tbuckley/cabot-search huggingface dataset:
Evaluation of the role of polymorphonuclear leukocytes on contractile function in myocardial reperfusion injury. Evidence for plasma-mediated leukocyte activation.
Authors: S M Shandelya, P Kuppusamy, M L Weisfeldt, J L Zweier
Journal: Circulation (1993)

BACKGROUND It has been hypothesized that chemotaxis and activation of polymorphonuclear leukocytes (PMNs) occur upon reperfusion of ischemic myocardium. Questions remain, however, regarding the mechanisms by which PMNs are chemotaxed and activated and how this process causes contractile failure. METHODS AND RESULTS Studies were performed in an isolated rat heart model in which the effects of isolated cellular or humoral factors could be studied. Isolated rat hearts were perfused by the method of Langendorff, subjected to 20 minutes of global ischemia, and reperfused with perfusate alone or with perfusate containing PMNs, plasma, PMNs plus plasma, or PMNs plus inactivated plasma (preheated to 56 degrees C for 30 minutes to denature complement) (n = 10 in each group). Left ventricular developed pressure (LVDP) was measured during 1 minute of preischemic control infusion and on reflow after a 20-minute period of global ischemia. Additional measurements of free-radical generation were also performed on the coronary effluent by electron paramagnetic resonance spectroscopy (EPR) with the spin trap 5,5'-dimethyl-1-pyrroline-N-oxide (DMPO). During control infusion, no significant alterations in LVDP were observed, and there was no measurable free-radical generation. Reperfusion with plasma or PMNs alone did not alter postischemic LVDP, whereas plasma and PMNs together caused marked injury. LVDP after 45 minutes of reflow with PMNs plus plasma was 31.9 +/- 6.1% of control compared with 60.6 +/- 9.9% with plasma, 64.5 +/- 8.8% with PMNs, and 63.6 +/- 7.2% with perfusate alone (p &lt; 0.01). With plasma, which was preheated to deplete complement, this injury was not seen; LVDP was 70.8 +/- 10.9%. EPR measurements with the spin trap DMPO in the absence of PMNs demonstrated that oxygen free-radical generation is observed only during the first 1-2 minutes of reflow. Upon reperfusion with PMNs and plasma, however, radical generation persisted for more than 10 minutes. Increased neutrophil accumulation was observed in the postischemic heart in the absence of plasma; however, plasma factors were required for neutrophil-mediated contractile failure. C5a alone did not cause significant injury, but in the presence of PMNs it effectively substituted for plasma, causing marked injury. CONCLUSIONS Thus, plasma factors, most likely complement, are required for neutrophil activation with oxygen free-radical generation and secondary contractile dysfunction.
TCT-330 Does Coronary Physiology or Anatomy Better Predict the Capacity of Stenting to Increase Flow?
Authors: Sukhjinder S. Nijjer, Sayan Sen, Ricardo Petraco, Tim P. van de Hoef, Martijn A. van Lavieren, Rasha Al-Lamee, Mauro Echavarria-Pinto, Darrel P. Francis, Carlo Di Mario, Javier Escaned, Jan Piek, Justin E. Davies
Journal: Journal of the American College of Cardiology (2014)
Epidermal naevi associated with extrahepatic portal venous obstruction, hypoplastic kidney and lymphangiectasia: a new syndromic variant?
Authors: T. Kaur, B. Kumar, Y.K. Chawwla
Journal: British Journal of Dermatology (2004)

Journal Article Epidermal naevi associated with extrahepatic portal venous obstruction, hypoplastic kidney and lymphangiectasia: a new syndromic variant? Get access T. Kaur, T. Kaur Departments of Dermatology, Venereology and Leprology and Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh, India Search for other works by this author on: Oxford Academic Google Scholar B. Kumar, B. Kumar Departments of Dermatology, Venereology and Leprology and Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh, India Bhushan Kumar, E‐mail: kumarbhushan@hotmail.com Search for other works by this author on: Oxford Academic Google Scholar Y.K. Chawwla Y.K. Chawwla Departments of Dermatology, Venereology and Leprology and Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh, India Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 150, Issue 3, 1 March 2004, Pages 618–619, https://doi.org/10.1111/j.1365-2133.2004.05841.x Published: 01 March 2004
Post-competition blood lactate concentrations in competitive track cyclists
Authors: E. R. Burke, S. Fleck, T. Dickson
Journal: British Journal of Sports Medicine (1981)

Blood lactate (BL) concentrations were measured in 19 competitive cyclists after 4 competitive track events (kilometre, individual and team pursuit, and match sprints) during the US National Championships. A total of 34 samples were drawn. Our purpose was to investigate the share of anaerobic metabolism in the various events. The greatest mean BL concentration (16.94 mM/l) was found after the kilometre, with one individual recording a value of 18.22 mM/l. A low correlation coefficient for BL versus total riding time was found in the 6 samples drawn during the kilometre (r=0.51) and the 12 samples drawn during the individual pursuit (r=0.44). BL concentrations in all four events were not significantly different (p&lt;0.05) from each other. High values for BL were found in the match sprints (7 samples, mean 13.65 mM/l) an event lasting approximately 11 seconds. The mean BL in the kilometre (6 samples, 16.94 mM/l), individual pursuit (12 samples, 15.18 mM/l), and team pursuit (5 samples, 12.08 mM/l) compare favourably to the values reported for a variety of exercise modes of similar time, except running. While there is increased muscle mass in running, this fact alone may not explain the lower BL values in cycling. It is suggested that lower BL levels may be attributed to prolonged contraction-relaxation phase during cycling causing decreased blood flow to the leg.
THE PATHOLOGIC CHANGES OF THE ST. LOUIS TYPE OF ACUTE ENCEPHALITIS
Authors: HOWARD ANDERSON McCORDOCK
Journal: JAMA (1934)

A large number of autopsies was secured during the recent St. Louis epidemic of acute encephalitis, the result mainly of the cooperation of the various public health offices, the general medical profession and the public. Sufficient material was obtained for a complete study of sixty-three cases. The thoracic and abdominal organs and portions of the spinal cord were examined in addition to the brain in about 90 per cent of the autopsies. An adequate neuropathologic study of all this material has not yet been accomplished, but a few representative cases have been studied in detail and a sufficient number of sections from the others have been examined to obtain a fair understanding of the pathologic alterations in this type of encephalitis. The essential pathologic process is an acute nonsuppurative inflammation of the central nervous system characterized by severe vascular congestion with occasional petechial hemorrhages, cellular infiltration of the nervous tissue
Sleep-Deprived Young Drivers and the Risk for Crash
Authors: Alexandra L. C. Martiniuk, Teresa Senserrick, Serigne Lo, Ann Williamson, Wei Du, Ronald R. Grunstein, Mark Woodward, Nick Glozier, Mark Stevenson, Robyn Norton, Rebecca Q. Ivers
Journal: JAMA Pediatrics (2013)

Short sleep duration is common in adolescents and young adults, and short sleep duration is a risk factor for motor vehicle crash.To assess the association between hours of sleep and the risk for motor vehicle crash, including the time of day of crash and types of crash (single, multiple vehicle, run off road, and intersection).Prospective cohort study.New South Wales, Australia.Questionnaire responses were obtained from 20,822 newly licensed drivers aged 17 to 24 years. Participants held a first-stage provisional license between June 2003 and December 2004 prospectively linked to licensing and police-reported crash data, with an average of 2 years of follow-up. Analyses were conducted on a subsample of 19,327 participants for which there was full information.Sleeping 6 or fewer hours per night.The main outcome variable was police-reported crash. Multivariable Poisson regression models were used to investigate the role of sleep duration on the risk for crash.On average, those who reported sleeping 6 or fewer hours per night had an increased risk for crash compared with those who reported sleeping more than 6 hours (relative risk [RR], 1.21; 95% CI, 1.04-1.41). Less weekend sleep was significantly associated with an increased risk for run-off-road crashes (RR, 1.55; 95% CI, 1.21-2.00). Crashes for individuals who had less sleep per night (on average and on weekends) were significantly more likely to occur between 8 pm and 6 am (RR, 1.86; 95% CI, 1.11-3.13, for midnight to 5:59 am and RR, 1.66; 95% CI, 1.15-2.39, for 8:00 pm to 11:59 pm).Less sleep per night significantly increased the risk for crash for young drivers. Less sleep on weekend nights increased the risk for run-off-road crashes and crashes occurring in the late-night hours. This provides rationale for governments and health care providers to address sleep-related crashes among young drivers.
ST2 as a Marker for Risk of Therapy-Resistant Graft-versus-Host Disease and Death
Authors: Mark T. Vander Lugt, Thomas M. Braun, Samir Hanash, Jerome Ritz, Vincent T. Ho, Joseph H. Antin, Qing Zhang, Chee-Hong Wong, Hong Wang, Alice Chin, Aurélie Gomez, Andrew C. Harris, John E. Levine, Sung W. Choi, Daniel Couriel, Pavan Reddy, James L.M. Ferrara, Sophie Paczesny
Journal: New England Journal of Medicine (2013)

No plasma biomarkers are associated with the response of acute graft-versus-host disease (GVHD) to therapy after allogeneic hematopoietic stem-cell transplantation.We compared 12 biomarkers in plasma obtained a median of 16 days after therapy initiation from 10 patients with a complete response by day 28 after therapy initiation and in plasma obtained from 10 patients with progressive GVHD during therapy. The lead biomarker, suppression of tumorigenicity 2 (ST2), was measured at the beginning of treatment for GVHD in plasma from 381 patients and during the first month after transplantation in three independent sets totaling 673 patients to determine the association of this biomarker with treatment-resistant GVHD and 6-month mortality after treatment or transplantation.Of the 12 markers, ST2 had the most significant association with resistance to GVHD therapy and subsequent death without relapse. As compared with patients with low ST2 values at therapy initiation, patients with high ST2 values were 2.3 times as likely to have treatment-resistant GVHD (95% confidence interval [CI], 1.5 to 3.6) and 3.7 times as likely to die within 6 months after therapy (95% CI, 2.3 to 5.9). Patients with low ST2 values had lower mortality without relapse than patients with high ST2 values, regardless of the GVHD grade (11% vs. 31% among patients with grade I or II GVHD and 14% vs. 67% among patients with grade III or IV GVHD, P<0.001 for both comparisons). Plasma ST2 values at day 14 after transplantation were associated with 6-month mortality without relapse, regardless of the intensity of the conditioning regimen.ST2 levels measured at the initiation of therapy for GVHD and during the first month after transplantation improved risk stratification for treatment-resistant GVHD and death without relapse after transplantation. (Funded by the National Institutes of Health.)
Anticardiolipin antibodies in acute myeloid leukemia: Prevalence and clinical significance
Authors: Izidore S. Lossos, Vered Bogomolski-Yahalom, Yaacov Matzner
Journal: American Journal of Hematology (1998)

This prospective study was designed to explore the prevalence and the clinical and prognostic significance of anticardiolipin (ACL) antibodies in patients with acute myeloid leukemia (AML). The study includes 37 consecutive AML patients >15 years old without previous history of thromboembolism, recurrent fetal loss, or autoimmune disease and with no evidence of infection at the time of enrollment. ACL antibodies were found in 25 patients (68%). None of the patients had high positive titers; 8 had moderately positive while 17 had low positive ACL antibody titers. ACL antibody positivity did not predict response to chemotherapy and was not correlated with age, gender, FAB class, platelet and white blood cell counts at presentation, and the risk of thromboembolism. ACL antibody titers did correlate, however, with AML activity in the majority of patients (93%) during 4-19 months of follow up. These results demonstrate a high prevalence of ACL antibodies in AML patients and suggest that serum ACL antibodies may be a useful adjunct in predicting relapse and documenting disease activity and therapy response.
Leucocytosis is not a manifestation of rejection.
Authors: A S Daar, P J Morris, D O Oliver
Journal: BMJ (1977)

The leucocyte response to allograft rejection was retrospectively analysed in 80 rejection episodes that occurred in 50 patients. There was no significant change in leucocyte count in 32 rejection episodes. In 27 there was a fall in leucocyte count of more than 20% and in only 21 was there a rise in count of more than 20%. Thus leucocytosis seems not to be a manifestation of rejection; indeed, it is the least common response, a fall in the count being commoner. The results also suggest that the prognosis for the graft is poorer when the leucocyte count falls significantly.
Regular aspirin use and myocardial infarction.
Authors: H Jick, O S Miettinen
Journal: BMJ (1976)

Current therapies are less effective for treating sustained/permanent versus paroxysmal atrial fibrillation (AF). We and others have previously shown that histone deacetylase (HDAC) inhibition reverses structural and electrical atrial remodeling in mice with inducible, paroxysmal-like AF. Here, we hypothesize an important, specific role for class I HDACs in determining structural atrial alterations during sustained AF. The class I HDAC inhibitor <i>N</i>-acetyldinaline [4-(acetylamino)-<i>N</i>-(2-amino-phenyl) benzamide] (CI-994) was administered for 2 weeks (1 mg/kg/day) to Hopx transgenic mice with atrial remodeling and inducible AF and to dogs with atrial tachypacing-induced sustained AF. Class I HDAC inhibition prevented atrial fibrosis and arrhythmia inducibility in mice. Dogs were divided into three groups: 1) sinus rhythm, 2) sustained AF plus vehicle, and 3) sustained AF plus CI-994. In group 3, the time in AF over 2 weeks was reduced by 30% compared with group 2, along with attenuated atrial fibrosis and intra-atrial adipocyte infiltration. Moreover, group 2 dogs had higher atrial and serum inflammatory cytokines, adipokines, and atrial immune cells and adipocytes compared with groups 1 and 3. On the other hand, groups 2 and 3 displayed similar left atrial size, ventricular function, and mitral regurgitation. Importantly, the same histologic alterations found in dogs with sustained AF and reversed by CI-994 were also present in atrial tissue from transplanted patients with chronic AF. This is the first evidence that, in sustained AF, class I HDAC inhibition can reduce the total time of fibrillation, atrial fibrosis, intra-atrial adipocytes, and immune cell infiltration without significant effects on cardiac function.
Intracranial leukaemia and the cerebrospinal fluid.
Authors: R G Rawbone, M T Shaw, K D Bagshawe
Journal: BMJ (1972)

Neuromodulators released during and after a fearful experience promote the consolidation of long-term memory for that experience. Because overconsolidation may contribute to the recurrent and intrusive memories of post-traumatic stress disorder, neuromodulatory receptors provide a potential pharmacological target for prevention. Stimulation of muscarinic receptors promotes memory consolidation in several conditioning paradigms, an effect primarily associated with the M<sub>1</sub> receptor (M<sub>1</sub>R). However, neither inhibiting nor genetically disrupting M<sub>1</sub>R impairs the consolidation of cued fear memory. Using the M<sub>1</sub>R agonist cevimeline and antagonist telenzepine, as well as M<sub>1</sub>R knock-out mice, we show here that M<sub>1</sub>R, along with β<sub>2</sub>-adrenergic (β<sub>2</sub>AR) and D<sub>5</sub>-dopaminergic (D<sub>5</sub>R) receptors, regulates the consolidation of cued fear memory by redundantly activating phospholipase C (PLC) in the basolateral amygdala (BLA). We also demonstrate that fear memory consolidation in the BLA is mediated in part by neuromodulatory inhibition of the M-current, which is conducted by KCNQ channels and is known to be inhibited by muscarinic receptors. Manipulating the M-current by administering the KCNQ channel blocker XE991 or the KCNQ channel opener retigabine reverses the effects on consolidation caused by manipulating β<sub>2</sub>AR, D<sub>5</sub>R, M<sub>1</sub>R, and PLC. Finally, we show that cAMP and protein kinase A (cAMP/PKA) signaling relevant to this stage of consolidation is upstream of these neuromodulators and PLC, suggesting an important presynaptic role for cAMP/PKA in consolidation. These results support the idea that neuromodulatory regulation of ion channel activity and neuronal excitability is a critical mechanism for promoting consolidation well after acquisition has occurred.
The peripheral myelin protein gene PMP–22 is contained within the Charcot–Marie–Tooth disease type 1A duplication
Authors: V. Timmerman, E. Nelis, W. Van Hul, B.W. Nieuwenhuijsen, K.L. Chen, S. Wang, K. Ben Othman, B. Cullen, R.J. Leach, C.O. Hanemann, P. De Jonghe, P. Raeymaekers, G-J.B. van Ommen, J-J. Martin, H.W. Müller, J.M. Vance, K.H. Fischbeck, C. Van Broeckhoven
Journal: Nature Genetics (1992)
Observations on THE SYMPATHETIC NERVOUS SYSTEM
Authors: W. J. Mayo
Journal: BMJ (1930)

HE that does nliot go beyond the facts w-ill seldom get as far as the facts" (Huxley).In research this axiom tells thle story.Star ting by deductionis from facts, scientific imzlagilnation develops hypotheses, which are prov-ed or dispro-ed through that form of inductive philosophy hich we call research.Although we desire positive results, negative results have value, and often negativity itself starts a niew (leduction whiclh leads to the truth.The hi.story of our unider staniding of the synmpathetic nervous sy-steiim w-ell illustrates the value of both positivce and negative scientific contributions.
Evidence based medicine: does it make a difference?
Authors: David P Kernick
Journal: BMJ (2005)

Evidence based medicine: does it make a difference? Use wiselyEditor-The term "evidence based medicine" entered the scientific lexicon only a little more than a decade ago. 1 What caused its remarkable spread, and what are the implications of its broad and rapid diffusion?The team that coined the term at first considered using the phrase "scientific medicine" but rejected it because it implied that other approaches were by definition unscientific. 2However, critics have argued that the term evidence based medicine carries a similar moral valence and linguistic slipperiness. 3 Who could argue against the notion of providing care that integrates individual clinical skill and the best external evidence? 4 Originally developed as a method for teaching medical residents, evidence based medicine is being applied ever more broadly to the organisation and delivery of medical services.Multiple stakeholders now seek to assume its mantle for purposes that often contradict its original intent.Managers, equating lack of evidence with lack of effectiveness, use it as a rationale for cutting services.Industry generates evidence of questionable quality to promote its products.Medical researchers come to believe that they hold a monopoly on generating and interpreting evidence.Evidence based medicine, developed as a means of taming the unscientific and messy world of clinical practice, has itself entered the unscientific and messy world of politics. 5ike any technology, evidence based medicine carries risks and benefits and can be used appropriately or inappropriately.Overly inclusive definitions threaten to deprive the term of meaning, and unchecked use increases the risk of misuse.In the past decade, evidence based medicine has contributed much to how we teach, deliver, and think about clinical services.In the coming decade, we must continue to ensure that it is not only used widely but wisely.
Community health services.
Authors: J. Neuberger
Journal: BMJ (1992)

The Tomlinson report, with its emphasis on primary and community care, offers great scope to community health services, for long the poor relation of the NHS, and particularly poorly resourced in London. The aim is to create services that break down the barriers between primary, secondary, and tertiary health care and concentrate on providing high quality care tailored to individual patients' needs. Thus a range of flexible options needs to be developed between acute hospital based care and the standard home care arrangements currently provided by district nurses. Examples, include hospital at home schemes, nursing beds, and rehabilitation beds. Together community and primary care services need to consider weekend coverage, to conduct research, and to become a setting for education. The infrastructure for primary and community care must, however, be put in place before acute facilities are shut.
The Editorial Team reflects on 2003: our first year “in office”
Authors: H Piper
Journal: Cardiovascular Research (2003)

At the end of last year, when a truck arrived from the previous Cardiovascular Research editorial office in Amsterdam with four filing cabinets full of manuscripts, we all swallowed hard with the thought of what lay ahead. We rolled up our sleeves, however, and got right to work. Looking back, the experience of those first 6 weeks was quite different from the routine of the Editorial Office today. In January, our fax machine was constantly running out of paper, and courier companies would have to come two or three times a day to deliver and pick up manuscripts. The induction of the electronic manuscript handling system in February radically changed all of that.

Submission is now carried out … 

*Corresponding author. Tel.: +49-641-994-7242; fax: +49-641-994-7209. CVR{at}physiologie.med.uni-giessen.de
Neuropathy in experimental diabetes: an animal model.
Authors: J Jakobsen, K Lundbaek
Journal: BMJ (1976)

A morphometric study of the common peroneal nerve in early experimental diabetes in rats showed that fibre size was diminished. The reduction in the size of the axon was twice that of the myelin sheath. This may contribute to the understanding of the impaired motor conduction velocity found in diabetics shortly after the onset of their disease.