tbuckley/cabot-search huggingface dataset:
Clinical characteristics and sleep discorded breathing in an elderly population referred for sleep study
Authors: Eleni Perantoni, Stavros Tryfon, Konstantina Nikolaou, Venetia Tsara
Journal: European Respiratory Journal (2014)

The aim of the study was to assess the severity of sleep disordered breathing in elderly patients with a history of daytime sleepiness and snoring.  Methods. We studied retrospectively 177 subjects over 70 years old, who were referred for a polysomnography study. Anthropometric characteristics, smoking habit, alcohol consumption were reported. Daily sleepiness was estimated subjectively by their perception and objectively by the Epworth Sleepiness Scale (ESS).  Results. The patients were 145 men and 32 women aged 74.5±3.1y , with a BMI of 31.1±8.4kg/m2. Former smokers were 10.2% and social alcohol consumers 15.8%. The ESS was 9±5.5 while the 40.1% of them reported daytime sleepiness.  In the 95.5% of patients an AHI>5/h was found. Mild SAS (AHI 5-15/h) was found in 13% , moderate (AHI 15-30/h) in 18.6% and severe (AHI>30/h) in 63.3 % of patients. Patients with severe SAS were more obese and a significant difference in BMI was observed between them and moderate SAS patients (BMI 32.9±5.2kg/m2 and 29.7±4.6 kg/m2 respectively, p   For all patients there was a positive correlation between AHI and BMI (r=0.400 p  Conclusion. Severe SAS was common in the elderly population referred for sleep study despite the mild symptoms. Obesity was found as a predictor positively correlated with the severity of the SAS.
Chronic arthritis before 1876: early British cases suggesting rheumatoid arthritis.
Authors: G O Storey, M Comer, D L Scott
Journal: Annals of the Rheumatic Diseases (1994)

Is rheumatoid arthritis (RA) a recent disease or do its roots lie in antiquity?There are several reasons to believe that RA may be a modem disease first seen in the mid-nineteenth century which could have followed the social changes of the industrial revolution.'But is this actually the case?Although the term 'rheumatoid arthritis' was only proposed by Garrod in 1876,2 much evidence indicates that RA existed before 1800.Rothschild et al3 found features of an erosive arthropathy in six pre- historic skeletons, though 3000 subterranean years could cause some bone changes.The illness of Constantine IX, described by Psellus (1 063)4 had features of a chronic inflammatory illness such as RA.4The disease of Desiderus Erasmus (1466-1536), reported by Appel- boom and others,5 had similar features.Sie- brandus Sisilius, a 17th century Dutch priest, had evidence of rheumatoid arthritis of the robust type shown in a portrait described by Dequeker.6The description of RA by Landr& Beauvais7 in 1800 is generally accepted as the modem disease but was this the first report?To evaluate if RA existed before the mid-1800s we reviewed medical writing before 1850 and examined diagnostic registers and case histories from archives at London hospitals after 1700.
Pristimerin induces apoptosis in imatinib-resistant chronic myelogenous leukemia cells harboring T315I mutation by blocking NF-κB signaling and depleting Bcr-Abl
Authors: Zhongzheng Lu, Yanli Jin, Chun Chen, Juan Li, Qi Cao, Jingxuan Pan
Journal: Molecular Cancer (2010)

Chronic myelogenous leukemia (CML) is characterized by the chimeric tyrosine kinase Bcr-Abl. Bcr-Abl-T315I is the notorious point mutation that causes resistance to imatinib and the second generation tyrosine kinase inhibitors, leading to poor prognosis. CML blasts have constitutive p65 (RelA NF-kappaB) transcriptional activity, and NF-kappaB may be a potential target for molecular therapies in CML that may also be effective against CML cells with Bcr-Abl-T315I.In this report, we discovered that pristimerin, a quinonemethide triterpenoid isolated from Celastraceae and Hippocrateaceae, inhibited growth and induced apoptosis in CML cells, including the cells harboring Bcr-Abl-T315I mutation. Additionally, pristimerin inhibited the growth of imatinib-resistant Bcr-Abl-T315I xenografts in nude mice. Pristimerin blocked the TNFalpha-induced IkappaBalpha phosphorylation, translocation of p65, and expression of NF-kappaB-regulated genes. Pristimerin inhibited two steps in NF-kappaB signaling: TAK1TauIKK and IKKTauIkappaBalpha. Pristimerin potently inhibited two pairs of CML cell lines (KBM5 versus KBM5-T315I, 32D-Bcr-Abl versus 32D-Bcr-Abl-T315I) and primary cells from a CML patient with acquired resistance to imatinib. The mRNA and protein levels of Bcr-Abl in imatinib-sensitive (KBM5) or imatinib-resistant (KBM5-T315I) CML cells were reduced after pristimerin treatment. Further, inactivation of Bcr-Abl by imatinib pretreatment did not abrogate the TNFalpha-induced NF-kappaB activation while silencing p65 by siRNA did not affect the levels of Bcr-Abl, both results together indicating that NF-kappaB inactivation and Bcr-Abl inhibition may be parallel independent pathways.To our knowledge, this is the first report to show that pristimerin is effective in vitro and in vivo against CML cells, including those with the T315I mutation. The mechanisms may involve inhibition of NF-kappaB and Bcr-Abl. We concluded that pristimerin could be a lead compound for further drug development to overcome imatinib resistance in CML patients.
Cigarette tar yields in relation to mortality from lung cancer in the cancer prevention study II prospective cohort, 1982-8
Authors: Jeffrey E Harris, Michael J Thun, Alison M Mondul, Eugenia E Calle
Journal: BMJ (2004)

To assess the risk of lung cancer in smokers of medium tar filter cigarettes compared with smokers of low tar and very low tar filter cigarettes.Analysis of the association between the tar rating of the brand of cigarette smoked in 1982 and mortality from lung cancer over the next six years. Multivariate proportional hazards analyses used to assess hazard ratios, with adjustment for age at enrollment, race, educational level, marital status, blue collar employment, occupational exposure to asbestos, intake of vegetables, citrus fruits, and vitamins, and, in analyses of current and former smokers, for age when they started to smoke and number of cigarettes smoked per day.Cancer prevention study II (CPS-II).364 239 men and 576 535 women, aged > or = 30 years, who had either never smoked, were former smokers, or were currently smoking a specific brand of cigarette when they were enrolled in the cancer prevention study.Death from primary cancer of the lung among participants who had never smoked, former smokers, smokers of very low tar (< or = 7 mg tar/cigarette) filter, low tar (8-14 mg) filter, high tar (> or = 22 mg) non-filter brands and medium tar conventional filter brands (15-21 mg).Irrespective of the tar level of their current brand, all current smokers had a far greater risk of lung cancer than people who had stopped smoking or had never smoked. Compared with smokers of medium tar (15-21 mg) filter cigarettes, risk was higher among men and women who smoked high tar (> or = 22 mg) non-filter brands (hazard ratio 1.44, 95% confidence interval 1.20 to 1.73, and 1.64, 1.26 to 2.15, respectively). There was no difference in risk among men who smoked brands rated as very low tar (1.17, 0.95 to 1.45) or low tar (1.02, 0.90 to 1.16) compared with those who smoked medium tar brands. The same was seen for women (0.98, 0.80 to 1.21, and 0.95, 0.82 to 1.11, respectively).The increase in lung cancer risk is similar in people who smoke medium tar cigarettes (15-21 mg), low tar cigarettes (8-14 mg), or very low tar cigarettes (< or = 7 mg). Men and women who smoke non-filtered cigarettes with tar ratings > or = 22 mg have an even higher risk of lung cancer.
Ischemic and Pharmacological Preconditioning in Girardi Cells and C2C12 Myotubes Induce Mitochondrial Uncoupling
Authors: Jan Minners, Lydia Lacerda, Joy McCarthy, James J. Meiring, Derek M. Yellon, Michael N. Sack
Journal: Circulation Research (2001)

Pharmacological uncoupling of mitochondrial oxidation from phosphorylation promotes preconditioning-like cardioprotection in the isolated rat heart. We hypothesized that modest mitochondrial uncoupling may be a critical cellular event in orchestrating preconditioning. Human-derived Girardi cells and murine C2C12 skeletal myotubes were preconditioned using simulated ischemia, adenosine, and diazoxide. Cell viability after 6 hours of simulated ischemia was measured using lactate dehydrogenase release and propidium iodide uptake. Mitochondrial inner membrane potential (ΔΨm) was investigated by flow cytometry, cellular ATP by recombinant firefly-luciferase bioluminescence, and cellular oxygen consumption using oximetry. Preconditioning enhanced cell viability with attenuation of lactate dehydrogenase release (≥30%, P &lt;0.05 versus ischemic controls) and a reduction in propidium iodide uptake by ≥26% versus ischemic controls after simulated ischemia in both cell lines. In Girardi cells, preconditioning induced the following phenotype immediately before index ischemia: (1) decreased ΔΨm (JC-1: simulated ischemia 90±3%, adenosine 82±7%, diazoxide 87±4%, versus control 100%, P &lt;0.05); (2) attenuation in cellular ATP levels (CTL 0.21±0.03 nmol/L ATP/μg protein, simulated ischemia 0.12±0.02, adenosine 0.15±0.02, diazoxide 0.11±0.02, P &lt;0.05); and (3) enhanced cellular oxygen consumption (control 2.3±0.1 nmol/L oxygen/min/1×10 6 cells, simulated ischemia 3.1±0.1, adenosine 3.1±0.3, diazoxide 2.6±0.2, P &lt;0.05). Cytoprotection, mitochondrial depolarization, and enhanced oxygen consumption were attenuated by the putative mitochondrial K ATP -channel antagonist 5-hydroxydecanoate. The uncoupled phenotype in response to preconditioning was similarly observed in C2C12 myotubes. The present study suggests that modest mitochondrial uncoupling represents a unifying cellular response which may be important in directing preconditioning-mediated cytoprotection.
Adverse Event Reporting in Publications Compared With Sponsor Database for Cancer Clinical Trials
Authors: Orit Scharf, A. Dimitrios Colevas
Journal: Journal of Clinical Oncology (2006)

Prospectively planned collection and analysis of adverse event (AE) data are essential parts of well-conducted clinical trials. The AE data in a trial sponsor's database should be comparable with what is stipulated in the protocol and with the AE data published. We examined whether the published AE data differ from those in the sponsor's database and from the data collection requirements stated in study protocols.We searched the National Cancer Institute (NCI) Clinical Data Update System (CDUS) for studies that used the Common Toxicity Criteria version 2.0 and for which a final study publication was available. We extracted from the protocols information pertaining to AE collection and reporting methods and compared it with the methods cited in the article. We also compared the AE data in the trial publication with the AE data submitted by the investigators to CDUS.We identified 22 studies meeting the criteria for this review. There was considerable inconsistency between AE collection and reporting methods cited in the protocols versus final publications. AE data in the article and CDUS were not identical. Twenty-seven percent of article high-grade AEs could not be matched to agent-attributable AEs in the CDUS. Twenty-eight percent of CDUS high-grade AEs could not be matched to AEs in the corresponding article. In 14 of 22 articles, the number of high-grade AEs in CDUS differed from the number in the articles by 20% or more.Lack of consistency in and reporting of AEs are associated with NCI database and trial publication AE data discrepancy.
learning colour words is slow: a cross-situational learning account
Authors: paul vogt, andrew d. m. smith
Journal: Behavioral and Brain Sciences (2005)

research into child language reveals that it takes a long time for children to learn the correct mapping of colour words. steels &amp; belpaeme's (s&amp;b's) guessing game, however, models fast learning of words. we discuss computational studies based on cross-situational learning, which yield results that are more consistent with the empirical child language data than those obtained by s&amp;b.
The Editor, 'The British Journal of Dermatology'. Napkin psoriasis
Authors: G. Auckland
Journal: British Journal of Dermatology (1967)

Journal Article The Editor, ‘The British Journal of Dermatology’. Napkin psoriasis Get access G. Auckland G. Auckland Manchester and Salford, Hospital for Skin Diseases, Quay St., Manchester, 2 Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 79, Issue 4, 1 April 1967, Pages 244–245, https://doi.org/10.1111/j.1365-2133.1967.tb11483.x Published: 01 April 1967
Association between LDL-C and Risk of Myocardial Infarction in CKD
Authors: Marcello Tonelli, Paul Muntner, Anita Lloyd, Braden Manns, Scott Klarenbach, Neesh Pannu, Matthew James, Brenda Hemmelgarn
Journal: Journal of the American Society of Nephrology (2013)

LDL cholesterol (LDL-C) is an important marker of coronary risk in the general population, but its utility in people with CKD is unclear. We studied 836,060 adults from the Alberta Kidney Disease Network with at least one measurement of fasting LDL-C, estimated GFR (eGFR), and proteinuria between 2002 and 2009. All participants were free of stage 5 CKD at cohort entry. We followed participants from first eGFR measurement to March 31, 2009; we used validated algorithms applied to administrative data to ascertain primary outcome (hospitalization for myocardial infarction) and Cox regression to calculate adjusted hazard ratios (HRs) for myocardial infarction by LDL-C categories within eGFR strata. During median follow-up of 48 months, 7762 patients were hospitalized for myocardial infarction, with incidence highest among participants with the lowest eGFR. Compared with 2.6–3.39 mmol/L (referent), the risk associated with having LDL-C above 4.9 mmol/L seemed greatest for GFR≥90 ml/min per 1.73 m2 and least for eGFR=15–59.9 ml/min per 1.73 m2. Specifically, the adjusted HRs (95% confidence intervals) of myocardial infarction associated with LDL-C of ≥4.9 compared with 2.6–3.39 mmol/L in participants with eGFR=15–59.9, 60–89.9, and ≥90 ml/min per 1.73 m2 were 2.06 (1.59, 2.67), 2.30 (2.00, 2.65), and 3.01 (2.46, 3.69). In conclusion, the association between higher LDL-C and risk of myocardial infarction is weaker for people with lower baseline eGFR, despite higher absolute risk of myocardial infarction. Increased LDL-C may be less useful as a marker of coronary risk among people with CKD than the general population.
A New Anatomical Framework for Neuropsychiatric Disorders and Drug Abuse
Authors: Lennart Heimer
Journal: American Journal of Psychiatry (2003)

Histotechnological breakthroughs in the late 1960s paved the way for anatomical discoveries that led to the concepts of the ventral striatal-pallidal system and the extended amygdala. These two macro-anatomical systems, together with the basal nucleus of Meynert, represent the main components of the new anatomy of the basal forebrain. The concept of the ventral striatal-pallidal system provided the first indication of the existence of parallel cortical-striatal-pallidal-thalamic-cortical circuits, which in turn led to the theory of segregated cortical-subcortical reentrant circuits as a conceptual framework for the study of neuropsychiatric disorders. The multifarious symptoms of neuropsychiatric disorders, however, cannot be understood unless the extended amygdala, the basal nucleus of Meynert, and the septal-diagonal band system are also included in such deliberations. All of these systems serve as output channels for activities in the greater limbic lobe, which usually is critically involved in neuropsychiatric disorders. Within the context of the new anatomy of the basal forebrain, structures such as the accumbens, the olfactory tubercle, and the amygdala have lost legitimacy as independent functional-anatomical units at the same time as the major components of the last uncharted territory of the human brain, the substantia innominata, have been identified.
Reduced bone density in cystic fibrosis: F508 mutation is an independent risk factor
Authors: S. J. King, D. J. Topliss, T. Kotsimbos, I. B. Nyulasi, M. Bailey, P. R. Ebeling, J. W. Wilson
Journal: European Respiratory Journal (2005)

The aim of this cross-sectional study was to determine the prevalence and identify determinants of reduced bone mineral density (BMD) in adults with cystic fibrosis (CF). Adults (88) with CF (mean± sd age 29.9±7.7 yrs; forced expiratory volume in one second (FEV1) 58.2±21.5% of the predicted value) were studied. BMD at the lumbar spine (LS) and femoral neck (FN) and body composition were measured using dual-energy X-ray absorptiometry. Blood and urine were analysed for hormones, bone turnover markers, and the cytokines tumour necrosis factor-α, and interleukin-6 and -1β. FEV1 (% pred); CF genotype; malnutrition; history of growth, development or weight gain delays; and corticosteroid use were analysed. BMD Z-scores were −0.58±1.30 (mean± sd ) at the LS and −0.24±1.19 at the FN. Z-scores of &lt;−2.0 were found in 17% of subjects. Subjects who were homozygous or heterozygous for the ΔF508 mutation exhibited significantly lower Z-scores than those with no ΔF508 allele. Multiple linear regression showed that the ΔF508 genotype and male sex were independently associated with lower BMD at both sites. Other factors also independently associated with lower BMD included malnutrition, lower 25-hydroxyvitamin D level, lower fat-free mass and lower FEV1 (% pred). In conclusion, reduced bone mineral density in cystic fibrosis is associated with a number of factors, including ΔF508 genotype, male sex, greater lung disease severity and malnutrition.
Stem cells, angiogenesis and muscle healing: a potential role in massage therapies?
Authors: Thomas M Best, Burhan Gharaibeh, Johnny Huard
Journal: British Journal of Sports Medicine (2012)

Skeletal muscle injuries are among the most common and frequently disabling injuries sustained by athletes. Repair of injured skeletal muscle is an area that continues to present a challenge for sports medicine clinicians and researchers due, in part, to complete muscle recovery being compromised by development of fibrosis leading to loss of function and susceptibility to re-injury. Injured skeletal muscle goes through a series of coordinated and interrelated phases of healing including degeneration, inflammation, regeneration and fibrosis. Muscle regeneration initiated shortly after injury can be limited by fibrosis which affects the degree of recovery and predisposes the muscle to reinjury. It has been demonstrated in animal studies that antifibrotic agents that inactivate transforming growth factor (TGF)-β1 have been effective at decreasing scar tissue formation. Several studies have also shown that vascular endothelial growth factor (VEGF) can increase the efficiency of skeletal muscle repair by increasing angiogenesis and, at the same time, reducing the accumulation of fibrosis. We have isolated and thoroughly characterised a population of skeletal muscle-derived stem cells (MDSCs) that enhance repair of damaged skeletal muscle fibres by directly differentiating into myofibres and secreting paracrine factors that promote tissue repair. Indeed, we have found that MDSCs transplanted into skeletal and cardiac muscles have been successful at repair probably because of their ability to secrete VEGF that works in a paracrine fashion. The application of these techniques to the study of sport-related muscle injuries awaits investigation. Other useful strategies to enhance skeletal muscle repair through increased vascularisation may include gene therapy, exercise, neuromuscular electrical stimulation and, potentially, massage therapy. Based on recent studies showing an accelerated recovery of muscle function from intense eccentric exercise through massage-based therapies, we believe that this treatment modality offers a practical and non-invasive form of therapy for skeletal muscle injuries. However, the biological mechanism(s) behind the beneficial effect of massage are still unclear and require further investigation using animal models and potentially randomised, human clinical studies.
Carotid artery intima-media thickness in polycystic ovary syndrome: a systematic review and meta-analysis
Authors: Michelle L. Meyer, Angela M. Malek, Robert A. Wild, Mary T. Korytkowski, Evelyn O. Talbott
Journal: Human Reproduction Update (2011)

BACKGROUNDPolycystic ovary syndrome (PCOS) is a common reproductive endocrine disorder associated with cardiovascular disease (CVD) risk factors and metabolic disturbances. This systematic review and meta-analysis was conducted to determine whether carotid intima-media thickness (CIMT), a marker of subclinical atherosclerosis, is higher in women with PCOS compared with women without PCOS.
Should patients with chronic obstructive pulmonary disease be prescribed a resistance-training programme?
Authors: T. P. Grove
Journal: British Journal of Sports Medicine (2008)

Chronic obstructive pulmonary disease (COPD) has long been recognised to affect the pulmonary system. However, a growing body of evidence is now emerging, which indicates that skeletal muscle dysfunction (SMD) is becoming a key feature of COPD.1 SMD is related to the loss of muscle mass and strength, which are significant predictors of poor healthrelated quality of life (HRQoL), mortality and subsequent increased healthcare costs in COPD patients.2,–,4 SMD usually affects the muscles of ambulation by altering their structure and biochemical function.1 Tissue biopsies taken from the quadriceps muscles have shown a greater predominance towards fatiguable Type IIb muscle fibres and a reduction in Type I muscle fibres, along with lower oxidative enzyme concentrations, mitochondria and lower muscle fibre-to-capillary ratios.1 5,–,7 The shift in Type IIb muscle fibres along with lower oxidative enzyme concentrations cause early lactic acid production at lower exercise levels due to anaerobic metabolism.8

Despite the greater predominance of Type IIb muscle fibres, there also appears to be a deficit in muscle strength in COPD patients. An observational study has demonstrated that respiratory disease patients have on average a 19% overall lower muscle strength score on four resistance exercises (knee extensions, leg curls, chest press and seated row) when compared with healthy subjects.9

Traditionally, most …
Pentoxifylline inhibits interleukin-2-induced toxicity in C57BL/6 mice but preserves antitumor efficacy.
Authors: M J Edwards, B T Heniford, E A Klar, K W Doak, F N Miller
Journal: Journal of Clinical Investigation (1992)

Interleukin 2 (IL-2) mediates the regression of metastatic cancer but clinical use has been limited due to associated toxicities. Tumor necrosis factor (TNF) is an important mediator of IL-2 toxicity and may have a limited role in IL-2 antitumor efficacy. Because pentoxifylline (PTXF) inhibits TNF production, we hypothesized that PTXF would ameliorate IL-2 toxicity without compromising antitumor efficacy. Four groups of female C57BL/6 mice with pulmonary metastases from a 3-methylcholanthrene-induced fibrosarcoma (MCA-105) and four groups of nontumored mice were treated every 6 h for 4 d by intraperitoneal injections of either IL-2 alone, IL-2 and PTXF, PTXF alone, or equal volumes of saline. Upon completion of therapy, we found that PTXF suppressed many of the IL-2-induced effects including TNF production, lymphocytic infiltration of multiple organs, multiple organ edema, hepatic dysfunction, leukopenia, and thrombocytopenia. Tumor response was determined 21 d after cessation of therapy by quantitating the number and surface area of pulmonary metastases. PTXF preserved antitumor efficacy while reducing the morbidity and mortality caused by IL-2 treatment. These data strongly support the use of PTXF in extending the therapeutic index of IL-2 in the treatment of cancer.