tbuckley/cabot-search huggingface dataset:
Inflammation, Residual Kidney Function, and Cardiac Hypertrophy Are Interrelated and Combine Adversely to Enhance Mortality and Cardiovascular Death Risk of Peritoneal Dialysis Patients
Authors: Angela Yee-Moon Wang, Mei Wang, Jean Woo, Christopher Wai-Kei Lam, Siu-Fai Lui, Philip Kam-Tao Li, John E. Sanderson
Journal: Journal of the American Society of Nephrology (2004)

ABSTRACT. C-reactive protein (CRP), the prototype marker of inflammation, and cardiac hypertrophy are important prognostic indicators in dialysis patients. Residual renal function (RRF) has also been shown to influence survival of peritoneal dialysis (PD) patients. This study examined the relations between inflammation, RRF, and left ventricular hypertrophy (LVH) and determined whether inflammation, RRF, and LVH combine adversely to predict the outcomes of PD patients. A prospective observational study was performed in 231 chronic PD patients. Left ventricular mass index (LVMi), residual glomerular filtration rate (GFR), CRP, hemoglobin, serum albumin, and BP were determined at study baseline and related to outcomes. On univariate analysis, age (P = 0.002), dialysis duration (P = 0.004), coronary artery disease (P < 0.001), pulse pressure (P < 0.001), hemoglobin (P < 0.001), serum albumin (P = 0.032), log-CRP (P < 0.001), and GFR (P < 0.001) were significantly associated with log-LVMi. Log-CRP was positively correlated with pulse pressure (R = 0.218, P = 0.001) and negatively correlated with GFR (R = −0.272, P < 0.001). Multivariate analysis showed that log-CRP (P = 0.008) and RRF (P = 0.003) remained associated with log-LVMi independent of hemoglobin, serum albumin, arterial pulse pressure, and coronary artery disease. After follow-up for 30 ± 14 mo, 34.2% patients had died. CRP, RRF, and LVMi each were significantly predictive of all-cause mortality and cardiovascular death. Kaplan-Meier analysis showed a significant increase in all-cause (P < 0.0001) and cardiovascular mortality (P < 0.0001) as the number of risk factors, namely CRP ≥50th percentile, no RRF, and LVMi≥ 50th percentile increased with the 2-yr all-cause mortality and cardiovascular death reaching as high as 61% and 46%, respectively, for patients who had all three risk factors. Compared with patients with none of the three risk factors, those with all three risk factors had an adjusted hazards ratio of 6.94 (P < 0.001) and 5.43 (P = 0.001) for all-cause mortality and cardiovascular mortality, respectively. In conclusion, inflammation, RRF, and LVH are interrelated and combine adversely to increase mortality and cardiovascular death risk of PD patients.
&lt;italic&gt;In Vitro&lt;/italic&gt; “Spontaneous” Neoplastic Transformation of Mouse Fibroblasts in Diffusion Chambers&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: Giorgio Parmiani, Giusi Carbone, Richmond T. Prehn
Journal: JNCI Journal of the National Cancer Institute (1971)

Mouse fibroblasts may undergo spontaneous neoplastic transformation in a few weeks in vitro, but not as rapidly as when in diffusion chambers in vivo. To study the critical factors determining the first phenomenon, muscle cells of newborn mice were seeded in diffusion chambers placed either in petri dishes or in the peritoneal cavity of syngeneic mice. During 8–36 weeks in vitro and 8–46 weeks in vivo, the chambers were recovered and opened at 4-week intervals. The Millipore filters on which cells were growing were implanted subcutaneously into immunodepressed syngeneic mice. No tumors were obtained from the cells cultivated in diffusion chambers in vivo, whereas tumors appeared in the assay mice transplanted with cells cultivated in chambers in vitro. These results show that the fluid environment bathing the cells profoundly affects the latent period of “spontaneous” neoplastic transformation.
Mechanisms of genetic resistance to Friend virus leukemia in mice. IV. Identification of a gene (Fv-3) regulating immunosuppression in vitro, and its distinction from Fv-2 and genes regulating marrow allograft reactivity.
Authors: V Kumar, L Goldschmidt, J W Eastcott, M Bennett
Journal: The Journal of Experimental Medicine (1978)

Friend leukemia viru (FV) suppresses the proliferative response of normal lymphocytes to mitogens. The in vitro suppressive effect of FV on lymphocyte mitogenesis is mediated by T-suppressor cells and is under host genetic control. Lymphocytes from strains of mice of the C57BL background (e.g., C57BL/6) are resistant while cells from other strains (e.g., 129 and DBA/2) are susceptible. Genetic analyses utilizing resistant and susceptible parental strains, their F1, intercross and backcross progeny indicated that susceptibility to in vitro suppression is regulated by a single autosomal gene, dominant for susceptibility to suppression. This gene, which is not linked to the H-2 complex, segregated independently of the Fv-2 gene which controls resistance to spleen focus formation in vivo. The gene is also unlinked to the Ir-like genes which regulate the ability of H-2d mice to reject H-2b bone marrow grafts. The gene is therefore designated as Fv-3. Fv-3 may mediate its effect by regulating the numbers and/or functions of T-suppressor cells.
Dermoscopy of naevoid melanoma
Authors: R. Marchiori Bakos
Journal: British Journal of Dermatology (2015)

Journal Article Dermoscopy of naevoid melanoma Get access R. Marchiori Bakos R. Marchiori Bakos Department of Dermatology Hospital de Clínicas de Porto Alegre Universidade Federal do Rio Grande do Sul Porto Alegre Brazil Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 172, Issue 4, 1 April 2015, Pages 848–849, https://doi.org/10.1111/bjd.13656 Published: 01 April 2015
Monocyte chemotactic protein 3 is a most effective basophil- and eosinophil-activating chemokine.
Authors: C A Dahinden, T Geiser, T Brunner, V von Tscharner, D Caput, P Ferrara, A Minty, M Baggiolini
Journal: The Journal of Experimental Medicine (1994)

CC chemokines constitute a novel class of cytokines that attract and activate monocytes and lymphocytes, as well as basophil and eosinophil leukocytes, with distinct target cell profiles, and are believed to be involved in the regulation of different types of inflammation. The action of the recently identified monocyte chemotactic protein 3 (MCP-3) on human basophil and eosinophil function was studied and compared with that of other CC chemokines. In basophils, MCP-3, MCP-1, RANTES, and macrophage inflammatory protein (MIP)-1 alpha all induced cytosolic-free calcium concentration ([Ca2+]i) changes and, with different efficacies, chemotaxis (RANTES = MCP-3 >> MCP-1 > MIP-1 alpha), histamine release (MCP-1 = MCP-3 >> RANTES > MIP-1 alpha), and leukotriene C4 formation, after IL-3 pretreatment (MCP-1 = MCP-3 >> RANTES > MIP-1 alpha). Thus, MCP-3 was as effective as MCP-1 as an inducer of mediator release, and as effective as RANTES as a stimulus of basophil migration. In contrast to MCP-1, MCP-3 was also a stimulus for eosinophils, and induced [Ca2+]i changes and chemotaxis as effectively as RANTES, which is the most potent chemotactic cytokine for these cells. Desensitization of the transient changes in [Ca2+]i was used to assess receptor usage. In basophils, stimulation with MCP-3 prevented responsiveness to MCP-1 and RANTES, but not to MIP-1 alpha. No single CC chemokine (except for MCP-3 itself) affected the response to MCP-3, however, which was prevented only when the cells were prestimulated with both MCP-1 and RANTES. In eosinophils, by contrast, cross-desensitization between RANTES and MCP-3 was obtained. RANTES and to a lesser extent MCP-3 also desensitized eosinophils toward MIP-1 alpha. The desensitization data suggest the existence of three chemokine receptors: (a) a MCP-1 receptor expressed on basophils but not eosinophils that is activated by MCP-1 and MCP-3; (b) a RANTES receptor in basophils and eosinophils that is activated by RANTES and MCP-3; and (c) a MIP-1 alpha receptor that is activated by MIP-1 alpha, RANTES and, more weakly, by MCP-3. This study shows that MCP-3 combines the properties of RANTES, a powerful chemoattractant, and MCP-1, a highly effective stimulus of mediator release, and thus has a particularly broad range of activities toward both human basophil and eosinophil leukocytes.
Self-deception, social desirability, and psychopathology
Authors: Antonio Preti, Paola Miotto
Journal: Behavioral and Brain Sciences (2011)

Abstract Social desirability can be conceived as a proxy for self-deception, as it involves a positive attribution side and a denial side. People with mental disorders have lower scores on measures of social desirability, which could depend on cognitive load caused by symptoms. This suggests that self-deception is an active strategy and not merely a faulty cognitive process.
Statin-Dependent Suppression of the Akt/Mammalian Target of Rapamycin Signaling Cascade and Programmed Cell Death 4 Up-Regulation in Renal Cell Carcinoma
Authors: Jennifer Woodard, Antonella Sassano, Nissim Hay, Leonidas C. Platanias
Journal: Clinical Cancer Research (2008)

Abstract Purpose: Statins are pharmacologic inhibitors of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase with potent regulatory effects on cholesterol biosynthesis in vitro and in vivo. There is accumulating evidence that, beyond their cholesterol-lowering properties, statins inhibit cell proliferation and promote apoptosis of malignant cells in vitro, but the mechanisms by which they generate such responses remain to be defined. Experimental Design: Combinations of experimental approaches were used, including immunoblotting and cell proliferation and apoptosis assays. Results: We provide evidence that fluvastatin is a potent inducer of apoptosis and suppresses proliferation of renal cell carcinoma (RCC) cells in vitro. Such effects are mediated by direct targeting of the Akt/mammalian target of rapamycin (mTOR) pathway, as evidenced by the suppression of phosphorylation/activation of Akt, resulting in inhibition of its downstream effectors, mTOR and p70 S6 kinase. In addition, fluvastatin blocks the mTOR-dependent phosphorylation/deactivation of the translational repressor eukaryotic initiation factor 4E (eIF4E)-binding protein, leading to the formation of eIF4E-binding protein-eIF4E complexes that suppress initiation of cap-dependent mRNA translation. Importantly, inhibition of p70 S6 kinase activity by fluvastatin results in the up-regulation of expression of programmed cell death 4 (PDCD4), a tumor suppressor protein with inhibitory effects on the translation initiation factor eIF4A, suggesting a mechanism for the generation of antitumor responses. Conclusions: Altogether, our findings establish that fluvastatin exhibits potent anti-RCC activities via inhibitory effects on the Akt/mTOR pathway and raise the possibility that combinations of statins and Akt inhibitors may be of future therapeutic value in the treatment of RCC.
Activation of Thermogenesis in Brown Adipose Tissue and Dysregulated Lipid Metabolism Associated with Cancer Cachexia in Mice
Authors: Maria Tsoli, Melissa Moore, Dominic Burg, Arran Painter, Ryland Taylor, Sarah H. Lockie, Nigel Turner, Alessandra Warren, Greg Cooney, Brian Oldfield, Stephen Clarke, Graham Robertson
Journal: Cancer Research (2012)

Abstract Cancer cachexia/anorexia is a complex syndrome that involves profound metabolic imbalances and is directly implicated as a cause of death in at least 20% to 30% of all cancers. Brown adipose tissue (BAT) plays a key role in thermogenesis and energy balance and potentially contributes to the physiologic perturbations associated with cachexia. In this study, we investigated the impact of cachexia-inducing colorectal tumor on BAT in mice. We found that brown adipocytes were smaller and exhibited profound delipidation in cachectic tumor–bearing mice. Diurnal expression profiling of key regulators of lipid accumulation and fatty acid β-oxidation and their corresponding target genes revealed dramatic molecular changes indicative of active BAT. Increased Ucp1, Pbe, and Cpt1α expression at specific points coincided with higher BAT temperatures during the dark cycle, suggestive of a temporal stimulation of thermogenesis in cachexia. These changes persisted when cachectic mice were acclimatized to 28°C confirming inappropriate stimulation of BAT despite thermoneutrality. Evidence of inflammatory signaling also was observed in the BAT as an energetically wasteful and maladaptive response to anorexia during the development of cachexia. Cancer Res; 72(17); 4372–82. ©2012 AACR.
Reduction of arteriosclerotic nanoplaque formation and size by fluvastatin in a receptor-based biosensor model
Authors: G Siegel
Journal: Cardiovascular Research (2003)

Proteoheparan sulfate can be adsorbed onto a methylated silica surface in a monomolecular layer via its transmembrane hydrophobic protein core domain. Due to electrostatic repulsion, its anionic glycosaminoglycan side chains are stretched out into the blood substitute solution, thereby representing a receptor site for specific lipoprotein binding through basic amino acid-rich residues within their apolipoproteins. The binding process was studied by ellipsometric techniques suggesting that HDL has a high binding affinity and a protective effect on interfacial heparan sulfate proteoglycan layers with respect to LDL and Ca2+ complexation. LDL was found to be deposited strongly at the proteoheparan sulfate-coated surface, particularly in the presence of Ca2+, apparently through complex formation ‘proteoglycan–low density lipoprotein–calcium’. This ternary complex build-up may be interpreted as arteriosclerotic nanoplaque formation on the molecular level responsible for the arteriosclerotic primary lesion. In a receptor-based biosensor application, this system was tested on its reliability to unveil possible acute pleiotropic effects of the lipid lowering drug fluvastatin. The VLDL/IDL/LDL and VLDL/IDL/LDL/HDL plasma fractions from a high risk patient with dyslipoproteinaemia and type 2 diabetes mellitus showed the start of arteriosclerotic nanoplaque formation at a normal blood Ca2+ concentration, with a strong increase at higher Ca2+ concentrations. Nanoplaque formation and size of the HDL-containing lipid fraction remained well below that of the LDL-containing lipid fraction. Fluvastatin, whether applied acutely to the patient (one single 80 mg slow release matrix tablet) or in a 2-month medication regimen, markedly slowed down this process of ternary aggregational nanoplaque build-up and substantially inhibited nanoplaque size development at all Ca2+ concentrations used. The acute action gave no significant change in lipid concentrations of the patient. Furthermore, after nanoplaque generation, fluvastatin, similar to HDL, was able to reduce nanoplaque formation and size. These immediate effects of fluvastatin have to be taken into consideration when interpreting the clinical outcome of long-term studies.
No evidence for association of the KLF12 gene with rheumatoid arthritis in a large UK cohort
Authors: S. Eyre, E. Flynn, P. Martin, A. Hinks, A. G. Wilson, A. W. Morgan, P. Emery, S. Steer, L. J. Hocking, D. M. Reid, P. Harrison, P. Wordsworth, W. Thomson, J. Worthington, A. Barton
Journal: Annals of the Rheumatic Diseases (2009)

Genome-wide association studies (GWAS) have heralded a major breakthrough in the search for genes underlying rheumatoid arthritis (RA). Indeed, GWAS in UK, US and Swedish populations have identified a number of confirmed RA loci.1 Recently, a modestly-sized GWAS was undertaken in a Spanish population comprising 400 patients with RA and 400 controls.2 Association with the KLF12 gene was detected (p=6.5×10−6) and subsequently replicated in an independent cohort of 410 Spanish patients with RA and 394 controls (p=0.01). The most strongly associated single nucleotide polymorphism (SNP) was rs1324913 mapping to intron 1 of the KLF12 gene. The KLF12 protein is a repressor for a transcriptional regulatory factor, AP-2α, which has been implicated in the control of inflammation. Other SNPs at this locus also showed weak evidence for association with RA in UK …
Quantitative assays for hepatitis C virus in serum as predictors of the long-term response to interferon
Authors: Yasushi Shiratori, Naoya Kato, Osamu Yokosuka, Etsuko Hashimoto, Naoaki Hayashi, Akira Nakamura, Manabu Asada, Hisamoto Kuroda, Hitoshi Ohkubo, Yasuyuki Arakawa, Akisuke Iwama, Masao Omata
Journal: Journal of Hepatology (1997)
Conditional Deletion of <i>c-myc</i> Does Not Impair Liver Regeneration
Authors: Feng Li, Yan Xiang, James Potter, Ramani Dinavahi, Chi V. Dang, Linda A. Lee
Journal: Cancer Research (2006)

The oncogene c-myc encodes a transcription factor that has long been considered essential to liver regeneration, the process by which fully differentiated hepatocytes proliferate in an attempt to maintain a normal functional mass in response to hepatic injury. Experimental liver regeneration can be induced upon 70% partial hepatectomy and is accompanied by an increase in c-myc expression accompanying the synchronous entry of remaining hepatocytes into the cell cycle. Because liver regeneration is an essential process for achieving liver homeostasis, therapies directed at reducing MYC expression in hepatocellular carcinoma are fraught with the theoretical possibility of injuring adjacent noncancerous liver cells, thereby restricting the liver's normal regenerative response to injury. To determine if intact c-myc is required for liver regeneration, we reduced hepatic c-myc in c-myc(fl/fl) mice using an adenoviral vector that expresses Cre recombinase. Despite a 90% decrease in hepatic expression of c-myc, restoration of liver mass 7 days later was not compromised. Reconstituted liver retained the same decrease in hepatic c-myc, indicating that hepatocytes deficient in c-myc were able to proliferate in response to partial hepatectomy. Although c-myc is required for embryonic development, our findings indicate that it is not required for the maintenance of the adult liver.
Older Adults, “Malignant” Left Ventricular Hypertrophy, and Associated Cardiac-Specific Biomarker Phenotypes to Identify the Differential Risk of New-Onset Reduced Versus Preserved Ejection Fraction Heart Failure
Authors: Stephen L. Seliger, James de Lemos, Ian J. Neeland, Robert Christenson, John Gottdiener, Mark H. Drazner, Jarett Berry, John Sorkin, Christopher deFilippi
Journal: JACC Heart Failure (2015)
Brain Function in Problem Children and Controls: Psychometric, Neurological, and Electroencephalographic Comparisons
Authors: ABRAHAM WIKLER, JOAN F. DIXON, JOSEPH B. PARKER
Journal: American Journal of Psychiatry (1970)

Psychometric, neurological, and EEG studies were made of 24 children with scholastic-behavioral problems but no classical evidence of neurological disease and of 24 matched controls. Differences between the two groups were significant in all three measures, giving evidence of brain dysfunction in the groups with scholastic-behavioral problems. Two subgroups—hyperactive and nonhyperactive—each with characteristics suggesting a different syndrome, are described.
Palaeopathology of spinal osteophytosis, vertebral ankylosis, ankylosing spondylitis, and vertebral hyperostosis.
Authors: J Rogers, I Watt, P Dieppe
Journal: Annals of the Rheumatic Diseases (1985)

Five hundred and sixty intact skeletons and several thousand disarticulated vertebrae have been examined with special reference to spinal fusion. In period they ranged from a 21st dynasty Egyptian mummy to a mid-19th century skeleton. Osteophytes were found in about half of the specimens, as reported previously. Fifteen skeletons with extensive blocks of spinal fusion were also identified. Sacroiliitis was present in two, but the asymmetrical spinal disease and peripheral joint changes suggested Reiter9s disease or psoriatic spondylitis rather than ankylosing spondylitis. The remaining 13 had typical features of Forrestier9s disease, and extraspinal findings indicative of diffuse idiopathic skeletal hyperostosis (DISH) were also common. A review of the available literature suggests that many palaeopathological specimens previously reported as anklylosing spondylitis are examples of DISH or other seronegative spondylarthropathies. The antiquity and palaeopathology of AS needs reappraisal.
Fecal Occult Blood Screening in the Minnesota Study: Role of Chance Detection of Lesions
Authors: F. Ederer, T. R. Church, J. S. Mandel
Journal: JNCI Journal of the National Cancer Institute (1997)

In the Minnesota Colon Cancer Control Study, annual fecal occult blood testing reduced mortality from colorectal cancer by at least 33.4%. Some attribute a large part of this reduction to chance detection of cancers by colonoscopies; rehydration of guaiac test slides greatly increased positivity and consequently the number of colonoscopies performed. This study was conducted to determine how much of the reduction resulted from chance detection.We used a mathematical model developed by Lang and Ransohoff to estimate the proportion of the 33.4% mortality attainable by chance alone. Applying the model requires the specification of five parameters: duration of follow-up, rate of compliance with fecal occult blood testing, rate of compliance with colonoscopy, positivity rate, and efficacy of colonoscopy in reducing colorectal cancer mortality. We took values for four of the five parameters directly from the Minnesota study. For the fifth parameter, efficacy of colonoscopy, we selected a value of 60%, based on the conclusions of another study. Whereas the Lang-Ransohoff model selects persons for colonoscopy by chance alone, those with bleeding cancers would also be selected by sensitive fecal occult blood testing. We therefore adjusted the result of the Lang-Ransohoff model for this dual detectability.We found that 16%-25% of the reduction in colorectal cancer deaths effected by fecal occult blood testing in the Minnesota study was due to chance detection; the remainder was due to sensitive detection.Chance played a minor role in the detection of colorectal cancers by fecal occult blood testing in the Minnesota study.
The role of neutropenia on outcomes of cancer patients with community-acquired pneumonia
Authors: S. Aliberti, J. A. Myers, P. Peyrani, F. Blasi, R. Menendez, P. Rossi, R. Cosentini, G. Lopardo, L. de Vedia, J. A. Ramirez
Journal: European Respiratory Journal (2008)

Although the presence of neutropenia may predispose cancer patients to develop community-acquired pneumonia, the role of neutropenia on their outcomes has not been investigated. The purpose of the present study was to compare clinical outcomes of cancer community-acquired pneumonia patients with and without neutropenia. Patients with cancer, identified in the Community-Acquired Pneumonia Organization database, were divided into two groups according to the type of cancer and the presence of neutropenia: patients with solid cancer without neutropenia versus those with functional or absolute neutropenia. Among the 3,106 community-acquired pneumonia patients enrolled, 135 had cancer without neutropenia and 75 had cancer with neutropenia. No significant difference was found between patients with and without neutropenia regarding mean time to clinical stability (5.4±2.7 versus 4.9±2.7 days, respectively), mean length of hospital stay (9.2±7.7 versus 9.9±9.6 days) and in-hospital mortality (18 versus 15%, respectively). Using a multiple logistic regression model, neutropenia was not associated with mortality in cancer patients when adjusting for significant covariates (odds ratio 1.30). Lack of neutropenia, during the initial evaluation of a cancer community-acquired pneumonia patient, should not be considered an indicator of better clinical outcome.