tbuckley/cabot-search huggingface dataset:
Morphological method for the diagnosis of human adult type hypolactasia.
Authors: L Maiuri, M Rossi, V Raia, F Paparo, S Coletta, F Mazzeo, A Breglia, S Auricchio
Journal: Gut (1994)

The primary adult type hypolactasia is the most common form of genetically determined disaccharidase deficiency. This study examined a large and homogeneous population of the south of Italy: surgical biopsy specimens of proximal jejunum from 178 adult subjects have been assayed for disaccharidase activities; the expression of lactase protein and lactase activity has also been investigated on tissue sections by immunomorphological and enzymohistochemical techniques. Histograms of lactase to sucrase ratio were found to provide a useful distribution of the lactase activity; a lactase to sucrase ratio of 0.17 was found to show discrimination between tissues with persistence of high lactase activity and tissues with adult type hypolactasia. In all 28 subjects with persistent high lactase activity, a uniform distribution of lactase protein and lactase activity in all villus enterocytes was detected, whereas in all 150 subjects with adult type hypolactasia a variable number of villus enterocytes failed to express the lactase. Moreover in hypolactasic samples the lactase activity on tissue sections was constantly detected later than in samples with persistent high lactase activity. The absolute correlation between the immunohistochemical and enzymohistochemical features and the assessment of lactase activity in intestinal homogenates suggests that the morphological criteria are an alternative method for the diagnosis of adult type hypolactasia in human biopsy specimens from proximal small jejunum.
Evaluation of Patients With Asymptomatic Microhematuria
Authors: David Kiragu, Adam S. Cifu
Journal: JAMA (2015)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Activity of interferon-α in relapsed patients with diffuse large B-cell and peripheral T-cell non-Hodgkin's lymphoma
Authors: J.O. Armitage, B. Coiffier
Journal: Annals of Oncology (2000)

Interferon-a has long been known to be an active agent in follicular lymphoma [1-3] and cutaneous T-cell lymphoma [4-6] in addition to a variety of other malignancies including hairy cell leukemia, chronic myeloid leukemia, multiple myeloma, malignant melanoma, and renal cell carcinoma [7-10]. However, it has been widely believed that interferon-a is not a useful agent in the management of patients with diffuse aggressive non-Hodgkin's lymphoma. This is despite the fact that early trials with interferon-a showed a modest response rate in aggressive lymphomas in relapse [11-13]. We became interested in the activity of interferon-a in patients with diffuse aggressive lymphoma after observing the patient described below. This led us to carry out a survey of oncologists worldwide in an attempt to identify similar patients.
Prevalence of increased serum total IgE and specific aeroallergen sensitivity in 5-8 year old Alaska Native children*1
Authors: G.J. Redding, R.J. Singleton, T.C. Lewis, P. Martinez, J. DeMain, B. Morray, H. Peters, L. Bulkow, C. Jones, D. Stamey, J.C. Butler
Journal: Journal of Allergy and Clinical Immunology (2004)
The role of metals in carcinogenesis: biochemistry and metabolism.
Authors: K W Jennette
Journal: Environmental Health Perspectives (1981)

The oxyanions of vanadium, chromium, molybdenum, arsenic, and selenium are stable forms of these elements in high oxidation states which cross cell membranes using the normal phosphate and/or sulfate transport systems of the cell. Once inside the cell, these oxyanions may sulfuryl transfer reactions. Often the oxyanions serve as alternate enzyme substrates but form ester products which are hydrolytically unstable compared with the sulfate and phosphate esters and, therefore, decompose readily in aqueous solution. Arsenite and selenite are capable of reacting with sulfhydryl groups in proteins. Some cells are able to metabolize redox active oxyanions to forms of the elements in other stable oxidation states. Specific enzymes may be involved in the metabolic processes. The metabolites of these elements may form complexes with small molecules, proteins and nucleic acids which inhibit their ability to function properly. The divalent ions of beryllium, manganese, cobalt, nickel, cadmium, mercury, and lead are stable forms of these elements which may mimic essential divalent ions such as magnesium, calcium, iron, copper, or zinc. These ions may complex small molecules, enzymes, and nucleic acids in such a way that the normal activity of these species is altered. Free radicals may be produced in the presence of these metal ions which damage critical cellular molecules.
BRAF Activation Induces Transformation and Then Senescence in Human Neural Stem Cells: A Pilocytic Astrocytoma Model
Authors: Eric H. Raabe, Kah Suan Lim, Julia M. Kim, Alan Meeker, Xing-gang Mao, Guido Nikkhah, Jarek Maciaczyk, Ulf Kahlert, Deepali Jain, Eli Bar, Kenneth J. Cohen, Charles G. Eberhart
Journal: Clinical Cancer Research (2011)

Abstract Purpose: BRAF is frequently activated by gene fusion or point mutation in pilocytic astrocytoma, the most common pediatric brain tumor. We investigated the functional effect of constitutive BRAF activation in normal human neural stem and progenitor cells to determine its role in tumor induction in the brain. Experimental Design: The constitutively active BRAFV600E allele was introduced into human neurospheres, and its effects on MAPK (mitogen-activated protein kinase) signaling, proliferation, soft agarose colony formation, stem cell phenotype, and induction of cellular senescence were assayed. Immunohistochemistry was used to examine p16INK4a levels in pilocytic astrocytoma. Results: BRAFV600E expression initially strongly promoted colony formation but did not lead to significantly increased proliferation. BRAFV600E-expressing cells subsequently stopped proliferating and induced markers of oncogene-induced senescence including acidic β-galactosidase, PAI-1, and p16INK4a whereas controls did not. Onset of senescence was associated with decreased expression of neural stem cell markers including SOX2. Primary pilocytic astrocytoma cultures also showed induction of acidic β-galactosidase activity. Immunohistochemical examination of 66 pilocytic astrocytomas revealed p16INK4a immunoreactivity in the majority of cases, but patients with tumors negative for p16INK4a had significantly shorter overall survival. Conclusions: BRAF activation in human neural stem and progenitor cells initially promotes clonogenic growth in soft agarose, suggesting partial cellular transformation, but oncogene-induced senescence subsequently limits proliferation. Induction of senescence by BRAF may help explain the low-grade pathobiology of pilocytic astrocytoma, whereas worse clinical outcomes associated with tumors lacking p16INK4a expression could reflect failure to induce senescence or an escape from oncogene-induced senescence. Clin Cancer Res; 17(11); 3590–9. ©2011 AACR.
Regulation of fibrillar collagen types I and III and basement membrane type IV collagen gene expression in pressure overloaded rat myocardium.
Authors: D Chapman, K T Weber, M Eghbali
Journal: Circulation Research (1990)

Left ventricular hypertrophy is based on cardiac myocyte growth. The hypertrophic process can be considered heterogeneous based on whether it also includes a remodeling and accumulation of fibrillar types I and III collagens that are responsible for impaired myocardial stiffness. In the heart, the messenger RNA (mRNA) for fibrillar collagen types I and III has been detected only in cardiac fibroblasts, whereas mRNA for basement membrane collagen type IV is present in both fibroblasts and myocytes. We studied the early and long-term expression of these collagenous proteins in rat myocardium after abdominal aortic banding with renal ischemia. Complementary DNA probes for rat pro-alpha 2 (I), mouse type III and mouse type IV collagens, and chicken beta-actin were used. Northern and dot blot analysis on total RNA extracted from left ventricular tissue indicated a sixfold increase in steady-state levels of mRNA for collagen type I on day 3 of abdominal aortic banding, which had declined to control levels by day 7 where it remained rather constant at 4 and 8 weeks. Type III collagen showed a similar pattern of gene expression after banding. mRNA levels for type IV collagen, on the other hand, were elevated on day 1 after banding, returning to control at day 7 and remaining constant. Actin mRNA levels also increased on day 1 of banding, followed by a rapid return to control levels. Monospecific antibody to types I and III collagens and immunofluorescent light microscopy on frozen sections of the myocardium revealed that at 1 week after banding, the distribution and density of these collagens were similar to those of control animals.(ABSTRACT TRUNCATED AT 250 WORDS)
Pseudo-occupational asthma.
Authors: K M Venables, A G Davison, K Browne, A J Newman Taylor
Journal: Thorax (1989)

A case is reported in which a pattern of work related asthma in a record of peak expiratory flow was artefactual. The patient had pronounced morning dips, which she recorded on working days, when she made the first recording at 0700 h, but not on holiday, when she stayed in bed longer. The case emphasises the need for clear instructions to patients about peak flow records.
Cholestenoic acids regulate motor neuron survival via liver X receptors
Authors: Spyridon Theofilopoulos, William J. Griffiths, Peter J. Crick, Shanzheng Yang, Anna Meljon, Michael Ogundare, Satish Srinivas Kitambi, Andrew Lockhart, Karin Tuschl, Peter T. Clayton, Andrew A. Morris, Adelaida Martinez, M. Ashwin Reddy, Andrea Martinuzzi, Maria T. Bassi, Akira Honda, Tatsuki Mizuochi, Akihiko Kimura, Hiroshi Nittono, Giuseppe De Michele, Rosa Carbone, Chiara Criscuolo, Joyce L. Yau, Jonathan R. Seckl, Rebecca Schüle, Ludger Schöls, Andreas W. Sailer, Jens Kuhle, Matthew J. Fraidakis, Jan-Åke Gustafsson, Knut R. Steffensen, Ingemar Björkhem, Patrik Ernfors, Jan Sjövall, Ernest Arenas, Yuqin Wang
Journal: Journal of Clinical Investigation (2014)

Cholestenoic acids are formed as intermediates in metabolism of cholesterol to bile acids, and the biosynthetic enzymes that generate cholestenoic acids are expressed in the mammalian CNS. Here, we evaluated the cholestenoic acid profile of mammalian cerebrospinal fluid (CSF) and determined that specific cholestenoic acids activate the liver X receptors (LXRs), enhance islet-1 expression in zebrafish, and increase the number of oculomotor neurons in the developing mouse in vitro and in vivo. While 3β,7α-dihydroxycholest-5-en-26-oic acid (3β,7α-diHCA) promoted motor neuron survival in an LXR-dependent manner, 3β-hydroxy-7-oxocholest-5-en-26-oic acid (3βH,7O-CA) promoted maturation of precursors into islet-1+ cells. Unlike 3β,7α-diHCA and 3βH,7O-CA, 3β-hydroxycholest-5-en-26-oic acid (3β-HCA) caused motor neuron cell loss in mice. Mutations in CYP7B1 or CYP27A1, which encode enzymes involved in cholestenoic acid metabolism, result in different neurological diseases, hereditary spastic paresis type 5 (SPG5) and cerebrotendinous xanthomatosis (CTX), respectively. SPG5 is characterized by spastic paresis, and similar symptoms may occur in CTX. Analysis of CSF and plasma from patients with SPG5 revealed an excess of the toxic LXR ligand, 3β-HCA, while patients with CTX and SPG5 exhibited low levels of the survival-promoting LXR ligand 3β,7α-diHCA. Moreover, 3β,7α-diHCA prevented the loss of motor neurons induced by 3β-HCA in the developing mouse midbrain in vivo.Our results indicate that specific cholestenoic acids selectively work on motor neurons, via LXR, to regulate the balance between survival and death.
Psychiatric Disorders in Later Life
Authors: R. S. Allison
Journal: BMJ (1952)

Social Survey, and to the Statistics Division of the Board of Trade for the provision of data, and to the Statistical Department of the Ministry of Labour for preparing the punched cards used in the mechanical analysis of the results.Finally, we wish to thank Miss Mama Buckatzsch, Miss Beryl lago, Miss Keena Jones, and Miss Rosemary Thomson, who inter- viewed the patients and, together with Mrs
The Antioxidant N-Acetylcysteine Induces Mesangial Cells to Create Three-Dimensional Cytoarchitecture That Underlies Cellular Differentiation
Authors: MASANORI KITAMURA
Journal: Journal of the American Society of Nephrology (1999)

Abstract. Prolonged culture of mesangial cells produces multifocal nodular structures, i.e. , “hillocks,” consisting of cells and extracellular matrix. Hillock formation is associated with induction of a differentiated phenotype of mesangial cells, with suppressed mitogenesis and downregulation of α-smooth muscle actin (α-SMA). Currently, little is understood regarding physiologically relevant factors that facilitate this cytodifferentiation. This study explores whether and how the cellular redox state modulates hillock formation. Exposure of confluent rat mesangial cells to the antioxidant N -acetylcysteine (NAC), an inducer of glutathione, dramatically facilitated hillock formation. This effect was mimicked by external addition of the reduced form of glutathione ethyl ester. In contrast, the oxidizing agents diamide and menadione inhibited the development of hillocks triggered by either NAC, glutathione, or prolonged culture. The induction of hillocks by NAC was correlated with downregulation of α-SMA as well as attenuated activity of the CArG box element (the cis -element relevant to the expression of the α-SMA gene and growth-associated genes). These results indicate that, by a redox-sensitive mechanism, NAC induces mesangial cells to create three-dimensional cytoarchitecture that underlies cellular differentiation.
Origins of Cardiac Fibroblasts
Authors: Elisabeth M. Zeisberg, Raghu Kalluri
Journal: Circulation Research (2010)

Cardiac fibroblasts play a critical role in maintenance of normal cardiac function. They are indispensable for damage control and tissue remodeling on myocardial injury and principal mediators of pathological cardiac remodeling and fibrosis. Despite their manyfold functions, cardiac fibroblasts remain poorly characterized in molecular terms. Evidence is evolving that cardiac fibroblasts are a heterogeneous population and likely derive from various distinct tissue niches in health and disease. Here, we review our emerging understanding of where cardiac fibroblasts come from, as well as how we can possibly use this knowledge to develop novel therapies for cardiac fibrosis.
Induction of the c-myc protooncogene after antigen binding to hapten-specific B cells.
Authors: E C Snow, J D Fetherston, S Zimmer
Journal: The Journal of Experimental Medicine (1986)

The stimulation of hapten-specific B cell populations with the thymus-dependent antigen, TNP-KLH, was found to induce elevated levels of c-myc mRNA by 2 h. A similar treatment with carrier protein alone did not elevate c-myc mRNA above the level seen in the nonstimulated, resting B cells. These results indicate that antigen binding to the sIg receptor, in the absence of Th cell involvement, directly signals the antigen-binding cell and implicates the active participation of sIg during the process of antigen-mediated B cell activation.
Activation of second messenger pathways in alveolar macrophages by endotoxin
Authors: M.M. Monick, G.W. Hunninghake
Journal: European Respiratory Journal (2002)

The alveolar macrophage plays an important role in immune surveillance of the lung. Early responses to infectious agents by macrophages can decrease tissue injury and promote recovery of the host. Macrophage responses to pathogens are the cornerstone of the innate or nonspecific immune system. In particular, the response of macrophages to endotoxin from Gram negative bacteria has been the focus of many recent studies. The recent discovery of the endotoxin receptor has accelerated the study of signalling in macrophages. This review focuses on the downstream events that occur following exposure of the alveolar macrophage to endotoxin.
Genetic Exceptionalism in Medicine: Clarifying the Differences between Genetic and Nongenetic Tests
Authors: Michael J. Green, Jeffrey R. Botkin
Journal: Annals of Internal Medicine (2003)

Predictive genetic tests are now available for assessing susceptibility to a variety of conditions, including breast and colon cancer, hemochromatosis, and Alzheimer and Huntington disease. Much controversy surrounds the application of these tests, stemming from their similarities to and differences from other tests commonly used in asymptomatic persons. Some have argued that genetic tests are unique and therefore justify special consideration with regard to informed consent and privacy. This paper examines the arguments for such genetic exceptionalism and concludes that no clear, significant distinctions between genetic and nongenetic tests justify a different approach to testing by clinicians. Nevertheless, with many genetic tests, the results may cause stigmatization, family discord, and psychological distress. Regardless of whether a test is genetic, when this combination of characteristics is present and when health care providers are not specifically trained to interpret results, testing should be performed with particular caution and the highest standards of informed consent and privacy protection should be applied.
Nitric oxide: inhibitory effects on endothelial cell calcium signaling, prostaglandin I2 production and nitric oxide synthase expression
Authors: K Takeuchi
Journal: Cardiovascular Research (2004)

Objective: Nitric oxide (NO) produced in large amounts by inducible nitric oxide synthase exerts many harmful effects such as stimulation of inflammation and induction of apoptosis. The effects of excessive NO production on functions of endothelial cells, the major physiological source of NO, are not completely known. The aim of this study was to investigate the role of NO on the regulation of endothelial cell Ca2+ signaling and endothelial cell function. Methods: Primary porcine aortic endothelial cells (PAECs) were used for all these studies. Intracellular Ca2+ concentrations ([Ca2+]i) were measured using fura-2/AM. Production of prostaglandin I2 (PGI2) and cyclic GMP were assessed using enzyme immunoassays, and endothelial NO synthase protein expression was evaluated by Western blotting. Results: Bradykinin (BK, 10 nM) and thapsigargin (TG, 1 μM) provoked large increases in [Ca2+]i. The NO donor NOC12 reduced these responses, respectively, by 21% and 31% at 100 μM, 60% and 55% at 300 μM, and 74% and 78% at 500 μM. These effects were also observed with other NO donors including spermine NONOate and NOC18, and were completely prevented by carboxy-PTIO (200 μM), an NO scavenger. 8-Bromo-cGMP, however, had no effects on BK- and TG-stimulated Ca2+ responses. A 30-fold increase in PGI2 production was observed in cells stimulated with BK. NOC12 again reduced this response by 12%, 54%, 83% and 95% at 10, 100, 300 and 500 μM, respectively. Endothelial NO synthase protein level was reduced by 2%, 15%, 36 and 47% after 2, 6, 12 and 24 h, respectively, of incubation with NOC18, a NO donor with long half-life. Conclusions: NO, when produced in large amounts, can inhibit agonist-induced Ca2+ responses independently of cyclic GMP, reduce the production of endothelium-derived relaxing factors (EDRFs) and interfere with endothelial NO synthase protein expression.
Randomized study of cyclophosphamide, doxorubicin, and vincristine versus etoposide and cisplatin versus alternation of these two regimens in extensive small-cell lung cancer: a phase III trial of the Southeastern Cancer Study Group.
Authors: B J Roth, D H Johnson, L H Einhorn, L P Schacter, N C Cherng, H J Cohen, J Crawford, J A Randolph, J L Goodlow, G O Broun
Journal: Journal of Clinical Oncology (1992)

PURPOSE The trial was undertaken to determine (1) the relative efficacy/toxicity of two commonly used combination chemotherapy regimens in patients with extensive small-cell lung cancer (SCLC) and (2) whether the rapid alternation of these two regimens could provide superior therapeutic results compared with either regimen alone. PATIENTS AND METHODS In this phase III trial, 437 eligible patients were stratified by performance status (PS) and sex and were randomly assigned to receive either 12 weeks of cisplatin and etoposide (EP); 18 weeks of cyclophosphamide, doxorubicin, and vincristine (CAV); or 18 weeks of alternation of these two regimens (CAV/EP). RESULTS There were no significant differences in treatment outcome for EP, CAV, or CAV/EP in terms of response rate (61%, 51%, 59%, respectively), complete response rate (10%, 7%, 7%, respectively), or median survival (8.6 months, 8.3 months, 8.1 months, respectively), with a non-statistically significant trend toward a longer median time to progression with alternating therapy (4.3 months, 4.0 months, 5.2 months, respectively). Crossover second-line chemotherapy given at progression produced low response rates and short survival, regardless of the regimen used. Myelosuppression was the dose-limiting toxicity for all patients, although the pattern and severity differed among the treatment arms. CONCLUSIONS The combination regimens EP and CAV can be considered equivalently effective induction therapies in extensive SCLC, and these two regimens are, to some degree, crossresistant. Alternating therapy provides no therapeutic advantage compared with the use of either of these regimens alone and should not be considered as standard treatment in this clinical setting.