age-standardised to the WHO world population, yearly stroke incidence rates were 108.6 per 100 000 (95% CI 89.0-130.9) in Hai and 315.9 per 100,000 (281.6-352.3) in Dar-es-Salaam.Age-standardised stroke incidence rates in Hai were similar to those seen in developed countries. However, age-standardised incidence rates in Dar-es-Salaam were higher than seen in most studies in developed countries; this could be because of a difference in the prevalence of risk factors and emphasises the importance of health screening at a community level. Health policy makers must continue to monitor the incidence of stroke in sub-Saharan Africa and should base future funding decisions on such data.The Wellcome Trust.
Does Juvenile Temporal Arteritis Exist?
Authors: Ulf de Faire
Journal: JAMA (1976)

To the Editor.—  In a recent issue ofThe Journal(234:496, 1975), Lie and his colleagues describe a juvenile form of temporal arteritis. All four cases (two young adults and two children) had a painless nodule in the temporal region. No characteristic symptoms of the classical form of temporal  were seen. Histologic examination of the lesions showed non-giant-cell granulomatous inflammation of the temporal arteries. The authors propose that these lesions might represent a new entity of juvenile temporal arteritis.  Temporal  and the closely related disorder of polymyalgia rheumatica have since long been considered age-related diseases. In the first report of temporal arteritis, by Hutchinson in 1890,1it was described as an arteritis of the aged. However, sometimes it seems to affect also people under the age of 50 years. The youngest patient so far reported with biopsy-verified temporal  is a 35-year old man.2Recently, we have
Influence of hyperthyroidism on splanchnic exchange of glucose and gluconeogenic precursors.
Authors: J Wahren, A Wennlund, L H Nilsson, P Felig
Journal: Journal of Clinical Investigation (1981)

Arterial concentrations and splanchnic exchange of glucose, amino acids, lactate, pyruvate, and glycerol were determined in 14 hyperthyroid patients and 12 healthy controls. Seven of the patients were restudied after 5-12 mo of medical management at which time there was chemical and clinical evidence of a euthyroid state. The arterial level of glucose was slightly higher (+10%) in the patient group and the glycerol concentration was three times greater among the patients. The plasma levels of the glycogenic amino acids, alanine, glycine, and serine were decreased by 20-30%, while the concentrations of leucine, isoleucine, and tyrosine were increased by 20-80%. The levels of lactate and pyruvate were similar in patients and controls as were insulin and glucagon concentrations. Splanchnic glucose output in the patient group was 35% lower than in controls. However, total splanchnic uptake of glucogenic precursors was 100% higher than in controls and showed a direct linear correlation with serum triiodothyronine. Total precursor uptake could account for 75% of splanchnic glucose output in the patients, compared to 26% in controls. The increase in uptake of lactate, alanine, and other amino acids was due to a 35-80% rise in splanchnic fractional extraction plus a 20% rise in estimated hepatic blood flow. When the patients were restudied after medical treatment splanchnic exchange of glucose and glucose precursors had reverted to normal values. The present findings demonstrate that in hyperthyroidism (a) total splanchnic glucose output is reduced in relation to controls, (b) splanchnic uptake of gluconeogenic precursors is accelerated, largely due to a rise in fractional extraction of precursor substrates and to a smaller extent, as a result of an increase in hepatic blood flow, and (c) these changes revert to normal when a euthyroid state has been achieved.
Development of Vaccines for High-Risk Ductal Carcinoma <i>In situ</i> of the Breast
Authors: Brian J. Czerniecki, Robert E. Roses, Gary K. Koski
Journal: Cancer Research (2007)

Abstract Certain ductal carcinoma in situ (DCIS) lesions overexpress the HER-2/neu receptor at this early stage of breast cancer development. Recently, we showed that a HER-2–targeted dendritic cell vaccine could be used to eliminate HER-2–overexpressing cells in patients that harbor these high-risk DCIS lesions. Our findings suggest that vaccinating such patients might diminish the risk of recurrence, protect against the development of invasive breast cancer, and minimize morbidity associated with current treatments. We discuss several implications of this work for developing effective cancer vaccines. [Cancer Res 2007;67(14):6531–4]
Combination of a Fusogenic Glycoprotein, Prodrug Activation, and Oncolytic Herpes Simplex Virus for Enhanced Local Tumor Control
Authors: Guy R. Simpson, Ziqun Han, Binlei Liu, Yibing Wang, Gregor Campbell, Robert S. Coffin
Journal: Cancer Research (2006)

Abstract We have previously developed an oncolytic herpes simplex virus-1 based on a clinical virus isolate, which was deleted for ICP34.5 to provide tumor selected replication and ICP47 to increase antigen presentation as well as tumor selective virus replication. A phase I/II clinical trial using a version of this virus expressing granulocyte macrophage colony-stimulating factor has shown promising results. The work reported here aimed to develop a version of this virus in which local tumor control was further increased through the combined expression of a highly potent prodrug activating gene [yeast cytosine deaminase/uracil phospho-ribosyltransferase fusion (Fcy::Fur)] and the fusogenic glycoprotein from gibbon ape leukemia virus (GALV), which it was hoped would aid the spread of the activated prodrug through the tumor. Viruses expressing the two genes individually or in combination were constructed and tested, showing (a) GALV and/or Fcy::Fur expression did not affect virus growth; (b) GALV expression causes cell fusion and increases the tumor cell killing at least 30-fold in vitro and tumor shrinkage 5- to 10-fold in vivo; (c) additional expression of Fcy::Fur combined with 5-fluorocytosine administration improves tumor shrinkage further. These results indicate, therefore, that the combined expression of the GALV protein and Fcy::Fur provides a highly potent oncolytic virus with improved capabilities for local tumor control. It is intended to enter the GALV/Fcy::Fur expressing virus into clinical development for the treatment of tumor types, such as pancreatic or lung cancer, where local control would be anticipated to be clinically advantageous. (Cancer Res 2006; 66(9): 4835-42)
Insights on altered mitochondrial function and dynamics in the pathogenesis of neurodegeneration
Authors: Joseph McInnes
Journal: Translational Neurodegeneration (2013)

In neurons, mitochondria are enriched to provide energy and calcium buffering required for synaptic transmission. Additionally, mitochondria localize to the synapse, where they are critical for the mobilization of reserve pool vesicles and for neurotransmitter release. Previously, functional defects in mitochondria were considered to be downstream effects of neurodegenerative diseases. However, more recent findings suggest mitochondria may serve as key mediators in the onset and progression of some types of neurodegeneration. In this review, we explore the possible roles of altered mitochondrial function and dynamics in the pathogenesis of neurodegenerative disorders, with a particular focus on Alzheimer's disease (AD) and Parkinson's disease (PD), which have highlighted the important role of mitochondria in neurodegeneration. While inheritable diseases like Charcot-Marie-Tooth disease type 2A are concretely linked to gene mutations affecting mitochondrial function, the cause of mitochondrial dysfunction in primarily sporadic diseases such as AD and PD is less clear. Neuronal death in PD is associated with defects in mitochondrial function and dynamics arising from mutations in proteins affecting these processes, including α-synuclein, DJ-1, LRRK2, Parkin and Pink1. In the case of AD, however, the connection between mitochondria and the onset of neurodegeneration has been less clear. Recent findings, however, have implicated altered function of ER-mitochondria contact sites and amyloid beta- and/or tau-induced defects in mitochondrial function and dynamics in the pathogenesis of AD, suggesting that mitochondrial defects may act as key mediators in the pathogenesis of AD as well. With recent findings at hand, it may be postulated that defects in mitochondrial processes comprise key events in the onset of neurodegeneration.
Intercellular adhesion molecule-1: a consistent inflammatory marker of the cutaneous radiation reaction both <i>in vitro</i> and <i>in vivo</i>
Authors: K. Müller, F.-M. Köhn, M. Port, M. Abend, M. Molls, J. Ring, V. Meineke
Journal: British Journal of Dermatology (2006)

Radiation damage to skin is a key diagnostic and prognostic parameter for patients accidentally exposed to radiation. Moreover, skin is a target organ for crucial side-effects of routine radiotherapy. The pathophysiology of the cutaneous radiation reaction is in many respects still unknown. The acute inflammatory radiation reaction of skin has been shown to involve alterations in cell-cell and cell-matrix interactions, which are mediated by cellular adhesion molecules.To evaluate the effect of ionizing radiation on intercellular adhesion molecule-1 (ICAM-1) expression in human skin cells.Dermal monolayer cells, a three-dimensional skin model and skin biopsies were investigated for ICAM-1 expression after ionizing radiation using flow cytometry, quantitative reverse transcription-polymerase chain reaction and immunohistochemistry. ICAM-1 expression in monolayer cells pretreated with protein kinase inhibitors and dexamethasone prior to irradiation was analysed by flow cytometry.Using different sources of skin cells, we demonstrated a consistent upregulation of both ICAM-1 mRNA and protein expression by ionizing radiation. Blocking experiments revealed that tumour necrosis factor-alpha, another ICAM-1 inducer, does not account for the effect of radiation. Radiation-induced upregulation of ICAM-1 expression was significantly attenuated by inhibitors to protein kinase C, mitogen-activated protein (MAP) ERK kinase, p38 MAP kinase and phosphatidylinositol 3-kinase. The anti-inflammatory agent dexamethasone suppressed the effect of radiation on ICAM-1 expression, suggesting its usefulness to treat the cutaneous radiation reaction.Our data suggest that ICAM-1 is a consistent inflammatory parameter of the cutaneous radiation reaction both in vitro and in vivo that might provide new therapeutic options for diagnosis and treatment of effects of radiation.