tbuckley/cabot-search huggingface dataset:
Translational Research Working Group Developmental Pathway for Immune Response Modifiers
Authors: Martin A. Cheever, Jeffrey Schlom, Louis M. Weiner, H. Kim Lyerly, Mary L. Disis, Addison Greenwood, Oren Grad, William G. Nelson
Journal: Clinical Cancer Research (2008)

The Translational Research Working Group (TRWG) was created as a national initiative to evaluate the current status of the investment of National Cancer Institute in translational research and envision its future. The Translational Research Working Group conceptualized translational research as a set of six developmental processes or pathways focused on various clinical goals. One of those pathways describes the development of immune response modifiers such as vaccines and cytokines. A hallmark of the Immune Response Modifier Developmental Pathway is the coordinated development of multiple components. The Immune Response Modifier Pathway was conceived not as a comprehensive description of the corresponding real-world processes but rather as a tool designed to facilitate movement of a candidate assay through the translational process to the point where it can be handed off for definitive clinical testing. This paper discusses key challenges associated with the immune response modifier agent development process in light of the pathway.
SKIN-DISEASES NAMED AFTER ENGLISHMEN.
Authors: HERMAN GOODMAN
Journal: British Journal of Dermatology (1925)

Journal Article SKIN‐DISEASES NAMED AFTER ENGLISHMEN. Get access HERMAN GOODMAN, B.S., M.D. HERMAN GOODMAN, B.S., M.D. New York City Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology and Syphilis, Volume 37, Issue 4, 1 April 1925, Pages 172–184, https://doi.org/10.1111/j.1365-2133.1925.tb09943.x Published: 01 April 1925
Can we determine a threshold level for allergenic foods by statistical analysis of published data in the literature?
Authors: C. Bindslev-Jensen, D. Briggs, M. Osterballe
Journal: Allergy (2002)

The aim of this paper was to investigate whether a statistical model could be developed to estimate a "threshold" dose for foods eliciting allergic reactions in susceptible patients. The threshold dose is defined to be one that elicits allergic reactions in a given (small) proportion of susceptible patients, using data from published studies.Based on data available from the literature, we developed a statistical model using the actual allergen content in the four foods, where data for allergen content are available (peanut, soy, egg, milk).The model demonstrated that the threshold doses giving a reaction of one in a million in susceptible patients were within the same order of magnitude for egg, milk and soy, but were an order of magnitude lower for peanut flour: 0.005 mg of cow's milk, 0.002 mg of fresh hen's egg, 0.0007 mg of peanut, or 0.0013 mg of soy flour.Although several assumptions were made in creating this statistical model, we demonstrated that the previously published differences in threshold doses for various foods can be largely eliminated by comparing actual allergen content; this may therefore serve as a model for further studies.
A PROSPECTIVE, BLINDED STUDY OF BIOIMPEDANCE VECTOR ANALYSIS AND BIOMARKER TESTING FOR THE PREDICTION OF WORSENING RENAL FUNCTION IN CONSECUTIVE PATIENTS WITH ACUTELY DECOMPENSATED HEART FAILURE: PRIMARY RESULTS OF THE BIOMONITORING AND CARDIORENAL SYNDROME IN HEART FAILURE (BIONICS-HF) TRIAL
Authors: Benedetta De Berardinis, Laura Magrini, Hanna K. Gaggin, Arianna Belcker, Benedetta Zancla, Alexandra Femia, Mandy Simon, Shweta Motiwala, Anju Bhardwaj, Blair Parry, Toby J. Nagurney, Salvatore Di Somma, James L. Januzzi
Journal: Journal of the American College of Cardiology (2013)
Middle T antigen-transformed endothelial cells exhibit an increased activity of nitric oxide synthase.
Authors: D Ghigo, M Arese, R Todde, A Vecchi, F Silvagno, C Costamagna, Q G Dong, M Alessio, R Heller, R Soldi, F Trucco, G Garbarino, G Pescarmona, A Mantovani, F Bussolino, A Bosia
Journal: The Journal of Experimental Medicine (1995)

Endothelioma cell lines transformed by polyoma virus middle T antigen (mTa) cause cavernous hemangiomas in syngeneic mice by recruitment of host cells. The production of nitric oxide (NO), as measured by nitrite and citrulline production, was significantly higher in mTa-transformed endothelial cells in comparison with nontransformed control cells. The maximal activity of NO synthase (NOS) was about 200-fold higher in cell lysates from the tEnd.1 endothelioma cell line than in lysates from nontransformed controls, whereas the affinity for arginine did not differ. The biochemical characterization of NOS and the study of mRNA transcripts indicate that tEnd.1 cells express both the inducible and the constitutive isoforms. NOS hyperactivity is not a simple consequence of cell transformation but needs a tissue-specific mTa expression. Since tEnd.1-conditioned medium induces NOS activity in normal endothelial cells, most likely NOS hyperactivity in endothelioma cells is attributable to the release of a soluble factor. This NOS-activating factor, which seems to be an anionic protein, could stimulate tEnd.1 cells to express NOS by an autocrine way. By the same mechanism, tEnd.1 cells could induce NOS in the neighboring endothelial cells, and NO release could play a role in the hemangioma development. Such hypothesis is confirmed by our in vivo experiments, showing that the administration of the NOS inhibitor L-canavanine to endothelioma-bearing mice significantly reduced both the volume and the relapse time of the tumor.
Home sweet home: how do virus specific T cells navigate to the skin?
Authors: Anthony L. Cunningham
Journal: Journal of Clinical Investigation (2002)

In mucosal immunology, the importance of homing of specific T and B lymphocyte memory cells back to their antigen’s tissue of origin has long been established (1). Elucidation of the mechanisms of such homing and their role in pathogenesis and immunodeficiency may provide targets for immunotherapy or vaccines (2). Recently, there has been intense interest in lymphocyte homing during the pathogenesis of inflammatory skin diseases, particularly the role of memory T cells carrying the cutaneous lymphocyte-associated antigen (CLA) marker.
The relationship of lower extremity alignments and anterior knee laxity to knee translations during a vertical drop landing
Authors: C A Myers, J E Giphart, M R Torry, K B Shelburne, S L Y Woo, J R Steadman
Journal: British Journal of Sports Medicine (2011)

Background Lower extremity alignment (LEA) measures have been linked to non-contact anterior cruciate ligament (ACL) injuries. High deceleration movements have been implicated in non-contact ACL injury mechanisms; and, evidence suggests that greater anterior tibial translation (ATT) may occur in healthy knees that demonstrate greater laxity compared to a stiff knee. Objective To determine the relationship between LEA measures, KT1000 anterior laxity values and ATT during landings using biplane fluoroscopy. Design Descriptive laboratory study. Setting Controlled laboratory setting. Subjects had a sport participation history at the high school or college level. Participants 16 healthy adults (10 females; 6 males). Assessment of risk factors KT1000 values and seven measures of LEA (pelvic angle, hip anteversion, Q-angle, genu recurvatum, tibial torsion, navicular drop and rear foot angle) were measured. Main outcome measurements Subjects performed a drop-landing (40 cm) while being filmed using a high speed, biplane fluoroscopy system. Initial, peak and excursions for ATT were calculated and regression analysis used to determine the relationships. Results KT1000 values were positively correlated with peak ATT values for group (r=0.89) and both genders (males, r=0.97; females, r=0.93) (p=&lt;0.0001). Navicular drop was also significantly correlated to maximal ATT (r=0.56) (p&lt;0.05). No other LEA was significantly correlated with initial, peak or range of ATT (all p&gt;0.05). Conclusion A strong relationship was observed between passive anterior knee laxity measured via KT1000 and ATT experienced during a landing activity in otherwise healthy persons. Navicular drop was significantly correlated with ATT during landing and is a relationship that warrants further investigation as it relates to ACL injury. Anterior knee laxity measured via the KT1000 should be considered in non-contact ACL injury risk assessment for all athletes.
Damage Induced in Sarcoma 37 with Podophyllin, Podophyllotoxin Alpha-Peltatin, Beta-Peltatin, and Quercetin&lt;xref ref-type="fn" rid="fn1"&gt;&lt;sup&gt;2&lt;/sup&gt;&lt;/xref&gt;
Authors: J. Leiter, V. Downing, J. L. Hartwell, M. J. Shear
Journal: JNCI Journal of the National Cancer Institute (1950)

Damage Induced in Sarcoma 37 with Podophyllin, Podophyllotoxin Alpha-Peltatin, Beta-Peltatin, and Quercetin Get access J. Leiter, J. Leiter Search for other works by this author on: Oxford Academic PubMed Google Scholar V. Downing, V. Downing Search for other works by this author on: Oxford Academic PubMed Google Scholar J. L. Hartwell, J. L. Hartwell Search for other works by this author on: Oxford Academic PubMed Google Scholar M. J. Shear M. J. Shear Chemotherapy Section, National Cancer Institute, National Institutes of Health, Public Health Service, Bethesda, Md. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 10, Issue 6, June 1950, Pages 1273–1293, https://doi.org/10.1093/jnci/10.6.1273 Published: 01 June 1950 Article history Received: 11 April 1950 Published: 01 June 1950
The adventitia: The outs and ins of vascular disease
Authors: P PAGANO, D GUTTERMAN
Journal: Cardiovascular Research (2007)

Long before it was established that the adventitia is a major source of vasoactive factors and a pivotal participant in vascular remodeling, it was noted that the changes occurring in the adventitia could be a signal of impending vascular disease, among them marked hypercellularity, increased connective tissue production, and clear signs of inflammation. Various forms of hypertension, atherosclerosis, and vascular injury are characterized by adventitial cell proliferation and increased leukocyte levels in the perivascular space. In 1915, Albutt [1] reported finding inflammatory cells in the perivascular adventitia of atherosclerotic arteries. Almost half a century later, Schwartz and Mitchell [2] showed a positive correlation between the magnitude of adventitial inflammation and the severity of atherosclerosis. However, for more than 30 years, these observations remained a curious, yet peculiar phenomenon that was largely ignored and generally considered irrelevant to homeostasis of the vessel wall. Until recently, doubts persisted that this outer segment of the blood vessel could have far-reaching effects on the vascular wall, including profound changes affecting medial smooth muscle and endothelial cell biology.

Over the past decade, however, a few landmark studies illustrated a highly important role for the adventitia in dysfunction, ranging from interference in endothelium-dependent responses to a direct contribution of adventitial myofibroblasts to restenosis. It is our expectation and hope that the reviews and original publications in this issue will shed important new light on an important role for the adventitia in vascular physiology and pathophysiology.

Maiellaro and Taylor [3] highlight the emerging new paradigm of vascular inflammation, describing an inward progression of inflammation from the adventitia toward the intima. Major strides have been made in revealing the identity of the adventitial cell population, which we now know includes monocytes, macrophages and T-cells together with increased differentiation of resident fibroblasts into myofibroblasts. Moreover, these changes were shown …
Nanoparticles functionalised with recombinant single chain Fv antibody fragments (scFv) for the magnetic resonance imaging of cancer cells
Authors: Kim L. Vigor, Panagiotis G. Kyrtatos, Shane Minogue, Khuloud T. Al-Jamal, Heide Kogelberg, Berend Tolner, Kostas Kostarelos, Richard H. Begent, Quentin A. Pankhurst, Mark F. Lythgoe, Kerry A. Chester
Journal: Biomaterials (2009)
Improvement in quality of life of patients with AL amyloidosis treated with high-dose melphalan and autologous stem cell transplantation
Authors: David C. Seldin, Jennifer J. Anderson, Vaishali Sanchorawala, Karim Malek, Daniel G. Wright, Karen Quillen, Kathleen T. Finn, John L. Berk, Laura M. Dember, Rodney H. Falk, Martha Skinner
Journal: Blood (2004)
A Role for Caspase-1 in Heart Failure
Authors: Sabine Merkle, Stefan Frantz, Michael P. Schön, Johann Bauersachs, Monika Buitrago, Robert J.A. Frost, Eva M. Schmitteckert, Martin J. Lohse, Stefan Engelhardt
Journal: Circulation Research (2007)

Apoptosis of cardiomyocytes is increased in heart failure and has been implicated in disease progression. The activation of "proapoptotic" caspases represents a key step in cardiomyocyte apoptosis. In contrast, the role of "proinflammatory" caspases (caspases 1, 4, 5, 11, 12) is unclear. Here, we study the cardiac function of caspase-1. Gene array analysis in a murine heart failure model showed upregulation of myocardial caspase-1. In addition, we found increased expression of caspase-1 protein in murine and human heart failure. Mice with cardiomyocyte-specific overexpression of caspase-1 developed heart failure in the absence of detectable formation of interleukin (IL)-1beta or IL-18 and inflammation. Transgenic caspase-1 induced primary cardiomyocyte apoptosis before structural and molecular signs of myocardial remodeling occurred. In contrast, deletion of endogenous caspase-1 was beneficial in the setting of myocardial infarction-induced heart failure. Furthermore, caspase-1-deficient mice were protected from ischemia/reperfusion-induced cardiomyocyte apoptosis. Studies in primary rat cardiomyocytes indicated that caspase-1 induces cardiomyocyte apoptosis primarily through activation of caspases-3 and -9. In contrast to previous findings, which imply a proinflammatory role of caspase-1, these data suggest a primary proapoptotic role for caspase-1 in cardiomyocytes. Our findings support a functional role for caspase-1-mediated myocardial apoptosis contributing to the progression of heart failure.
Terahertz pulsed imaging of basal cell carcinoma ex vivo and in vivo
Authors: V.P. Wallace, A.J. Fitzgerald, S. Shankar, N. Flanagan, R. Pye, J. Cluff, D.D. Arnone
Journal: British Journal of Dermatology (2004)

Background Terahertz radiation lies between the infrared and microwave regions of the electromagnetic spectrum and can be used to excite large amplitude vibrational modes of molecules and probe the weak interactions between them. Terahertz pulsed imaging (TPI) is a noninvasive imaging technique that utilises this radiaton. Objectives To determine whether TPI could differentiate between basal cell carcinoma (BCC) and normal tissue and to test whether it can help facilitate delineation of tumour margins prior to surgery. Methods A portable TPI system was used in the clinic to image 18 BCCs ex vivo and five in vivo. Results The diseased tissue showed a change in terahertz properties compared with normal tissue, manifested through a broadening of the reflected terahertz pulse. Regions of disease identified in the terahertz image correlated well with histology. Conclusions This study has confirmed the potential of TPI to identify the extent of BCC in vivo and to delineate tumour margins. Further clinical study of TPI as a surgical tool is now required.
P616 TGFβ1 STIMULATION OF HUMAN BONE MARROW MESENCHYMAL STEM CELLS (MSC) ENHANCES THEIR HEPATIC ENGRAFTMENT AND THERAPEUTIC EFFECT IN INJURED LIVER VIA UPREGULATION OF CXCR3 FUNCTION
Authors: A. Garg, N.J. Davies, V. Aldridge, A.L. King, S.T. Ward, K.-K. Li, R. Bernstein, S. Desai, J. Fear, P.F. Lalor, P.N. Newsome
Journal: Journal of Hepatology (2014)
Prospective observational study on the incidence of medication errors during simulated resuscitation in a paediatric emergency department
Authors: Eran Kozer, Winnie Seto, Zulfikaral Verjee, Chris Parshuram, Sohail Khattak, Gideon Koren, D Anna Jarvis
Journal: BMJ (2004)

<h3>Abstract</h3> <b>Objectives</b> To characterise the incidence and nature of medication errors during paediatric resuscitations. <b>Design</b> A prospective observational study of simulated emergencies. <b>Setting</b> Emergency department of a tertiary paediatric hospital. <b>Participants</b> Teams that included a clinician who commonly leads "real" resuscitations, at least two assisting physicians, and two or three paediatric nurses. <b>Interventions</b> The teams conducted eight mock resuscitations, including ordering medications. Exercises were videotaped and drugs ordered and administered during the resuscitation were recorded. Syringes and drugs prepared during the resuscitation were collected and analysed for concentrations and actual amounts. <b>Main outcome measures</b> Number and type of drug errors. <b>Results</b> Participants gave 125 orders for medications. In 21 (17%) of the orders the exact dose was not specified. Nine dosing errors occurred during the ordering phase. Of these errors, five were intercepted before the drug reached the patient. Four 10-fold errors were identified. In nine (16%) out of 58 syringes analysed, measured drug concentrations showed a deviation of at least 20% from the ordered dose. A large deviation (at least 50%) from the expected dose was found in four (7%) cases. <b>Conclusions</b> Medication errors commonly occur during all stages of paediatric resuscitation. Many errors could be detected only by analysing syringe content, suggesting that such errors may be a major source of morbidity and mortality in resuscitated children.
Biological Effects of the Neonatal Injection of 7,12-Dimethylbenz[&lt;italic&gt;a&lt;/italic&gt;]anthracene&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: J K Ball, D A Dawson
Journal: JNCI Journal of the National Cancer Institute (1969)

The neonatal injection of 7,12-dimethylbenz[a]anthracene (DMBA) in Swiss mice results in a very high incidence of thymic lymphomas. This paper presents a dose-response study to determine the relationship between toxicity and tumor incidence. Thirty μg DMBA resulted in a tumor incidence of 100%, but mortality was insignificant. Higher doses (50, 80 μg), although inducing tumors in 100% of the survivors, caused 26 and 63% mortality, respectively. Mice receiving 100 μg DMBA could be completely protected against lethal effects by the injection of normal syngeneic bone marrow or spleen cells. Thymic cells were ineffective. The cells in the bone marrow responsible for this protection could be concentrated 100-fold by centrifugation in a serum-albumin density gradient. Doses of 25 or 12 μg DMBA had no influence on whole-body or spleen weights or hemoglobin levels for the first 30 days after neonatal injection. Thymus weights were significantly decreased by both doses, starting 8–10 days post injection. The extent of the weight loss was independent of the dose. Bone marrow cellularity was also significantly reduced and the extent of the decrease depended on the dose of DMBA injected. Both doses suppressed bone marrow cellularity as early as 2 days after treatment. The permanent immunosuppression induced by DMBA could be reversed by the injection of normal syngeneic bone marrow and spleen cells but not with thymic implants. Bone marrow and spleen cells from DMBA-treated mice also did not affect restoration of the immunosuppression.
Quantitation of T-cell neogenesis in vivo after allogeneic bone marrow transplantation in adults
Authors: Ephraim P. Hochberg, Antoinette C. Chillemi, Catherine J. Wu, Donna Neuberg, Christine Canning, Kelly Hartman, Edwin P. Alyea, Robert J. Soiffer, Spyros A. Kalams, Jerome Ritz
Journal: Blood (2001)
NEUROBIOLOGY OF SPEECH PERCEPTION
Authors: R. Holly Fitch, Steve Miller, Paula Tallal
Journal: Annual Review of Neuroscience (1997)

▪ Abstract The mechanisms by which human speech is processed in the brain are reviewed from both behavioral and neurobiological perspectives. Special consideration is given to the separation of speech processing as a complex acoustic-processing task versus a linguistic task. Relevant animal research is reviewed, insofar as these data provide insight into the neurobiological basis of complex acoustic processing in the brain.
Liver Ultrastructure in Mitochondrial Urea Cycle Enzyme Deficiencies and Comparison with Reye's Syndrome
Authors: Patricia S. Latham, Douglas R. Labrecque, John W. Mcreynolds, Gerald Klatskin
Journal: Hepatology (1984)

The liver ultrastructural findings in two girls with partial carbamyl phosphate synthetase I (CPS) deficiency and their heterozygote parents and two siblings with ornithine transcarbamylase (OTC) deficiency are described. Liver ultrastructure in the four patients with inherited deficiencies of urea cycle enzymes showed minimal alterations with essentially normal mitochondria when biopsy was performed during periods of good control of their hyperammonemia. Mitochondrial ultrastructure was also essentially normal in the heterozygotes for carbamyl phosphate synthetase I deficiency. These findings are in contrast to the marked alterations in mitochondrial ultrastructure found in the study of two cases of Reye's syndrome in which severe depression of ornithine transcarbamylase and carbamyl phosphate synthetase I activities was noted.
Angiotensinogen gene G-6A polymorphism influences idiopathic pulmonary fibrosis disease progression
Authors: M. Molina-Molina, A. Xaubet, X. Li, A. Abdul-Hafez, K. Friderici, K. Jernigan, W. Fu, Q. Ding, J. Pereda, A. Serrano-Mollar, A. Casanova, E. Rodríguez-Becerra, F. Morell, J. Ancochea, C. Picado, B. D. Uhal
Journal: European Respiratory Journal (2008)

Angiotensin II is a growth factor that plays a key role in the physiopathology of idiopathic pulmonary fibrosis (IPF). A nucleotide substitution of an adenine instead of a guanine (G-6A) in the proximal promoter region of angiotensinogen (AGT), the precursor of angiotensin II, has been associated with an increased gene transcription rate. In order to investigate whether the G-6A polymorphism of the AGT gene is associated with IPF development, severity and progression, the present study utilised a case–control study design and genotyped G-6A in 219 patients with IPF and 224 control subjects. The distribution of G-6A genotypes and alleles did not significantly differ between cases and controls. The G-6A polymorphism of the AGT gene was not associated with disease severity at diagnosis. The presence of the A allele was strongly associated with increased alveolar arterial oxygen tension difference during follow-up, after controlling for the confounding factors. Higher alveolar arterial oxygen tension changes over time were observed in patients with the AA genotype (0.37±0.7 mmHg (0.049±0.093 kPa) per month) compared to GA genotype (0.12±1 mmHg (0.016±0.133 kPa) per month) and GG genotype (0.2±0.6 mmHg (0.027±0.080 kPa) per month). G-6A polymorphism of the angiotensinogen gene is associated with idiopathic pulmonary fibrosis progression but not with disease predisposition. This polymorphism could have a predictive significance in idiopathic pulmonary fibrosis patients.