tbuckley/cabot-search huggingface dataset:
A Role for Bone Morphogenetic Protein-4 in Lymph Node Vascular Remodeling and Primary Tumor Growth
Authors: Rae H. Farnsworth, Tara Karnezis, Ramin Shayan, Masataka Matsumoto, Cameron J. Nowell, Marc G. Achen, Steven A. Stacker
Journal: Cancer Research (2011)

Abstract Lymph node metastasis, an early and prognostically important event in the progression of many human cancers, is associated with expression of VEGF-D. Changes to lymph node vasculature that occur during malignant progression may create a metastatic niche capable of attracting and supporting tumor cells. In this study, we sought to characterize molecules expressed in lymph node endothelium that could represent therapeutic or prognostic targets. Differential mRNA expression profiling of endothelial cells from lymph nodes that drained metastatic or nonmetastatic primary tumors revealed genes associated with tumor progression, in particular bone morphogenetic protein-4 (BMP-4). Metastasis driven by VEGF-D was associated with reduced BMP-4 expression in high endothelial venules, where BMP-4 loss could remodel the typical high-walled phenotype to thin-walled vessels. VEGF-D expression was sufficient to suppress proliferation of the more typical BMP-4–expressing high endothelial venules in favor of remodeled vessels, and mechanistic studies indicated that VEGF receptor-2 contributed to high endothelial venule proliferation and remodeling. BMP-4 could regulate high endothelial venule phenotype and cellular function, thereby determining morphology and proliferation responses. Notably, therapeutic administration of BMP-4 suppressed primary tumor growth, acting both at the level of tumor cells and tumor stromal cells. Together, our results show that VEGF-D–driven metastasis induces vascular remodeling in lymph nodes. Furthermore, they implicate BMP-4 as a negative regulator of this process, suggesting its potential utility as a prognostic marker or antitumor agent. Cancer Res; 71(20); 6547–57. ©2011 AACR.
Autoantibodies to hLAMP-2 in ANCA-Negative Pauci-Immune Focal Necrotizing GN
Authors: Andrea Peschel, Neil Basu, Alexandra Benharkou, Ricarda Brandes, Markus Brown, Régis Dieckmann, Andrew J. Rees, Renate Kain
Journal: Journal of the American Society of Nephrology (2013)

Pauci-immune focal necrotizing GN (piFNGN) is usually associated with ANCAs that are thought to be pathogenic. However, 10%–15% of patients are ANCA negative and the cause of their injury is unknown. We previously reported a high frequency of autoantibodies to human lysosome-associated membrane protein-2 (hLAMP-2) in ANCA-associated piFNGN, and have now investigated whether the same is true in ANCA-negative patients. Of 11 patients, 8 (73%) had anti–hLAMP-2 antibodies detected by ELISA and confirmed by immunoblotting and indirect immunofluorescence. The autoantibodies from all 8 patients bound to native LAMP-2 purified from human glomeruli and recombinant hLAMP-2 expressed in ldlD cells, both with molecular masses of 110 kD. However, in contrast to anti–LAMP-2 antibodies from ANCA-positive patients, these antibodies from ANCA-negative patients failed to bind the more complexly glycosylated native neutrophil hLAMP-2 (190 kD). Treatment with the deglycosylating enzyme, endo-β-galactosidase, reduced the mass of neutrophil hLAMP-2 to 110 kD and enabled autoantibody binding. Similarly, pretreating neutrophils with endo-β-galactosidase or neuraminidase converted ANCA assay results from negative to positive. Finally, IgG from LAMP-2-positive ANCA-negative patients bound specifically to normal human kidney sections and to human glomerular endothelial cells in culture. In conclusion, in patients with ANCA-negative piFNGN, we have identified autoantibodies to hLAMP-2 that bind native glomerular but not neutrophil hLAMP-2, suggesting a role in pathogenesis.
Fc-Gamma-Receptor-IIb Is Required For The Immunomodulatory Actions Of Intravenous Immune Globulin In An Antigen-Driven Murine Model Of Allergic Airways Disease
Authors: Gabriel N. Kaufman, Amir Hossein Massoud, Ciriaco A. Piccirillo, Bruce D. Mazer
Journal: Journal of Allergy and Clinical Immunology (2014)
Early CPAP prevents evolution of acute lung injury in patients with hematologic malignancy
Authors: Vincenzo Squadrone, Massimo Massaia, Benedetto Bruno, Filippo Marmont, Michele Falda, Carlotta Bagna, Stefania Bertone, Claudia Filippini, Arthur S. Slutsky, Umberto Vitolo, Mario Boccadoro, V. Marco Ranieri
Journal: Intensive Care Medicine (2010)
The involvement of calpain-independent proteolysis of the tumor suppressor NF2 (merlin) in schwannomas and meningiomas
Authors: Yoriyoshi Kimura, Hisashi Koga, Norie Araki, Norifumi Mugita, Naoyuki Fujita, Hideo Takeshima, Tohru Nishi, Tetsumori Yamashima, Takaomi C. Saido, Toshiki Yamasaki, Kouzo Moritake, Hideyuki Saya, Mitsuyoshi Nakao
Journal: Nature Medicine (1998)
COMPLETE RESTORATION OF BURSA-DEPENDENT IMMUNE SYSTEM AFTER TRANSPLANTATION OF SEMIALLOGENEIC STEM CELLS INTO IMMUNODEFICIENT CHICKS
Authors: Paavo Toivanen, Auli Toivanen, Olli Vainio
Journal: The Journal of Experimental Medicine (1974)

For transplantation of semiallogeneic bursal stem cells into cyclophosphamide-treated 3-day old chicks, two lines of chickens homozygous at the major histocompatibility locus and their F(1) hybrids were used in reciprocal combinations. The semiallogeneic transplantations resulted in a complete restoration of antibody formation to sheep red blood cells (SRBC) and Brucella, of microscopic morphology of bursa fabricii, and of germinal center formation in the spleen. In contrast, allogeneic bursal stem cells were not effective in restoring secondary response to SRBC and germinal center formation, while they were able to reconstitute anti-Brucella responses and bursal morphology. These findings indicate an effective cooperation of donor and host cells leading to a complete restoration of the bursa-dependent lymphoid system, when the donor and recipient share at least one haplotype determining the major histocompatibility antigen complex.
Patients at lower risk of arrhythmia recurrence: a subgroup in whom implantable defibrillators may not offer benefit
Authors: Alfred P Hallstrom, John H McAnulty, Bruce L Wilkoff, Dean Follmann, Merritt H Raitt, Mark D Carlson, Anne M Gillis, Hue-Teh Shih, Judy L Powell, Hank Duff, Blair D Halperin
Journal: Journal of the American College of Cardiology (2001)
Human Th1 and Th2 lymphocytes: their role in the pathophysiology of atopy
Authors: G. Del Prete
Journal: Allergy (1992)

In human beings, as in mice, two distinct patterns of cytokine secretion have been defined among CD4 + helper T‐cell clones. Human type 1 helper (Th1), but not type 2 helper (Th2), cells produce interleukin‐2 (IL‐2), gamma‐interferon (IFN‐γ), and tumor necrosis factor‐β, whereas Th2, but not Th1, cells secrete IL‐4 and IL‐5, but not IL‐2 or IFN‐γ. Other cytokines, such as IL‐3, IL‐6, GM‐CSF, or TNF‐α, are produced by both Th1 and Th2 cells. The cells, a third Th subset, show combined production of Th1‐and Th2‐type cytokines. The different cytokine patterns are associated with different functions. In general, Th2 cells provide an excellent helper function for B‐cell antibody production, particularly of the IgE class. On the other hand, Th1 cells are responsible for delayed type hypersensitivity reactions and are cytolytic for autologous antigen‐presenting cells, including B cells. Most allergen‐ or helminth‐antigen‐specific human CD4 + T‐cell clones exhibit a Th2 phenotype, whereas most clones specific for bacterial antigens show a Th1 profile. Allergen‐specific Th2 cells seem to play a crucial role in atopy. These cells induce IgE production via IL‐4 and favor the proliferation, differentiation, and activation of eosinophils via IL‐5. In addition, Th2‐derived IL‐3 and IL‐4 are mast‐cell growth factors that act in synergy, at least in vitro. Recent evidence indicates that allergen‐specific Th2 cells are selectively enriched in tissues affected by allergic inflammation, such as the bronchial mucosa of subjects with allergic asthma. However, the reason why allergens preferentially expand Th2 cells in atopics is unknown. A number of factors may influence Th subset differentiation into Th1 or Th2 cells. At present, the IL‐4 produced in the microenvironment in which antigen is presented to Th cells seems to be the major factor favoring Th2 development. In this connection, the aberrant production of IL‐4 (and IL‐5) exhibited by T cells from atopics, even in response to bacterial antigens, may be of great importance.
Substitutes for Morphine and Heroin
Authors: G. N. Myers
Journal: BMJ (1933)

IMEICAL OjoRIqALno effect in prolonging the incubation period in monkeys.In an appendix to the memoir Major Malone gives reasons for believing that in the period 1925-30 any signifi- cant differences in the death rates of the various popula- tions studied were due to one exceptional conditionnamely, the method of treatment employed.If no signifi- cance carn be attached to these differences, it is deducible that no one treatment employed anywhere could be considered better than another.
Sympathetic and nonsympathetic neuropeptide Y-containing nerves in the rat myocardium and coronary arteries.
Authors: L A Corr, J A Aberdeen, P Milner, J Lincoln, G Burnstock
Journal: Circulation Research (1990)

We have examined the neuropeptide Y-containing intrinsic nerves of the heart in young (6-week-old) and adult (4-month-old) rats to determine whether they project to the coronary arteries or are capable of doing so if the neuropeptide Y-containing extrinsic nerves are removed. Chronic treatment of neonates with guanethidine was used to permanently destroy the sympathetic nerves. In the young treated animals, 33-54% of the neuropeptide Y remained in the heart despite a 90-99% reduction in norepinephrine; these proportions did not change in the animals that were allowed to develop to adulthood. The level of neuropeptide Y in the right atrium of young animals was unexpectedly high (252 +/- 28.7 pmol/g) compared with adults (75.4 +/- 18.8 pmol/g). The coronary arteries in the control rats received a moderately dense supply of neuropeptide Y-containing nerves; after guanethidine, all neuropeptide Y-containing nerves innervating the large coronary arteries disappeared, but some were still seen in association with small resistance vessels. No compensatory proliferation of the intrinsic neuropeptide Y-containing neurons occurred in the adult sympathectomized animals, and the intrinsic nerves did not reinnervate the large coronary arteries. These results are discussed in relation to the clinical syndrome of coronary artery spasm.
Management of treatment resistant inflammation of acute on chronic tophaceous gout with anakinra
Authors: D McGonagle, A L Tan, S Shankaranarayana, J Madden, P Emery, M F McDermott
Journal: Annals of the Rheumatic Diseases (2007)

We report a 74-year-old man with acute on chronic tophaceous gout in whom conventional treatments failed but who responded to treatment with the interleukin-1 receptor antagonist, anakinra. The patient presented in February 2004 with a severe flare of gout. Multiple joints were swollen, including the right fifth proximal interphalangeal (PIP), the left fourth PIP, and the first metatarsophalangeal (MTP) joints bilaterally. Apart from chronic tophaceous gout, he also had a history of membranous glomerulonephritis (for which he was on prednisolone 5 mg/day), hypertension, and ischaemic heart disease. Allopurinol had previously induced a severe anaphylactic reaction and his renal impairment was exacerbated by non-steroidal anti-inflammatory drugs.

On examination, the …
NIRS and IVUS for Characterization of Atherosclerosis in Patients Undergoing Coronary Angiography
Authors: Salvatore Brugaletta, Hector M. Garcia-Garcia, Patrick W. Serruys, Sanneke de Boer, Jurgen Ligthart, Josep Gomez-Lara, Karen Witberg, Roberto Diletti, Joanna Wykrzykowska, Robert-Jan van Geuns, Carl Schultz, Evelyn Regar, Henricus J. Duckers, Nicolas van Mieghem, Peter de Jaegere, Sean P. Madden, James E. Muller, Antonius F.W. van der Steen, Wim J. van der Giessen, Eric Boersma
Journal: JACC. Cardiovascular imaging (2011)
Medical Hazards of Obesity
Authors: F X Pi-Sunyer
Journal: Annals of Internal Medicine (1993)

The medical hazards of obesity are discussed. Risks include insulin resistance, diabetes mellitus, hypertriglyceridemia, decreased levels of high-density lipoprotein cholesterol, and increased levels of low-density lipoprotein cholesterol. Obesity is also associated with gallbladder disease and some forms of cancer as well as sleep apnea, chronic hypoxia and hypercapnia, and degenerative joint disease. Obesity is an independent risk factor for death from coronary heart disease. A central distribution of body fat enhances the risk for most of these conditions.
TWO CASES OF ACUTE PEMPHIGUS OF INFANTS
Authors: ARTHUR WHITFIELD
Journal: British Journal of Dermatology (1903)

Journal Article TWO CASES OF ACUTE PEMPHIGUS OF INFANTS Get access ARTHUR WHITFIELD, M.D., M.R.C.P. ARTHUR WHITFIELD, M.D., M.R.C.P. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 15, Issue 6, 1 June 1903, Pages 218–221, https://doi.org/10.1111/j.1365-2133.1903.tb16504.x Published: 01 June 1903
Maximal Diffusing Capacity of the Lung for Carbon Monoxide*
Authors: Robert L. Johnson, Harold F. Taylor, W. Harold Lawson
Journal: Journal of Clinical Investigation (1965)

During exercise pulmonary diffusing capacity for carbon monoxide and oxygen increases because the pulmonary capillary bed expands (1).It seems reasonable that there should be an upper limit to this expansion at which the diffusing ca- pacity reaches maximum.The apparent oxygen diffusing capacity (DLO2) has been noted to ap- proach a plateau or upper limit as the work load increases (2, 3), but a similar plateau for CO dif- fusing capacity has never been clearly demon- strated (1, 4) perhaps because it has not been measured at heavy enough work loads.Thus our purpose was to determine how high CO diffusing capacity can go as exercise work load increases and to see whether it reaches a plateau before the maximal tolerated work load is achieved.To accomplish this we measured apparent CO diffusing capacity (DLco) and pulmonary blood flow simultaneously in five normal adults, five normal children, and in three adult patients with mitral stenosis.Measurements were made at rest and at increasing treadmill work loads up to and beyond that causing maximal oxygen con- sumption.At rest and at maximal oxygen con- sumption the true membrane diffusing capacity for CO (DMco) and the pulmonary capillary blood volume (Vc) were estimated by the Roughton- Forster method (5).
180 ORAL L-ORNITHINE-L-ASPARTATE (LOLA) FOR PATIENTS WITH OVERT HEPATIC ENCEPHALOPATHY TREATED WITH LACTULOSE; A RANDOMIZED, DOUBLE-BLINDED, PLACEBO-CONTROLLED TRIAL
Authors: S. Nimanong, C. Siwaporn, I. Sansak, T. Tanwandee, P. Charatcharoenwitthaya, W. Chotiyaputta, K. Boonyapisit, N. Pausawasdi, W. Prachayakul, S. Pongprasobchai, S. Leelakusolvong, S. Manatsathit, U. Kachintorn
Journal: Journal of Hepatology (2010)
EBV Latent Membrane Protein 1 Effects on Plakoglobin, Cell Growth, and Migration
Authors: Kathy H.Y. Shair, Caroline I. Schnegg, Nancy Raab-Traub
Journal: Cancer Research (2008)

Latent membrane protein 1 (LMP1), the major oncoprotein of EBV, is likely responsible for many of the altered cellular growth properties in EBV-associated cancers, including nasopharyngeal carcinoma (NPC). In this study, the effects of LMP1 on cell growth and migration were studied in the context of the EBV-positive C666-1 NPC cell line. In the soft agar transformation and Transwell metastasis assays, LMP1 enhanced cell growth and migration through activation of phosphatidylinositol 3-kinase (PI3K)/Akt and nuclear factor-kappaB (NF-kappaB) signaling. Inhibitors of PI3K, Akt, and NF-kappaB signaling dramatically reduced these enhanced properties. An IkappaBalpha super-repressor also blocked these effects. However, constitutive activation of Akt alone did not alter cell growth, suggesting that both PI3K/Akt and NF-kappaB activation are required by LMP1. These enhanced effects required the full-length LMP1 encompassing both the PI3K/Akt-activating COOH-terminal activation region (CTAR) 1 and the nonredundant NF-kappaB-activating regions CTAR1 and CTAR2. LMP2A, a latent protein that is also frequently expressed in NPC, similarly activates the PI3K/Akt pathway; however, its overexpression in C666-1 cells did not affect cell growth or migration. LMP1 also decreased expression of the junctional protein plakoglobin, which was shown to be partially responsible for enhanced migration induced by LMP1. This study reveals that in epithelial cells the transforming properties of LMP1 require activation of both PI3K/Akt and NF-kappaB and shows that the loss of plakoglobin expression by LMP1 is a significant factor in the enhanced migration.
Race and Health Care — An American Dilemma?
Authors: H. Jack Geiger
Journal: New England Journal of Medicine (1996)

More than half a century has passed since the publication of Gunnar Myrdal's An American Dilemma, a monumental study that illuminated the profound disparity between this nation's democratic principles and egalitarian commitments and the realities of its racial policies and practices.1 Despite great improvements over the ensuing decades, race and social class have continued to be powerful and often divisive factors in our national life. It is hardly surprising, therefore, that they substantially influence the health status, access to health care, and scope and quality of health care of minority and poor populations.2 A recent search of the literature on . . .
Effects of serotonin on rat ileocolonic transit and fluid transfer in vivo: possible mechanisms of action.
Authors: L Oosterbosch, M von der Ohe, M A Valdovinos, L J Kost, S F Phillips, M Camilleri
Journal: Gut (1993)

The aim was to investigate the action of serotonin (5HT) on function of the ileocolonic junction (ICJ) in vivo. In anaesthetised rats, models were developed to study the effects of intra-aortic (ia) serotonin on ileocolonic and colonic transit, and the effects on transit of a number of 5HT receptor antagonists. In the first series of experiments, a bolus of saline labelled with 99mTc DTPA was instilled 20 cm proximal to the ICJ and transit was assessed three hours later by the geometric centre of the spread of isotope. In the second series, similar techniques were used on the postcaecal colon and transit assessed two hours later. In the third series of experiments, the effects of ia 5HT on ileal net fluid flux was evaluated by standard perfusion experiments with 14C polyethylene glycol (PEG) 4000 as a non-absorbable marker in rat plasma-like electrolyte solution. Compared with ia saline, 5HT accelerated ICJ transit significantly (p &lt; 0.05). This acceleration was comparable with the effect of ia bethanechol. The effects of 5HT on ICJ transit were inhibited by the intraperitoneal (ip) infusion of atropine, the 5HT receptor antagonists, methysergide, ketanserin, zacopride, and the 5HT4 agonist, SC53116. Methysergide, zacopride, and SC53116 given with ia 5HT slowed ICJ transit to rates below those of ia saline alone. When these same agents were given together with ia saline, the ICJ transit was not significantly altered. Serotonin, at the dose that accelerated ICJ transit, did not significantly alter colonic transit or ileal fluid transport. In conclusion, 5HT is a potent pharmacological stimulant of transit across the rat ICJ in vivo; the action of 5HT is mediated partly through muscarinic neurones and several 5HT receptor subtypes.
Racial Differences in Association of Elevated Interleukin-18 Levels With Type 2 Diabetes
Authors: Smita I. Negi, James S. Pankow, Karl Fernstrom, Ron C. Hoogeveen, Na Zhu, David Couper, Maria I. Schmidt, Bruce B. Duncan, Christie M. Ballantyne
Journal: Diabetes Care (2012)

OBJECTIVE Elevated plasma interleukin-18 (IL-18) has been linked to onset of diabetes mellitus (DM) and its complications. However, so far this association has been shown only in predominantly white populations. We examined IL-18 levels and their association with incident DM in a racially heterogeneous population. RESEARCH DESIGN AND METHODS In a nested case-cohort design representing a 9-year follow-up of 9,740 middle-aged, initially healthy, nondiabetic white and African American participants of the Atherosclerosis Risk in Communities Study, we selected and measured analytes on race-stratified (50% white, 50% African American) random samples of both cases of incident diabetes (n = 548) and eligible members of the full cohort (n = 536). RESULTS Baseline IL-18 levels were significantly higher in white participants compared with African American participants (P &amp;lt; 0.001). Although white participants in the fourth (versus first) quartile of IL-18 levels had a significant hazard ratio (HR) for developing DM (HR: 2.1, 95% CI: 1.3–3.4), after adjustment for age, sex, and study center, no difference was seen among African Americans (HR: 1.0, 95% CI: 0.6–1.7). Unlike those in African Americans, IL-18 levels in whites had a significant correlation with age (P &amp;lt; 0.01); anthropometric characteristics such as waist circumference (P &amp;lt; 0.001), height (P = 0.04), waist-to-hip ratio (P &amp;lt; 0.001), and BMI (P &amp;lt; 0.01); and total (P &amp;lt; 0.001) and high-molecular-weight (P &amp;lt; 0.001) adiponectin. CONCLUSIONS There are racial differences in levels of IL-18 and the association of IL-18 with risk factors and incident type 2 DM. In addition, there seems to be a complex interplay of inflammation and adiposity in the development of DM.
Fatal haemorrhage from Dieulafoy's disease of the bronchus
Authors: T S van der Werf, A Timmer, J G Zijlstra
Journal: Thorax (1999)

A 70 year old woman with a previous history of healed tuberculosis and suspected chronic obstructive pulmonary disease presented with recurrent haemoptysis and respiratory failure from a lobar pneumonia. Massive bleeding occurred when biopsy specimens were taken during bronchoscopy which was managed conservatively, but later there was a fatal rebleed from the same site. Two different Dieulafoy’s vascular malformations were found in the bronchial tree at necropsy, one of which was the biopsied lesion in the left upper lobe. This report confirms the possibility that vascular lesions occur in the bronchial tree. It is suggested that, if such lesions are suspected at bronchoscopy, bronchial and pulmonary arteriography with possible embolotherapy should be performed.