tbuckley/cabot-search huggingface dataset:
Risk factors for patellar tendinopathy in competitive volleyball players
Authors: R De Ridder, N Mahieu, L Reynaert, W Poppe, K Strubbe, A Cools, P Roosen
Journal: British Journal of Sports Medicine (2011)

Background Patellar tendinopathy (PT) is an important problem in a volleyball population. However, in order to optimize rehabilitation and prevention strategies, not all intrinsic risk factors are known. This study is the first study that takes the hip strength into account. Objective The objective is to identify some intrinsic risk factors of the lower limb for the development of PT in competitive volleyball players. Design Retrospective. Setting Eight male national volleyball teams participated in this study. Risk factors were assessed at the beginning of the season 2009–2010. By means of questionnaires, the participants injury history was documented. Participants A total of 71 male players (25.1±4.5 years) were included. Players with a history of surgery and pain on the moment of testing were excluded. Assessment of risk factors Muscle strength, muscle length and landing strategies were assessed. Main outcome measurements The strength of the hip muscles was measured with a hand-held dynamometer. Muscle length of gastrocnemius, soleus, hamstrings and quadriceps was determined by means of a plurimeter. A 2D video analyses was made of a vertical jump. Knee flexion angle, Q-angle and Ankle dorsiflexion angle during the landing were calculated. Results The players with a history of PT (&gt;6 months ago) displayed a significant greater ankle dorsiflexion ROM, a significant lower hip flexion strength and a significant shorter quadriceps. A logistic regression model indicated that a greater ankle dorsiflexion ROM and a lower hip flexion strength are predictors for occurrence of PT. Conclusions It can be concluded that a greater dorsiflexion ankle during landing and a lower hip flexion strength are associated with the occurrence of a PT. Future prospective studies should include, not only the knee, but also the hip and the ankle in their assessment.
Improving Publication Rates of Biomarker Results from Cancer Trials
Authors: Robert Iannone
Journal: Clinical Cancer Research (2012)

Abstract Mandatory nondiagnostic biopsies for biomarker research pose risk and inconvenience to patients with cancer that should be justified by the knowledge gained. This commentary reflects on the publication by Freeman and Kimmelman, which points to a potentially low publication rate of biomarker results from cancer clinical trials requiring nondiagnostic biopsies. Clin Cancer Res; 18(23); 6398–9. ©2012 AACR.
Lumleian Lectures, Delivered before the Royal College of Physicians
Authors: J. R. Reynolds
Journal: BMJ (1867)

THE object pf this lecture is tozshq that there exists a radical diference 4etweep the.$endemcifs og, sciertific study and of.legal practice; the tendeacy,of gcience is to deStroy' artifirial lines, that -of egal practice to create them.=It is only 'ecessayto glance at the scientific d6velopment of the present day in order tp illqstr4te this' position.Every scienee has, dAuring, its -progreas, to draw arti.ficial lines, and theiattempt of each eience is to mhke them as conformable Oas m3y be withAthe facts of nature.We mak6' use of suiih lines Itor the purposes of de- scription anq dtinctinp, and,th,lrs medine, bi logy, chemiitry, a4n physies, employ them to separte, from each other the materials, phenomena, and groips of phenomena, a history of whidh niAkes up thoe sciences.:By~means of artificial' linied
Immune recognition of <i>Pseudomonas aeruginosa</i> mediated by the IPAF/NLRC4 inflammasome
Authors: Fayyaz S. Sutterwala, Lilia A. Mijares, Li Li, Yasunori Ogura, Barbara I. Kazmierczak, Richard A. Flavell
Journal: The Journal of Experimental Medicine (2007)

Pseudomonas aeruginosa is a Gram-negative bacterium that causes opportunistic infections in immunocompromised individuals. P. aeruginosa employs a type III secretion system to inject effector molecules into the cytoplasm of the host cell. This interaction with the host cell leads to inflammatory responses that eventually result in cell death. We show that infection of macrophages with P. aeruginosa results in activation of caspase-1 in an IPAF-dependent, but flagellin-independent, manner. Macrophages deficient in IPAF or caspase-1 were markedly resistant to P. aeruginosa–induced cell death and release of the proinflammatory cytokine interleukin (IL)-1β. A subset of P. aeruginosa isolates express the effector molecule exoenzyme U (ExoU), which we demonstrate is capable of inhibiting caspase-1–driven proinflammatory cytokine production. This study shows a key role for IPAF and capase-1 in innate immune responses to the pathogen P. aeruginosa, and also demonstrates that virulent ExoU-expressing strains of P. aeruginosa can circumvent this innate immune response.
MRL-<i>lpr/lpr</i> Mice Exhibit a Defect in Maintaining Developmental Arrest and Follicular Exclusion of Anti–double-stranded DNA B Cells
Authors: Laura Mandik-Nayak, Su-jean Seo, Caroline Sokol, Kathryn M. Potts, Anh Bui, Jan Erikson
Journal: The Journal of Experimental Medicine (1999)

A hallmark of systemic lupus erythematosus and the MRL murine model for lupus is the presence of anti–double-stranded (ds)DNA antibodies (Abs). To identify the steps leading to the production of these Abs in autoimmune mice, we have compared the phenotype and localization of anti-dsDNA B cells in autoimmune (MRL+/+ and lpr/lpr) mice with that in nonautoimmune (BALB/c) mice. Anti-dsDNA B cells are actively regulated in BALB/c mice as indicated by their developmental arrest and accumulation at the T–B interface of the splenic follicle. In the MRL genetic background, anti-dsDNA B cells are no longer developmentally arrested, suggesting an intrinsic B cell defect conferred by MRL background genes. With intact Fas, they continue to exhibit follicular exclusion; however, in the presence of the lpr/lpr mutation, anti-dsDNA B cells are now present in the follicle. Coincident with the altered localization of anti-dsDNA B cells is a follicular infiltration of CD4 T cells. Together, these data suggest that MRL mice are defective in maintaining the developmental arrest of autoreactive B cells and indicate a role for Fas in restricting entry into the follicle.
Effect of influenza vaccination on excess deaths occurring during periods of high circulation of influenza: cohort study in elderly people
Authors: Ben G Armstrong, Punam Mangtani, Astrid Fletcher, Sari Kovats, Anthony McMichael, Sam Pattenden, Paul Wilkinson
Journal: BMJ (2004)

<h3>Abstract</h3> <b>Objective</b> To estimate the protection against death provided by vaccination against influenza. <b>Design</b> Prospective cohort follow up supplemented by weekly national counts of influenza confirmed in the community. <b>Setting</b> Primary care. <b>Participants</b> 24 535 patients aged over 75 years from 73 general practices in Great Britain. <b>Main outcome measure</b> Death. <b>Results</b> In unvaccinated members of the cohort daily all cause mortality was strongly associated with an index of influenza circulating in the population (mortality ratio 1.16, 95% confidence interval 1.04 to 1.29 at 90th centile of circulating influenza). The association was strongest for respiratory deaths but was also present for cardiovascular deaths. In contrast, in vaccinated people mortality from any cause was not associated with circulating influenza. The difference in patterns between vaccinated and unvaccinated people could not easily be due to chance (P = 0.02, all causes). <b>Conclusions</b> This study, using a novel and robust approach to control for confounding, provides robust evidence of a protective effect on mortality of vaccination against influenza.
Distribution of serum IgE in children and adolescents aged 7 to 16 years in Copenhagen, in relation to factors of importance
Authors: V. Backer, C. S. Ulrik, D. Wendelboe, N. Bach‐Mortensen, K. K. Hansen, E. M. Laursen, A. Dirksen
Journal: Allergy (1992)

The distribution of total serum‐IgE and factors of importance for the level of IgE was studied in a random sample of 508 children and adolescents, aged 7–16 years, from Copenhagen. A detailed history about asthma, rhinitis, dermatitis and urticaria was obtained, and a physical examination, skin prick test with 9 common allergens, lung function test, bronchial challenge with inhaled histamine and exercise, and measurement of IgE (kU/1) were performed. The distribution of IgE among children and adolescents was found to exhibit a log normal distribution and a positive skin prick test, allergic symptoms, a family history of allergic diseases, age and smoking were found to be significantly related to an increased level of IgE. No relationship was found between increased bronchial responsiveness and IgE. The geometric mean of “normal” values of IgE (* 1 SD and *2 SD) of the Danish children and adolescents was 18 kU/1 (*4.7, * 18.2), suggesting that normal IgE values were within 330 kU/1. Measurement of IgE as the only screening for allergic disease is unreliable, as the predictive value of an elevated IgE in population samples was found to be 50%, whereas misclassification (1‐specificity) of asymptomatic subjects as allergic because of an increased IgE was low (4%). In conclusion, total IgE is highly influenced by allergen skin reactivity. Further, this study suggests that normal IgE values were within 330 kU/1, although the range was wide.
Metabolism of β-sitosterol in man
Authors: Gerald Salen, E. H. Ahrens, Scott M. Grundy
Journal: Journal of Clinical Investigation (1970)

The metabolism of β-sitosterol was compared to that of cholesterol in 12 patients. Sterol balance methods were supplemented by radiosterol studies, with the following results. (a) Plasma concentrations of β-sitosterol ranged from 0.30 to 1.02 mg/100 ml plasma in patients on intakes of β-sitosterol typical of the American diet. Plasma levels were raised little when intakes were increased greatly, and on fixed intakes they were constant from week to week. On diets devoid of plant sterols, the plasma and feces rapidly became free of β-sitosterol. (b) The percentage of esterified β-sitosterol in the plasma was the same as for cholesterol. However, the rate of esterification of β-sitosterol was slower than that for cholesterol. (c) Specific activity-time curves after simultaneous pulse labeling with β-sitosterol-3H and cholesterol-14C conformed to two-pool models. The two exponential half-lives of β-sitosterol were much shorter than for cholesterol, and pool sizes were much smaller. Values of turnover for β-sitosterol obtained by the sterol balance method agreed closely with those derived by use of the two-pool model. There was no endogenous synthesis of β-sitosterol in the patients studied; hence, daily turnover of β-sitosterol equaled its daily absorption. Absorption of β-sitosterol was 5% (or less) of daily intake, while cholesterol absorption ranged from 45 to 54% of intake. (d) About 20% of the absorbed β-sitosterol was converted to cholic and chenodeoxycholic acids. The remainder was excreted in bile as free sterol; this excretion was more rapid than that of cholesterol. (e) The employment of β-sitosterol as an internal standard to correct for losses of cholesterol in sterol balance studies is further validated by the results presented here.
Radioautographic Study of Aortic Plaque Formation
Authors: I. GORDON FELS, KANABROCKI THADDEUS
Journal: Circulation Research (1959)

Radioautographic evidence using Ca 45 Cl 2 is presented to demonstrate that the aorta has an inherent ability to bind calcium ion regardless of age, sex or species. The binding occurs primarily in the intima and is not homogeneously distributed. Experiments with boiled aorta suggest that the primary substance responsible is collagen. The binding of calcium by the aorta has a marked effect upon the stability of emulsions. A theory of arterial plaque formation is presented.
Histone deacetylase activity is essential for the expression of <i>HoxA9</i> and for endothelial commitment of progenitor cells
Authors: Lothar Rössig, Carmen Urbich, Thomas Brühl, Elisabeth Dernbach, Christopher Heeschen, Emmanouil Chavakis, Ken-ichiro Sasaki, Diana Aicher, Florian Diehl, Florian Seeger, Michael Potente, Alexandra Aicher, Lucia Zanetta, Elisabetta Dejana, Andreas M. Zeiher, Stefanie Dimmeler
Journal: The Journal of Experimental Medicine (2005)

The regulation of acetylation is central for the epigenetic control of lineage-specific gene expression and determines cell fate decisions. We provide evidence that the inhibition of histone deacetylases (HDACs) blocks the endothelial differentiation of adult progenitor cells. To define the mechanisms by which HDAC inhibition prevents endothelial differentiation, we determined the expression of homeobox transcription factors and demonstrated that HoxA9 expression is down-regulated by HDAC inhibitors. The causal involvement of HoxA9 in the endothelial differentiation of adult progenitor cells is supported by the finding that HoxA9 overexpression partially rescued the endothelial differentiation blockade induced by HDAC inhibitors. Knockdown and overexpression studies revealed that HoxA9 acts as a master switch to regulate the expression of prototypical endothelial-committed genes such as endothelial nitric oxide synthase, VEGF-R2, and VE-cadherin, and mediates the shear stress–induced maturation of endothelial cells. Consistently, HoxA9-deficient mice exhibited lower numbers of endothelial progenitor cells and showed an impaired postnatal neovascularization capacity after the induction of ischemia. Thus, HoxA9 is regulated by HDACs and is critical for postnatal neovascularization.
Diminished atherosclerotic arterial calcifications in asthma
Authors: E. C. Lasser, C. Berry, K. Kortman
Journal: Allergy (1987)

Twenty‐seven patients beyond the age of 50 were radiographically compared with age‐and sex‐matched controls for the degree of calcified therosclerotic plaque formation in the aorta and its major pelvic branches. Significantly less calcification was present in the aorta, iliac and hypogastric arteries of the asthmatics ( P = 0.01). Previous studies in other asthmatic patients have shown elevated endogenous heparin‐like material to be present in their plasma. It is peculated that diminished atherosclerosis in asthmatic patients might be a consequence of elevated circulating endogenous heparin‐like material.
Nitric oxide donating compounds stimulate human colonic ion transport in vitro.
Authors: W A Stack, B Filipowicz, C J Hawkey
Journal: Gut (1996)

Nitric oxide (NO) has been recently implicated as a possible mediator of bowel inflammation and has also been shown to stimulate electrogenic chloride secretion in rat and guinea pig intestine. This study therefore investigated the effect on two NO donors, sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine (SNAP) on human colonic ion transport.Changes in short circuit current (delta SCC) in response to nitric oxide donating compounds were measured in muscle stripped normal human colon mounted in Ussing chambers. The ion species and intracellular mechanisms responsible for delta SCC evoked by SNP were investigated.Basolateral SNP caused a progressive rise in delta SCC over the range 10(-7) to 10(-4)M (ED50 = 2.5 x 10(-5)M). SNAP 10(-4)M also evoked a qualitatively similar delta SCC compared with SNP 10(-4)M. Basolateral SNP evoked a greater delta SCC than apical and this was significantly attenuated by bumetanide 10(-4)M (52.9 +/- 10.1%) and in chloride free media (68.3 +/- 7.3%). delta SCC response to SNP was not significantly changed by basolateral 4-acetamido-4'-isothio-cyano-2,2'disulphonic acid stillbene (SITS 10(-3)M) an inhibitor of sodium/bicarbonate exchange, or apical amiloride 10(-5)M an inhibitor of sodium absorption. SNP induced delta SCC was also significantly reduced by piroxicam (mean (SEM)) 10(-5)M (57.9 (11.9)%), nordihydroguaretic acid 10(-4)M (48.0 (12.9)%), tetrodotoxin (TTX 10(-6)M, 52.3 (9.1)%), and practically abolished by TTX and piroxicam together (96.8 (3.3)%).NO donors stimulate human colonic ion transport in vitro. For SNP, increased delta SCC is at least due in part to chloride secretion, and the response seems to be transduced through enteric nerves and by local prostanoid synthesis. This study provides evidence that NO may be another important mediator of ion transport in human colon.
Regulation of intercellular adhesion molecule-1 (ICAM-1) in ischemic and reperfused canine myocardium.
Authors: G L Kukielka, H K Hawkins, L Michael, A M Manning, K Youker, C Lane, M L Entman, C W Smith, D C Anderson
Journal: Journal of Clinical Investigation (1993)

Previous studies in vitro have shown an important role for intercellular adhesion molecule-1 (ICAM-1) in adherence interactions of canine neutrophils with canine jugular vein endothelial cells and in cytotoxicity of canine neutrophils for adult cardiac myocytes. To evaluate the regulation of ICAM-1 in myocardial inflammation and its role in the pathogenesis of myocardial ischemia and reperfusion, a series of in vivo and ex vivo studies were performed in canine animals. Systemic administration of LPS elicited ICAM-1 mRNA in several tissues, including myocardium, which demonstrated increasing ICAM-1 staining on intercalated discs of cardiac myocytes. In ischemia and reperfusion protocols: (a) ICAM-1 mRNA was found in ischemic segments within 1 h of reperfusion and in both ischemic and normally perfused segments by 24 h of reperfusion; (b) expression of ICAM-1 was detected in cardiac myocytes in the ischemic region by 6 h of reperfusion; increased expression was seen thereafter as a function of time; (c) post-ischemic (but not preischemic) cardiac lymph collected at intervals from 1 to 24 h after reperfusion elicited ICAM-1 mRNA, ICAM-1 expression, and ICAM-1-dependent neutrophil adhesion in canine jugular vein endothelial cells and in cardiac myocytes with peak cytokine activity seen by 1 h; (d) extravascular localization of neutrophils was detected in ischemic areas only, and was associated with endothelium bearing high levels of ICAM-1 within 1 h of reperfusion; infiltration increased thereafter in association with increasing levels of ICAM-1 mRNA in myocardial segments and increasing levels of ICAM-1 expression on cardiac myocytes. These findings provide the first direct evidence for inflammatory regulation of ICAM-1 in ischemic and reperfused canine myocardium. They support the hypothesis that ICAM-1 participates in neutrophil-mediated myocardial damage.
Concurrent Scarlatina and Enteric Fever
Authors: E. M. D. Cosgrave
Journal: BMJ (1897)

ALTHOUGH many cases sre on record of convalescents from enteric fever contracting scarlatina, and on the other hand of convalescents from scarlatina contracting enteric, true con- currence, that is, tlce incubation and pyrexial stages of the two diseases occurring simultaneously, is not common, and has only lately been recorded, and that in but few instances.A convenient starting point which sums up previous know- ledge is a paper 2 by Murellison, who, writing in 1859, says that in ten years he saw only one case of scarlatina contract- ing enteric fever, and that supervened on the twenty-sixth day; he gives, however, some cases of scarlatina supervening in enteric, but goes on to say, " No cases have hitherto been published s-howing the possibility of these two diseases coexisting."This extreme view he afterwards modified, and in his classic work on fevers 3 says, " In the London Fever Hospital, where it was the practice to treat all forms of fever in the same wards, it was not uncommon for a patient suffering from enteric fever to contract scarlet fever, and I have notes of eight cases in which the eruptions of the two diseases co- existed."Murchison gives notes of two of these cases; in one the scarlatina eruption came out late in enteric-probably in the third week; and in the other case it appeared on the twenty-second day.On the other hand Murchison says4 " scarlatina appears indeed to predispose to enteric fever.
Effect of angiotensin II on uterine and systemic vasculature in pregnant sheep.
Authors: R P Naden, C R Rosenfeld
Journal: Journal of Clinical Investigation (1981)

The response of uteroplacental blood flow (UBF) to angiotensin II is controversial. Moreover, the relationship of the uterine and systemic responses to infused angiotensin II is not well understood. Thus, in eight chronically instrumented, near-term pregnant sheep, we have determined the relationships between the dose and duration of constant systemic infusions of angiotensin II ([Val5] ANG II) and changes in UBF, uterine vascular resistance (UVR), mean arterial pressure (MAP), and systemic vascular resistance (SVR). [Val5] ANG II caused dose-dependent increases in UVR and MAP at all doses studied (P less than 0.05). The response in UBF was bidirectional, with increases at doses less than or equal to 1.15 microgram/min and decreases at greater than or equal to 2.29 micrograms/min (P less than 0.05). Increases in UBP occurred when the relative rise (delta) in MAP greater than delta UVR, whereas UBF was unchanged when delta MAP = delta UVR and decreased when delta MAP less than delta UVR. SVR also rose in a dose-dependent fashion (P less than 0.05); delta SVR was greater than delta UVR at doses less than or equal to 2.29 micrograms [Val5] ANG II/min (P less than 0.01). In studies of the effect of duration of [Val5] ANG II infusions, UBF increased at all doses during the 1st min, followed by stabilization at 4--5 min, with eventual decreases at doses greater than or equal to 2.29 micrograms/min and increases at doses less than 2.29 micrograms/min. The relationship between the changes in MAP and UVR to the response of UBF was as noted above. It is evident that (a) [Val5] NAG II is uterine vasoconstrictor, (b) changes in UBF are dependent upon relative changes in perfusion pressure and UVR, which in turn are dependent upon both the dose and duration of a [Val5] ANG II infusion, and (c) the uteroplacental vasculature is relatively refractory to the vasoconstricting effects of low doses of [Val5] ANG II.
Impaired Phosphatidylcholine Biosynthesis Reduces Atherosclerosis and Prevents Lipotoxic Cardiac Dysfunction in ApoE <sup>−/−</sup> Mice
Authors: Laura K. Cole, Vernon W. Dolinsky, Jason R.B. Dyck, Dennis E. Vance
Journal: Circulation Research (2011)

Phosphatidylcholine (PC) is the predominant phospholipid component of circulating lipoproteins. The majority of PC is formed by the choline pathway. However, approximately one-third of hepatic PC can also be synthesized by phosphatidylethanolamine N-methyltransferase (PEMT). PEMT is required for normal secretion of very-low-density lipoproteins from the liver. We hypothesized that lack of PEMT would attenuate atherosclerosis and improve myocardial function.Investigate the contribution of PEMT to atherosclerotic lesion formation and cardiac function in mice that lack apolipoprotein E.Mice deficient in apolipoprotein E (Pemt(+/+)/Apoe(-/-)) and mice lacking both PEMT and apoE (Pemt(-/-)/Apoe(-/-)) were fed a chow diet for 1 year. The atherogenic lipoprotein profile of plasma of Apoe(-/-) mice was significantly improved by PEMT deficiency, with lower levels of triacylglycerol (45%) and cholesterol (≈25%) in the very-low-density lipoprotein and low-density/intermediate-density lipoprotein fractions, respectively (P < 0.05). Atherosclerotic lesion area was reduced by ≈30%, and aortic cholesteryl ester and cholesterol content were also reduced by ≈40% by PEMT deficiency (P < 0.05). By in vivo echocardiography, we detected a ≈50% improvement in systolic function in the Pemt(-/-)/Apoe(-/-) compared with Pemt(+/+)/Apoe(-/-) mice (P < 0.05). This was accompanied by a significant reduction in cardiac triacylglycerol (34%) in mice lacking PEMT.These results indicate that treatment strategies aimed at inhibition of PEMT might prevent the accumulation of cardiac triacylglycerol that predisposes individuals to compromised cardiac function.