tbuckley/cabot-search huggingface dataset:
Pregnancy in past or present lupus nephritis: a study of 32 pregnancies from a single centre
Authors: D L. T. Huong
Journal: Annals of the Rheumatic Diseases (2001)

<h3>OBJECTIVE</h3> To study maternal and fetal outcome in women with past or present histologically proven systemic lupus erythematosus (SLE) nephritis. <h3>METHOD</h3> Retrospective study of 32 pregnancies in 22 women with past or present histologically proven SLE nephritis in a single French centre. <h3>RESULTS</h3> Pregnancy (25 planned and 7 not planned) occurred in a mean (SD) of 8 (5) years after SLE diagnosis and 6 (4) years after renal disease onset. Seven occurred in women with antiphospholipid syndrome. At pregnancy onset, all but one woman had creatininaemia below 100 μmol/l, five had proteinuria &gt;0.5 g/day, none had hypertension. Twelve pregnancies occurred in women previously treated with immunosuppressant drugs. Treatment comprised prednisone (n=31), hydroxychloroquine (n=11), aspirin (n=22), heparin (n=12), and azathioprine in one patient with steroid resistant nephrotic syndrome disclosing SLE. No therapeutic abortion was done. During pregnancy or the postpartum period, or both, proteinuria &gt;0.5 g/day occurred in 10 women (five related to pre-eclampsia, four to renal flare, one to stable nephrotic syndrome). One flare consisted of mild arthralgias. Pregnancy outcome comprised one feto-maternal death in SLE disclosed by pregnancy, five embryonic losses, two fetal deaths, and 18 premature (one neonatal death) and six full term births. No criterion appeared to influence fetal survival significantly. At long term, one patient died during an SLE flare, three women had renal relapses. At the last visit, all had creatininaemia below 100 μmol/l except one woman with creatinine level 115 μmol/l, nine had proteinuria &gt;0.5 g/day, and one was treated for hypertension. <h3>CONCLUSION</h3> Pregnancy need not be discouraged in women with a history of SLE nephritis with normal or mildly impaired renal function. Deterioration of renal function rarely occurs. However, these pregnancies are at high risk of pre-eclampsia and prematurity.
Evaluation of the cardiovascular health study (CHS) instrument and the Vulnerable Elders Survey-13 (VES-13) in elderly cancer patients. Are we still missing the right screening tool?
Authors: L. Biganzoli, L. Boni, D. Becheri, E. Zafarana, C. Biagioni, S. Cappadona, E. Bianchini, C. Oakman, S.U. Magnolfi, A. Di Leo, G. Mottino
Journal: Annals of Oncology (2012)
Dap10 and Dap12 Form Distinct, but Functionally Cooperative, Receptor Complexes in Natural Killer Cells
Authors: Jun Wu, Holly Cherwinski, Thomas Spies, Joseph H. Phillips, Lewis L. Lanier
Journal: The Journal of Experimental Medicine (2000)

Many of the activating receptors on natural killer (NK) cells are multisubunit complexes composed of ligand-binding receptors that are noncovalently associated with membrane-bound signaling adaptor proteins, including CD3ζ, FcεRIγ, DAP12, and DAP10. Because the DAP10 and DAP12 genes are closely linked, expressed in NK cells, and have remarkably similar transmembrane segments, it was of interest to determine the specificity of their interactions with ligand-binding receptors and to examine their signaling properties. Despite their similarities, DAP10, DAP12, FcεRIγ, and CD3ζ form specific receptor complexes with their ligand-binding partners in NK cells and transfectants. The transmembrane regions of DAP10 and DAP12 are sufficient to confer specific association with their partners. Although cross-linking of either DAP10- or DAP12-associated receptors has been shown to be sufficient to trigger NK cell–mediated cytotoxicity against Fc receptor–bearing cells, substantial synergy was observed in the induction of cytokine production when both receptors were engaged. Activation of the Syk/ZAP70 tyrosine kinases by the immunoreceptor tyrosine-based activation motif–containing DAP12 adaptor and of the phosphatidylinositol 3-kinase pathway by the YxNM-containing DAP10 adaptor may play an important role in the stimulation of NK cells and T cells.
Pulmonary vasoconstriction produced by protamine and protamine-heparin complex in the isolated cat lung perfused with blood or dextran
Authors: J. JASTRZEBSKI, P. HILGARD, M. K. SYKES
Journal: Cardiovascular Research (1975)

Injections of protamine sulphate, protamine-heparin complex, and the supernatant from this mixture produced a rise in pulmonary artery pressure during constant flow perfusion in the isolated cat lung. The rise in pressure occurred with both blood and dextran perfusates. This suggests that the pulmonary vasoconstriction produced by protamine may be partly due to a direct action on the pulmonary vasculature or to the release of vasoactive substances from the lungs.
Reference Values and Determinants Of Fractional Concentration Of Exhaled Nitric Oxide (FeNO) In Healthy Children
Authors: Young Ho Jung, Hyun Ju Cho, Ji-Won Kwon, Song I. Yang, Eun Lee, Hyung Young Kim, Ju-Hee Seo, Byoung-Ju Kim, Hyo-Bin Kim, So Yeon Lee, Dae Jin Song, Woo Kyung Kim, Gwang Cheon Jang, Jung Yeon Shim, Soo-Jong Hong
Journal: Journal of Allergy and Clinical Immunology (2014)
Central infusion of aldosterone synthase inhibitor attenuates left ventricular dysfunction and remodelling in rats after myocardial infarction
Authors: B. S. Huang, R. A. White, M. Ahmad, J. Tan, A. Y. Jeng, F. H.H. Leenen
Journal: Cardiovascular Research (2008)

Blockade of mineralocorticoid receptors in the central nervous system (CNS) prevents sympathetic hyperactivity and improves left ventricle (LV) function in rats post-myocardial infarction (MI). We examined whether aldosterone produced locally in the brain may contribute to the activation of mineralocorticoid receptors in the CNS.Two days after coronary artery ligation, Wistar rats received an intra-cerebroventricular (icv) infusion via osmotic mini-pumps of the aldosterone synthase inhibitor FAD286 at 100 microg/kg/day or vehicle for 4 weeks. LV function was assessed by echocardiography at 2 and 4 weeks, and by Millar catheter at 4 weeks. At 4 weeks post-MI, aldosterone in the hippocampus was increased by 70% and tended to increase in the hypothalamus by 20%. These increases were prevented by FAD286. Across groups, aldosterone in the hippocampus and hypothalamus showed a high correlation. There were no differences in brain corticosterone levels. Compared to sham rats, at both 2 and 4 weeks post-MI rats treated with vehicle showed increased LV dimensions and decreased LV ejection fraction. Icv infusion of FAD286 attenuated these changes in LV dimensions and ejection fraction by approximately 30%. At 4 weeks post-MI, LV peak systolic pressure (LVPSP) and dP/dt(max/min) were decreased and LV end-diastolic pressure (LVEDP) was increased. In rats treated with icv FAD286, LVPSP and dP/dt(min) remained normal and LVEDP and dP/dt(max) were markedly improved. Post-MI increases in cardiac fibrosis and cardiomyocyte diameter were substantially attenuated by icv FAD286.These data suggest that aldosterone produced locally in the brain acts as the main agonist of mineralocorticoid receptors in the CNS and contributes substantially to the progressive heart failure post MI.
Immune Cell Toll-Like Receptor 4 Is Required for Cardiac Myocyte Impairment During Endotoxemia
Authors: Samantha A. Tavener, Elizabeth M. Long, Stephen M. Robbins, Krista M. McRae, Holly Van Remmen, Paul Kubes
Journal: Circulation Research (2004)

The aim of this study was to investigate the importance of Toll-like receptor 4 (TLR4) signaling on cardiac myocytes versus immune cells in lipopolysaccharide (LPS)-induced cardiac dysfunction. Cardiac myocytes isolated from LPS-treated C57Bl/6 mice showed reduced shortening and calcium transients as compared with myocytes from untreated mice. In addition, LPS-treated C57Bl/6 mice showed impaired cardiac mitochondrial function, including reduced respiration and reduced time of induction of permeability transition. All of the aforementioned cardiac dysfunction was dependent on TLR4, because LPS-treated TLR4-deficient mice did not have reduced myocyte shortening or mitochondrial dysfunction. To evaluate the role of cardiac myocyte versus leukocyte TLR4, LPS was injected into chimeric mice with TLR4-positive leukocytes and TLR4-deficient myocytes. These mice showed reduced myocyte shortening in response to LPS. Myocytes from chimeric mice with TLR4-deficient leukocytes and TLR4-positive myocytes had no response to LPS. In addition, isolated myocytes from C57Bl/6 mice subsequently treated with LPS and serum for various times did not have reduced shortening, despite the presence of TLR4 mRNA and protein, as determined by reverse-transcription polymerase chain reaction and fluorescent-activated cell sorting. In fact, cardiac myocytes had equivalent amounts of TLR4 as endothelium; however, only the latter is responsive to LPS. Furthermore, signaling pathways downstream of TLR4 were not activated during direct LPS treatment of myocytes. In conclusion, TLR4 on leukocytes, and not on cardiac myocytes, is important for cardiac myocyte impairment during endotoxemia.
THE RATIO OF CONTRAST MEDIA VOLUME TO ESTIMATED GLOMERULAR FILTRATION RATE AS A NEW MARKER TO PREVENT CONTRAST INDUCED NEPHROPATHY IN PATIENTS WITH PERCUTANEOUS CORONARY INTERVENTION
Authors: Soichiro Ebisawa, Masashi Kimura, Tsuyoshi Ito, Maoto Habara, Tairo Kurita, Nobuyoshi Tanaka, Kenya Nasu, Tatsuya Ito, Yoshihisa Kinoshita, Etsuo Tsuchikane, Mitsuyasu Terashima, Yasushi Asakura, Osamu Kato, Takahiko Suzuki
Journal: Journal of the American College of Cardiology (2011)
Circulating ghrelin levels in patients with inflammatory bowel disease
Authors: M Peracchi
Journal: Gut (2006)

Ghrelin, the gut-brain peptide recently identified as the natural endogenous ligand for growth hormone secretagogue receptors, exerts various endocrine and non-endocrine effects, including control of food intake and energy homeostasis.1 It could also play a role in modulating immune responses and inflammatory processes.1 Indeed, ghrelin exerts potent anti-inflammatory effects in vitro and in vivo,1–5 and high circulating ghrelin levels have been found in rats with septic shock, cysteamine induced duodenal ulcers, and adjuvant induced arthritis.4–6 Also, we have recently demonstrated that in patients with newly diagnosed coeliac disease, circulating ghrelin levels are abnormally high, correlate positively with intestinal mucosal lesion severity, and normalise in successfully gluten free diet treated patients.7 However, normal or even decreased ghrelin levels have been found in other inflammatory diseases, including rheumatoid arthritis and Helicobacter pylori associated …
Microbiota and diabetes: an evolving relationship
Authors: Herbert Tilg, Alexander R Moschen
Journal: Gut (2014)

The gut microbiota affects numerous biological functions throughout the body and its characterisation has become a major research area in biomedicine. Recent studies have suggested that gut bacteria play a fundamental role in diseases such as obesity, diabetes and cardiovascular disease. Data are accumulating in animal models and humans suggesting that obesity and type 2 diabetes (T2D) are associated with a profound dysbiosis. First human metagenome-wide association studies demonstrated highly significant correlations of specific intestinal bacteria, certain bacterial genes and respective metabolic pathways with T2D. Importantly, especially butyrate-producing bacteria such as <i>Roseburia intestinalis</i> and <i>Faecalibacterium prausnitzii</i> concentrations were lower in T2D subjects. This supports the increasing evidence, that butyrate and other short-chain fatty acids are able to exert profound immunometabolic effects. Endotoxaemia, most likely gut-derived has also been observed in patients with metabolic syndrome and T2D and might play a key role in metabolic inflammation. A further hint towards an association between microbiota and T2D has been derived from studies in pregnancy showing that major gut microbial shifts occurring during pregnancy affect host metabolism. Interestingly, certain antidiabetic drugs such as metformin also interfere with the intestinal microbiota. Specific members of the microbiota such as <i>Akkermansia muciniphila</i> might be decreased in diabetes and when administered to murines exerted antidiabetic effects. Therefore, as a ‘gut signature’ becomes more evident in T2D, a better understanding of the role of the microbiota in diabetes might provide new aspects regarding its pathophysiological relevance and pave the way for new therapeutic principles.
RNA Editome Imbalance in Hepatocellular Carcinoma
Authors: Lihua Qi, Tim Hon Man Chan, Daniel G. Tenen, Leilei Chen
Journal: Cancer Research (2014)

Abstract Adenosine-to-inosine conversion (A-to-I editing), a posttranscriptional modification on RNA, contributes to extensive transcriptome diversity. A-to-I editing is a hydrolytic deamination process, catalyzed by adenosine deAminase acting on double-stranded RNA (ADAR) family of enzymes. ADARs are essential for normal mammalian development, and disturbance in RNA editing has been implicated in various pathologic disorders, including cancer. Thanks to next-generation sequencing, rich databases of transcriptome evolution for cancer development at the resolution of single nucleotide have been generated. Extensive bioinformatic analysis revealed a complex picture of RNA editing change during transformation. Cancer displayed global hypoediting of Alu-repetitive elements with gene-specific editing pattern. In particular, hepatocellular carcinoma editome is severely disrupted and characterized by hyper- and hypoediting of different genes, such as hyperedited AZIN1 (antizyme inhibitor 1) and FLNB (filamin B, β) and hypoedited COPA (coatomer protein complex, subunit α). In hepatocellular carcinoma, not only the recoding editing in exons, but also the editing in noncoding regions (e.g., Alu-repetitive elements and microRNA) displays such complex editing pattern with site-specific editing trend. In this review, we will discuss current research progress on the involvement of abnormal A-to-I editing in cancer development, more specifically on hepatocellular carcinoma. Cancer Res; 74(5); 1301–6. ©2014 AACR.
Epigenetic inactivation of SFRP genes allows constitutive WNT signaling in colorectal cancer
Authors: Hiromu Suzuki, D Neil Watkins, Kam-Wing Jair, Kornel E Schuebel, Sanford D Markowitz, Wei Dong Chen, Theresa P Pretlow, Bin Yang, Yoshimitsu Akiyama, Manon van Engeland, Minoru Toyota, Takashi Tokino, Yuji Hinoda, Kohzoh Imai, James G Herman, Stephen B Baylin
Journal: Nature Genetics (2004)
Bioterrorism, Public Health, and Civil Liberties
Authors: George J Annas
Journal: New England Journal of Medicine (2002)

In the wake of the September 11, 2001, terrorist attacks, the Centers for Disease Control and Prevention proposed a model act for the states that specifies steps to be taken to contain an epidemic resulting from a bioterrorist attack. The act would grant broad powers to the states in the event of public health emergencies arising from bioterrorism. Annas discusses the trade-off between civil liberties and the need to protect the health of the public in the event of bioterrorism. His underlying premise is that the model act, despite being revised in December 2001, goes too far.
A BALANCED CONCEPT OF CHILD TRAINING WITH SOCIAL IMPLICATIONS
Authors: FREDERIC T. ZIMMERMAN, BESSIE B. BURGEMEISTER
Journal: American Journal of Psychiatry (1953)

We have presented a balanced concept of child training based on our observations of the dynamics of life in the retarded-child family and the known data of animal experimentation. Since the preservation of a culture depends on the efficacy of transmission of its ideals through its children, we have attempted to explore the possible sociological implications connected with child training.
Metabolic Syndrome and Diabetes Are Associated With an Increased Likelihood of Inducible Myocardial Ischemia Among Patients With Subclinical Atherosclerosis
Authors: Nathan D. Wong, Alan Rozanski, Heidi Gransar, Romalisa Miranda-Peats, Xingping Kang, Sean Hayes, Leslee Shaw, John Friedman, Donna Polk, Daniel S. Berman
Journal: Diabetes Care (2005)

OBJECTIVE—Coronary artery calcification (CAC) is associated with cardiac events and the likelihood of inducible myocardial ischemia. Because metabolic syndrome contributes to atherosclerosis, we assessed whether it also influences the relationship between CAC levels and myocardial ischemia. RESEARCH DESIGN AND METHODS—We evaluated 1,043 patients without known coronary artery disease (CAD) who underwent stress myocardial perfusion scintigraphy (MPS) and computed tomography. Metabolic syndrome was defined by modified National Cholesterol Education Program criteria. Metabolic abnormalities were present in 313 patients (30%), including 140 with diabetes (with or without metabolic syndrome) and 173 who had metabolic syndrome without diabetes. RESULTS—Although CAC scores &amp;lt;100 identified a low likelihood (∼2%) of ischemia, the presence (versus absence) of metabolic abnormalities (metabolic syndrome or diabetes) was a predictor of more frequent ischemia among patients with CAC scores of 100–399 (13.0 vs. 3.6%, P &amp;lt; 0.02) and CAC scores ≥400 (23.4 vs. 13.6%, P = 0.03). Similar trends were observed when patients with metabolic syndrome and diabetes were considered separately. Multiple logistic regression revealed the odds of MPS ischemia to be 4.3-fold greater per SD of log CAC (P &amp;lt; 0.001) and 2.0-fold greater in the presence of metabolic abnormalities (P &amp;lt; 0.01). CONCLUSIONS— Among patients with CAC scores ≥100, metabolic abnormalities, and even metabolic syndrome in the absence of diabetes predicted a higher likelihood of inducible ischemia. These findings suggest the need for assessment of metabolic status when interpreting the results of CAC imaging among patients undergoing such testing because of suspected CAD.
Cardiac Growth Factors in Human Hypertrophy
Authors: Gian Gastone Neri Serneri, Pietro Amedeo Modesti, Maria Boddi, Ilaria Cecioni, Rita Paniccia, Mirella Coppo, Giorgio Galanti, Ignazio Simonetti, Simone Vanni, Letizia Papa, Brunella Bandinelli, Angela Migliorini, Alessandra Modesti, Massimo Maccherini, Guido Sani, Michele Toscano
Journal: Circulation Research (1999)

Abstract —The aim of the present study was to investigate whether and which cardiac growth factors are involved in human hypertrophy, whether growth factor synthesis is influenced by overload type and/or by the adequacy of the hypertrophy, and the relationships between cardiac growth factor formation and ventricular function. Cardiac growth factor formation was assessed by measuring aorta-coronary sinus concentration gradient in patients with isolated aortic stenosis (n=26) or regurgitation (n=15) and controls (n=12). Gene expression and cellular localization was investigated in ventricular biopsies using reverse transcriptase–polymerase chain reaction and in situ hybridization. Cardiac hypertrophy with end-systolic wall stress &lt;90 kdyne/cm 2 was associated with a selective increased formation of insulin-like growth factor (IGF)-I in aortic regurgitation and of IGF-I and endothelin (ET)-1 in aortic stenosis. mRNA levels for IGF-I and preproET-1 were elevated and mainly expressed in cardiomyocytes. At stepwise analysis, IGF-I formation was correlated to the mean velocity of circumferential fiber shortening ( r =0.86, P &lt;0.001) and ET-1 formation to relative wall thickness ( r =0.82, P &lt;0.001). When end-systolic wall stress was &gt;90 kdyne/cm 2 , IGF-I and ET-1 synthesis by cardiomyocytes was no longer detectable, and only angiotensin (Ang) II was generated, regardless of the type of overload. The mRNA level for angiotensinogen was high, and the mRNA was exclusively expressed in the interstitial cells. Ang II formation was positively correlated to end-systolic stress ( r =0.89, P &lt;0.001) and end-diastolic stress ( r =0.84, P &lt;0.001). Multivariate stepwise analysis selected end-systolic stress as the most predictive variable and left ventricular end-diastolic pressure as the independent variable for Ang II formation ( r =0.93, P &lt;0.001). In conclusion, the present results indicate that the course of human left ventricular hypertrophy is characterized by the participation of different cardiac growth factors that are selectively related both to the type of hemodynamic overload and to ventricular function.
MASL1 induces erythroid differentiation in human erythropoietin-dependent CD34+ cells through the Raf/MEK/ERK pathway
Authors: Chutima Kumkhaek, Wulin Aerbajinai, Wenli Liu, Jianqiong Zhu, Naoya Uchida, Roger Kurlander, Matthew M. Hsieh, John F. Tisdale, Griffin P. Rodgers
Journal: Blood (2013)
Breast Cancer Prognosis and Occult Lymph Node Metastases, Isolated Tumor Cells, and Micrometastases
Authors: M. de Boer, J. A. A. M. van Dijck, P. Bult, G. F. Borm, V. C. G. Tjan-Heijnen
Journal: JNCI Journal of the National Cancer Institute (2010)

The prognostic relevance of isolated tumor cells and micrometastases in lymph nodes from patients with breast cancer has become a major issue since the introduction of the sentinel lymph node procedure. We conducted a systematic review of this issue.Studies published from January 1, 1977, until August 11, 2008, were identified by use of MEDLINE, EMBASE, and the Cochrane Library. A total of 58 studies (total number of patients = 297,533) were included and divided into three categories according to the method for pathological assessment of the lymph nodes: cohort studies with single-section pathological examination of axillary lymph nodes (n = 285,638 patients), occult metastases studies with retrospective examination of negative lymph nodes by step sectioning and/or immunohistochemistry (n = 7740 patients), and sentinel lymph node biopsy studies with intensified work-up of the sentinel but not of the nonsentinel lymph nodes (n = 4155 patients). We used random-effects meta-analyses to calculate pooled estimates of the relative risks (RRs) of 5- and 10-year disease recurrence and death and the multivariably corrected pooled hazard ratio (HR) of overall survival of the cohort studies.In the cohort studies, the presence (vs the absence) of metastases of 2 mm or less in diameter in axillary lymph nodes was associated with poorer overall survival (pooled HR of death = 1.44, 95% confidence interval [CI] = 1.29 to 1.62). In the occult metastases studies, the presence (vs the absence) of occult metastases was associated with poorer 5-year disease-free survival (pooled RR = 1.55, 95% CI = 1.32 to 1.82) and overall survival (pooled RR = 1.45, 95% CI = 1.11 to 1.88), although these endpoints were not consistently assessed in multivariable analyses. Sentinel lymph node biopsy studies were limited by small patient groups and short follow-up.The presence (vs the absence) of metastases of 2 mm or less in diameter in axillary lymph nodes detected on single-section examination was associated with poorer disease-free and overall survival.