tbuckley/cabot-search huggingface dataset:
Thermographic Patterns of Angina Pectoris
Authors: CONSTANTINE POTANIN, DAVID HUNT, L. THOMAS SHEFFIELD
Journal: Circulation (1970)

Liquid crystals, encapsulated onto black Mylar tapes, were used as cutaneous temperature sensors in 50 male patients, who had thermographic examinations while they were being exercised on the treadmill, in an attempt to induce angina pectoris. Twenty-eight of the group remained free of pain and the exercise thoracic thermogram was essentially unchanged from the control or resting state. Twenty-two patients developed angina pectoris during exercise, of whom 21 had associated ST depression in the electrocardiogram, and 17 thermographic abnormalities. When the pain was unilateral (nine patients), skin coolness was invariable and was within the distribution of the pain. When the pain was central (13 patients), skin coolness was present in some of the patients (eight of 13) and was not always within the area of pain. When present, the skin coolness was transient and settled within minutes of relief of pain.
Murine gammaherpes virus as a cofactor in the development of pulmonary fibrosis in bleomycin resistant mice
Authors: S.S. Lok, Y. Haider, D. Howell, J.P. Stewart, P.S. Hasleton, J.J. Egan
Journal: European Respiratory Journal (2002)

Studies of human tissue have suggested an association between productive Epstein Barr virus and idiopathic pulmonary fibrosis (IPF). However, a pathogenic role for the virus has not been established. This study was undertaken to develop an animal model, which would explore the association between viral infection and pulmonary fibrosis. BALB/c mice (n=30), resistant to bleomycin, were primed with murine gammaherpesvirus 68 and then given intraperitoneal bleomycin. The mice were sacrificed at 28 days after bleomycin and their lungs assessed histologically and biochemically. Lung pathology was scored 0-3 for fibrotic and inflammatory change. BALB/c mice given virus and bleomycin showed more lung fibrosis (median score 2.2) compared to those given bleomycin alone (median 0), virus alone (median 0.2) or phosphate-buffered saline (PBS) control (median 0). Similarly mice given both virus and bleomycin showed more lung inflammation (median score 1.9) compared to those given bleomycin (median 0.5), virus (median 0.8), or PBS control (median 0.2). There was a significant difference in collagen content between the bleomycin and virus group (mean 1.86 mg) compared to the belomycin alone group (mean 1.52 mg). These results suggest that virus alone does not result in pulmonary fibrosis but that replicating virus in the presence of an exogenous injury may promote the development of pulmonary fibrosis.
Cast of Complex Congenital Heart Malformation in a Living Patient
Authors: Sibylle Mottl-Link, Thomas Boettger, Julia J. Krueger, Urte Rietdorf, Bernhard Schnackenburg, Peter Ewert, Felix Berger, Eike Nagel, Hans-Peter Meinzer, Amy Juraszek, Titus Kuehne, Ivo Wolf
Journal: Circulation (2005)
Hepatic mycobacterial disease and aids
Authors: Richard W. Light
Journal: Hepatology (1990)

We reviewed the clinical data, hepatic histology, and microbiological features of 21 patients with previously documented acquired immune deficiency syndrome who had liver biopsies. Diagnoses of specific infections were made on liver biopsy in 11/21 patients (57%). Granulomas were found in 10/21 patients (48%) and were most often a manifestation of infection with Mycobacterium avium-intracellulare. Elevated levels of serum alkaline phosphatase and longer duration of diagnosed illness were significantly associated with the presence of granulomatous disease.
Got a match? Home oxygen therapy in current smokers
Authors: Y Lacasse
Journal: Thorax (2006)

The problems of providing home oxygen therapy to active smokers

The recent death of two patients registered in our respiratory home care programme stimulated this reflection regarding oxygen therapy in current smokers. Both had oxygen dependent chronic obstructive pulmonary disease (COPD) and died from severe burns and inhalation injury that occurred while they were receiving oxygen through their home oxygen concentrator. The inquiries revealed that both were smoking when the accidents happened and that their oxygen concentrator was functioning properly.

Contrary to popular belief, oxygen is not explosive. Rather, oxygen accelerates combustion and is therefore an obvious fire hazard. Several reports underlining the risks of burn in patients who smoke while receiving oxygen have been published.1 Reports of death are rare, however. Nevertheless, the proportion of active smokers among patients who receive long term oxygen therapy (LTOT) is almost never mentioned in the current literature. In the few reports that courageously and specifically addressed this issue, the proportion reached almost 20%.2 Such is our own experience.3 Those who report that none of their patients on home oxygen therapy currently smokes do not know their patients well.

Smokers get home oxygen therapy because physicians prescribe it. Why is that so? An explanation may be that, in the British Medical Council’s trial of LTOT in COPD, smoking was not an exclusion criterion even if, at study entry, all patients were “urged …
Morphology and a Limited Number of Immunohistochemical Markers May Efficiently Subtype Non–Small-Cell Lung Cancer
Authors: Giulio Rossi, Mauro Papotti, Mattia Barbareschi, Paolo Graziano, Giuseppe Pelosi
Journal: Journal of Clinical Oncology (2009)

reported on the high sensitivity andspeciﬁcityofhsa-miR-205expressioninsquamouscellcarcinomaof the lung. This method provides an accurate subclassiﬁcationof non–small-cell lung cancer (NSCLC) in the light of novelhistology-based therapeutic strategies, such as antiangiogeneticagents, multityrosine kinase inhibitors, and pemetrexed.
Interventions to Promote Physical Activity and Dietary Lifestyle Changes for Cardiovascular Risk Factor Reduction in Adults
Authors: Nancy T. Artinian, Gerald F. Fletcher, Dariush Mozaffarian, Penny Kris-Etherton, Linda Van Horn, Alice H. Lichtenstein, Shiriki Kumanyika, William E. Kraus, Jerome L. Fleg, Nancy S. Redeker, Janet C. Meininger, JoAnne Banks, Eileen M. Stuart-Shor, Barbara J. Fletcher, Todd D. Miller, Suzanne Hughes, Lynne T. Braun, Laurie A. Kopin, Kathy Berra, Laura L. Hayman, Linda J. Ewing, Philip A. Ades, J. Larry Durstine, Nancy Houston-Miller, Lora E. Burke
Journal: Circulation (2010)

A pproximately 79 400 000 American adults, or 1 in 3, have cardiovascular disease (CVD). 1 CVD accounts for 36.3% or 1 of every 2.8 deaths in the United States and is the leading cause of death among both men and women in the United States, killing an average of 1 American every 37 seconds. 1 Older adults, some ethnic minority populations, and socioeconomically disadvantaged individuals have an increased prevalence of CVD and vascular/metabolic risk factors such as hypertension, dyslipidemia, and diabetes; are more likely to have Ն2 risk factors; and are at increased risk of being sedentary, overweight or obese, and having unhealthy dietary habits. 2-10Black and Hispanic immigrants are initially at lower risk for vascular/metabolic risk factors and CVD than US-born black and Hispanic individuals, 2 but as they adapt to the diet and activity habits of this country, the prevalence of vascular/metabolic risk factors increases. 3Each of these issues emphasizes the importance of interventions to promote physical activity (PA) and healthy diets in all American adults.Even modest sustained lifestyle changes can substantially reduce CVD morbidity and mortality.Because many of the beneficial effects of lifestyle changes accrue over time, long-term adherence maximizes individual and population benefits.Interventions targeting dietary patterns, weight reduction, and new PA habits often result in impressive rates of initial behavior changes, but frequently are not translated into long-term behavioral maintenance. 4Both adoption and maintenance of new cardiovascular risk-reducing behaviors pose challenges for many individuals.According to the National Center for Health Statistics, life expectancy could increase byThe American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel.Specifically, all members of the writing group are required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest.
Liver hepatocyte growth factor does not always correlate with hepatocellular proliferation in human liver lesions: Its specific receptorc-met does
Authors: A D'Errico, M Fiorentino, A Ponzetto, Y Daikuhara, H Tsubouchi, C Brechot, J Scoazec, W F Grigioni
Journal: Hepatology (1996)

Increased levels of expression of hepatocyte growth factor (HGF) and its specific receptor c–met have been shown in the liver of several benign and malignant pathologies, both in experimental models and humans. We investigated by immunohistochemistry the presence of both HGF and c–met protoocogene product ( c–met pp) in 20 hepatocellular carcinomas (HCCs), 5 focal nodular hyperplasias (FNHs), 4 cases of fulminant hepatitis (FH), and 1 case of regenerated liver. The c–met protooncogene product was expressed in all cases with marked overexpression in the HCCs and in ductular metaplasia. HGF was detected in the Ito cells of all cases and in neoplastic hepatocytes of 9 of 20 HCCs (45%). The proliferative index of each lesion was evaluated by means of the polyclonal antibody anti–cyclin A. When the level of expression of HGF and c–met protooncogene product with the percentage of cyclin A+ nuclei were compared, the closest relationship was between c–met protooncogene product and cyclin A+ nuclei were compared, the closest relationship was between c–met protooncogene product and cyclin A. In 11 of 20 HCCs (55%), there wa no correlation between HGF positivity and cyclin A. This seems to suggest that, independently of the levels of native liver HGF, c–met protooncogene product is the most active modulator of liver cell proliferation.
Microsomal specificity underlying the differing hepatic formation of bilirubin glucuronide and glucose conjugates by rat and dog
Authors: Ursula Sommerer, Ellen R. Gordon, Carl A. Goresky
Journal: Hepatology (1988)

Bilirubin monoglucuronide monoglucoside diester is one of the principal bilirubin conjugates in dog bile (and a lesser conjugate, in human bile), and bilirubin diglucoside is an occasional trace conjugate in dog bile whereas, in contrast, neither is detectable in rat bile. In order to investigate, in comparative fashion, the factors underlying the formation of glucuronide and glucose-containing conjugates, hepatic microsomes were isolated by differential centrifugation from the livers of both normal mongrel dogs and Sprague-Dawley rats, and their formation of bilirubin conjugates examined, in the presence of varying levels of UDP-glucuronate and UDP-glucose. Bilirubin and its conjugates were extracted and separated by high-performance liquid chromatography; a new methodology was devised, which clearly separates bilirubin diglucoside from bilirubin monoglucuronide, as well as bilirubin diglucuronide, the mixed monoglucuronide monoglucoside conjugate and bilirubin monoglucoside. At bilirubin levels of 12.5 μ M , in the presence of equal amounts of both UDP-glucuronate and UDP-glucose, dog microsomes formed substantial amounts of both bilirubin diglucuronide and the mixed monoglucuronide-monoglucoside conjugate, and minor amounts of bilirubin monoglucuronide and bilirubin diglucoside. Microsomes from rat liver, under similar conditions, formed only bilirubin diglucuronide and bilirubin monoglucuronide. When only UDP-glucose was present, dog microsomes formed predominantly diglucoside and rat, predominantly monoglucoside. The findings imply that it is not the availability of the UDP-glycoside but rather the preference of the microsomal enzymic system for the different glycosidic nucleotides which dictates the varieties of bilirubin conjugates ordinarily formed in these two species.
Genetic studies to identify genes underlying menopausal age
Authors: Helen S Kok, Kristel M van Asselt, Yvonne T van der Schouw, Petra H M Peeters, Cisca Wijmenga
Journal: Human Reproduction Update (2005)

Menopausal age is important as a retrospective marker for ovarian senescence, an early menopausal age is associated with an increased risk of cardiovascular diseases and osteoporosis, whereas a later menopausal age has been associated with an increased risk of breast cancer. The worldwide average for age at natural menopause is approximately 51 years and is more or less normally distributed with a range roughly between 40 and 60 years. Environmental factors explain only a small part of the variance and it has been proposed that genetic factors are the main source of variation. Menopausal age may be considered a continuous complex trait. Complex traits are defined as traits that are influenced by both multiple genetic and environmental factors. A category of complex traits comprises those that are measured on a continuous scale. The genomic loci that make up the genetic component are called 'quantitative trait loci' or QTLs. The first linkage study on menopausal age suggests that the involvement of the X-chromosome may not be limited to premature ovarian failure (POF), but may influence the broader spectrum of menopausal age. A potentially new locus for variation in menopausal age was allocated to chromosome 9. Further studies need to identify new candidate genes to help unravel the pathophysiology of menopausal age. It is becoming increasingly clear that, in any speciality, it should be acknowledged that genetic factors are involved in many traits and that uncovering these factors may provide insight into pathogenesis and ultimately advance prevention and treatment of disease. In this review we discuss methods and basic principles of gene finding for such traits, exemplified by menopausal age as phenotype. Furthermore, we give an overview of the state of the art of candidate gene studies and linkage studies.
1-Methoxy-Canthin-6-One Induces c-Jun NH2-Terminal Kinase–Dependent Apoptosis and Synergizes with Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand Activity in Human Neoplastic Cells of Hematopoietic or Endodermal Origin
Authors: Massimo Ammirante, Rita Di Giacomo, Laura De Martino, Alessandra Rosati, Michela Festa, Antonio Gentilella, Maria Carmela Pascale, Maria Antonietta Belisario, Arturo Leone, Maria Caterina Turco, Vincenzo De Feo
Journal: Cancer Research (2006)

We investigated the effects of 1-methoxy-canthin-6-one, isolated from the medicinal plant Ailanthus altissima Swingle, on apoptosis in human leukemia (Jurkat), thyroid carcinoma (ARO and NPA), and hepatocellular carcinoma (HuH7) cell lines. Cultures incubated with the compound showed >50% of sub-G1 (hypodiploid) elements in flow cytometry analysis; the apoptosis-inducing activity was evident at <10 micromol/L and half-maximal at about 40 micromol/L 1-methoxy-canthin-6-one. The appearance of hypodiploid elements was preceded by mitochondrial membrane depolarization, mitochondrial release of cytochrome c, and Smac/DIABLO and procaspase-3 cleavage. We subsequently investigated the effect of 1-methoxy-canthin-6-one in combination with human recombinant tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in the four cell lines. Suboptimal concentrations (10 micromol/L 1-methoxy-canthin-6-one and 0.25 ng/mL TRAIL, respectively) of the two agents, unable to elicit apoptosis when used alone, induced mitochondrial depolarization, activation of caspase-3, and 45% to 85% of sub-G1 elements when added together to the cells. The synergism seemed to rely partly on the enhanced expression of TRAIL receptor 1 (TRAIL-R1; DR4), analyzed by immunofluorescence, by 1-methoxy-canthin-6-one. Cell incubation with 1-methoxy-canthin-6-one resulted in activating c-Jun NH2-terminal kinase (JNK), as revealed by Western blotting; induction of apoptosis and TRAIL-R1 up-regulation by 1-methoxy-canthin-6-one were >80% prevented by the addition of the JNK inhibitor (JNKI) SP600125JNKI, indicating that both effects were almost completely mediated by JNK activity. On the other hand, synergism with TRAIL was reduced by about 50%, suggesting that besides up-regulating TRAIL-R1, 1-methoxy-canthin-6-one could influence other factor(s) that participated in TRAIL-induced apoptosis. These findings indicate that 1-methoxy-canthin-6-one can represent a candidate for in vivo studies of monotherapies or combined antineoplastic therapies.
Endometrial receptivity: Clinical assessment in relation to fertility, infertility, and antifertility
Authors: Annu Makker, M.M. Singh
Journal: Medicinal Research Reviews (2006)

Fertility in humans and other mammalian species depends absolutely on synchronous events that render the developing blastocyst and the receiving uterus competent for implantation. Endometrial receptivity is defined as the period during which the endometrial epithelium acquires functional, but transient, ovarian steroid-dependent status supportive to blastocyst acceptance and implantation. Once inside the uterus, the blastocyst is surrounded by an intact luminal epithelium, which is considered to act as barrier to its attachment, except for this short period of high endometrial receptivity to blastocyst signal(s). Its transport and permeability properties, in conjunction with cellular action of the endometrium and the embryo, have been suggested to influence creation and maintenance of informational and nutritional status of uterine luminal milieu. This period, also termed as the 'window of implantation,' is limited to days 20–24 of menstrual cycle in humans. However, establishment of endometrial receptivity is still a biological mystery that remains unsolved despite marked advances in our understanding of endometrial physiology following extensive research associated with its development and function. This review deals with various structural, biochemical, and molecular events in the endometrium coordinated within the implantation window that constitute essential elements in the repertoire that signifies endometrial receptivity and is aimed to achieve a better understanding of its relationship to fertility, infertility, and for the development of targeted antifertility agents for human use and welfare. © 2006 Wiley Periodicals, Inc.
Stimulation of hepatocarcinogenesis by neutrophils upon induction of oncogenic kras expression in transgenic zebrafish
Authors: Chuan Yan, Xiaojing Huo, Shu Wang, Yi Feng, Zhiyuan Gong
Journal: Journal of Hepatology (2015)

Chronic inflammation is a major etiological factor for hepatocellular carcinoma (HCC), but how immune cells respond in the initiation of hepatocarcinogenesis remains uncharacterized. This study aims to investigate the response and roles of neutrophils in early hepatocarcinogenesis.By inducible expression of oncogenic kras(V12) in hepatocytes in transgenic zebrafish combined with live imaging of neutrophils in transparent larvae, the response of neutrophils to oncogenic liver was characterized and their roles investigated by pharmaceutical and genetic manipulations.We found a rapid recruitment of neutrophils to the liver upon induction of kras(V12) expression. Pharmaceutical stimulation of neutrophils resulted in further increases of neutrophils in oncogenic livers, liver size and tumor severity, while inhibition of neutrophils caused decreases of liver-associated neutrophils and liver size. Time-lapse video indicated that neutrophils had a stagnant migratory pattern meandering along the tumor edge but became relatively stationary upon entering the kras(V12)-expressing liver. Both oncogenic hepatocytes and tumor-associated neutrophils (TANs) were isolated via fluorescence-activated cell sorting. Molecular analyses indicated a pro-inflammatory microenvironment, as marked by increased tgfβ1a expression in kras(V12)-expressing hepatocytes and a loss of anti-tumor activities in TANs. Depletion of Tgf-β significantly reduced the number of TANs and the size of oncogenic liver.An inflammatory cue from oncogenic hepatocytes upon induction of kras(V12) expression causes a rapid recruitment of neutrophils to oncogenic liver and the neutrophils play a promoting role in early hepatocarcinogenesis.
Analgesic effects of branding in treatment of headaches.
Authors: A Branthwaite, P Cooper
Journal: BMJ (1981)

The effect of branding--that is, the labelling and marketing--of a well-known proprietary analgesic used to treat headaches was studied in a sample of women given a branded or unbranded form with either an inert or an active formulation. The sample was also divided according to whether the subjects were regular users of the brand or users of other brands. The findings showed that branded tablets were overall significantly more effective than unbranded tablets in relieving headaches. Differential effects were observed: the effects of branding were more noticeable one hour after the tablets were taken compared with 30 minutes; in the women given the placebo; and in the users of the brand compared with the users of other brands. It is hypothesised that these effects are due to increased confidence in obtaining relief with a well-known brand, and that branding has an analgesic effect that interacts with the analgesic effects of placebos and active ingredients.
The different clinical faces of obstructive sleep apnoea: a cluster analysis
Authors: Lichuan Ye, Grace W. Pien, Sarah J. Ratcliffe, Erla Björnsdottir, Erna Sif Arnardottir, Allan I. Pack, Bryndis Benediktsdottir, Thorarinn Gislason
Journal: European Respiratory Journal (2014)

Although commonly observed in clinical practice, the heterogeneity of obstructive sleep apnoea (OSA) clinical presentation has not been formally characterised. This study was the first to apply cluster analysis to identify subtypes of patients with OSA who experience distinct combinations of symptoms and comorbidities. An analysis of baseline data from the Icelandic Sleep Apnoea Cohort (822 patients with newly diagnosed moderate-to-severe OSA) was performed. Three distinct clusters were identified. They were classified as the "disturbed sleep group" (cluster 1), "minimally symptomatic group" (cluster 2) and "excessive daytime sleepiness group" (cluster 3), consisting of 32.7%, 24.7% and 42.6% of the entire cohort, respectively. The probabilities of having comorbid hypertension and cardiovascular disease were highest in cluster 2 but lowest in cluster 3. The clusters did not differ significantly in terms of sex, body mass index or apnoea-hypopnoea index. Patients with OSA have different patterns of clinical presentation, which need to be communicated to both the lay public and the professional community with the goal of facilitating care-seeking and early identification of OSA. Identifying distinct clinical profiles of OSA creates a foundation for offering more personalised therapies in the future.
Is the international staging system superior to the Durie–Salmon staging system? A comparison in multiple myeloma patients undergoing autologous transplant
Authors: P N Hari, M-J Zhang, V Roy, W S Pérez, A Bashey, L B To, G Elfenbein, C O Freytes, R P Gale, J Gibson, R A Kyle, H M Lazarus, P L McCarthy, G A Milone, S Pavlovsky, D E Reece, G Schiller, J Vela-Ojeda, D Weisdorf, D Vesole
Journal: Leukemia (2009)