tbuckley/cabot-search huggingface dataset:
Effect of 12 weeks of moderate–intensity resistance training on arterial stiffness: a randomised controlled trial in women aged 32–59 years
Authors: M Yoshizawa, S Maeda, A Miyaki, M Misono, Y Saito, K Tanabe, S Kuno, R Ajisaka
Journal: British Journal of Sports Medicine (2008)

Background: Resistance training has been increasingly incorporated into the overall exercise programme because of its effect on muscle strength, functional capacity and osteoporosis. High-intensity resistance training increases arterial stiffness. However, the effect of moderate-intensity resistance training on arterial stiffness is unknown. Objective: To determine whether 12 weeks of moderate-intensity resistance training increases arterial stiffness in middle-aged women. Methods: 35 middle-aged women (age range 32 to 59 years) volunteered to participate. The subjects were randomly assigned to one of three groups: resistance training (RT) group, aerobic exercise training (AET) group or control group. The RT and AET groups performed 12 weeks of moderate-intensity resistance training or aerobic exercise training (two days/week). Results: In the RT group, one-repetition maximum strength significantly increased after the intervention. Interestingly, aortic (carotid–femoral) pulse wave velocity (PWV; an index of arterial stiffness), and peripheral (femoral–ankle) PWV did not change with moderate-intensity resistance training. In contrast, in the AET group, carotid–femoral PWV significantly decreased after the intervention. Resistance training and aerobic exercise training did not affect blood pressure. Conclusions: This study found that moderate-intensity resistance training did not increase arterial stiffness in middle-aged women, which may have great importance for health promotion with resistance training.
Circulating glucose levels modulate neural control of desire for high-calorie foods in humans
Authors: Kathleen A. Page, Dongju Seo, Renata Belfort-DeAguiar, Cheryl Lacadie, James Dzuira, Sarita Naik, Suma Amarnath, R. Todd Constable, Robert S. Sherwin, Rajita Sinha
Journal: Journal of Clinical Investigation (2011)

Obesity is a worldwide epidemic resulting in part from the ubiquity of high-calorie foods and food images. Whether obese and nonobese individuals regulate their desire to consume high-calorie foods differently is not clear. We set out to investigate the hypothesis that circulating levels of glucose, the primary fuel source for the brain, influence brain regions that regulate the motivation to consume high-calorie foods. Using functional MRI (fMRI) combined with a stepped hyperinsulinemic euglycemic-hypoglycemic clamp and behavioral measures of interest in food, we have shown here that mild hypoglycemia preferentially activates limbic-striatal brain regions in response to food cues to produce a greater desire for high-calorie foods. In contrast, euglycemia preferentially activated the medial prefrontal cortex and resulted in less interest in food stimuli. Indeed, higher circulating glucose levels predicted greater medial prefrontal cortex activation, and this response was absent in obese subjects. These findings demonstrate that circulating glucose modulates neural stimulatory and inhibitory control over food motivation and suggest that this glucose-linked restraining influence is lost in obesity. Strategies that temper postprandial reductions in glucose levels might reduce the risk of overeating, particularly in environments inundated with visual cues of high-calorie foods.
Flavopiridol Targets c-KIT Transcription and Induces Apoptosis in Gastrointestinal Stromal Tumor Cells
Authors: Elliot B. Sambol, Grazia Ambrosini, Rula C. Geha, Peter T. Kennealey, Penelope DeCarolis, Rachael O'Connor, Yuhsin V. Wu, Monica Motwani, Jin-Hong Chen, Gary K. Schwartz, Samuel Singer
Journal: Cancer Research (2006)

Abstract Gastrointestinal stromal tumors (GIST) are characterized by activating mutations in the c-KIT gene which confers ligand-independent activation of the KIT receptor. Imatinib mesylate has been shown to effectively block constitutively active KIT and delay tumor growth. However, resistance to imatinib mesylate is emerging as a major clinical problem and novel therapies are needed. We report that treatment of GIST cells with the transcriptional inhibitor flavopiridol, initially down-regulates the antiapoptotic proteins bcl-2, mcl-1, and X-linked inhibitor of apoptosis protein which occurs as early as 4 hours after exposure. This is followed at 24 hours by the transcriptional suppression of KIT resulting in poly(ADP-ribose) polymerase cleavage and apoptosis. To separate the apoptotic effect of KIT suppression relative to the down-regulation of antiapoptotic proteins, we used small interfering RNA–directed knockdown of KIT. Results show that focused suppression of KIT alone is sufficient to induce apoptosis in GIST cells, but not to the same extent as flavopiridol. In contrast, imatinib mesylate, which inhibits KIT kinase activity but does not suppress total KIT expression, fails to cause apoptosis. We also show that flavopiridol suppresses KIT mRNA expression through positive transcriptional elongation factor inhibition and decreases KIT promoter activity. This causes a global decrease in the level of functionally mature KIT at the cell surface, resulting in a decrease in autophosphorylation at tyrosine residues 703 and 721, which characterizes activated KIT. Our results indicate that targeting KIT expression and these antiapoptotic proteins with flavopiridol represents a novel means to disrupt GIST cell dependence on KIT signaling and collectively renders these cells sensitive to apoptosis. (Cancer Res 2006; 66(11): 5858-66)
Social Marketing: Its Place in Public Health
Authors: Jack C. Ling, Barbara A.K. Franklin, Janis F. Lindsteadt, Susan A.N. Gearon
Journal: Annual Review of Public Health (1992)

In recent decades, public health policy and practice have been increasingly challenged by globalization, even as global financing for health has increased dramatically. This article discusses globalization and its health challenges from a vantage of ...Read More
Abnormal heart rate variability in patients with sarcoidosis
Authors: Elias Giallafos, Vasilios Kouranos, Anastasios Kalianos, Georgios Kaltsakas, Ilias Peros, David Tsoukas, George Dionelis, Charalampos Kostopoulos, Eleutherios Stamboulis, Nikos Koulouris, Aggeliki Rapti
Journal: European Respiratory Journal (2012)

Background: Heart Rate Variability (HRV) can predict cardiovascular events, especially sudden cardiac death and ventricular arrhythmias. Aim of this study was the evaluation of HRV indices in sarcoidosis (Sarc).  Methods: 180 biopsy proven Sarc patients who were not taking antiarrhythmic drugs were included in this study. They were compared with 72 sex and age matched healthy subjects. All participants had pulmonary function tests, cardiac ultrasound, 24-hour Holter monitoring and cardiac MRI and were classified to group A (healthy), group B (cardiac-free Sarc) or group C (cardiac Sarc). The average heart rate (mean HR), the maximum and minimum heart rate (maxHR and minHR), the root mean square of SD of RR (RMSSD) and the standard deviation of all normal to normal NN intervals (SDRR) were calculated during 24-hour Holter monitoring.  Results:  In bivariate analysis, SDRR is correlated with age (p=0.001, r=-.397), FVC(p=0.001, r=.242), FEV1(p=0.001, r=.261), TLC(p=0.001, r=.290) and DLCO (p=0.0001, r=.264).  Conclusion: HRV is decreased in patients with systemic sarcoidosis compared to the control group. SDRR is significantly decreased in patients with cardiac sarcoidosis and is correlated with lung function indices.
A patient with pancreatitis, anaemia and an intrathoracic tumour
Authors: D. Kügler, D. Jäger, J. Barth
Journal: European Respiratory Journal (2006)

<h3>Abstract</h3> A label-free procedure to identify single amino acids (AAs) for protein sequencing is developed in theory and simulated in part. A terminal AA cleaved from a protein/peptide, a tRNA, its cognate amino-acyl tRNA synthetase (AARS), and adenosine triphosphate (ATP) are brought together in a container where tRNA, if cognate, gets charged with AA and adenosine monophosphate (AMP) is released. The released AMP (and any free AA and ATP molecules) filters into the <i>cis</i> chamber of an adjoining electrolytic cell (e-cell) from where they pass through a nanopore into the <i>trans</i> chamber. Addition of NaOH to the container deacylates the tRNA if it is charged. The resulting free AA passes into the <i>cis</i> chamber of the e-cell, translocates into <i>trans</i>, and causes a current blockade; AA is immediately known from the identity of the tRNA (the two are cognate). If the tRNA is not charged there is no AA bound to it so AA remains unidentified. In this approach there is no need to distinguish among the 20 AAs by blockade size; it suffices to distinguish blockades from noise: thus a high-precision analog measurement has been transformed into a low-precision binary one. Identification is accurate because of tRNA superspecificity (the tRNA charging error rate is &lt; 1/350); parallel execution with 20 different tRNAs can identify AA in one cycle. This is a <i>de novo</i> method in which no prior information about the protein is used or needed.
The chemokine CCL18 characterises<i>Pseudomonas</i>infections in cystic fibrosis lung disease
Authors: Andreas Hector, Carolin Kröner, Melanie Carevic, Martina Bakele, Nikolaus Rieber, Joachim Riethmüller, Matthias Griese, Gernot Zissel, Dominik Hartl
Journal: European Respiratory Journal (2014)

Cystic fibrosis (CF) lung disease is characterised by chronic Pseudomonas aeruginosa infection and leukocyte infiltration. Chemokines recruit leukocytes to sites of infection. Gene expression analysis identified the chemokine CCL18 as upregulated in CF leukocytes. We hypothesised that CCL18 characterises infection and inflammation in patients with CF lung disease. Therefore, we quantified CCL18 protein levels in the serum and airway fluids of CF patients and healthy controls, and studied CCL18 protein production by airway cells ex vivo . These studies demonstrated that CCL18 levels were increased in the serum and airway fluids from CF patients compared with healthy controls. Within CF patients, CCL18 levels were increased in P. aeruginosa -infected CF patients. CCL18 levels in the airways, but not in serum, correlated with severity of pulmonary obstruction in CF. Airway cells isolated from P. aeruginosa -infected CF patients produced significantly higher amounts of CCL18 protein compared with airway cells from CF patients without P. aeruginosa infection or healthy controls. Collectively, these studies show that CCL18 levels characterise chronic P. aeruginosa infection and pulmonary obstruction in patients with CF. CCL18 may, thus, serve as a potential biomarker and therapeutic target in CF lung disease.
Label-retaining liver cancer cells are relatively resistant to sorafenib
Authors: Hong-Wu Xin, Chenwi M Ambe, Danielle M Hari, Gordon W Wiegand, Tyler C Miller, Jin-Qiu Chen, Andrew J Anderson, Satyajit Ray, John E Mullinax, Tomotake Koizumi, Russell C Langan, Douglas Burka, Michelle A Herrmann, Paul K Goldsmith, Alexander Stojadinovic, Udo Rudloff, Snorri S Thorgeirsson, Itzhak Avital
Journal: Gut (2013)

<h3>Objective</h3> The standard therapy for advanced hepatocellular carcinoma (HCC) is sorafenib, with most patients experiencing disease progression within 6 months. Label-retaining cancer cells (LRCC) represent a novel subpopulation of cancer stem cells (CSC). The objective was to test whether LRCC are resistant to sorafenib. <h3>Methods</h3> We tested human HCC derived LRCC and non-LRCC before and after treatment with sorafenib. <h3>Results</h3> LRCC derived from human HCC are relatively resistant to sorafenib. The proportion of LRCC in HCC cell lines is increased after sorafenib while the general population of cancer cells undergoes growth suppression. We show that LRCC demonstrate improved viability and toxicity profiles, and reduced apoptosis, over non-LRCC. We show that after treatment with sorafenib, LRCC upregulate the CSC marker aldehyde dehydrogenase 1 family, wingless-type MMTV-integration-site family, cell survival and proliferation genes, and downregulate apoptosis, cell cycle arrest, cell adhesion and stem cells differentiation genes. This phenomenon was accompanied by non-uniform activation of specific isoforms of the sorafenib target proteins extracellular-signal-regulated kinases and v-akt-murine-thymoma-viral-oncogene homologue (AKT) in LRCC but not in non-LRCC. A molecular pathway map for sorafenib treated LRCC is proposed. <h3>Conclusions</h3> Our results suggest that HCC derived LRCC are relatively resistant to sorafenib. Since LRCC can generate tumours with as few as 10 cells, our data suggest a potential role for these cells in disease recurrence. Further investigation of this phenomenon might provide novel insights into cancer biology, cancer recurrence and drug resistance with important implications for the development of novel cancer therapies based on targeting LRCC.
Prevention of Tunneled Hemodialysis Catheter-Related Infections Using Catheter-Restricted Filling with Gentamicin and Citrate
Authors: Gursharan K Dogra, Helen Herson, Brian Hutchison, Ashley B Irish, Christopher H Heath, Clay Golledge, Grant Luxton, Harry Moody
Journal: Journal of the American Society of Nephrology (2002)

In the west of Scotland use of a single intragenic restriction fragment length polymorphism (F9(VIII)/TaqI) allowed definitive genetic counselling for 45% of females at risk of being carriers for haemophilia B. Two further intragenic RFLPs, F9(VIII)/XmnI) and F9(VIII)/DdeI, have been applied to this population and by using all three polymorphisms the carrier status could be determined in 68% of females at risk. Linkage disequilibrium was apparent between these three RFLPs, and in the west of Scotland the single most clinically useful polymorphism was F9(VIII)/TaqI followed by F9(VIII)/DdeI and then F9(VIII)/XmnI. Overall, prenatal diagnosis by DNA analysis could be offered to 31 of 37 (84%) carriers (obligate and detected) in these families.
Regulatory, Effector, and Cytotoxic T Cell Profiles in Long-Term Kidney Transplant Patients
Authors: Joanna Ashton-Chess, Emilie Dugast, Robert B. Colvin, Magali Giral, Yohann Foucher, Anne Moreau, Karine Renaudin, Christophe Braud, Anne Devys, Sophie Brouard, Jean-Paul Soulillou
Journal: Journal of the American Society of Nephrology (2009)

Animal studies have suggested a potential role for regulatory T cells (Tregs) in allograft tolerance, but these FOXP3+ cells seem to be an inherent component of acute rejection (AR) in human recipients of renal transplants. The balance between regulatory cells and effector/cytotoxic cells may determine graft outcome; this balance has not been described for chronic allograft injury. We investigated the expression of key regulatory, effector, and cytotoxic transcripts (i.e., FOXP3, T-bet, and granzyme B, respectively) in the grafts and peripheral blood of long-term-surviving renal transplant patients. We found that, whereas neither intragraft nor peripheral blood FOXP3 or T-bet mRNA could distinguish between rejection and nonrejection status, granzyme B (GrzB) mRNA could: It was significantly increased in the graft and significantly decreased in the peripheral blood of patients with chronic antibody-mediated rejection (CAMR). Quantifying peripheral blood GrzB mRNA demonstrated potential to aid in the noninvasive diagnosis of CAMR. In summary, these data affirm GrzB as a marker not only for AR but also for CAMR. In addition, we identified several previously unreported clinical or demographic factors influencing regulatory/effector/cytotoxic profiles in the peripheral blood, highlighting the necessity to consider confounding variables when considering the use of potential biomarkers, such as FOXP3, for diagnosis or prognosis in kidney transplantation.
The Giant Protein Titin
Authors: Henk L. Granzier, Siegfried Labeit
Journal: Circulation Research (2004)

The sarcomere contains, in addition to thin and thick filaments, a filament composed of the giant protein titin (also known as connectin). Titin molecules anchor in the Z-disc and extend to the M-line region of the sarcomere. The majority of titin’s I-band region functions as a molecular spring. This spring maintains the precise structural arrangement of thick and thin filaments, and gives rise to passive muscle stiffness; an important determinant of diastolic filling. Earlier work on titin has been reviewed before. In this study, our main focus is on recent findings vis-à-vis titin’s molecular spring segments in cardiac titins, including the discovery of fetal cardiac isoforms with novel spring elements. We also discuss new insights regarding the role of titin as a biomechanical sensor and signaling molecule. We will end with focusing on the rapidly growing knowledge regarding titinopathies.
Iron Homeostasis and the Inflammatory Response
Authors: Marianne Wessling-Resnick
Journal: Annual Review of Nutrition (2010)

Iron and its homeostasis are intimately tied to the inflammatory response. The adaptation to iron deficiency, which confers resistance to infection and improves the inflammatory condition, underlies what is probably the most obvious link: the anemia of inflammation or chronic disease. A large number of stimulatory inputs must be integrated to tightly control iron homeostasis during the inflammatory response. In order to understand the pathways of iron trafficking and how they are regulated, this article presents a brief overview of iron homeostasis. A major focus is on the regulation of the peptide hormone hepcidin during the inflammatory response and how its function contributes to the process of iron withdrawal. The review also summarizes new and emerging information about other iron metabolic regulators and effectors that contribute to the inflammatory response. Potential benefits of treatment to ameliorate the hypoferremic condition promoted by inflammation are also considered.
Necrotizing vasculitis and severe atherosclerosis: resolution of the vasculitis following surgery
Authors: P. Berbis, P. Piquet, C. Mercier, Y. Privat
Journal: British Journal of Dermatology (1990)

Journal Article Necrotizing vasculitis and severe atherosclerosis: resolution of the vasculitis following surgery Get access P. Berbis, P. Berbis Clinique Dermatologique, Hotel Dieu, 6 Place Daviel, 13002 Marseille. Search for other works by this author on: Oxford Academic Google Scholar P. Piquet, P. Piquet Service de Chirugie Vasculae, Hopital de la Conception, 147 Bd Baille, 13005 Marseille, France Search for other works by this author on: Oxford Academic Google Scholar C. Mercier, C. Mercier Service de Chirugie Vasculae, Hopital de la Conception, 147 Bd Baille, 13005 Marseille, France Search for other works by this author on: Oxford Academic Google Scholar Y. Privat Y. Privat Clinique Dermatologique, Hotel Dieu, 6 Place Daviel, 13002 Marseille. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 122, Issue 1, 1 January 1990, Pages 120–121, https://doi.org/10.1111/j.1365-2133.1990.tb08254.x Published: 01 January 1990
Ophthalmic Medical Practitioners' Fees
Authors: P. R. Day
Journal: BMJ (1966)

True in a vocation one does not expect to earn as much as if the work was not " vocational."But one must have some reward, and this in a vocation is the satisfac- tion of a good job well done.If this is denied (60 patients in the surgery, 40 children. in the classroom) no vocational approach is possible.
Extensive and coordinated transcription of noncoding RNAs within cell-cycle promoters
Authors: Tiffany Hung, Yulei Wang, Michael F Lin, Ashley K Koegel, Yojiro Kotake, Gavin D Grant, Hugo M Horlings, Nilay Shah, Christopher Umbricht, Pei Wang, Yu Wang, Benjamin Kong, Anita Langerød, Anne-Lise Børresen-Dale, Seung K Kim, Marc van de Vijver, Saraswati Sukumar, Michael L Whitfield, Manolis Kellis, Yue Xiong, David J Wong, Howard Y Chang
Journal: Nature Genetics (2011)
Cyclooxygenase 1 and cyclooxygenase 2 expression is abnormally regulated in human nasal polyps
Authors: Joaquim Mullol, Joan C. Fernàndez-Morata, Jordi Roca-Ferrer, Laura Pujols, Antoni Xaubet, Pedro Benitez, Cesar Picado
Journal: Journal of Allergy and Clinical Immunology (2002)
Response to Letters Regarding Article, “Anticoagulation and Survival in Pulmonary Arterial Hypertension: Results From the Comparative, Prospective Registry of Newly Initiated Therapies for Pulmonary Hypertension (COMPERA)”
Authors: Karen M. Olsson, Marion Delcroix, H. Ardeschir Ghofrani, Henning Tiede, Doerte Huscher, Rudolf Speich, Ekkehard Grünig, Gerd Staehler, Stephan Rosenkranz, Michael Halank, Matthias Held, Tobias J. Lange, Juergen Behr, Hans Klose, Martin Claussen, Ralf Ewert, Christian F. Opitz, C. Dario Vizza, Laura Scelsi, Anton Vonk-Noordegraaf, Harald Kaemmerer, J. Simon R. Gibbs, Gerry Coghlan, Joanna Pepke-Zaba, Uwe Schulz, Matthias Gorenflo, David Pittrow, Marius M. Hoeper
Journal: Circulation (2014)
Velocity associated characteristics of force production in college weight lifters
Authors: H Kanehisa, T Fukunaga
Journal: British Journal of Sports Medicine (1999)

To determine velocity specific isokinetic forces and cross sectional areas of reciprocal muscle groups in Olympic weight lifters.The cross sectional area of the flexor or extensor muscles of the elbow or knee joint was determined by a B-mode ultrasonic apparatus in 34 college weight lifters and 31 untrained male subjects matched for age. Maximum voluntary force produced in the flexion and extension of the elbow and knee joints was measured on an isokinetic dynamometer at 60, 180, and 300 degrees/s.The average cross sectional area was 31-65% higher, and the force was 19-62% higher in weight lifters than in the untrained subjects. The ratio of force to cross sectional area was the same in both groups. The weight lifters showed a lower velocity associated decline in force than untrained subjects in the elbow and knee flexors but not in the extensors.These results indicate that for muscle contractions with velocities between 60 degrees/s and 300 degrees/s the difference in isokinetic force between weight lifters and untrained subjects can be primarily attributed to the difference in the muscle cross sectional area. However, the lower velocity associated decline in force implies that weight lifters may have a higher force per cross sectional area than untrained subjects at velocities above 300 degrees/s.
Metastatic squamous cell carcinoma of the nail bed: a presenting sign of lung cancer
Authors: S.E. Chang, J.H. Choi, K.J. Sung, K.C. Moon, J.K. Koh
Journal: British Journal of Dermatology (1999)

Journal Article Metastatic squamous cell carcinoma of the nail bed: a presenting sign of lung cancer Get access S.E. Chang, S.E. Chang Department of Dermatology, Asan Medical Center, College of Medicine, University of Ulsan, 388‐1 Poongnap‐dong, Songpa‐gu, Seoul 138‐040, Korea Search for other works by this author on: Oxford Academic Google Scholar J.H. Choi, J.H. Choi Department of Dermatology, Asan Medical Center, College of Medicine, University of Ulsan, 388‐1 Poongnap‐dong, Songpa‐gu, Seoul 138‐040, Korea Search for other works by this author on: Oxford Academic Google Scholar K.J. Sung, K.J. Sung Department of Dermatology, Asan Medical Center, College of Medicine, University of Ulsan, 388‐1 Poongnap‐dong, Songpa‐gu, Seoul 138‐040, Korea Search for other works by this author on: Oxford Academic Google Scholar K.C. Moon, K.C. Moon Department of Dermatology, Asan Medical Center, College of Medicine, University of Ulsan, 388‐1 Poongnap‐dong, Songpa‐gu, Seoul 138‐040, Korea Search for other works by this author on: Oxford Academic Google Scholar J.K. Koh J.K. Koh Department of Dermatology, Asan Medical Center, College of Medicine, University of Ulsan, 388‐1 Poongnap‐dong, Songpa‐gu, Seoul 138‐040, Korea Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 141, Issue 5, 1 November 1999, Pages 939–940, https://doi.org/10.1046/j.1365-2133.1999.03182.x Published: 01 November 1999