tbuckley/cabot-search huggingface dataset:
MANTLE CELL LYMPHOMA–CASE SERIES AND REVIEW
Authors: V Kalansooriya, C Ozo, I Mainie
Journal: Gut (2013)

Introduction Mantle cell lymphoma (MCL) of the colon may present with features mimicking inflammatory bowel disease. We present two cases of patients with a history of MCL presenting with lower GI symptoms undergoing colonoscopy. Aims/Background Colonoscopy findings of 2 cases discussed were consistent with inflammatory bowel disease; although immunohistochemical studies of tissue biopsies proved to be Mantle Cell Lymphoma. Method Patient records of two cases presenting with lower GI symptoms and colonoscopy findings of colitis were reviewed along with literature review of Mantle Cell lymphoma. Results Median age for presentation of MCL as late 6th or 7th decade and to be extremely rare under 30 years, Extra nodal site involvement is very common with gastro intestinal tract being the most common. Patients with GI tract involvement largely remain asymptomatic although subset of patients (approximately 10%) present with the syndrome known as Multiple Lymphomatous Polyposis (MLP- polypoid tumour masses throughout GI tract excluding oesophagus and anus), can be associated with GI symptoms. Conclusion MCL's tropism for GI tract is recently recognized. Microscopic involvement of GI tract is found in patients free of GI symptoms. Findings consistent with the case described here, where initial diagnosis by endoscopist was of colitis, are rarely documented.
Does Gastroscopy Induce Myocardial Ischemia in Patients With Coronary Heart Disease?
Authors: J. Schenck, C.-H. Müller, H. Lübbers, R. Mahlke, D. Lehnick, P. G. Lankisch
Journal: Endoscopy (2000)

Background and Study Aims: Gastroscopy has been reported to be dangerous for unstable patients with coronary heart disease (CHD). The aims of this study were to find out whether endoscopy is equally liable to cause myocardial ischemia in stable CHD patients, and whether this can be predicted prior to endoscopy, and to find out the frequency of abnormal findings in patients for whom a secondary prophylaxis with acetylsalicylic acid (ASA) is indicated.
National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: Clinical Utilization of Cardiac Biomarker Testing in Heart Failure
Authors: W.H. Wilson Tang, Gary S. Francis, David A. Morrow, L. Kristin Newby, Christopher P. Cannon, Robert L. Jesse, Alan B. Storrow, Robert H. Christenson, Robert H. Christenson, Fred S. Apple, Christopher P. Cannon, Gary S. Francis, Robert L. Jesse, David A. Morrow, L. Kristin Newby, Jan Ravkilde, Alan B. Storrow, W.H. Wilson Tang, Alan H.B. Wu
Journal: Circulation (2007)
A Novel Pathway Involving Melanoma Differentiation Associated Gene-7/Interleukin-24 Mediates Nonsteroidal Anti-inflammatory Drug–Induced Apoptosis and Growth Arrest of Cancer Cells
Authors: Luiz F. Zerbini, Akos Czibere, Yihong Wang, Ricardo G. Correa, Hasan Otu, Marie Joseph, Yuko Takayasu, Moriah Silver, Xuesong Gu, Kriangsak Ruchusatsawat, Linglin Li, Devanand Sarkar, Jin-Rong Zhou, Paul B. Fisher, Towia A. Libermann
Journal: Cancer Research (2006)

Numerous studies show that nonsteroidal anti-inflammatory drugs (NSAIDs) are effective in chemoprevention or treatment of cancer. Nevertheless, the mechanisms underlying these antineoplastic effects remain poorly understood. Here, we report that induction of the cancer-specific proapoptotic cytokine melanoma differentiation associated gene-7/interleukin-24 (MDA-7/IL-24) by several NSAIDs is an essential step for induction of apoptosis and G(2)-M growth arrest in cancer cells in vitro and inhibition of tumor growth in vivo. We also show that MDA-7/IL-24-dependent up-regulation of growth arrest and DNA damage inducible 45 alpha (GADD45alpha) and GADD45gamma gene expression is sufficient for cancer cell apoptosis via c-Jun NH(2)-terminal kinase (JNK) activation and growth arrest induction through inhibition of Cdc2-cyclin B checkpoint kinase. Knockdown of GADD45alpha and GADD45gamma transcription by small interfering RNA abrogates apoptosis and growth arrest induction by the NSAID treatment, blocks JNK activation, and restores Cdc2-cyclin B kinase activity. Our results establish MDA-7/IL-24 and GADD45alpha and GADD45gamma as critical mediators of apoptosis and growth arrest in response to NSAIDs in cancer cells.
PERCUTANEOUS ABSORPTION OF SODIUM FUSIDATE AND FUSIDIC ACID*
Authors: C. F. H. VICKERS
Journal: British Journal of Dermatology (1969)

SUMMARY.— Evidence is presented that the antibiotic substances sodium fusidate and fusidic acid are both capable of penetrating intact human skin at a rate similar to that seen with glucocorticoids. This is the first experimental in vitro evidence of the penetration of a topically applied antibiotic: the techniques employed depended on the measurement of C14‐labelled material, and upon microbiological assay.
Influenza vaccination reduced cardiovascular events in patients hospitalized with an acute coronary syndrome
Authors: Henry S. Sacks
Journal: Annals of Internal Medicine (2011)

Source Citation Phrommintikul A, Kuanprasert S, Wongcharoen W, et al. Influenza vaccination reduces cardiovascular events in patients with acute coronary syndrome. Eur Heart J. 2011;32:1730-5. 21289042
Controlled trial of methotrexate versus 10-deazaaminopterin in the treatment of rheumatoid arthritis.
Authors: G.S Alarcón, O Castañeda, M.G Nair, M Ferrándiz, W.J Koopman, C.L Krumdieck
Journal: Annals of the Rheumatic Diseases (1992)

A 15 week double blind controlled trial of methotrexate and 10-deazaaminopterin for the treatment of rheumatoid arthritis (RA) was performed in 26 patients. Significant improvement in all measured clinical parameters was observed in the two patient groups. The drugs were well tolerated; only one patient (10-deazaaminopterin) withdrew from the study because of side effects. It is concluded that, in the context of this relatively short clinical trial, 10-deazaaminopterin is at least as beneficial as methotrexate in the treatment of RA.
Jones' Own Fracture
Authors: Stanley P. Bohrer
Journal: JAMA (1986)

<h3>To the Editor.—</h3> I congratulate Keene and Lange<sup>1</sup>for clearly distinguishing between the Jones' fracture (fracture of the diaphysis of the fifth metatarsal about 2 cm distal to the tuberosity) and avulsion fractures of the tuberosity. Too many textbooks of radiology and orthopedics erroneously refer to all such fractures as Jones' fractures. Keene and Lange and others<sup>2,3</sup>call the Jones' fracture a<i>stress</i>fracture from repetitive trauma. While this may be true, it is not always so. It can be due to an acute injury. Jones himself,<sup>4,5</sup>reporting on his own injury and others, explained that, "whilst dancing, I trod on the outer side of my foot, my heel at the moment being off the ground. Something gave way midway down my foot...." Perhaps this fracture, which can be complete or incomplete when first seen, can be a stress fracture or an acute indirect trauma fracture (as
Postoperative Course of Patients during Hospitalization following Renal Transplantation
Authors: Fritz A. Muthny
Journal: Psychotherapy and Psychosomatics (1984)

The results presented here are based on a longitudinal study on 33 patients who were first interviewed on dialysis and followed up over the hospitalization period following cadaver renal transplantation. The emotional state of the patients before and after surgery is described, three typical postoperative courses are shown. Possible predictors for the mastering of stressful events in this stage are delineated based on the previous interview on dialysis. The findings confirm that many patients experience substantial strain on dialysis and during their inpatient care after transplantation. Despite this, the predominant feeling of most of the patients in this period is hope. The results stress the importance of psychological assessment prior to transplantation in order to identify patients with psychosocial risk factors. This may enhance adequate preparation for possible strains occurring in transplantation and provide more efficient psychological aids.
SLITRK6 mutations cause myopia and deafness in humans and mice
Authors: Mustafa Tekin, Barry A. Chioza, Yoshifumi Matsumoto, Oscar Diaz-Horta, Harold E. Cross, Duygu Duman, Haris Kokotas, Heather L. Moore-Barton, Kazuto Sakoori, Maya Ota, Yuri S. Odaka, Joseph Foster, F. Basak Cengiz, Suna Tokgoz-Yilmaz, Oya Tekeli, Maria Grigoriadou, Michael B. Petersen, Ajith Sreekantan-Nair, Kay Gurtz, Xia-Juan Xia, Arti Pandya, Michael A. Patton, Juan I. Young, Jun Aruga, Andrew H. Crosby
Journal: Journal of Clinical Investigation (2013)

Myopia is by far the most common human eye disorder that is known to have a clear, albeit poorly defined, heritable component. In this study, we describe an autosomal-recessive syndrome characterized by high myopia and sensorineural deafness. Our molecular investigation in 3 families led to the identification of 3 homozygous nonsense mutations (p.R181X, p.S297X, and p.Q414X) in SLIT and NTRK-like family, member 6 (SLITRK6), a leucine-rich repeat domain transmembrane protein. All 3 mutant SLITRK6 proteins displayed defective cell surface localization. High-resolution MRI of WT and Slitrk6-deficient mouse eyes revealed axial length increase in the mutant (the endophenotype of myopia). Additionally, mutant mice exhibited auditory function deficits that mirrored the human phenotype. Histological investigation of WT and Slitrk6-deficient mouse retinas in postnatal development indicated a delay in synaptogenesis in Slitrk6-deficient animals. Taken together, our results showed that SLITRK6 plays a crucial role in the development of normal hearing as well as vision in humans and in mice and that its disruption leads to a syndrome characterized by severe myopia and deafness.
Effects of vascular trauma and transient myocardial ischaemia on coronary venous prostaglandin levels in the dog
Authors: I. A BAILEY, F. CAREY, D. HAWORTH, H. J SMITH
Journal: Cardiovascular Research (1983)

The plasma concentrations of immunoreactive thromboxane B2 and 6-keto-prostaglandin-F1 alpha were determined in coronary venous blood sampled from open-chested, anaesthetised beagle dogs by local vein catheterisation. Thromboxane levels were high immediately following catheterisation (2.08 +/- 0.75 ng X ml-1, mean +/- SEM, n = 6) and fell over 25 min to 0.48 +/- 0.07 ng X ml-1. Initial trauma of the coronary veins (agitation of the catheter) produced a large but variable increase to 5.13 +/- 2.27 ng X ml-1 (0.1 greater than P greater than 0.05) within 2 min, but arterial trauma (repeated momentary occlusions) produced 0.4 +/- 0.03 ng X ml-1, a value not significantly different from control. After 7 min ischaemia an increase to 0.98 +/- 0.26 ng X ml-1 was detected (P less than 0.05). Reperfusion after 15 min ischaemia caused a fall to 0.43 +/- 0.09 ng X ml-1 at 2 min. In contrast, 6-keto-prostaglandin-F1 alpha levels varied little with trauma but increased to 0.64 +/- 0.14 ng X ml-1 (P less than 0.01) within 2 min ischaemia, remaining elevated. On reperfusion, levels fell to 0.27 +/- 0.06 ng X ml-1 (P less than 0.05) at 2 min, progressively increasing to 0.35 +/- 0.05 ng X ml-1 at 30 min. We conclude that intimal trauma of coronary veins induced thromboxane release and that the physical effects of venous sampling may contribute to apparent thromboxane release from ischaemic muscle. Although transient arterial and venous trauma had no significant effect on 6-keto-prostaglandin-F1 alpha, it is still possible that its release during ischaemia may follow prolonged arterial clamping.
Evidence that blood ionized calcium can regulate serum 1,25(OH)2D3 independently of parathyroid hormone and phosphorus in the rat.
Authors: D A Bushinsky, G S Riera, M J Favus, F L Coe
Journal: Journal of Clinical Investigation (1985)

This study asks whether arterial blood ionized calcium concentration (Ca++) can regulate the serum level of 1,25-dihydroxy-vitamin D3 [1,25(OH)2D3] independently of serum phosphorus and parathyroid hormone (PTH). We infused either PTH (bovine 1-34, 10 U/kg body wt/h) or saline into awake and unrestrained rats for 24 h, through a chronic indwelling catheter. PTH raised total serum calcium and arterial blood ionized calcium, yet serum 1,25(OH)2D3 fell from 35 +/- 6 (mean +/- SEM, n = 10) with saline to 12 +/- 3 pg/ml (n = 11, P less than 0.005 vs. saline). To determine if the decrease in serum 1,25(OH)2D3 was due to the elevated Ca++, we infused PTH into other rats for 24 h, along with varying amounts of EGTA. Infusion of PTH + 0.67 micron/min EGTA reduced Ca++, and 1,25(OH)2D3 rose to 90 +/- 33 (P less than 0.02 vs. PTH alone). PTH + 1.00 micron/min EGTA lowered Ca++ more, and 1,25(OH)2D3 increased to 148 +/- 29 (P less than 0.01 vs. saline or PTH alone). PTH + 1.33 micron/min EGTA lowered Ca++ below values seen with saline or PTH alone, and 1,25(OH)2D3 rose to 267 +/- 46 (P less than 0.003 vs. all other groups). Thus, during PTH infusion lowering Ca++ with EGTA raised 1,25(OH)2D3 progressively. There were no differences in serum phosphorus concentration or in arterial blood pH in any group infused with PTH. The log of serum 1,25(OH)2D3 was correlated inversely with Ca++ in all four groups infused with PTH (r = -0.737, n = 31, P less than 0.001), and also when the saline group was included (r = -0.677, n = 41, P less than 0.001). The results of this study indicate that serum 1,25(OH)2D3 may be regulated by Ca++ independent of PTH and serum phosphorus levels in the rat. Since 1,25(OH)2D3 regulates gastrointestinal calcium absorption, there may be direct feedback control of 1,25(OH)2D3, by its regulated ion, Ca++.
CESAREAN SECTION AS A METHOD OF TREATMENT FOR PLACENTA PREVIA.
Authors: WILLIAM J. GILLETTE
Journal: JAMA (1901)

During the past ten or twelve years, the question of Cesarean section in the treatment of placenta previa has been from time to time brought to the attention of the profession. Those discussing it have strongly opposed or advocated it; but the probabilities are, like all new departures in medicine, it has not escaped the fate of being judged either too harshly or with too much favor. Lawson Tait<sup>1</sup>was one of its strong advocates, and a short time before his death, in an article on "The Treatment of Unavoidable Hemorrhage by Removal of the Uterus," he took the ground that the only safe treatment for placenta previa is the operation of Porro-Cesarean section. The profession has been slow in accepting this doctrine, and probably never will; for it is the experience of all, that where the placenta is laterally attached, and the cervix easily dilatable, delivery may be
Europe fragmented over embryonic stem cell research
Authors: Karen Birmingham
Journal: Journal of Clinical Investigation (2003)

Embryonic stem cell (ES) research: California endorses it, and New Jersey, New York, and Massachusetts seem likely to follow suit, even though the next session of Congress may see it banned at a federal level. But problems establishing a consensus on regulation for this type of study aren't limited to the United States. The European Union also has a major problem on its hands with ES research. New guidelines proposed by the European Commission last month, aimed at appeasing Catholic countries and stemming a scientific ‘brain drain,’ are set to be vehemently opposed by some member states.

“It’s an absolute disaster,” says Christine Mummery, a senior investigator at the Hubrecht Laboratorium in the Netherlands. Her country, along with Sweden, Finland, Greece, and Britain, permits the derivation of cell lines from embryos left over from in vitro fertilization research, so-called supernumerary embryos. However, at the present time, a moratorium on EC funding means that she is reliant on ready-made Australian/Singaporean cell lines, as she has no money to derive her own lines.

The one-year moratorium was introduced in September last year when the European Council of Science Ministers approved Europe’s current four-year research program (Sixth Framework). The moratorium was instigated on the understanding that provisions for funding ES research would be established before the end of 2003. These were announced on July 9, and, if ratified, they will form the guidelines under which some forms of ES research will receive EU backing. The problem is that countries that have banned embryo research — notably Germany, Italy, Austria, and Ireland — do not want their communal EU taxes supporting this work in other countries and are likely to oppose the guidelines.
Hemodynamic Stress Echocardiography in Patients Supported With a Continuous-Flow Left Ventricular Assist Device
Authors: Mads Andersen, Finn Gustafsson, Per Lav Madsen, Patrice Brassard, Anette Schophuus Jensen, Niels Secher, Christian Hassager, Nikolai Nordsborg, Jacob Eifer Møller
Journal: JACC. Cardiovascular imaging (2010)
Comparative Safety and Efficacy of Fluticasone Propionate plus Salmeterol via Diskus® Versus Fluticasone Propionate in Subjects with Asthma Greater than or Equal to 55 and 65 Years of Age
Authors: H ORTEGA, D STEMPEL, L SUTTON, W LINCOURT, L FRITH, R FORTH, W BUSSE
Journal: Journal of Allergy and Clinical Immunology (2008)
Ibuprofen Inhibits Survival of Bladder Cancer Cells by Induced Expression of the p75NTR Tumor Suppressor Protein
Authors: Fatima Khwaja, Jeff Allen, John Lynch, Peter Andrews, Daniel Djakiew
Journal: Cancer Research (2004)

Abstract Nonsteroidal anti-inflammatory drugs (NSAIDs) are used to reduce inflammation and as analgesics by inhibition of cyclooxygenase-2. At higher concentrations, some NSAIDs inhibit proliferation and induce apoptosis of cancer cells. Although several molecular mechanisms have been postulated to explain the anticancer effects of NSAIDs, they do not involve merely the inhibition of cyclooxygenase-2, and a more proximate initiator molecule may be regulated by NSAIDs to inhibit growth. The p75 neurotrophin receptor (p75NTR) is a proximate cell membrane receptor glycoprotein that has been identified as a tumor and metastasis suppressor. We observed that NSAID treatment of cell lines from bladder and other organs induced expression of the p75NTR protein. Of the different types of NSAIDs examined, ibuprofen was more efficacious than aspirin and acetaminophen and comparable with (R)-flurbiprofen and indomethacin in induction of p75NTR protein expression. This rank order NSAID induction of the p75NTR protein correlated with the ability of these NSAIDs to reduce cancer cell survival. To examine a mechanistic relationship between ibuprofen induction of p75NTR protein and inhibition of survival, bladder cancer cells were transfected with ponasterone A-inducible vectors that expressed a death domain-deleted (ΔDD) or intracellular domain-deleted (ΔICD) p75NTR product that acts as a dominant negative antagonist of the intact p75NTR protein. Expression of ΔDD and ΔICD rescued cells from ibuprofen inhibition of growth. These observations suggest that p75NTR is an important upstream modulator of the anticancer effects of NSAIDs and that ibuprofen induction of the p75NTR protein establishes an alternate mechanism by which ibuprofen may exert an anticancer effect.
Neurofibromin-Deficient Myeloid Cells Are Critical Mediators of Aneurysm Formation In Vivo
Authors: Fang Li, Brandon D. Downing, Lucy C. Smiley, Julie A. Mund, Matthew R. DiStasi, Waylan K. Bessler, Kara N. Sarchet, Daniel M. Hinds, Lisa M. Kamendulis, Cynthia M. Hingtgen, Jamie Case, D. Wade Clapp, Simon J. Conway, Brian K. Stansfield, David A. Ingram
Journal: Circulation (2013)

Background— Neurofibromatosis type 1 (NF1) is a genetic disorder resulting from mutations in the NF1 tumor suppressor gene. Neurofibromin, the protein product of NF1 , functions as a negative regulator of Ras activity in circulating hematopoietic and vascular wall cells, which are critical for maintaining vessel wall homeostasis. NF1 patients have evidence of chronic inflammation resulting in the development of premature cardiovascular disease, including arterial aneurysms, which may manifest as sudden death. However, the molecular pathogenesis of NF1 aneurysm formation is unknown. Method and Results— With the use of an angiotensin II–induced aneurysm model, we demonstrate that heterozygous inactivation of Nf1 ( Nf1 +/– ) enhanced aneurysm formation with myeloid cell infiltration and increased oxidative stress in the vessel wall. Using lineage-restricted transgenic mice, we show that loss of a single Nf1 allele in myeloid cells is sufficient to recapitulate the Nf1 +/– aneurysm phenotype in vivo. Finally, oral administration of simvastatin or the antioxidant apocynin reduced aneurysm formation in Nf1 +/– mice. Conclusion— These data provide genetic and pharmacological evidence that Nf1 +/– myeloid cells are the cellular triggers for aneurysm formation in a novel model of NF1 vasculopathy and provide a potential therapeutic target.
Methyldopa-Induced Decrease in Mental Activity
Authors: Sheldon Adler
Journal: JAMA (1974)

Five professional people, including three physicians, an engineer, and an accountant, reported severe changes in mental acuity, including lack of concentrating ability, amnesia-like episodes, difficulty in simple calculations, and problems in reading. Each was taking methyldopa at normal dosages, and when treatment with this drug was discontinued the mental symptoms disappeared within 96 hours. These cases emphasize the importance of questioning patients taking methyldopa about difficulties in mentation. (<i>JAMA</i>230:1428-1429, 1974)
Expanded Fc receptor bearing 'third population' lymphocytes in rheumatoid arthritis: analysis by cell partitioning in two-polymer aqueous phase systems.
Authors: J P Michalski, S Zanki, H Walter
Journal: Annals of the Rheumatic Diseases (1988)

ground were awakened to the dynamic factors that needed to be considered in interpreting results; clinicians were resolved to dissect arthritic condi- tions further on clinical grounds so that both disciplines could work together in attempting a more careful correlation of clinical, laboratory, and radiological changes with precise pathological fea- tures of the diseases studied.The next conference in the series will be held on 4 May 1989 at Harrogate, and the subject will be announced shortly.
Hormone-Replacement Therapy — Breast versus Heart versus Bone
Authors: Nancy E. Davidson
Journal: New England Journal of Medicine (1995)

Thanks to many public health advances, in the developed countries the average woman will be postmenopausal for about one third of her life. As a consequence, she and her physician will ultimately need to make a decision about postmenopausal estrogen-replacement therapy. This treatment has been used for several decades, but there is a surprising lack of consensus about when and how to use it. The initial goal of estrogen-replacement therapy was to alleviate menopausal symptoms. More recently, the possibility has emerged that estrogen can reduce morbidity and mortality from ischemic heart disease and osteoporosis. However, women and their physicians must . . .
Ultrasound-based molecular imaging and specific gene delivery to mesenteric vasculature by endothelial adhesion molecule targeted microbubbles in a mouse model of Crohn's disease
Authors: José L. Tlaxca, Joshua J. Rychak, Peter B. Ernst, Prasad R. Konkalmatt, Talent I. Shevchenko, Theresa T. Pizzaro, Jesús Rivera-Nieves, Alexander L. Klibanov, Michael B. Lawrence
Journal: Journal of Controlled Release (2012)