tbuckley/cabot-search huggingface dataset:
The Formation of Immunogenic Major Histocompatibility Complex Class II–Peptide Ligands in Lysosomal Compartments of Dendritic Cells Is Regulated by Inflammatory Stimuli
Authors: Kayo Inaba, Shannon Turley, Tomonori Iyoda, Fumiya Yamaide, Susumu Shimoyama, Caetano Reis e Sousa, Ronald N. Germain, Ira Mellman, Ralph M. Steinman
Journal: The Journal of Experimental Medicine (2000)

During their final differentiation or maturation, dendritic cells (DCs) redistribute their major histocompatibility complex (MHC) class II products from intracellular compartments to the plasma membrane. Using cells arrested in the immature state, we now find that DCs also regulate the initial intracellular formation of immunogenic MHC class II–peptide complexes. Immature DCs internalize the protein antigen, hen egg lysozyme (HEL), into late endosomes and lysosomes rich in MHC class II molecules. There, despite extensive colocalization of HEL protein and MHC class II products, MHC class II–peptide complexes do not form unless the DCs are exposed to inflammatory mediators such as tumor necrosis factor α, CD40 ligand, or lipoplolysaccharide. The control of T cell receptor (TCR) ligand formation was observed using the C4H3 monoclonal antibody to detect MHC class II–HEL peptide complexes by flow cytometry and confocal microscopy, and with HEL-specific 3A9 transgenic T cells to detect downregulation of the TCR upon MHC–peptide encounter. Even the binding of preprocessed HEL peptide to MHC class II is blocked in immature DCs, including the formation of C4H3 epitope in MHC class II compartments, suggesting an arrest to antigen presentation at the peptide-loading step, rather than an enhanced degradation of MHC class II–peptide complexes at the cell surface, as described in previous work. Therefore, the capacity of late endosomes and lysosomes to produce MHC class II–peptide complexes can be strictly controlled during DC differentiation, helping to coordinate antigen acquisition and inflammatory stimuli with formation of TCR ligands. The increased ability of maturing DCs to load MHC class II molecules with antigenic cargo contributes to the &amp;gt;100-fold enhancement of the subsequent primary immune response observed when immature and mature DCs are compared as immune adjuvants in culture and in mice.
Peripherally Induced Foxp3+ Regulatory T Cells Mediates The Immunomodulatory Effect Of Intravenous Immunoglobulin In An Experimental Model Of Allergic Airway Disease
Authors: Amir Hossein Massoud, Gabriel N. Kaufman, Ciriaco Piccirillo, Bruce D. Mazer
Journal: Journal of Allergy and Clinical Immunology (2014)
Monobenzylether of hydroquinone
Authors: B. Bentley-Phillips
Journal: British Journal of Dermatology (1978)

Journal Article Monobenzylether of hydroquinone Get access B. Bentley‐Phillips B. Bentley‐Phillips Dermatology Clinic, King Edward VIII Hospital, Congella, Durban 4001, South Africa. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 99, Issue 6, 1 December 1978, Page 719, https://doi.org/10.1111/j.1365-2133.1978.tb07069.x Published: 01 December 1978
Report: Sports Medicine Seminar--Manila, December 1981
Authors: H. E. Robson
Journal: British Journal of Sports Medicine (1982)

The assembly of the nations of South East Asia for the 11th SEA Games held in the Philippines from December 6th gave a good opportunity for the doctors, physiotherapists and others engaged professionally in the scientific aspects of sport to get together for a short seminar on sports medicine.The venue was the magnificent Philippine International Convention Centre, equipped to take at least half a dozen conferences of a hundred people minimum at the same time, and with excellent lecture room facilities.Unfortunately, like so many places in the world in the 1980s, it was necessary for armed guards to carry out a security check of all entering the building, including a search of brief cases and handbags.
Atrial natriuretic peptide decreases circulatory capacitance in areflexic rats.
Authors: N C Trippodo, F E Cole, E D Frohlich, A A MacPhee
Journal: Circulation Research (1986)

The short-term hemodynamic response to atrial natriuretic peptide appears to be partly mediated by decreased venous return, which could result from increased circulatory capacitance or decreased blood volume. To determine if rat atrial natriuretic peptide 99-126 (0.5 microgram/kg/min IV for 30-70 minutes) dilated capacitance vessels or decreased blood volume, mean circulatory filling pressure (measured during brief circulatory arrest by inflating an intraatrial balloon) and blood volume (51Cr-erythrocytes) were measured in anesthetized rats. Mean circulatory filling pressure, central venous pressure, and blood volume decreased by 0.4 mm Hg, 0.5 mm Hg, and 3.4 ml/kg, respectively. To determine the total circulatory pressure-volume relationship without influence from autonomic reflexes, mean circulatory filling pressure and blood volume were measured in spinal-cord-transected rats before and immediately after infusing or withdrawing 5 ml blood. Atrial natriuretic peptide decreased mean circulatory filling pressure, central venous pressure, and blood volume by 0.9 mm Hg, 1.7 mm Hg, and 8.0 ml/kg, respectively, and displaced the pressure-volume relationship toward the pressure axis by decreasing extrapolated unstressed volume. Similar results were obtained in spinal-cord-transected rats that had initial vascular tone restored to a greater level by norepinephrine infusion. In anephric rats, atrial natriuretic peptide decreased central venous pressure by 0.3 mm Hg and blood volume by 1.6 ml/kg. The results indicate that short-term infusion of atrial natriuretic peptide reduced circulatory capacitance in rats and suggest that this reduction resulted from diminished blood volume due to urinary fluid loss followed by passive vascular recoil and active venoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)
Competitive match-play tennis under heat stress: a challenge for all players
Authors: Julien D Périard, Michael F Bergeron
Journal: British Journal of Sports Medicine (2014)

In January 2014, the heat took over centre court and the rest of the grounds during the first week of the Australian Open in Melbourne. Following days of scorching hot weather and air temperatures nearing 43°C, play was suspended for several hours when the ‘Extreme Heat Policy’ was invoked. This entailed a stoppage in play, except that sets in progress had to carry on until completion, along with closing of the roofs over the arenas so that some matches could continue. The stoppage of play, however, occurred only after a plastic bottle had reportedly started melting on court, a ball boy and a male player fainted, a female player experienced cramping and vomiting and several notable players voiced their concerns regarding the appropriateness and safety of continuing to compete in such conditions. Further examination of the rules governing the suspension of play is seemingly warranted, in the context of balancing players’ health and performance. This sequence of events played out on the international stage in Australia is mirrored each year around the world in numerous other much lower profile events, consistently and convincingly demonstrating the challenges and consequences of competing under excessive heat stress. Arguably, the current guidelines and practices for effectively and safely playing tennis in the heat, or the thresholds to suspend play, may not be adequate and sufficiently evidence based.

Competitive match-play tennis is multifactorial, underpinned by an integrated array of complex physiological, biomechanical, cognitive and psychological processes. Players must have an appropriate balance of particular physical attributes such as speed, agility, power, muscular endurance and a high level of overall aerobic fitness, as well as a keen-sustained capacity to constantly anticipate, quickly react and make numerous ongoing split-second decisions.1 When undertaken in hot and/or humid conditions, all of these essential processes are challenged, with further …
IFN-γ inhibits liver progenitor cell proliferation in HBV-infected patients and in 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet-fed mice
Authors: Hong-lei Weng, De-chun Feng, Svetlana Radaeva, Xiao-ni Kong, Lei Wang, Yan Liu, Qi Li, Hong Shen, Yun-peng Gao, Roman Müllenbach, Stefan Munker, Tong Huang, Jia-lin Chen, Vincent Zimmer, Frank Lammert, Peter R. Mertens, Wei-min Cai, Steven Dooley, Bin Gao
Journal: Journal of Hepatology (2013)
Frozen shoulder: prospective clinical study with an evaluation of three treatment regimens.
Authors: D Y Bulgen, A I Binder, B L Hazleman, J Dutton, S Roberts
Journal: Annals of the Rheumatic Diseases (1984)

Forty-two patients with frozen shoulder were followed up closely for eight months. They were all taught pendular exercises and randomly allocated to one of four treatment groups: (a) intraarticular steroids, (b) mobilisations , (c) ice therapy, (d) no treatment. This study has shown that there is little long-term advantage in any of the treatment regimens but that steroid injections may benefit pain and range of movement in the early stages of the condition.
Effect of resistance training during hospitalization in the systemic inflammation, functional capacity and muscle strength in COPD patients
Authors: Rodrigo Borges, Celso R.F. Carvalho
Journal: European Respiratory Journal (2011)

Background:  Resistance training (RT) during hospitalization improves skeletal muscle strength; however its effect on systemic inflammation and to modify the level of activity remains unknown.   Objective:  Our aim was to evaluate the effect of RT in the systemic inflammation and functional capacity in COPD patients during and after hospitalization.   Methods:  Twenty nine out 102 patients hospitalized due to COPD exacerbation were randomly assigned to either Control (CG) or RT (RTG) groups. They were evaluated on the 2nd day of hospitalization, at hospital discharge and after 30 days. It was evaluated systemic inflammatory markers (TNF-α, RCP, IL1β, IL-12p70, IL-6, IL-8, IL10), level of physical activity, health-related quality of life (HRQL), and upper and lower limbs muscle strength.   Results:  Patients from RTG showed an improvement in the lower limb muscle strength, in the six-minute walking test (6MWT) and in all domains of HRQL (p   Conclusion:  Our results suggest that resistance training during hospitalization improves lower limbs muscle strength, health-related quality of life and physical capacity; however does not change either systemic inflammatory levels or physical activity during or after hospital discharge.  Supported by FAPESP
Germline CBL mutations cause developmental abnormalities and predispose to juvenile myelomonocytic leukemia
Authors: Charlotte M Niemeyer, Michelle W Kang, Danielle H Shin, Ingrid Furlan, Miriam Erlacher, Nancy J Bunin, Severa Bunda, Jerry Z Finklestein, Kathleen M Sakamoto, Thomas A Gorr, Parinda Mehta, Irene Schmid, Gabriele Kropshofer, Selim Corbacioglu, Peter J Lang, Christoph Klein, Paul-Gerhard Schlegel, Andrea Heinzmann, Michaela Schneider, Jan Starý, Marry M van den Heuvel-Eibrink, Henrik Hasle, Franco Locatelli, Debbie Sakai, Sophie Archambeault, Leslie Chen, Ryan C Russell, Stephanie S Sybingco, Michael Ohh, Benjamin S Braun, Christian Flotho, Mignon L Loh
Journal: Nature Genetics (2010)
Results of the First Phase I Clinical Trial of the Novel Ii-Key Hybrid Preventive HER-2/<i>neu</i>Peptide (AE37) Vaccine
Authors: Jarrod P. Holmes, Linda C. Benavides, Jeremy D. Gates, Mark G. Carmichael, Matthew T. Hueman, Elizabeth A. Mittendorf, James L. Murray, Asna Amin, Dianna Craig, Eric von Hofe, Sathibalan Ponniah, George E. Peoples
Journal: Journal of Clinical Oncology (2008)

Purpose HER-2/neu is overexpressed in breast cancer and is the source of immunogenic peptides. CD4 + T-helper peptides for HER-2/neu are being evaluated in vaccine trials. The addition of Ii-Key, a four–amino-acid LRMK modification, increases vaccine potency when compared with unmodified class II epitopes. We present the results of the first human phase I trial of the Ii-Key hybrid HER-2/neu peptide (AE37) vaccine in disease-free, node-negative breast cancer patients. Patients and Methods The dose escalation trial included five dose groups, to determine safety and optimal dose of the hybrid peptide (100 μg, 500 μg, 1,000 μg) and granulocyte-macrophage colony-stimulating factor (GM-CSF; range, 0 to 250 μg). In the event of significant local toxicity, GM-CSF (or peptide in absence of GM-CSF) was reduced by 50%. Immunologic response was monitored by delayed-type hypersensitivity and [ 3 H]thymidine proliferative assays for both the hybrid AE37 (LRMK-positive HER-2/neu:776-790) and AE36 (unmodified HER-2/neu:776-790). Results All 15 patients completed the trial with no grade 3 to 5 toxicities. Dose reductions occurred in 47% of patients. In the second group (peptide, 500 μg; GM-CSF, 250 μg), all patients required dose reductions, prompting peptide-only inoculations in the third group. The vaccine induced dose-dependent immunologic responses in vitro and in vivo to AE37, as well as AE36. Conclusion The hybrid AE37 vaccine seems safe and well tolerated with minimal toxicity if properly dosed. AE37 is capable of eliciting HER-2/neu–specific immune responses, even without the use of an adjuvant. This trial represents the first human experience with the Ii-Key modification, and to our knowledge, AE37 is the first peptide vaccine to show potency in the absence of an immunoadjuvant.
A Feasibility Study of Bevacizumab plus Dose-Dense Doxorubicin–Cyclophosphamide (AC) Followed by Nanoparticle Albumin–Bound Paclitaxel in Early-Stage Breast Cancer
Authors: Heather L. McArthur, Hope Rugo, Benjamin Nulsen, Laura Hawks, Jill Grothusen, Michelle Melisko, Mark Moasser, Matthew Paulson, Tiffany Traina, Sujata Patil, Qin Zhou, Richard Steingart, Chau Dang, Monica Morrow, Peter Cordeiro, Monica Fornier, John Park, Andrew Seidman, Diana Lake, Theresa Gilewski, Maria Theodoulou, Shanu Modi, Gabriella D'Andrea, Nancy Sklarin, Mark Robson, Mary Ellen Moynahan, Steven Sugarman, Jane E. Sealey, John H. Laragh, Carmen Merali, Larry Norton, Clifford A. Hudis, Maura N. Dickler
Journal: Clinical Cancer Research (2011)

Bevacizumab confers benefits in metastatic breast cancer but may be more effective as adjuvant therapy. We evaluated the cardiac safety of bevacizumab plus dose-dense doxorubicin-cyclophosphamide (ddAC) → nanoparticle albumin-bound (nab)-paclitaxel in human epidermal growth factor receptor 2 normal early-stage breast cancer.Eighty patients with normal left ventricular ejection fraction (LVEF) were enrolled. Bevacizumab was administered for 1 year, concurrently with ddAC → nab-paclitaxel then as a single agent. LVEF was evaluated at months 0, 2, 6, 9, and 18. This regimen was considered safe if fewer than three cardiac events or fewer than two deaths from left ventricular dysfunction occurred. Correlative studies of cardiac troponin (cTn) and plasma renin activity (PRA) were conducted.The median age was 48 years (range, 27-75 years), and baseline LVEF was 68% (53%-82%). After 39 months' median follow-up (5-45 months): median LVEF was 68% (53%-80%) at 2 months (n = 78), 64% (51%-77%) at 6 months (n = 66), 63% (48%-77%) at 9 months (n = 61), and 66% (42%-76%) at 18 months (n = 54). One patient developed symptomatic LV dysfunction at month 15. Common toxicities necessitating treatment discontinuation were hypertension (HTN, 4%), wound-healing complications (4%), and asymptomatic LVEF declines (4%). Neither cTn nor PRA predicted congestive heart failure (CHF) or HTN, respectively.Bevacizumab with ddAC → nab-paclitaxel had a low rate of cardiac events; cTn and PRA levels are not predictive of CHF or HTN, respectively. The efficacy of bevacizumab as adjuvant treatment will be established in several ongoing phase III trials.
Pancreatic carcinoma with polyarthritis, fat necrosis, and high serum lipase and trypsin activity.
Authors: R J van Klaveren, P H de Mulder, A M Boerbooms, C A van de Kaa, U J van Haelst, D J Wagener, J C Hafkenscheid
Journal: Gut (1990)

A 46 year old white man presented with subcutaneous and intramedullary fat necrosis, destructive polyarthritis, and osteolytic bone lesions, complicating a poorly differentiated adenocarcinoma of the tail of the pancreas with metastases in the liver and omentum. There was a 100-fold increase in serum lipase and trypsin activity. His condition deteriorated rapidly, was characterised by rapid tumour growth, formation of ascites, a 20 kg weight loss, extensive subcutaneous fat necrosis, and fistula formation in the left calf. Treatment with 5-fluorouracil 300 mg/m2 on days 1-5 and doxorubicin 50 mg/m2 and cisplatin 100 mg/m2 on day 1, every three weeks, was well tolerated and resulted in rapid clinical improvement. After three courses of treatment a partial remission was seen and after seven courses further improvement occurred with a return to normal of serum lipase and trypsin activity. One year after starting chemotherapy the tumour relapsed but responded again to chemotherapy (epirubicin 40 mg/m2 and carboplatin 300 mg/m2 on day 1, every three weeks).
Impact of Platelet Reactivity on Cardiovascular Outcomes in Patients With Type 2 Diabetes Mellitus and Coronary Artery Disease
Authors: Dominick J. Angiolillo, Esther Bernardo, Manel Sabaté, Pilar Jimenez-Quevedo, Marco A. Costa, Jorge Palazuelos, Rosana Hernández-Antolin, Raul Moreno, Javier Escaned, Fernando Alfonso, Camino Bañuelos, Luis A. Guzman, Theodore A. Bass, Carlos Macaya, Antonio Fernandez-Ortiz
Journal: Journal of the American College of Cardiology (2007)
C5a Receptor Mediates Neutrophil Activation and ANCA-Induced Glomerulonephritis
Authors: Adrian Schreiber, Hong Xiao, J. Charles Jennette, Wolfgang Schneider, Friedrich C. Luft, Ralph Kettritz
Journal: Journal of the American Society of Nephrology (2008)

Anti-neutrophil cytoplasmic autoantibody (ANCA)-induced necrotizing crescentic glomerulonephritis (NCGN) requires complement participation in its pathogenesis. We tested the hypothesis that the anaphylatoxin C5a is pivotal to disease induction via the neutrophil C5a receptor (C5aR). Supernatants from ANCA-activated neutrophils activated the complement cascade in normal serum, producing C5a. This conditioned serum primed neutrophils for ANCA-induced respiratory burst; neutrophil C5aR blockade abrogated this priming, but C3aR blockade did not. Furthermore, recombinant C5a but not C3a dosage-dependently primed neutrophils for ANCA-induced respiratory burst. To test the role of C5aR in a model of NCGN, we immunized myeloperoxidase-deficient mice with myeloperoxidase, irradiated them, and transplanted bone marrow from wild-type mice or C5aR-deficient mice into them. All mice that received wild-type marrow (six of six) but only one of eight mice that received C5aR-deficient marrow developed NCGN (P < 0.05). Albuminuria and neutrophil influx into glomeruli were also significantly attenuated in the mice that received C5aR-deficient marrow (P < 0.05). In summary, C5a and the neutrophil C5aR may compose an amplification loop for ANCA-mediated neutrophil activation. The C5aR may provide a new therapeutic target for ANCA-induced necrotizing crescentic glomerulonephritis.
Diabetic Cardiovascular Autonomic Neuropathy
Authors: Aaron I. Vinik, Dan Ziegler
Journal: Circulation (2007)

O ne of the most overlooked of all serious complications of diabetes is cardiovascular autonomic neuropathy (CAN), [1][2][3] which encompasses damage to the autonomic nerve fibers that innervate the heart and blood vessels, resulting in abnormalities in heart rate control and vascular dynamics. 4he present report discusses the clinical manifestations (eg, resting tachycardia, orthostasis, exercise intolerance, intraoperative cardiovascular liability, silent myocardial infarction [MI], and increased risk of mortality) in the presence of CAN.It also demonstrates that autonomic dysfunction can affect daily activities of individuals with diabetes and may invoke potentially life-threatening outcomes.Advances in technology, built on decades of research and clinical testing, now make it possible to objectively identify early stages of CAN with the use of careful measurement of autonomic function and to provide therapeutic choices that are based on symptom control and that might abrogate the underlying disorder. Epidemiology of CANLittle information exists as to frequency of CAN in representative diabetic populations.This is further complicated by the differences in the methodology used and the lack of standardization.Fifteen studies using different end points report prevalence rates of 1% to 90%. 1 The heterogenous methodology makes it difficult to compare epidemiology across different studies.CAN may be present at diagnosis, and prevalence increases with age, duration of diabetes, and poor glycemic control.CAN also cosegregates with distal symmetric polyneuropathy, microangiopathy, and macroangiopathy.Age, diabetes, obesity, and smoking are risk factors for reduced heart rate variability (HRV) 5 in type 2 diabetes.Thus, there may be selectivity and sex-related differences among the various cardiovascular risk factors as to their influence on autonomic dysfunction. 6HbA1c, hypertension, distal symmetrical polyneuropathy, retinopathy, and exposure to hyperglycemia were shown to be risk factors for developing CAN in type 1 diabetes. 7 Clinical Manifestations of CAN Resting TachycardiaWhereas abnormalities in HRV are early findings of CAN, resting tachycardia and a fixed heart rate are characteristic late findings in diabetic patients with vagal impairment. 8esting heart rates of 90 to 100 bpm and occasional heart rate increments up to 130 bpm occur.The highest resting heart rates have been found in patients with parasympathetic damage, occurring earlier in the course of CAN than sympathetic nerve function; in those with evidence for combined vagal and sympathetic involvement, the rate returns toward normal but remains elevated.A fixed heart rate that is unresponsive to moderate exercise, stress, or sleep indicates almost complete cardiac denervation. 8Thus, heart rate may not provide a reliable diagnostic criterion of CAN in the absence of other causes unless it is increased by more than 100 bpm.
Adenovirus infection and disease in paediatric haematopoietic stem cell transplant patients: clues for antiviral pre-emptive treatment
Authors: L. Feghoul, S. Chevret, A. Cuinet, J.-H. Dalle, M. Ouachée, K. Yacouben, M. Fahd, V. Guérin-El Khourouj, J. Roupret-Serzec, G. Sterkers, A. Baruchel, F. Simon, J. LeGoff
Journal: Clinical Microbiology and Infection (2015)
Histone deacetylation in epigenetics: An attractive target for anticancer therapy
Authors: Antonello Mai, Silvio Massa, Dante Rotili, Ilaria Cerbara, Sergio Valente, Riccardo Pezzi, Silvia Simeoni, Rino Ragno
Journal: Medicinal Research Reviews (2005)

The reversible histone acetylation and deacetylation are epigenetic phenomena that play critical roles in the modulation of chromatin topology and the regulation of gene expression. Aberrant transcription due to altered expression or mutation of genes that encode histone acetyltransferase (HAT) or histone deacetylase (HDAC) enzymes or their binding partners, has been clearly linked to carcinogenesis. The histone deacetylase inhibitors are a new promising class of anticancer agents (some of which in clinical trials), that inhibit the proliferation of tumor cells in culture and in vivo by inducing cell-cycle arrest, terminal differentiation, and/or apoptosis. This report reviews the chemistry and the biology of HDACs and HDAC inhibitors, laying particular emphasis on agents actually in clinical trials for cancer therapy and on new potential anticancer lead compounds more selective and less toxic. © 2005 Wiley Periodicals, Inc.