tbuckley/cabot-search huggingface dataset:
The additional effects of swiss ball use during the wall squat exercise on lowerlimb muscle activity
Authors: E Hinds
Journal: British Journal of Sports Medicine (2011)

Objective To investigate whether the addition of a swiss ball to a wall squat exercise has any effect on the levels of lower limb muscle activity at varying angles of knee flexion. Design An observational study with repeated measures design. Methods Measures were made of both legs of 14 healthy subjects (3 female, 11 male) mean height, age and weight were 31 years, 175 cm, 73 kg respectively. Each subject performed the wall squat exercise to 60°, 90° and 110° of knee flexion, with and without a swiss ball. Electromyographical (EMG) muscle activity was collected from vastus medialis, vastus lateralis, rectus femoris, semitendinosus, bicep femoris, internal oblique, gluteus maximus and gluteus medius. A pelvis and lower limb motion capture protocol was used to enable the EMG to be referenced to position. The EMG data was rectified and smoothed using a root mean square method. Analysis was made of the EMG data to determine whether the addition of the swiss ball resulted in any significant changes in muscle activity and also to identify whether there was a significant difference in muscle activity between the three angles of knee flexion used during the test. Results The addition of the swiss ball to the wall squat exercise resulted in a significant increase in muscle activity of vastus medialis at 60° and 90° of knee flexion (Z=−4.053 and 3.643 respectively, p&lt;0.002), vastus lateralis at 60°, 90° and 110° of knee flexion (Z=−3.142, −3.142, −3.142 respectively, p=0.002), semitendinosus at 60°, 90° and 110° of knee flexion(Z=−3.388, −3.075, −4.213, p=0.002) and internal oblique at 90°of knee flexion (Z=−3.074, p=0.002). Conclusion The addition of the swiss ball to the wall squat exercise does increase muscle activity of the some of the lower limb muscles. However, the effects appear to be dependant on the muscles investigated and the angle of knee flexion to which the exercise is performed. The swiss ball cannot be generalised as a means of increasing lower limb muscle activity during the wall squat but the study indicates that it does play a role in increasing the muscle activity of specific muscles.
Transmission of mitochondrial DNA following assisted reproduction and nuclear transfer
Authors: E.C. Spikings, J. Alderson, J.C.St. John
Journal: Human Reproduction Update (2006)

Mitochondria are the organelles responsible for producing the majority of a cell's ATP and also play an essential role in gamete maturation and embryo development. ATP production within the mitochondria is dependent on proteins encoded by both the nuclear and the mitochondrial genomes, therefore co-ordination between the two genomes is vital for cell survival. To assist with this co-ordination, cells normally contain only one type of mitochondrial DNA (mtDNA) termed homoplasmy. Occasionally, however, two or more types of mtDNA are present termed heteroplasmy. This can result from a combination of mutant and wild-type mtDNA molecules or from a combination of wild-type mtDNA variants. As heteroplasmy can result in mitochondrial disease, various mechanisms exist in the natural fertilization process to ensure the maternal-only transmission of mtDNA and the maintenance of homoplasmy in future generations. However, there is now an increasing use of invasive oocyte reconstruction protocols, which tend to bypass mechanisms for the maintenance of homoplasmy, potentially resulting in the transmission of either form of mtDNA heteroplasmy. Indeed, heteroplasmy caused by combinations of wild-type variants has been reported following cytoplasmic transfer (CT) in the human and following nuclear transfer (NT) in various animal species. Other techniques, such as germinal vesicle transfer and pronuclei transfer, have been proposed as methods of preventing transmission of mitochondrial diseases to future generations. However, resulting embryos and offspring may contain mtDNA heteroplasmy, which itself could result in mitochondrial disease. It is therefore essential that uniparental transmission of mtDNA is ensured before these techniques are used therapeutically.
Iron deficiency in pulmonary arterial hypertension: a potential therapeutic target
Authors: C.J. Rhodes, J. Wharton, L. Howard, J.S.R. Gibbs, A. Vonk-Noordegraaf, M.R. Wilkins
Journal: European Respiratory Journal (2011)

Iron deficiency is known to be common and detrimental in chronic left heart failure, where parenteral iron treatment has been shown to improve exercise capacity, New York Heart Association functional class and patient wellbeing. There is now increasing interest in the role of iron in the natural history of pulmonary arterial hypertension (PAH). Iron availability influences the pulmonary vasoconstrictor response to hypoxia and accumulating evidence indicates that iron deficiency is prevalent in idiopathic and heritable forms of PAH, iron status being related to exercise capacity, symptoms and poorer survival in patients with idiopathic PAH (IPAH). Potential mechanisms behind iron deficiency in IPAH include inhibition of dietary iron uptake by the master iron regulator hepcidin. High hepcidin levels underlie the anaemia of chronic disease. Possible stimuli of the observed high levels of hepcidin in IPAH include dysfunctional bone morphogenetic protein receptor type II signalling and inflammation. Iron status may influence outcomes through modulation of the pulmonary circulation as well as myocardial and skeletal muscle function. Two parallel studies, from our centre (Hammersmith Hospital, London, UK) and others in the UK and Amsterdam (the Netherlands), investigating the safety and potential benefit of iron supplementation in patients with PAH are currently under way.
Strong group-level traits and selection-transmission thickets
Authors: Jeffrey C. Schank
Journal: Behavioral and Brain Sciences (2014)

Abstract I suggest that we should distinguish between weak and strong group-level traits. It is the latter that are especially problematic for developing models of cultural evolution. Using Campbell's notion of vicarious selection mechanisms, I argue that these mechanisms become intertwined with other group-level traits resulting in selection-transmission thickets that are obstacles to modeling cultural evolution.
Adrenal glucocorticoids have a key role in circadian resynchronization in a mouse model of jet lag
Authors: Silke Kiessling, Gregor Eichele, Henrik Oster
Journal: Journal of Clinical Investigation (2010)

Jet lag encompasses a range of psycho- and physiopathological symptoms that arise from temporal misalignment of the endogenous circadian clock with external time. Repeated jet lag exposure, encountered by business travelers and airline personnel as well as shift workers, has been correlated with immune deficiency, mood disorders, elevated cancer risk, and anatomical anomalies of the forebrain. Here, we have characterized the molecular response of the mouse circadian system in an established experimental paradigm for jet lag whereby mice entrained to a 12-hour light/12-hour dark cycle undergo light phase advancement by 6 hours. Unexpectedly, strong heterogeneity of entrainment kinetics was found not only between different organs, but also within the molecular clockwork of each tissue. Manipulation of the adrenal circadian clock, in particular phase-shifting of adrenal glucocorticoid rhythms, regulated the speed of behavioral reentrainment. Blocking adrenal corticosterone either prolonged or shortened jet lag, depending on the time of administration. This key role of adrenal glucocorticoid phasing for resetting of the circadian system provides what we believe to be a novel mechanism-based approach for possible therapies for jet lag and jet lag-associated diseases.
Identification of the In Vivo Role of a Viral bcl-2
Authors: Shivaprakash Gangappa, Linda F. van Dyk, Travis J. Jewett, Samuel H. Speck, Herbert W. Virgin
Journal: The Journal of Experimental Medicine (2002)

Many γ-herpesviruses encode candidate oncogenes including homologues of host bcl-2 and cyclin proteins (v-bcl-2, v-cyclin), but the physiologic roles of these genes during infection are not known. We show for the first time in any virus system the physiologic role of v-bcl-2. A γ-herpesvirus v-bcl-2 was essential for efficient ex vivo reactivation from latent infection, and for both persistent replication and virulence during chronic infection of immunocompromised (interferon [IFN]-γ−/−) mice. The v-cyclin was also critical for the same stages in pathogenesis. Strikingly, while the v-bcl-2 and v-cyclin were important for chronic infection, these genes were not essential for viral replication in cell culture, viral replication during acute infection in vivo, establishment of latent infection, or virulence during acute infection. We conclude that v-bcl-2 and v-cyclin have important roles during latent and persistent γ-herpesvirus infection and that herpesviruses encode genes with specific roles during chronic infection and disease, but not acute infection and disease. As γ-herpesviruses primarily cause human disease during chronic infection, these chronic disease genes may be important targets for therapeutic intervention.
Paralytic rabies after a two week holiday in India
Authors: Tom Solomon, Denise Marston, Macpherson Mallewa, Tim Felton, Steve Shaw, Lorraine M McElhinney, Kumar Das, Karen Mansfield, Jane Wainwright, Georges Ng Man Kwong, Anthony R Fooks
Journal: BMJ (2005)

Rabies is an acute infection of the central nervous system (CNS) and caused by rabies virus or related members of the genus Lyssavirus , family Rhabdoviridae.1 The virus is usually transmitted through a dog bite and produces one of the most important viral encephalitides worldwide, with at least 40 000 deaths reported annually.2 However, it is rare in the United Kingdom, where just 12 cases have been reported since 19773: 11 were imported from overseas, and one occurred in a bat handler infected in Scotland with European bat lyssavirus type 2a.4 Most UK patients presented with furious rabies, which is characterised by hydrophobia and spasms. We report a case of paralytic rabies in a tourist after a two week holiday in Goa, India.



Fig 2 
Phylogenetic tree depicting the relation between the rabies virus sequence amplified from our patient (RV1964—boxed) and other viruses originating in Asia. The horizontal branch lengths represent the extent of difference between the strains (expressed as nucleotide substitutions per nucleotide site), and the closer viruses are on the tree, the more closely they are related



A woman in her late 30s was admitted to her local general hospital under the orthopaedic surgeons, with lower back pain radiating to the left leg. The pain had started four days earlier, was severe and shooting in nature, and was getting worse. She had been seen twice in casualty in the preceding days, and by the time of admission she was unable to walk. She also had a headache and had vomited once. Three and a half months before admission, during a two week holiday to Goa, India, she had been bitten by a dog; she was walking in the street when a puppy on a lead nipped her on the left leg. There was a slight …
Studies on the molecular mechanisms of human Fc receptor-mediated phagocytosis. Amplification of ingestion is dependent on the generation of reactive oxygen metabolites and is deficient in polymorphonuclear leukocytes from patients with chronic granulomatous disease.
Authors: H D Gresham, J A McGarr, P G Shackelford, E J Brown
Journal: Journal of Clinical Investigation (1988)

Human PMN and monocytes both possess a mechanism for amplifying Fc receptor-mediated phagocytic function, which is dependent on activation of the respiratory burst. The pathway for augmentation of phagocytosis requires superoxide anion, hydrogen peroxide, and lactoferrin and is independent of the hydrogen peroxide-MPO-halide system. In neither cell type is this mechanism induced upon exposure to the opsonized target. PMN require an additional signal for stimulation of the respiratory burst; this is not true of monocytes. On the other hand, monocytes require an exogenous source of lactoferrin in order to activate this pathway for enhanced ingestion. The dependence of this pathway for both PMN and monocytes on superoxide anion, hydrogen peroxide, and cell-bound lactoferrin is consistent with a role for locally generated reactive oxygen metabolites, possibly hydroxyl radicals, in phagocytosis amplification. Patients with chronic granulomatous disease, who are genetically deficient in the ability to activate the respiratory burst, are unable to amplify Fc receptor-mediated phagocytosis. Thus, these patients may have a previously unrecognized defect in the recruitment of phagocytic function at inflammatory sites.
Head-to-Head Comparison of Sirolimus- and Paclitaxel-Eluting Stent in the Same Diabetic Patient With Multiple Coronary Artery Lesions
Authors: Fabrizio Tomai, Bernhard Reimers, Leonardo De Luca, Alfredo R. Galassi, Achille Gaspardone, Anna S. Ghini, Valeria Ferrero, Luca Favero, Gaetano Gioffrè, Francesco Prati, Corrado Tamburino, Flavio Ribichini
Journal: Diabetes Care (2007)

It is still controversial whether sirolimus-eluting stent (SES) and paclitaxel-eluting stent (PES) are equally effective in patients with diabetes. In these patients, multiple individual variables may be responsible for neointimal hyperplasia, thus making difficult the comparison of the two drug-eluting stents (DES).We designed a prospective, randomized study to compare the efficacy in prevention of restenosis of SES and PES, both implanted in the same diabetic patient with multiple de novo coronary artery lesions undergoing elective percutaneous coronary intervention. We enrolled 60 patients with diabetes with at least two significant de novo angiographic stenoses in different coronary segments. The primary end point was in-stent late luminal loss (LLL) at 8-month angiographic follow-up.A total of 120 lesions were successfully treated with the randomly assigned DES (SES, n = 60; PES, n = 60). In-stent LLL was lower in the SES than in the PES group (0.26 +/- 0.4 vs. 0.50 +/- 0.6 mm; P = 0.01). Coronary lesions treated with SES presented a reduced in-stent LLL in 40 (68%) patients, while PES resulted in a lower in-stent LLL in 19 (32%) patients (P = 0.0002). At multivariable analysis, the type of DES implanted was the only independent predictor of in-stent LLL (odds ratio 2.3 [95% CI 1.1-5.0]; P = 0.03).SES directly compared with PES in the same diabetic patient is associated with a decrease in the extent of in-stent LLL at 8 months, suggesting a reduced risk of restenosis.
Costs of telaprevir-based triple therapy for hepatitis C: $189,000 per sustained virological response
Authors: Kian Bichoupan, Valerie Martel-Laferriere, David Sachs, Michel Ng, Emily A. Schonfeld, Alexis Pappas, James Crismale, Alicia Stivala, Viktoriya Khaitova, Donald Gardenier, Michael Linderman, Ponni V. Perumalswami, Thomas D. Schiano, Joseph A. Odin, Lawrence Liu, Alan J. Moskowitz, Douglas T. Dieterich, Andrea D. Branch
Journal: Hepatology (2014)

In registration trials, triple therapy with telaprevir (TVR), pegylated interferon (Peg-IFN), and ribavirin (RBV) achieved sustained virological response (SVR) rates between 64% and 75%, but the clinical effectiveness and economic burdens of this treatment in real-world practice remain to be determined. Records of 147 patients who initiated TVR-based triple therapy at the Mount Sinai Medical Center (May-December 2011) were reviewed. Direct medical costs for pretreatment, on-treatment, and posttreatment care were calculated using data from Medicare reimbursement databases, RED Book, and the Healthcare Cost and Utilization Project database. Costs are presented in 2012 U.S. dollars. SVR (undetectable hepatitis C virus [HCV] RNA 24 weeks after the end of treatment) was determined on an intention-to-treat basis. Cost per SVR was calculated by dividing the median cost by the SVR rate. Median age of the 147 patients was 56 years (interquartile range [IQR] = 51–61), 68% were male, 19% were black, 11% had human immunodeficiency virus/HCV coinfection, 36% had advanced fibrosis/cirrhosis (FIB-4 scores ≥3.25), and 44% achieved an SVR. The total cost of care was $11.56 million. Median cost of care was $83,721 per patient (IQR = $66,652-$98,102). The median cost per SVR was $189,338 (IQR = $150,735-$221,860). Total costs were TVR (61%), IFN (24%), RBV (4%), adverse event management (8%), professional fees (2%), and laboratory tests (1%). Conclusions : TVR and Peg-IFN accounted for 85% of costs. Pharmaceutical prices and the low (44%) SVR rate, in this real-world study, were major contributors to the high cost per SVR. (Hepatology 2014;60:1187–1195)
Measurement and Interpretation of the Ankle-Brachial Index
Authors: Victor Aboyans, Michael H. Criqui, Pierre Abraham, Matthew A. Allison, Mark A. Creager, Curt Diehm, F. Gerry R. Fowkes, William R. Hiatt, Björn Jönsson, Philippe Lacroix, Benôıt Marin, Mary M. McDermott, Lars Norgren, Reena L. Pande, Pierre-Marie Preux, H.E. (Jelle) Stoffers, Diane Treat-Jacobson
Journal: Circulation (2012)
Combined Statin and Niacin Therapy Remodels the High-Density Lipoprotein Proteome
Authors: Pattie S. Green, Tomas Vaisar, Subramaniam Pennathur, J. Jacob Kulstad, Andrew B. Moore, Santica Marcovina, John Brunzell, Robert H. Knopp, Xue-Qiao Zhao, Jay W. Heinecke
Journal: Circulation (2008)

Boosting low high-density lipoprotein (HDL) levels is a current strategy for preventing clinical events that result from cardiovascular disease. We previously showed that HDL(3) of subjects with coronary artery disease is enriched in apolipoprotein E and that the lipoprotein carries a distinct protein cargo. This observation suggests that altered protein composition might affect the antiatherogenic and antiinflammatory properties of HDL. We hypothesized that an intervention that increases HDL levels-combined statin and niacin therapy-might reverse these changes.HDL(3) isolated from 6 coronary artery disease subjects before and 1 year after combination therapy was analyzed by liquid chromatography-Fourier transform-mass spectrometry. Alterations in protein composition were detected by spectral counting and confirmed with extracted ion chromatograms. We found that combination therapy decreased the abundance of apolipoprotein E in HDL(3) while increasing the abundance of other macrophage proteins implicated in reverse cholesterol transport. Treatment-induced decreases in apolipoprotein E levels of HDL(3) were validated biochemically in a second group of 18 coronary artery disease subjects. Interestingly, the changes in HDL(3) proteome with niacin/statin treatment resulted in a protein composition that more closely resembled that of HDL(3) in healthy control subjects.Combined statin and niacin therapy partially reverses the changes in the protein composition seen in HDL(3) in coronary artery disease subjects. Our observations raise the possibility that quantifying the HDL proteome could provide insights into the therapeutic efficacy of antiatherosclerotic interventions.
Murder and Gun Control
Authors: JUDGE GEORGE EDWARDS
Journal: American Journal of Psychiatry (1972)

Most people incorrectly believe that murder by strangers, with robbery as a motive, poses a most serious threat in the U.S. The evidence shows that murder ranks relatively low on the list of causes of violent death and that most victims are relatives or friends of the murderer. The "mythology" of murder has caused many people to purchase arms as a means of self-defense when in fact this greatly increases the hazard to themselves and their families. The author recommends more stringent gun control legislation.
Genomic risk factors in sudden infant death syndrome
Authors: David W Van Norstrand, Michael J Ackerman
Journal: Genome Medicine (2010)

Sudden infant death syndrome (SIDS) is a major contributor to postneonatal infant death, and is the third leading cause of infant mortality in the USA. While public health efforts have reduced these deaths in recent years, the pathogenesis of SIDS remains unclear. Epidemiological data on SIDS-related deaths have suggested genetic factors, and many studies have attempted to identify SIDS-associated genes. This has resulted in a large body of literature implicating various genes and their encoded proteins and signaling pathways in numerous cohorts of various sizes and ethnicities. This review has undertaken a systematic evaluation of these studies, identifying the pathways that have been implicated in these studies, including central nervous system pathways, cardiac channelopathies, immune dysfunction, metabolism/energy pathways, and nicotine response. This review also explores how new genomic techniques will aid in advancing our knowledge of the genomic risk factors associated with SIDS, including SNPs and copy number variation. Last, this review explores how the current information can be applied to aid in our assessment of the at risk infant population.
Real-time Pathology to Guide Breast Surgery: Seeing Alone Is Not Believing
Authors: Irving J. Bigio
Journal: Clinical Cancer Research (2012)

Abstract Tissue diagnostic techniques based on optical spectroscopy, in various incarnations, are approaching clinical reality for intraoperative guidance of surgical procedures. Examination of tissue properties by elastic light-scattering spectroscopy may constitute a preferable alternative to frozen-section pathology or touch imprint cytology for intraoperative assessment of resection margins during breast-conserving surgery. Clin Cancer Res; 18(22); 6083–5. ©2012 AACR.