tbuckley/cabot-search huggingface dataset:
Assisted reproduction: the epigenetic perspective
Authors: Bernhard Horsthemke, Michael Ludwig
Journal: Human Reproduction Update (2005)

Developmental pathways in humans and other organisms are buffered against changes in genotype and environment. Therefore, it should not come as a surprise that most of the children conceived by assisted reproduction technology (ART) are healthy, although ART bypasses a lot of biological filters and subjects the gametes and the early embryo to environmental stress. If, however, the buffer breaks down, the development of certain tissues or organs may follow abnormal trajectories. We argue that both normal and abnormal development in children conceived by ART can be explained by epigenetic mechanisms, which control the establishment and maintenance of gene expression patterns in the placenta and fetus. Imprinted genes are of special importance in this respect. There is increasing evidence that genetic factors in infertile couples as well as environmental factors (hormones and culture media) can have adverse effects on epigenetic processes controlling implantation, placentation, organ formation and fetal growth. In addition, loss of epigenetic control may expose hidden genetic variation.
Monocyte Selectivity and Tissue Localization Suggests a Role for Breast and Kidney–Expressed Chemokine (Brak) in Macrophage Development
Authors: Isabel Kurth, Katharina Willimann, Patrick Schaerli, Thomas Hunziker, Ian Clark-Lewis, Bernhard Moser
Journal: The Journal of Experimental Medicine (2001)

Although numerous chemokines act on monocytes, none of them is specific for these cells. Here, we show that breast and kidney–expressed chemokine (BRAK) is a highly selective monocyte chemoattractant. Migration efficacy and Bordetella pertussis toxin–sensitive Ca2+ mobilization responses to BRAK were strongly enhanced after treatment of monocytes with the cyclic AMP–elevating agents prostaglandin E2 and forskolin. BRAK is the first monocyte-selective chemokine, as other types of blood leukocytes or monocyte-derived dendritic cells and macrophages did not respond. Expression in normal skin keratinocytes and dermal fibroblasts as well as lamina propria cells in normal intestinal tissues suggests a homeostatic rather than an inflammatory function for this chemokine. In addition, macrophages were frequently found to colocalize with BRAK-producing fibroblasts. We propose that BRAK is involved in the generation of tissue macrophages by recruiting extravasated precursors to fibroblasts, which are known to secrete essential cytokines for macrophage development.
RUBELLA VIRUS CARRIER CULTURES DERIVED FROM CONGENITALLY INFECTED INFANTS
Authors: William E. Rawls, Joseph L. Melnick
Journal: The Journal of Experimental Medicine (1966)

Spontaneous rubella carrier cultures derived from tissues of infants with congenital rubella were studied in an attempt to elucidate a possible mechanism for viral persistence observed in these infants. Chronically infected cells were found to have a reduced growth rate and the cultures appeared to have a shortened life span. The rubella carrier state was not dependent on serum inhibitors or rubella antibodies. Virtually every cell in the carrier population was found to be producing virus. The carrier cultures could not be cured by rubella antibodies. The rubella-infected cells were resistant to superinfection with vesicular stomatitis virus and herpes simplex virus but were susceptible to infection with echovirus 11. The replication of vesicular stomatitis virus was apparently blocked at an intracellular site, for the virus readily adsorbed to the chronically infected cells and entered into an eclipse phase; however no infectious virus developed. No evidence of interferon production by these cells could be obtained. It is postulated that clones of rubella-infected cells in vivo, with properties similar to those in carrier cultures developed in vitro from tissues of in utero infected infants, might explain the observed viral persistence noted in congenital rubella.
Microalbuminuria correlates with intestinal histopathological grading in patients with inflammatory bowel disease.
Authors: N Mahmud, G S McDonald, D Kelleher, D G Weir
Journal: Gut (1996)

It has previously been shown that microalbuminuria is a useful disease activity marker for inflammatory bowel disease (IBD). Microalbuminuria correlates strongly with the markers of clinical and laboratory disease activity such as erythrocyte sedimentation rate (ESR), and C reactive protein (CRP). The aim of this study was to discover if microalbuminuria accurately reflects the intestinal inflammation by correlating it with intestinal inflammation using a standard histopathological grading system in patients with ulcerative colitis and Crohn's colitis. Forty two patients with IBD who had undergone endoscopic examination of the entire colon for the assessment of severity and extent of the disease (Crohn's colitis (n = 21), ulcerative colitis (n = 21)) were recruited to the study. Patients with small bowel Crohn's disease were not studied. Twenty four patients had left sided colonic disease and 18 patients had extensive colonic disease. Each patient's colonic biopsy specimens were scored blindly by a histopathologist and a composite score was compiled on the basis of the severity of changes in the enterocytes and crypts and the cellularity of the lamina propria. A clinical disease activity was obtained using the simple index of Harvey and Bradshaw. Microalbuminuria was measured in all patients by an immunoturbiditimetric method. ESR and CRP were also measured, as indicators of acute phase response in the same patients. It was found that patients with active IBD had higher concentrations of microalbuminuria compared with those patients in remission (median 222 micrograms/min (range 40-686 micrograms/min) v median 96 micrograms/min (range 30-376 micrograms/min); p < 0.001)). Significantly higher concentrations of microalbuminuria were also detected in patients with extensive colonic IBD compared with those patients with left sided disease (median 297 micrograms/min (range 132-686 micrograms/min) v median 101 micrograms/min (range 30-433 micrograms/min); p < 0.001)). A strong positive correlation was seen between microalbuminuria and intestinal histopathological score in IBD patient groups with left sided colitis (r = 0.77; p < 0.001) and extensive disease (r = 0.71; p < 0.01). The standard histopathological grading system correlated with the clinical disease activity (r = 0.64; p < 0.005) and CRP (r = 0.62; p < 0.02), however, it did not correlate with ESR. In conclusion, the strong correlation of microalbuminuria with a standard intestinal histopathological grading system suggests that microalbuminuria accurately reflects the severity of colonic inflammation in patients with Crohn's colitis and ulcerative colitis.
Cytokine profile of bronchoalveolar lavage in systemic sclerosis with interstitial lung disease: comparison with usual interstitial pneumonia
Authors: F Meloni, R Caporali, A Marone Bianco, E Paschetto, M Morosini, A M Fietta, F Bobbio-Pallavicini, E Pozzi, C Montecucco
Journal: Annals of the Rheumatic Diseases (2004)

Interstitial lung disease (ILD), which often develops in systemic sclerosis (SSc), is associated with a better prognosis than idiopathic usual interstitial pneumonia (UIP) because only a limited number of patients with SSc progress to end stage fibrosis.1,2 Mechanisms driving the fibrotic evolution of ILD are still poorly understood, but, recently, on the basis of animal models, a pathogenetic role has been ascribed to an imbalance in the local Th1/Th2 response, with an expansion of the Th2 profile.3

We studied the cytokine profile of bronchoalveolar lavage fluid (BALF) of 28 patients with SSc-ILD (6 men, 22 women; mean (SD) age 50.3 (8.9) years). All patients with SSc satisfied the preliminary American College of Rheumatology (ACR) criteria for classification of the disease,4 and respiratory disease was defined on the basis of functional tests and high resolution computed tomography findings as at least grade 1 …
Art and Psychosis
Authors: M Malliarou, Captain Hellenic Navy, Lieutenant Hellenic Navy
Journal: JAMA (1999)

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
Aspergillus species recombinant antigens for serodiagnosis of farmer's lung disease
Authors: Laurence Millon, Sandrine Roussel, Benedicte Rognon, Manfredo Quadroni, Karin Salamin, Gabriel Reboux, Coralie Barrera, Jean-Marc Fellrath, John D. Aubert, Jean-Charles Dalphin, Michel Monod
Journal: Journal of Allergy and Clinical Immunology (2012)
Anti-inflammatory actions of benzoyl peroxide: effects on the generation of reactive oxygen species by leucocytes and the activity of protein kinase C and calmodulin
Authors: L. HEGEMANN, S.M. TOSO, K. KITAY, C.F. WEBSTER
Journal: British Journal of Dermatology (1994)

Journal Article Anti‐inflammatory actions of benzoyl peroxide: effects on the generation of reactive oxygen species by leucocytes and the activity of protein kinase C and calmodulin Get access L. HEGEMANN, L. HEGEMANN Departments of Dermatology, Thomas Jefferson University, Philadelphia, Pennsylvania, U.S.A. and University of Vienna, Vienna, Austria Dr L. Hegemann, Department of Dermatology, Dermatopharmacology Unit, University Hospital of Vienna, Währinger Gürtel 18–20, 1090 Vienna, Austria. Search for other works by this author on: Oxford Academic Google Scholar S.M. TOSO, S.M. TOSO Departments of Dermatology, Thomas Jefferson University, Philadelphia, Pennsylvania, U.S.A. and University of Vienna, Vienna, Austria Search for other works by this author on: Oxford Academic Google Scholar K. KITAY, K. KITAY Departments of Dermatology, Thomas Jefferson University, Philadelphia, Pennsylvania, U.S.A. and University of Vienna, Vienna, Austria Search for other works by this author on: Oxford Academic Google Scholar C.F. WEBSTER C.F. WEBSTER Departments of Dermatology, Thomas Jefferson University, Philadelphia, Pennsylvania, U.S.A. and University of Vienna, Vienna, Austria Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 130, Issue 5, 1 May 1994, Pages 569–575, https://doi.org/10.1111/j.1365-2133.1994.tb13101.x Published: 01 May 1994 Article history Accepted: 10 September 1993 Published: 01 May 1994
Rebound Increase in Thrombin Generation and Activity After Cessation of Intravenous Heparin in Patients With Acute Coronary Syndromes
Authors: Christopher B. Granger, Julie M. Miller, Edwin G. Bovill, Andras Gruber, Russell P. Tracy, Mitchell W. Krucoff, Cindy Green, Eric Berrios, Robert A. Harrington, E. Magnus Ohman, Robert M. Califf
Journal: Circulation (1995)

Background The abrupt cessation of heparin and other thrombin inhibitors when used to treat acute coronary syndromes has been accompanied by a clustering of thrombotic events. It is unknown whether these events are the result of inadequate antithrombin therapy or whether they represent a rebound increase in thrombin activity. This study was designed to determine whether there is a true rebound, as defined by an increase followed by a subsequent decrease, in thrombin activity after discontinuation of intravenous heparin therapy. Methods and Results Thirty-five patients with recent acute myocardial infarction or unstable angina who had received at least 48 hours of intravenous heparin were studied. Patients underwent ST-segment monitoring, and blood samples for determination of thrombin generation and activity were drawn at 0, 3, 6, 10, and 24 hours after heparin discontinuation. Median aPTT was 65 seconds before heparin discontinuation. Median fibrinopeptide A increased from 9.5 to 16.9 ng/mL at 3 hours ( P &lt;.0004) and returned to 10.5 by 24 hours. Prothrombin fragment 1.2 likewise transiently increased, from 0.34 to 0.51 nmol/L at 6 hours ( P &lt;.0002). Modified antithrombin III decreased over time ( P &lt;.002), and activated protein C increased from 2.3 to 4.5 ng/mL at 3 hours ( P &lt;.001). Although there were no clinical thrombotic events in the first 24 hours, 4 patients had evidence of ischemia by ST-segment monitoring at a median of 12 hours after heparin discontinuation. The degree of increase in fibrinopeptide A and prothrombin fragment 1.2 was not found to be associated with baseline diagnosis, duration of heparin therapy, baseline level of antithrombin III, or activated protein C. Conclusions This study demonstrates a transient rebound increase in thrombin activity as well as in activated protein C upon abrupt discontinuation of intravenous heparin. Clinicians should be vigilant for associated thrombotic events. Further investigation of the significance, mechanism, and possible prevention of this rebound phenomenon is needed.
Expression of Hepatocyte Growth Factor and Its Receptor Met in Wilms' Tumors and Nephrogenic Rests Reflects Their Roles in Kidney Development
Authors: Raisa Vuononvirta, Neil J. Sebire, Boo Messahel, Nina Perusinghe, Jorge S. Reis-Filho, Kathy Pritchard-Jones, Gordan M. Vujanic, Chris Jones
Journal: Clinical Cancer Research (2009)

Hepatocyte growth factor (HGF) and its receptor Met are known to play diverse roles in both organogenesis and cancer. Wilms' tumor (WT) is a prototype for the link between abrogated development and neoplasia, with dysregulation of growth factor/receptor pathways playing key roles. Despite this, an understanding of the HGF/Met axis in the process is lacking.Observing copy number alterations at the loci for these genes in WTs and their precursor lesions nephrogenic rests, we examined protein expression by immunohistochemistry and investigated the effects of HGF on an in vitro model of kidney development.HGF was preferentially expressed in the blastemal cells of nephrogenic rests but not WTs. Met expression was infrequent and restricted to well-differentiated epithelial cells and stroma in both lesions. In an independent cohort of favorable histology WTs on a tissue microarray, HGF was expressed in 15 of 193 (8%) cases and correlated with a predominance of epithelial cells, whereas Met expression was observed in 25 of 179 (14%) cases and was associated with stromal subtypes. In a mouse mesonephric cell line model, we observed Met expression in culture conditions reflecting both mesenchymal and epithelial differentiation, whereas HGF was up-regulated in association with acquisition of a more epithelial-like phenotype. This could be mimicked by exogenous exposure of mesenchymal-like cells to recombinant HGF.These data show that the relatively infrequent expression of HGF and Met in WT tumorigenesis reflects their roles in nephrogenesis, particularly the mesenchymal-to-epithelial transition, rather than a dependence on oncogenic signaling pathways.
Differential expression of DKK-1 binding receptors on stromal cells and myeloma cells results in their distinct response to secreted DKK-1 in myeloma
Authors: Xiaoyi Dun, Hua Jiang, Jianfeng Zou, Jun Shi, Lili Zhou, Rong Zhu, Jian Hou
Journal: Molecular Cancer (2010)

Abstract Background The canonical Wnt signaling is concurrently important for osteoblast differentiation and myeloma cell proliferation. Its activation in myeloma cells and its inhibition in osteoblasts and their progenitors have been identified in the previous studies. Osteoblast progenitors and myeloma cells from a myeloma patient share the same bone marrow (BM) microenvironment, but respond differently to DKK-1 secreted by myeloma cells. The mechanisms remain unclear. Methods Primary multiple myeloma (MM) cells were isolated from BM mononuclear cells of 12 MM patients. Human bone marrow stromal cells (SCs) were obtained from BM adherent cells of these MM patients and 10 healthy donors. The mRNA expression levels of DKK-1 binding receptor LRP5/6 and Kremen1/2 (Krm1/2) were analyzed by Real-time PCR in human myeloma cell line (HMCL) RPMI-8226, NCI-H929, U266, LP-1, CZ-1, KM-3, Sko-007, primary myeloma cells and SCs from 12 MM patients and SCs from 10 healthy donors. The binding capability of DKK-1 binding receptors to DKK-1 on primary myeloma cells and SCs was detected by flow cytometry assay. Results The mRNA expression levels of DKK-1 binding receptor LRP5/6 and Krm1/2 in SCs from patients with MM were significantly higher than those in myeloma cells and in SCs from healthy donors. The binding capability to DKK-1of DKK-1 binding receptors on SCs from MM patients was obviously higher than those on myeloma cells and SCs from healthy donors by flow cytometry assay. Similar to the effects of coculture with rhDKK1, coculture of SCs from healthy donors with myeloma cells in the presence or absence of a Transwell insert did up-regulate SCs' mRNA levels of LRP5/6 and Krm1/2, and down-regulate their mRNA levels of β-catenin. Conclusion Compared with myeloma cells, the SCs from MM patients overexpress DKK-1 binding receptors LRP5/6 and Krm1/2 in response to DKK-1 secreted by myeloma cells, which results in intracellular Wnt signaling inhibition. Our study provides a novel insight into mechanisms of myeloma associated osteolytic lesions.
Catastrophic rugby injuries of the spinal cord: changing patterns of injury.
Authors: A T Scher
Journal: British Journal of Sports Medicine (1991)

In reports from the UK and New Zealand, it is noted that the incidence of rugby injuries to the cervical spinal cord has dropped and that the percentage of players injured in the tackle has similarly decreased. In contrast, this does not appear to be the pattern in South Africa and an analysis has therefore been made of 40 rugby players sustaining injuries to the spinal cord during the period 1985 to 1989. The radiological appearances on admission have been correlated with the circumstances of injury, associated orthopaedic injuries and neurological deficits. The tackle was responsible for the majority of injuries, causing more than the scrum. Tackles were also responsible for more cases of complete, permanent quadriplegia than the scrum. The commonest cause of injury in players being tackled was the high tackle around the neck, while the commonest cause of injury in players making the tackle was the dive tackle. This survey has shown that the tackle is now the major cause of spinal cord injury in South African rugby, in contrast to earlier analyses in which the scrum was identified as the most common cause.
Initiation of Atrial Fibrillation by Ectopic Beats Originating From the Pulmonary Veins
Authors: Shih-Ann Chen, Ming-Hsiung Hsieh, Ching-Tai Tai, Chin-Feng Tsai, V. S. Prakash, Wen-Chung Yu, Tsui-Lieh Hsu, Yu-An Ding, Mau-Song Chang
Journal: Circulation (1999)

Background —Atrial fibrillation (AF) can be initiated by ectopic beats originating from the atrial or great venous tissues. This study investigated the anatomic characteristics and electrophysiological properties of pulmonary veins (PVs), as well as the possible mechanisms and response to drugs of ectopic foci, and assessed the effects of radiofrequency (RF) ablation on AF initiated by ectopic beats originating from PVs. Methods and Results —Seventy-nine patients with frequent episodes of paroxysmal AF and 10 control patients were included. Distal PVs showed the shortest effective refractory periods (ERPs), and right superior PVs showed a higher incidence of intra-PV conduction block than left superior PVs. Superior and left PVs had longer myocardial sleeves than inferior and right PVs, respectively. These electrophysiological characteristics were similar between AF and control patients. Propranolol, verapamil, and procainamide suppressed ectopic beats that originated from the PVs. Of 116 ectopic foci that initiated AF, 103 (88.8%) originated from PVs. A mean of 7±3 RF applications completely eliminated 110 ectopic foci (94.8%). During the 6±2-month follow-up period, 68 patients (86.1%) were free of AF without any antiarrhythmic drugs. Follow-up transesophageal echocardiogram showed 42.4% of ablated PVs had focal stenosis. One patient had mild exertional dyspnea after ablation, but it resolved 3 months later; 1 patient had onset of mild exertional dyspnea 5 months after ablation. Conclusions —Electrophysiological characteristics of PVs are different from those in the atria. Ectopic beats from PVs can initiate AF, and β-adrenergic receptor blocker, calcium channel blockers, and sodium channel blockers can suppress these ectopic beats. Careful mapping and elimination of these ectopic foci can cure paroxysmal AF.
Residual sleepiness in patients with OSA on CPAP
Authors: J. R. Stradling
Journal: European Respiratory Journal (2009)

To the Editors: 

Pepin et al. 1 recently published a very interesting study of residual excessive sleepiness (RES) in 502 patients with obstructive sleep apnoea treated successfully with continuous positive airway pressure (CPAP). They concluded that a significant percentage (about 6–12%, depending on inclusion criteria) had RES. They concluded that, since about 230,000 French patients are on CPAP, a minimum of 13,800 might suffer …
B cell activating factor belonging to the TNF family might be a useful biomarker in interstitial lung diseases associated with connective tissue diseases
Authors: Tstuomu Hamada, Tomohiro Kumamoto, Asami Harumatsu, Keiko Mizuno, Takuya Samukawa, Ikkou Higashimoto, Masaki Watanabe, Hiromasa Inoue
Journal: European Respiratory Journal (2013)

Background; B cell-activating factor belonging to the TNF family (BAFF) is a vital homeostatic cytokine for B cells and has been associated with autoimmune disease. We have shown that the elevation of serum BAFF in patients with interstitial lung disease associated with connective tissue disease (CTD-ILD). However, BAFF has not been confirmed as a disease severity for CTD-ILD.  Aim; The aim of this study was to investigate the potential of serum BAFF as a biomarker and to confirm its correlation with disease severity in patients with CTD-ILD.  Methods; Sixty-seven patients with IIP (n=19), undifferentiated CTD-ILD (n=14), and CTD-ILD (n=34) who visited our institution were enrolled. Twenty-one healthy volunteers were included as a control group. Serum BAFF levels were measured by ELISA. Expression of BAFF in the lung was evaluated by immunohistochemistry.  Results; Serum BAFF levels were significantly elevated in patients with CTD-ILD (2.2±1.1 ng/ml) compared with IIP (1.1±0.4 ng/ml, p  Conclusion: BAFF in serum might be a useful candidate biomarker with which to distinguish CTD-ILD from IIP.