tbuckley/cabot-search huggingface dataset:
Leucocytoclastic vasculitis after coronary bypass artery grafting
Authors: J. George, Y. Levy, A. Afec, R. Yaniv, Y. Shoenfeld
Journal: British Journal of Dermatology (1996)

Journal Article Leucocytoclastic vasculitis after coronary bypass artery grafting Get access J. George, J. George Department of Medicine ‘B’ and the Unit of Autoimmune Disease Research, Sheba Medical Center, Tel‐Hashomer, Sackler Faculty of Medicine, Tel‐Aviv University, Tel‐Aviv, Israel Search for other works by this author on: Oxford Academic Google Scholar Y. Levy, Y. Levy Department of Medicine ‘B’ and the Unit of Autoimmune Disease Research, Sheba Medical Center, Tel‐Hashomer, Sackler Faculty of Medicine, Tel‐Aviv University, Tel‐Aviv, Israel Search for other works by this author on: Oxford Academic Google Scholar A. Afec, A. Afec Department of Medicine ‘B’ and the Unit of Autoimmune Disease Research, Sheba Medical Center, Tel‐Hashomer, Sackler Faculty of Medicine, Tel‐Aviv University, Tel‐Aviv, Israel Search for other works by this author on: Oxford Academic Google Scholar R. Yaniv, R. Yaniv Department of Medicine ‘B’ and the Unit of Autoimmune Disease Research, Sheba Medical Center, Tel‐Hashomer, Sackler Faculty of Medicine, Tel‐Aviv University, Tel‐Aviv, Israel Search for other works by this author on: Oxford Academic Google Scholar Y. Shoenfeld Y. Shoenfeld Department of Medicine ‘B’ and the Unit of Autoimmune Disease Research, Sheba Medical Center, Tel‐Hashomer, Sackler Faculty of Medicine, Tel‐Aviv University, Tel‐Aviv, Israel Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 135, Issue 6, 1 December 1996, Pages 1015–1016, https://doi.org/10.1046/j.1365-2133.1996.d01-1122.x Published: 01 December 1996
Respiratory muscle function and free radicals: from cell to COPD
Authors: L. M A Heunks
Journal: Thorax (2000)

Respiratory muscle dysfunction in chronic obstructive pulmonary disease (COPD)Dysfunction of the respiratory muscles, especially the diaphragm, is known to occur in patients with severe chronic obstructive pulmonary disease (COPD). [1]2][3] Weakness of the diaphragm is part of a generalised process involving all (respiratory and peripheral) skeletal muscles.Causative factors for respiratory muscle dysfunction in COPD include disturbances in electrolytes, 4 hypercapnia, 5 forward failure, 6 and prolonged use of oral corticosteroids. 7In addition, the altered geometry of the thorax in severe emphysema compromises the ventilatory pump function of the diaphragm. 8Malnutrition, which frequently occurs in moderate to severe COPD, 9 could also play a part in respiratory muscle dysfunction.Recent studies have indicated that wasting of fat free mass in COPD is associated with peripheral skeletal muscle weakness. 10However, few data are available regarding the eVects of malnutrition on respiratory muscle strength.Maximal inspiratory pressure (PImax) in nutritionally depleted patients with COPD (forced expiratory volume in one second (FEV 1 ) 45.5 (15.1)% predicted) was lower than in nondepleted patients, but this did not reach statistical significance. 9ittle is known about the underlying mechanisms of muscle dysfunction and the structural alterations that occur in the diaphragm with COPD.Levine et al 11 have shown that the diaphragm in patients with severe COPD (FEV 1 33 (4)% predicted) has a higher proportion of type I (slow) fibres and a lower proportion of type II (fast) fibres than in those without COPD.It has recently been shown that a strong correlation exists between pulmonary functional residual capacity and the proportion of slow myosin heavy chain fibres in the diaphragm. 12This fast to slow fibre transition in the diaphragm can be regarded as an advantageous adaptation since it will attenuate fatiguability of the diaphragm. 13However, eventually most patients with COPD die from respiratory muscle failure.Apparently, at some point clinical relevant respiratory muscle dysfunction occurs in COPD.It has been shown that, besides slow to fast fibre transition, other processes also occur in the diaphragm.For instance, Campbell et al 14 found that in 17 of 22
Transforming Growth Factor-β1 Suppresses Airway Hyperresponsiveness in Allergic Airway Disease
Authors: John F. Alcorn, Lisa M. Rinaldi, Elizabeth F. Jaffe, Mirjam van Loon, Jason H. T. Bates, Yvonne M. W. Janssen-Heininger, Charles G. Irvin
Journal: American Journal of Respiratory and Critical Care Medicine (2007)

Rationale: Asthma is characterized by increases in airway resistance, pulmonary remodeling, and lung inflammation. The cytokine transforming growth factor (TGF)-β has been shown to have a central role in asthma pathogenesis and in mouse models of allergic airway disease.Objectives: To determine the contribution of TGF-β to airway hyperresponsiveness (AHR), we examined the time course, source, and isoform specificity of TGF-β production in an in vivo mouse asthma model. To then elucidate the function of TGF-β in AHR, inflammation, and pulmonary fibrosis, we examined the effects of blocking TGF-β signaling with neutralizing antibody.Methods: Mice were sensitized and challenged with ovalbumin (OVA) to establish allergic airway disease. TGF-β activity was neutralized by intranasal administration of monoclonal antibody.Measurements and Main Results: TGF-β1 protein levels were increased in OVA-challenged lungs versus naive controls, and airway epithelial cells were shown to be a likely source of TGF-β1. In addition, TGF-β1 levels were elevated in OVA-exposed IL-5–null mice, which fail to recruit eosinophils into the airways. Neutralization of TGF-β1 with specific antibody had no significant effect on airway inflammation and eosinophilia, although anti–TGF-β1 antibody enhanced OVA-induced AHR and suppressed pulmonary fibrosis.Conclusions: These data show that TGF-β1 is the main TGF-β isoform produced after OVA challenge, with a likely cellular source being the airway epithelium. The effects of blocking TGF-β1 signaling had differential effects on AHR, fibrosis, and inflammation. While TGF-β neutralization may be beneficial to abrogating airway remodeling, it may be detrimental to lung function by increasing AHR.
Splenectomy for refractory Evans' syndrome associated with antiphospholipid antibodies: report of two cases
Authors: J. Font
Journal: Annals of the Rheumatic Diseases (2000)

The main haematological manifestations seen in patients with antiphospholipid antibodies (aPL) are thrombocytopenia, usually mild, and haemolytic anaemia with a positive Coombs test. Owing to the shared characteristics with idiopathic thrombocytopenic purpura, similar rules are followed in the treatment of these cytopenias. Two patients with severe aPL associated cytopenias, who required splenectomy after being refractory to steroids, immunosuppressive agents, and other treatments (intravenous gammaglobulin, danazol), are described, and previously reported cases are reviewed.
Upfront triple combination therapy in pulmonary arterial hypertension: a pilot study
Authors: Olivier Sitbon, Xavier Jaïs, Laurent Savale, Vincent Cottin, Emmanuel Bergot, Elise Artaud Macari, Hélène Bouvaist, Claire Dauphin, François Picard, Sophie Bulifon, David Montani, Marc Humbert, Gérald Simonneau
Journal: European Respiratory Journal (2014)

Patients with severe pulmonary arterial hypertension (PAH) in New York Heart Association (NYHA) functional class (FC) III/IV have a poor prognosis, despite survival benefits being demonstrated with intravenous epoprostenol. In this pilot study, the efficacy and safety of a triple combination therapy regimen in patients with severe PAH was investigated. Data from newly diagnosed NYHA FC III/IV PAH patients (n=19) initiated on upfront triple combination therapy (intravenous epoprostenol, bosentan and sildenafil) were collected retrospectively from a prospective registry. Significant improvements in 6-min walk distance and haemodynamics were observed after 4 months’ triple combination therapy in 18 patients (p&lt;0.01); 17 patients had improved to NYHA FC I or II. One patient was not included in the month 4 assessment (due to an emergency lung transplant in month 3). At the final evaluation (mean± sd 32±19 months), all 18 patients had sustained clinical and haemodynamic improvement. Overall survival estimates for the triple combination cohort were 100% at 1, 2 and 3 years. Expected survival calculated from the French equation was 75% (95% CI 68–82%), 60% (95% CI 50–70%) and 49% (95% CI 38–60%) at 1, 2 and 3 years, respectively. This pilot study provides preliminary evidence of the long-term benefits of upfront triple combination therapy in patients with severe PAH.
Ductal pancreatic cancer modeling and drug screening using human pluripotent stem cell– and patient-derived tumor organoids
Authors: Ling Huang, Audrey Holtzinger, Ishaan Jagan, Michael BeGora, Ines Lohse, Nicholas Ngai, Cristina Nostro, Rennian Wang, Lakshmi B Muthuswamy, Howard C Crawford, Cheryl Arrowsmith, Steve E Kalloger, Daniel J Renouf, Ashton A Connor, Sean Cleary, David F Schaeffer, Michael Roehrl, Ming-Sound Tsao, Steven Gallinger, Gordon Keller, Senthil K Muthuswamy
Journal: Nature Medicine (2015)
Effective photodynamic therapy of actinic keratoses and Bowen’s disease using microneedle perforation
Authors: G. Kolde, E. Rowe, H. Meffert
Journal: British Journal of Dermatology (2012)

Journal Article Effective photodynamic therapy of actinic keratoses and Bowen’s disease using microneedle perforation Get access G. Kolde, G. Kolde Dermatologic Center Berlin, Potsdamer Chaussee 80, D‐14129 Berlin, Germany E‐mail: gerhard.kolde@arcor.de Search for other works by this author on: Oxford Academic Google Scholar E. Rowe, E. Rowe Dermatologic Center Berlin, Potsdamer Chaussee 80, D‐14129 Berlin, Germany E‐mail: gerhard.kolde@arcor.de Search for other works by this author on: Oxford Academic Google Scholar H. Meffert H. Meffert Dermatologic Center Berlin, Potsdamer Chaussee 80, D‐14129 Berlin, Germany E‐mail: gerhard.kolde@arcor.de Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 168, Issue 2, 1 February 2013, Pages 450–452, https://doi.org/10.1111/j.1365-2133.2012.11153.x Published: 01 February 2013
A Prospective Randomized Trial of Teflon Versus Polyethylene Stents for Distal Malignant Biliary Obstruction
Authors: A. M. van Berkel, C. Boland, W. K. Redekop, J. J. G. H. M. Bergman, A. K. Groen, G. N. J. Tytgat, K. Huibregtse
Journal: Endoscopy (1998)

Background and Study Aims: Clogging of biliary stents continues to be a major clinical problem. Different polymer materials may have different effects on clogging.In vitrostudies have shown a direct relation between the frictional coefficient of a polymer and the amount of encrusted material. Teflon appeared to be the best polymer for biliary stents. Two different types of stents made of Teflon have been tested in clinical practice and showed favourable patency rates. However, a randomized trial has never been performed. We compared the patency of an Amsterdam-type polyethylene stent with a Teflon stent in a prospective randomized trial.
Diabetic Endothelial Nitric Oxide Synthase Knockout Mice Develop Advanced Diabetic Nephropathy
Authors: Takahiko Nakagawa, Waichi Sato, Olena Glushakova, Marcelo Heinig, Tracy Clarke, Martha Campbell-Thompson, Yukio Yuzawa, Mark A. Atkinson, Richard J. Johnson, Byron Croker
Journal: Journal of the American Society of Nephrology (2007)

Ca<sup>2+</sup> channels in distinct subcellular compartments of neurons mediate voltage-dependent Ca<sup>2+</sup> influx, which integrates synaptic responses, regulates gene expression, and initiates synaptic transmission. Antibodies that specifically recognize the α<sub>1</sub> subunits of class A, B, C, D, and E Ca<sup>2+</sup> channels have been used to investigate the localization of these voltage-gated ion channels on spinal motor neurons, interneurons, and nerve terminals of the adult rat. Class A P/Q-type Ca<sup>2+</sup> channels were present mainly in a punctate pattern in nerve terminals located along the cell bodies and dendrites of motor neurons. Both smooth and punctate staining patterns were observed over the surface of the cell bodies and dendrites with antibodies to class B N-type Ca<sup>2+</sup>channels, indicating the presence of these channels in the cell surface membrane and in nerve terminals. Class C and D L-type and class E R-type Ca<sup>2+</sup> channels were distributed mainly over the cell soma and proximal dendrites. Class A P/Q-type Ca<sup>2+</sup> channels were present predominantly in the presynaptic terminals of motor neurons at the neuromuscular junction. Occasional nerve terminals innervating skeletal muscles from the hindlimb were labeled with antibodies against class B N-type Ca<sup>2+</sup> channels. Staining of the dorsal laminae of the rat spinal cord revealed a complementary distribution of class A and class B Ca<sup>2+</sup> channels in nerve terminals in the deeper versus the superficial laminae. Many of the nerve terminals immunoreactive for class B N-type Ca<sup>2+</sup> channels also contained substance P, an important neuropeptide in pain pathways, suggesting that N-type Ca<sup>2+</sup> channels are predominant at synapses that carry nociceptive information into the spinal cord.
Association Between Hepatitis C Virus and Non-Hodgkin's Lymphomas
Authors: Mariano Provencio, Antonio Sánchez, Félix Bonilla, Pilar España
Journal: Journal of Clinical Oncology (2006)

TO THE EDITOR: In the February 20, 2006, issue of the Journal of Clinical Oncology, Besson et al reported that the Groupe d Etude des Lymphomes de l Adulte found differences in clinical presentation and worsened prognosis in 26 patients with diffuse large-cell lymphoma (DLCL) and hepatitis C virus infection (HCV) compared with DLCL HCV-negative patients. Only patients who were included in the clinical trial were studied and the prevalence in the population selected was 0.5%. Our group examined 114 patients with non-Hodgkin’s lymphoma who were not selected, except for the exclusion of patients who were seropositive against the AIDS virus and parenteral drug addicts. We detected 15 HCV positives (13%). We did not find significant differences in relation to the presence or absence of HCV infection in the clinical presentation, nor did we find any association between highor low-malignancy grade. We did find a significant difference in global survival between the eight DLCL patients who were HCV positive (75% at 2 years; 95% CI, 45% to 100%) and the 50 DLCL patients who were HCV negative (94% at 2 years; 95% CI, 87% to 100%; P .022). We found no relation between HCV infection and survival in the rest of the patients grouped as low-grade lymphomas. In our experience the percentage of HCV infection is similar in highand low-grade lymphomas, and prognosis is no worse in the latter. We found a greater prevalence of HCV infection and lymphomas than that reported for the selected population studied by Groupe d Etude des Lymphomes de l Adulte.
A lasting legacy from Tony Blair? NHS culture change
Authors: Jeffrey Braithwaite
Journal: Journal of the Royal Society of Medicine (2011)

He appeared to be talking off the cuff, but ever since he uttered the words, philosophers have been debating whether his language refers to some sort of deeper epistemological truth, a kind of new philosophy for the age. In other areas of life, serendipity appears everywhere: celebrated examples are Fleming’s discovery of Penicillium notatum on an overnight petri dish, and Penzias and Wilson’s accidental detection of the cosmic microwave background radiation from the noise emanating from their radiometer’s antennae. Tony Blair has done something similar in his new autobiography Tony Blair: a journey. Most of the 718-page monolith is relatively easily disposed of: it is his version of events during his prime ministership, 1997–2007, a lot of which we knew. Yet in an intriguing way it is compulsory reading as it gets into the mind of a key decisionmaker as he made the choices we agreed with or disputed, but regardless followed so closely. It is not nearly as self-serving, indulgent or religious as it could have been, or some have made out. That said, it has one section, buried in chapter 6, ‘Peace in Northern Ireland’, which may prove useful for improving the National Health Service (NHS) – or any large health organization. Following Blair’s account of the negotiations leading to the Good Friday Agreement by which the warring loyalist and republican parties, along with the British and Irish governments, came together to discuss the end of hostilities lies more than the germ of an idea about how to alter complex organizations. Blair presents 10 reasons why the agreement was successful, despite numerous setbacks and blind alleys. These principles are useful not only, as Blair intended, to be applied to other sticky political negotiations by those brokering peace among truculent, bellicose parties, but for longer-term cultural and organizational transformation. This type of change is badly needed in the NHS in substitution of, or as a replacement for, the structural change which is being sponsored by the Conservative–Liberal Democrat Coalition. Table 1 summarizes this proposal. Culture change involves concerted effort, usually over lengthy periods, to influence and shape behaviours and practices on the one hand, and attitudes and values on the other. It is readily conceptualized as an iceberg, with the visible portion, the organizational and clinical activities, above the waterline, and the invisible collective mental constructs, below. The idea is that both need re-orientation to render cultural renewal (Figure 1). Did Blair realize he had developed a yet-to-be tested but nevertheless promising new model for culture change across large complex systems? From a close reading of his book, it does not appear so. This is an unknown unknown: Blair did not say, and we are unable to confirm this. He looks to be genuine in his desire to leave recommendations for DECLARATIONS
Injectable Electronic Identification, Monitoring, and Stimulation Systems
Authors: Philip R. Troyk
Journal: Annual Review of Biomedical Engineering (1999)

▪ Abstract Historically, electronic devices such as pacemakers and neuromuscular stimulators have been surgically implanted into animals and humans. A new class of implants made possible by advances in monolithic electronic design and implant packaging is small enough to be implanted by percutaneous injection through large-gauge hypodermic needles and does not require surgical implantation. Among these, commercially available implants, known as radio frequency identification (RFID) tags, are used for livestock, pet, laboratory animal, and endangered-species identification. The RFID tag is a subminiature glass capsule containing a solenoidal coil and an integrated circuit. Acting as the implanted half of a transcutaneous magnetic link, the RFID tag is powered by and communicates with an extracorporeal magnetic reader. The tag transmits a unique identification code that serves the function of identifying the animal. Millions of RFID tags have been sold since the early 1980s. Based on the success of the RFID tags, research laboratories have developed injectable medical implants, known as micromodules. One type of micromodule, the microstimulator, is designed for use in functional-neuromuscular stimulation. Each microstimulator is uniquely addressable and could comprise one channel of a multichannel functional-neuromuscular stimulation system. Using bidirectional telemetry and commands, from a single extracorporeal transmitter, as many as 256 microstimulators could form the hardware basis for a complex functional-neuromuscular stimulation feedback-control system. Uses include stimulation of paralyzed muscle, therapeutic functional-neuromuscular stimulation, and neuromodulatory functions such as laryngeal stimulation and sleep apnea.
The Role of Undernutrition in the Pathogenesis of Diabetes Mellitus
Authors: R Harsha Rao
Journal: Diabetes Care (1984)

Recent epidemiologic studies show that diabetes mellitus is almost as prevalent in undernourished populations as it is in well-nourished ones, despite the virtual absence of obesity as an etiologic determinant in the former. Undernutrition itself may be the risk factor that replaces obesity in predisposing such populations to diabetes. The glucose intolerance of protein-energy malnutrition is known to be associated with structural changes in the beta cell, and in a significant proportion of undernourished subjects it is irreversible despite prolonged and vigorous nutritional rehabilitation. Chronic undernutrition over a lifetime may, therefore, be an important determinant of diabetes in an individual, either by progressively impairing beta cell function or by increasing the susceptibility of the individual to other genetic and environmental diabetogenic influences.
Mutations in BRAF and KRAS Converge on Activation of the Mitogen-Activated Protein Kinase Pathway in Lung Cancer Mouse Models
Authors: Hongbin Ji, Zhenxiong Wang, Samanthi A. Perera, Danan Li, Mei-Chih Liang, Sara Zaghlul, Kate McNamara, Liang Chen, Mitchell Albert, Yanping Sun, Ruqayyah Al-Hashem, Lucian R. Chirieac, Robert Padera, Roderick T. Bronson, Roman K. Thomas, Levi A. Garraway, Pasi A. Jänne, Bruce E. Johnson, Lynda Chin, Kwok-Kin Wong
Journal: Cancer Research (2007)

Abstract Mutations in the BRAF and KRAS genes occur in ∼1% to 2% and 20% to 30% of non–small-cell lung cancer patients, respectively, suggesting that the mitogen-activated protein kinase (MAPK) pathway is preferentially activated in lung cancers. Here, we show that lung-specific expression of the BRAF V600E mutant induces the activation of extracellular signal–regulated kinase (ERK)-1/2 (MAPK) pathway and the development of lung adenocarcinoma with bronchioloalveolar carcinoma features in vivo. Deinduction of transgene expression led to dramatic tumor regression, paralleled by dramatic dephosphorylation of ERK1/2, implying a dependency of BRAF-mutant lung tumors on the MAPK pathway. Accordingly, in vivo pharmacologic inhibition of MAPK/ERK kinase (MEK; MAPKK) using a specific MEK inhibitor, CI-1040, induced tumor regression associated with inhibition of cell proliferation and induction of apoptosis in these de novo lung tumors. CI-1040 treatment also led to dramatic tumor shrinkage in murine lung tumors driven by a mutant KRas allele. Thus, somatic mutations in different signaling intermediates of the same pathway induce exquisite dependency on a shared downstream effector. These results unveil a potential common vulnerability of BRAF and KRas mutant lung tumors that potentially affects rational deployment of MEK targeted therapies to non–small-cell lung cancer patients. [Cancer Res 2007;67(10):4933–9]