tbuckley/cabot-search huggingface dataset:
Ambulatory blood pressure monitoring for hypertension in general practice
Authors: R S Taylor, J Stockman, D Kernick, D Reinhold, A C Shore, J E Tooke
Journal: Journal of the Royal Society of Medicine (1998)

Ambulatory blood pressure monitoring (ABPM) is being increasingly used in general practice. There is at present little published evidence regarding the clinical utility of ABPM in the care of patients with established hypertension in this setting. We examined this issue by undertaking ABPM in a group of patients with established hypertension. 40 patients (aged 33–60 years) currently being treated for hypertension were randomly selected from a general practice list and underwent a single 24-hour ABPM study. ABPM values were compared with clinic blood pressure (CBP) values obtained on the day of monitoring together with previous readings taken by the general practitioner (GP). In the case of mean arterial pressure, 24-hour, awake and asleep ABPM values were found to underestimate CBP values by 14 mmHg (95% confidence interval 11–16 mmHg), 9 mmHg (95% Cl 6–12 mmHg) and 24 mmHg (95% Cl 21–27 mmHg), respectively. When used to classify blood pressure control, ABPM values produced equivalent results to CBP except by the criterion of BP load, for which 24-hour ABPM showed a higher rate of unsatisfactory control. 5 patients classified by CBP to have satisfactory BP control according to current international guidelines were found to have unsatisfactory BP control by ABPM. This study demonstrates the potential value of ABPM in patients with essential hypertension in a general practice setting. ABPM provided information over and above that obtained by CBP in a substantial proportion of patients.
Primary hepatocellular carcinoma and hepatitis B infection during childhood
Authors: Tzee Chung Wu, Myron J. Tong, Betau Hwang, Shou-Dong Lee, Mu Mei Hu
Journal: Hepatology (1987)

Twenty pediatric patients with primary hepatocellular carcinoma in Taiwan were tested for HBsAg, and all were found to be positive. The youngest case was 8 months of age, five cases occurred between 9 and 10 years of age, and 14 cases occurred between 11 and 16 years of age. The serum alpha-fetoprotein was elevated in all 20 primary hepatocellular carcinoma patients, and the average survival of these cases after diagnosis was 4.7 months. Seventy per cent of the mothers of the pediatric primary hepatocellular carcinoma cases and 52.9% of their siblings who were tested also were positive for HBsAg. In addition, two families had clustering of primary hepatocellular carcinoma cases. The occurrence of primary hepatoceullar carcinoma in the pediatric age group suggests the need for close follow-up of young HBsAg-positive carriers. Also, prevention of perinatal transmission of hepatitis B virus by immunoprophylaxis will significantly decrease both the hepatitis B virus carrier rate and the incidence of primary hepatocellular carcinoma in the asian population.
The Influence of Innate and Adaptive Immune Responses on Atherosclerosis
Authors: Joseph L. Witztum, Andrew H. Lichtman
Journal: Annual Review of Pathology Mechanisms of Disease (2013)

Both the chronic development of atherosclerotic lesions and the acute changes in lesion phenotype that lead to clinical cardiovascular events are significantly influenced by the innate and adaptive immune responses to lipoprotein deposition and oxidation in the arterial wall. The rapid pace of discovery of mechanisms of immunologic recognition, effector functions, and regulation has significantly influenced the study of atherosclerosis, and our new knowledge is beginning to affect how we treat this ubiquitous disease. In this review, we discuss recent advances in our understanding of how innate and adaptive immunity contribute to atherosclerosis, as well as therapeutic opportunities that arise from this knowledge.
Sudden cardiac death: role of heart rate variability to identify patients at risk
Authors: Federico Lombardi, Timo H. Mäkikallio, Robert J. Myerburg, Heikki V. Huikuri
Journal: Cardiovascular Research (2001)

Time for primary review: 31 days. 

Sudden, unexpected cardiac death stands as one of the most important and unresolved problems in clinical cardiology also in the new millennium. Despite unanticipated advancement in the understanding of the mechanisms that concur to determine such a dramatic event [1], our capability of identifying patients at risk has not reached satisfactory levels. In most instances, our attention is focused on selected small subgroups of patients at highest risk while ignoring the majority of subjects in whom sudden cardiac death is the first and last manifestation of a cardiac disease [2].

In the last 20 years, the appraisal [3] of the pro-arrhythmic role exerted by transient or persistent alterations in sympathetic and vagal control mechanisms has stimulated the development of techniques capable of providing information on autonomic modulation and of its alteration in different clinical conditions such as ischemic heart disease, hypertension and congestive heart failure [4,5]. Among these methodologies, analysis of heart rate (HR) variability and of baroreflex sensitivity are the two that have provided the most interesting results in terms of feasibility, clinical results and predictive value [6,7].

The aim of the present article is to specifically address the value of HR variability analyses, not only for identifying patients at risk but also for describing changes in autonomic control mechanisms immediately prior to onset of malignant ventricular arrhythmias. A brief description of available methodologies, limitations of the study designs and of future directions in HR variability utilisation is also included.

There are numerous methods to describe regulation of HR and constant fluctuation of R—R intervals. An optimal method for clinical work would be an index that could be easily computed with a simple and widely available analysis method. Despite the efforts of the Task Force of the North American … 

* Corresponding author. Tel.: +358-8-315-4108; fax: 358-8-315-5599 heikki.huikuri{at}oulu.fi
Neoadjuvant cetuximab, twice-weekly gemcitabine, and intensity-modulated radiotherapy (IMRT) in patients with pancreatic adenocarcinoma
Authors: J.M. Pipas, B.I. Zaki, M.M. McGowan, M.J. Tsapakos, G.H. Ripple, A.A. Suriawinata, G.J. Tsongalis, T.A. Colacchio, S.R. Gordon, J.E. Sutton, A. Srivastava, K.D. Smith, T.B. Gardner, M. Korc, T.H. Davis, M. Preis, S.M. Tarczewski, T.A. MacKenzie, R.J. Barth
Journal: Annals of Oncology (2012)
Following the TRAIL from hepatitis C virus and alcohol to fatty liver
Authors: S C Afford
Journal: Gut (2005)

Tumour necrosis factor related apoptosis inducing ligand or TRAIL, is a novel mediator of fatty liver disease which may provide a mechanism to explain the development of steatosis in hepatitis C virus infection and in response to alcohol

Fatty liver or steatosis is a common finding in several liver diseases, most notably non-alcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD) but is also seen more frequently in chronic hepatitis C virus (HCV) related liver disease than would be predicted by simple concurrence of the two diseases.1 Several mechanisms have been proposed to explain why steatosis might develop in chronic viral infection, including direct effects of the virus on lipid metabolism, but none of these is entirely convincing. Furthermore, steatosis is not a benign lesion but one that contributes to the progression of fibrosis, not only in NAFLD and ALD but also in HCV, in part by increasing the sensitivity of the liver to oxidative stress and cytokine mediated injury.2 The paper by Mundt and colleagues3 in this issue of Gut provides novel mechanistic insights into why steatosis develops in HCV and how it might accentuate liver injury (see page 1590) . They have concentrated their efforts on a member of the tumour necrosis factor (TNF) superfamily called TRAIL or TNF related apoptosis inducing ligand. TRAIL is known to induce apoptosis in transformed cells and this group have previously shown TRAIL, acting through one of its receptors called TRAIL-DR5 or TRAIL-2, mediates hepatocyte apoptosis in viral hepatitis. What they now show is that this receptor-ligand pair can also mediate hepatic steatosis in both viral hepatitis and in response to alcohol.

The authors start with the observation that expression of TRAIL is increased in the livers of patients with HCV associated steatosis and they then proceed …
The fibrocyte in pulmonary hypertension: we seek him here, we seek him there
Authors: M.R. Toshner, N.W. Morrell
Journal: European Respiratory Journal (2011)

The fibrocyte is one of many populations of bone marrow-derived cells that can be detected in the peripheral blood and is considered to represent a mesenchymal progenitor cell [1]. The fibrocyte, as we currently understand this term, was originally described by Bucala et al. [2] in 1994 and is defined by the expression of a variety of cell surface antigens, including the stem cell marker CD34, the pan-leukocyte marker CD45, and monocyte markers CD14 and CD11. The fibroblast-like nature of these cells is evidenced by their expression of collagen I, collagen II and vimentin. In normal individuals, these cells comprise <0.5% of circulating leukocytes [3]. In animal models employing surgically implanted wound chambers, it can be shown that ∼16% of cells that accumulate over a number of days are putative blood-derived fibrocytes [4]. Similarly, CD34+ cells can be identified in human scar tissue, suggesting that these cells may contribute to tissue remodelling and repair [5]. Importantly, fibrocytes can be isolated and grown in culture [2]. Since these early observations, fibrocytes have been implicated in the tissue remodelling that occurs in a variety of human diseases, including idiopathic pulmonary fibrosis, asthma, pulmonary hypertension, atherosclerosis and renal fibrosis [6]. Their potential role in the pathobiology of these diseases extends beyond the accumulation of fibroblasts in scar tissue and is now thought to include regulation of fibrogenesis by the secretion of cytokines and growth factors, the production of extracellular matrix and secretion of matrix metalloproteinases [7]. In addition, they act as antigen presenting cells and promote angiogenesis …
Exacerbation of atopic dermatitis on grass pollen exposure in an environmental challenge chamber
Authors: Thomas Werfel, Annice Heratizadeh, Margarete Niebuhr, Alexander Kapp, Lennart Matthias Roesner, Annika Karch, Veit J. Erpenbeck, Christian Lösche, Thomas Jung, Norbert Krug, Philipp Badorrek, Jens M. Hohlfeld
Journal: Journal of Allergy and Clinical Immunology (2015)
JunD attenuates phenylephrine-mediated cardiomyocyte hypertrophy by negatively regulating AP-1 transcriptional activity
Authors: D HILFIKERKLEINER, A HILFIKER, M CASTELLAZZI, K WOLLERT, C TRAUTWEIN, H SCHUNKERT, H DREXLER
Journal: Cardiovascular Research (2006)

Objective Mice deficient for the AP-1 transcription factor JunD, the only Jun protein constitutively expressed and clearly detectable in the mammalian heart, develop enhanced cardiac hypertrophy in response to chronic pressure overload. Catecholamines inducing α-adrenergic receptor-mediated signaling have been implicated in the neurohumoral response to pressure overload and the development of left ventricular hypertrophy. In the present study we analyzed the mechanistic role of JunD in cardiomyocyte hypertrophy in vitro in response to α-adrenergic agonist phenylephrine (PE).
A Comparison of the Metabolism of Radioactive 17-Isoaldosterone and Aldosterone Administered Intravenously and Orally to Normal Human Subjects*
Authors: C. Flood, G. Pincus, J. F. Tait, S. A. S. Tait, S. Willoughby
Journal: Journal of Clinical Investigation (1967)

After intravenous and oral administration of radioactive aldosterone to normal subjects, 7.3 +/- 0.4 (SE) and 5.4 +/- 0.5 (SE)%, respectively, of the dose was recovered from a 48-hour collection of urine as aldosterone released by mild acid hydrolysis (from aldosterone 18-glucuronide), and 35 +/- 5 (SE) and 39 +/- 4 (SE)%, respectively, was recovered as tetrahydroaldosterone after incubation with beta-glucuronidase.After intravenous and oral administration of 17-isoaldosterone-4-(14)C to a similar group of subjects, 35 +/- 3 (SE) and 53 +/- 4 (SE)%, respectively, of the dose was recovered as 17-isoaldosterone released by acid and less than 5% as total metabolites after incubation with beta-glucuronidase. No detectable radioactivity (< 0.5%) could be recovered as tetrahydroaldosterone or as a compound with the expected chromatographic properties of tetrahydro-17-isoaldosterone. The total radioactivity in the neutral extracts was also relatively small (< 2%) after administration of either labeled aldosterone or 17-isoaldosterone. The radioactivity as aldosterone in the neutral extract was much lower after oral [0.017 +/- 0.003 (SE)%] than after intravenous [0.21 +/- 0.04 (SE)%] administration of labeled aldosterone. The radioactivity as 17-isoaldosterone in the neutral extract was similar after intravenous [0.20 +/- 0.02 (SE)%] and after oral [0.38 +/- 0.18 (SE)%] administration of 17-isoaldosterone. These results indicated that, due to lack of A-ring reduction of the molecule and the consequent slowing of hepatic clearance, 17-isoaldosterone is converted to an acid-labile conjugate (presumably 17-isoaldosterone 18-glucuronide) as the major metabolite. 17-Isoaldosterone was not secreted or converted to aldosterone to any significant extent in the normal subjects investigated.
Models of liver fibrosis: exploring the dynamic nature of inflammation and repair in a solid organ
Authors: John P. Iredale
Journal: Journal of Clinical Investigation (2007)

Models of liver fibrosis, which include cell culture models, explanted and biopsied human material, and experimental animal models, have demonstrated that liver fibrosis is a highly dynamic example of solid organ wound healing. Recent work in human and animal models has shown that liver fibrosis is potentially reversible and, in specific circumstances, demonstrates resolution with a restoration of near normal architecture. This Review highlights the manner in which studies of models of liver fibrosis have contributed to the paradigm of dynamic wound healing in this solid organ.
IL-1β-induced activation of p38 promotes metastasis in gastric adenocarcinoma via upregulation of AP-1/c-fos, MMP2 and MMP9
Authors: Qiaojia Huang, Fenghua Lan, Xiaoting Wang, Yinghao Yu, Xuenong Ouyang, Feng Zheng, Junyong Han, Youdong Lin, Yanchuan Xie, Feilai Xie, Wei Liu, Xiaoli Yang, Han Wang, Lihong Dong, Lie Wang, Jianming Tan
Journal: Molecular Cancer (2014)

Interleukin-1β (IL-1β) has been implicated in the progression of gastric adenocarcinoma (GA); however, the molecular mechanisms of action of IL-1β in GA are poorly characterized. P38 and JNK are the major MAPK family members that regulate IL-1β signaling pathways. Here, we investigated the role of both p38 and JNK in IL-1β-induced GA cell migration, invasion and metastatic potential. The effects of IL-1β-induced p38 and JNK activation in GA cells were determined using in vitro Transwell migration and invasion assays of MKN-45 and AGS cells, or an in vivo metastasis assay in nude mice. The IL-1β-induced p38 signaling pathway was further characterized in GA cells. Activation of the IL-1β/p38 signaling pathway was also assessed in human primary GA tissues by immunohistochemistry. IL-1β-induced activation of p38 increased GA cell migration and invasion in vitro and promoted the metastatic potential of GA cells in vivo; these effects were attenuated by p38 siRNA or the p38 inhibitor SB202190. MMP2 or MMP9 siRNAs and the MMP2/9 inhibitor BiPS also inhibited IL-1β-induced GA cell migration and invasion in vitro. IL-1β-induced p38 activation significantly increased MMP2 and MMP9 mRNA and protein expression and activity. Luciferase reporter assays demonstrated that the activator protein-1 (AP-1) and the AP-1 binding sites of the MMP9 promoter (−670/MMP9) were activated by IL-1β-induced p38 activation. Phospho-p38 was significantly upregulated in human GA tissues (compared to matched non-neoplastic tissues), and significantly associated with lymph node metastasis, and invasion beyond the serosa. Expression of phospho-p38 significantly correlated with IL-1β, MMP2, MMP9, and c-fos expression in both human GA tissues and GA cell metastases in the lungs of nude mice. IL-1β was also capable of activating JNK in GA cells, but activation of JNK was not associated with GA cell migration and invasion. Therefore, IL-1β-induced the migration and invasion in GA cells were regulated by p38, but not by JNK. IL-1β-induced p38 activation and the IL-1β/p38/AP-1(c-fos)/MMP2 & MMP9 pathway play an important role in metastasis in GA; this pathway may provide a novel therapeutic target for GA.
The Clinical Significance of Biological Characteristics of the Cells in Acute Myeloid Leukemia
Authors: M R Baer, C D Bloomfield
Journal: Annual Review of Medicine (1991)

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of coronavirus disease 2019 (COVID-19), emerged in China in December 2019 and quickly spread around the globe, killing more than 4 million people and causing a severe economic crisis. ...Read More
American College of Cardiology/Society for Cardiac Angiography and Interventions Clinical Expert Consensus Document on Cardiac Catheterization Laboratory Standards41When citing this document, the American College of Cardiology and the Society for Cardiac Angiography and Interventions would appreciate the following citation format: Bashore TM, Bates ER, Berger PB, Clark DA, Cusma JT, Dehmer GJ, Kern MJ, Laskey WK, O’Laughlin MP, Oesterle S, Popma JJ. Cardiac catheterization laboratory standards…
Authors: Thomas M Bashore, Eric R Bates, Peter B Berger, David A Clark, Jack T Cusma, Gregory J Dehmer, Morton J Kern, Warren K Laskey, Martin P O’Laughlin, Stephen Oesterle, Jeffrey J Popma, Robert A O’Rourke, Jonathan Abrams, Eric R Bates, Bruce R Brodie, Pamela S Douglas, Gabriel Gregoratos, Mark A Hlatky, Judith S Hochman, Sanjiv Kaul, Cynthia M Tracy, David D Waters, William L Winters
Journal: Journal of the American College of Cardiology (2001)
Protective effect of different doses of terfenadine on the conjunctival provocation test
Authors: G. Ciprandi, S. Buscagiia, A. Iudice, G. W. Canonica
Journal: Allergy (1992)

The protective effect of terfenadine on inOammatory processes following the early phase of conjunctival provocation tests by specific allergen was assessed in 24 patients suffering from seasonal allergic rhinoconjunctivitis, in a single‐blind, randomized, placebo‐controlled, parallel‐group study. Patients were randomly assigned to four treatment groups, each being given terfenadine 60, 120, 180 mg daily, or placebo, respectively, for 7 days, out of the pollen season. Clinical severity (burning, itching, lacrimation and hyperemia), and number of inflammatory cells obtained by conjunctival scraping (neutrophils, eosinophils, lymphocytes, and monocytes) were evaluated before and after treatment. Pre‐treatment with terfenadine resulted in a significantly higher allergen threshold dose than placebo (p&lt;0.01), regardless of drug dose. Patients given terfenadine experienced a significant reduction (p&lt;0.03) in conjunctival symptom severity, as compared with placebo, following conjunctival challenge. Accordingly, the number of inflammatory cells in terfenadine‐treated patients was significantly lower (p&lt;0.01) than in the placebo‐treated after the conjunctival provocation test. The results of this study suggest that terfenadine has a significant protective effect on the early‐phase cellular and clinical events of conjunctival reaction induced by allergen challenge in atopic patients.
Estrogen Signaling in Livers of Male Mice With Hepatocellular Carcinoma Induced by Exposure to Arsenic In Utero
Authors: M. P. Waalkes, J. Liu, H. Chen, Y. Xie, W. E. Achanzar, Y.-S. Zhou, M.-L. Cheng, B. A. Diwan
Journal: JNCI Journal of the National Cancer Institute (2004)

Exposure of pregnant mice to inorganic arsenic induces a spectrum of tumors, including hepatocellular carcinoma (HCC), in their adult offspring similar to that induced by exposing adult mice to estrogenic compounds. To investigate whether arsenic exposure in utero causes altered estrogen signaling, we examined expression of estrogen receptor-alpha (ER-alpha), cyclin D1 (an estrogen-responsive hepatic oncogene), and several cytochrome P450 genes (with sexually dimorphic liver expression patterns) in livers from adult male mice with in utero arsenic-induced HCC.Quantitative real-time reverse transcription-polymerase chain reaction was used to evaluate gene expression in livers of adult male mice that had (i.e., exposed mice; n = 8) or had not (i.e., control mice; n = 5) been exposed to arsenic in utero. DNA methylation status of portions of the ER-alpha and cyclin D1 gene promoters in liver tissue was measured using methylation-specific polymerase chain reaction. Statistical tests were two-sided.ER-alpha mRNA levels were 3.1-fold (95% confidence interval [CI] = 2.0-fold to 4.3-fold) higher in livers of exposed mice than in those of control mice, and cyclin D1 levels were 3.0-fold (95% CI = 1.7-fold to 4.3-fold) higher. Exposed mice showed a feminized expression pattern of several cytochrome P450 genes, expressing the female-dominant CYP2A4 (P =.017 versus control) and CYP2B9 (P<.001) genes at 8.7 and 10.5 times, respectively, the level in control mice and expressing the male-dominant CYP7B1 at approximately one-fourth the level in control mice(P =.0012). Exposed mice exhibited reduced (by approximately 90%) methylation of the ER-alpha gene promoter in liver DNA as compared with control mice; the cyclin D1 gene promoter was not methylated in either exposed or control mice.Altered estrogen signaling may play a role in induction of HCC by arsenic exposure in utero. Specifically, overexpression of ER-alpha, potentially through promoter region hypomethylation, in livers of such mice may be linked to the hepatocarcinogenicity of arsenic.
Support for multiple classes of local expression clusters in Drosophila melanogaster, but no evidence for gene order conservation
Authors: Claudia C Weber, Laurence D Hurst
Journal: Genome biology (2011)

Abstract Background Gene order in eukaryotic genomes is not random, with genes with similar expression profiles tending to cluster. In yeasts, the model taxon for gene order analysis, such syntenic clusters of non-homologous genes tend to be conserved over evolutionary time. Whether similar clusters show gene order conservation in other lineages is, however, undecided. Here, we examine this issue in Drosophila melanogaster using high-resolution chromosome rearrangement data. Results We show that D. melanogaster has at least three classes of expression clusters: first, as observed in mammals, large clusters of functionally unrelated housekeeping genes; second, small clusters of functionally related highly co-expressed genes; and finally, as previously defined by Spellman and Rubin, larger domains of co-expressed but functionally unrelated genes. The latter are, however, not independent of the small co-expression clusters and likely reflect a methodological artifact. While the small co-expression and housekeeping/essential gene clusters resemble those observed in yeast, in contrast to yeast, we see no evidence that any of the three cluster types are preserved as synteny blocks. If anything, adjacent co-expressed genes are more likely to become rearranged than expected. Again in contrast to yeast, in D. melanogaster , gene pairs with short intergene distance or in divergent orientations tend to have higher rearrangement rates. These findings are consistent with co-expression being partly due to shared chromatin environment. Conclusions We conclude that, while similar in terms of cluster types, gene order evolution has strikingly different patterns in yeasts and in D. melanogaster , although recombination is associated with gene order rearrangement in both.