tbuckley/cabot-search huggingface dataset:
Caffeine Can Decrease Insulin Sensitivity in Humans
Authors: Gerben B. Keijzers, Bastiaan E. De Galan, Cees J. Tack, Paul Smits
Journal: Diabetes Care (2002)

OBJECTIVE—Caffeine is a central stimulant that increases the release of catecholamines. As a component of popular beverages, caffeine is widely used around the world. Its pharmacological effects are predominantly due to adenosine receptor antagonism and include release of catecholamines. We hypothesized that caffeine reduces insulin sensitivity, either due to catecholamines and/or as a result of blocking adenosine-mediated stimulation of peripheral glucose uptake. RESEARCH DESIGN AND METHODS—Hyperinsulinemic-euglycemic glucose clamps were used to assess insulin sensitivity. Caffeine or placebo was administered intravenously to 12 healthy volunteers in a randomized, double-blind, crossover design. Measurements included plasma levels of insulin, catecholamines, free fatty acids (FFAs), and hemodynamic parameters. Insulin sensitivity was calculated as whole-body glucose uptake corrected for the insulin concentration. In a second study, the adenosine reuptake inhibitor dipyridamole was tested using an identical protocol in 10 healthy subjects. RESULTS—Caffeine decreased insulin sensitivity by 15% (P &amp;lt; 0.05 vs. placebo). After caffeine administration, plasma FFAs increased (P &amp;lt; 0.05) and remained higher than during placebo. Plasma epinephrine increased fivefold (P &amp;lt; 0.0005), and smaller increases were recorded in plasma norepinephrine (P &amp;lt; 0.02) and blood pressure (P &amp;lt; 0.001). Dipyridamole did not alter insulin sensitivity and only increased plasma norepinephrine (P &amp;lt; 0.01). CONCLUSIONS—Caffeine can decrease insulin sensitivity in healthy humans, possibly as a result of elevated plasma epinephrine levels. Because dipyridamole did not affect glucose uptake, peripheral adenosine receptor antagonism does not appear to contribute to this effect.
Sources of individual differences in depressive symptoms: analysis of two samples of twins and their families
Authors: K S Kendler, E E Walters, K R Truett, A C Heath, M C Neale, N G Martin, L J Eaves
Journal: American Journal of Psychiatry (1994)

Self-reported symptoms of depression are commonly used in mental health research to assess current psychiatric state, yet wide variation in these symptoms among individuals has been found in both clinical and epidemiologic populations. The authors sought to understand, from a genetic-epidemiologic perspective, the sources of individual differences in depressive symptoms.Self-reported symptoms of depression were assessed in two samples of twins and their spouses, parents, siblings, and offspring: one sample contained volunteer twins recruited through the American Association of Retired Persons and their relatives (N = 19,203 individuals) and the other contained twins from a population-based twin registry in Virginia and their relatives (N = 11,242 individuals). Model fitting by an iterative, diagonal, weighted least squares method was applied to the 80 different family relationships in the extended twin-family design.Independent analyses of the two samples revealed that the level of depressive symptoms was modestly familial, and familial resemblance could be explained solely by genetic factors and spousal resemblance. The estimated heritability of depressive symptoms was between 30% and 37%. There was no evidence that the liability to depressive symptoms was environmentally transmitted from parents to offspring or was influenced by environmental factors shared either generally among siblings or specifically between twins. With correction for unreliability of measurement, genetic factors accounted for half of the stable variance in depressive symptoms.Depressive symptoms in adulthood partly reflect enduring characteristics of temperament that are substantially influenced by hereditary factors but little, or not at all, by shared environmental experiences in the family of origin.
Trends in U.S. Pleural Mesothelioma Incidence Rates Following Simian Virus 40 Contamination of Early Poliovirus Vaccines
Authors: H. D. Strickler, J. J. Goedert, S. S. Devesa, J. Lahey, J. F. Fraumeni, P. S. Rosenberg
Journal: JNCI Journal of the National Cancer Institute (2002)

Poliovirus vaccines that were used during the late 1950s and early 1960s were contaminated with simian virus 40 (SV40), a monkey virus that is tumorigenic in rodents. SV40 DNA sequences have been detected in some human cancers, especially pleural mesotheliomas, although results are conflicting. We examined the relationship between SV40-contaminated poliovirus vaccine exposure and subsequent rates of pleural mesothelioma in the United States.We used data from the Surveillance, Epidemiology, and End Results Program to estimate age- and sex-specific pleural mesothelioma incidence rates per 10(5) person-years (py) from 1975 through 1997 and the Poisson distribution to determine 95% confidence intervals (CIs) for each rate. The prevalence, by birth cohort, of poliovirus vaccine exposure during the period of widespread SV40 contamination was determined from published survey data. Trends in mesothelioma incidence rates were assessed by examining age- and sex-specific rates over calendar periods and with the use of the age-period-cohort model. Trends in mesothelioma incidence were then compared with trends in prevalence of exposure. All statistical tests were two-sided.The age-standardized pleural mesothelioma incidence rate for 1975 through 1997 was 1.29/10(5) py (95% CI = 1.24/10(5) to 1.34/10(5) py) in males and 0.21/10(5) py (95% CI = 0.20/10(5) to 0.23/10(5) py) in females. The rate in males increased from 0.79/10(5) py (95% CI = 0.62/10(5) to 1.0/10(5) py) in 1975 to a peak of 1.69/10(5) py (95% CI = 1.46/10(5) to 1.95/10(5) py) in 1992. Incidence rates increased the most among males who were 75 years of age or older, the age group least likely to have been immunized against poliovirus. Incidence rates among males in the age groups most heavily exposed to SV40-contaminated poliovirus vaccine remained stable or decreased from 1975 through 1997. Similar age-specific trends were observed among females. The age-period-cohort models for men and women also indicated that the trends in pleural mesothelioma incidence were not related to trends in exposure to SV40-contaminated poliovirus vaccine.Age-specific trends in U.S. pleural mesothelioma incidence rates are not consistent with an effect of exposure to SV40-contaminated poliovirus vaccine. Nonetheless, given reports of the detection of SV40 genomic DNA sequences in human mesotheliomas, monitoring of vaccine-exposed cohorts should continue.
Is Reliable In Vivo Detection of Stem Cell Viability Possible in a Large Animal Model of Myocardial Injury?
Authors: Phillip C. Yang
Journal: Circulation (2012)

I n vivo cellular and molecular imaging of the stem cells has been developed to characterize the biological processes at the most fundamental level in an intact, living organism.With the emergence of cell-based therapy in a failing heart, the capability to evaluate engraftment and survival of the transplanted stem cells in vivo represents a critical measure of therapeutic efficacy.The stem cells at the very least must survive to restore the injured myocardium. 1,2Cell viability signal holds physiological relevance because it may correlate with the resultant myocardial restoration.There are 2 primary considerations for in vivo imaging of stem cell viability in the heart: (1) amplification of molecular and cellular signals and(2) high spatial and temporal resolution imaging of the myocardium.It is widely acknowledged that there is no single imaging modality that will fulfill all needs of in vivo stem cell imaging.However, an imaging modality that optimizes the technical objectives may extract meaningful information on cellular and molecular events of the transplanted cells.The predominant imaging modalities to assess stem cell survival in vivo in preclinical models consist of radionuclide imaging, optical imaging, and MRI.These modalities are commonly used in small animal models.Direct transfer of in vivo cellular and molecular imaging techniques from small to large animal models, however, has not been straightforward.
Activity of telithromycin and seven other agents against 1034 pediatric Streptococcus pneumoniae isolates from ten central and eastern European centers
Authors: B. Bozdogan, P.C. Appelbaum, L.M. Kelly, D.B. Hoellman, A. Tambic-Andrasevic, L. Drukalska, W. Hryniewicz, H. Hupkova, M.R. Jacobs, J. Kolman, M. Konkoly-Thege, J. Miciuleviciene, M. Pana, L. Setchanova, J. Trupl, P. Urbaskova
Journal: Clinical Microbiology and Infection (2003)
Why does my shoulder hurt? A review of the neuroanatomical and biochemical basis of shoulder pain
Authors: Benjamin John Floyd Dean, Stephen Edward Gwilym, Andrew Jonathan Carr
Journal: British Journal of Sports Medicine (2013)

If a patient asks ‘why does my shoulder hurt?’ the conversation will quickly turn to scientific theory and sometimes unsubstantiated conjecture. Frequently, the clinician becomes aware of the limits of the scientific basis of their explanation, demonstrating the incompleteness of our understanding of the nature of shoulder pain. This review takes a systematic approach to help answer fundamental questions relating to shoulder pain, with a view to providing insights into future research and novel methods for treating shoulder pain. We shall explore the roles of (1) the peripheral receptors, (2) peripheral pain processing or ‘nociception’, (3) the spinal cord, (4) the brain, (5) the location of receptors in the shoulder and (6) the neural anatomy of the shoulder. We also consider how these factors might contribute to the variability in the clinical presentation, the diagnosis and the treatment of shoulder pain. In this way we aim to provide an overview of the component parts of the peripheral pain detection system and central pain processing mechanisms in shoulder pain that interact to produce clinical pain.
α <sub>7</sub> -Nicotinic Acetylcholine Receptors on Cerebral Perivascular Sympathetic Nerves Mediate Choline-Induced Nitrergic Neurogenic Vasodilation
Authors: Min-Liang Si, Tony J.F. Lee
Journal: Circulation Research (2002)

It has been suggested in isolated porcine cerebral arteries that stimulation by nicotine of α 7 -nicotinic acetylcholine receptors (α 7 -nAChRs) on sympathetic nerves, but not direct stimulation of parasympathetic nitrergic nerves, caused nitrergic neurogenic dilation. Direct evidence supporting this hypothesis has not been presented. The present study, which used in vitro tissue bath and confocal microscopy techniques, was designed to determine whether choline, a selective agonist for α 7 -nAChRs, induced sympathetic-dependent nitrergic dilation of porcine basilar arterial rings. Choline and several nAChR agonists induced exclusive relaxation of basilar arterial rings without endothelium. The relaxation was blocked by tetrodotoxin, nitro- l -arginine, guanethidine, and β 2 -adrenoceptor antagonists. Furthermore, the relaxation was blocked by methyllycaconitine and α-bungarotoxin (preferential α 7 -nAChR antagonists) and mecamylamine but was not affected by dihydro-β-erythroidine (a preferential α 4 -nAChR antagonist). Confocal microscopic study demonstrated that choline and nicotine induced significant calcium influx in cultured porcine superior cervical ganglionic cells but failed to affect calcium influx in cultured sphenopalatine ganglionic cells, providing direct evidence that choline and nicotine did not act directly on the parasympathetic nitrergic neurons. The increased calcium influx in superior cervical ganglionic cells was attenuated by α-bungarotoxin and methyllycaconitine but not by dihydro-β-erythroidine. These results support our hypothesis that activation of α 7 -nAChRs on cerebral perivascular sympathetic nerves causes calcium influx and the release of norepinephrine, which then act on presynaptic β 2 -adrenoceptors located on the neighboring nitrergic nerve terminals, resulting in NO release and vasodilation. Endogenous choline may play an important role in regulating cerebral sympathetic activity and vascular tone.
IRON, FERRITIN, AND NUTRITION
Authors: Elizabeth C. Theil
Journal: Annual Review of Nutrition (2004)

Ferritin, a major form of endogenous iron in food legumes such as soybeans, is a novel and natural alternative for iron supplementation strategies where effectiveness is limited by acceptability, cost, or undesirable side effects. A member of the nonheme iron group of dietary iron sources, ferritin is a complex with Fe3+ iron in a mineral (thousands of iron atoms inside a protein cage) protected from complexation. Ferritin illustrates the wide range of chemical and biological properties among nonheme iron sources. The wide range of nonheme iron receptors matched to the structure of the iron complexes that occurs in microorganisms may, by analogy, exist in humans. An understanding of the chemistry and biology of each type of dietary iron source (ferritin, heme, Fe2+ ion, etc.), and of the interactions dependent on food sources, genes, and gender, is required to design diets that will eradicate global iron deficiency in the twenty-first century.
P289 Carboxyhaemoglobin Levels In Emergency Department Patients: An Important Tool In Validating Smoking History And Detecting "missed Smokers"
Authors: R. Fowler
Journal: Thorax (2014)

<h3>Introduction</h3> Blood gas analysers in emergency departments (ED) routinely report carboxyhaemoglobin (COHb) levels, but unless environmental carbon monoxide poisoning is suspected, measurements are ignored, particularly when blood gases have been performed to check acid-base status. Raised initial COHb levels are likely to indicate highly nicotine dependent smokers needing specialist support to quit. <h3>Methods</h3> Data were obtained from 824 samples analysed in the ED in June 2013. There were 82 samples with COHb levels &gt;2.0%, including 66 from 55 identifiable patients. Only the first measurements were used. Records were requested and checked for diagnosis and smoking history. <h3>Results</h3> 42 records were retrieved. The highest initial COHb level was 13.5%; 15 had levels &gt;4.5%. There were eight confirmed COPD and two possible cases. Eleven patients presented with drug and alcohol poisoning. Table 1 lists diagnoses. 28/42 (66.7%) were current tobacco smokers; in 14 (33.3%) pack-years could be estimated. There was no smoking history recorded in seven patients. Seven others were recorded as non-smokers, but in five there was evidence to contradict this. One had an explanatory blood disorder, leaving one unexplained high level. Four patients smoked cannabis; all smoked tobacco cigarettes as well. Only 4/42 (10%) were referred to stop smoking services (SSS), though 10/42 (23.8%) were already known and one was referred subsequently. Two previous quitters had evidently relapsed. Of the remainder known to SSS, two self-referrers quit, three failed and eight missed appointments. In the largest group, those with drug or alcohol poisoning, smoking history was of poorer quality – pack-years could only be estimated in one case. Most had underlying mental health problems. None were referred to SSS. <h3>Conclusions</h3> 1. Patients with COHb levels &gt;2.0% are usually tobacco smokers. 2. Multiple substance dependence is common. Most have mental health problems and are rarely referred to SSS – a missed opportunity to improve life expectancy in this vulnerable population. 3. Carboxyhaemoglobin levels must be included in a systematic approach to identify people needing intensive support to quit smoking.
Nomenclature for diseases with IgA antikeratinocyte cell surface autoantibodies
Authors: T. Hashimoto, T. Nishikawa
Journal: British Journal of Dermatology (2015)

Journal Article Nomenclature for diseases with IgA antikeratinocyte cell surface autoantibodies Get access T. Hashimoto, T. Hashimoto Kurume University Institute of Cutaneous Cell Biology 67 Asahimachi, Kurume Fukuoka 830‐0011 Japan Search for other works by this author on: Oxford Academic Google Scholar T. Nishikawa T. Nishikawa Samoncho Dermatological Clinic Shinjuku Tokyo JapanDepartment of Dermatology Keio University School of Medicine Tokyo Japan Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 173, Issue 3, 1 September 2015, Pages 868–869, https://doi.org/10.1111/bjd.13813 Published: 01 September 2015
Zero reference level for right heart catheterisation
Authors: Gabor Kovacs, Alexander Avian, Andrea Olschewski, Horst Olschewski
Journal: European Respiratory Journal (2013)

Although in the pulmonary circulation small pressure differences may alter the categorisation of patients, there is no consensus on a standard zero reference level (ZRL). In the supine position, ZRL is mostly set at "5 cm below anterior thorax surface", "1/3 thoracic diameter below anterior thorax surface", "mid-thoracic level" or "10 cm above table level". We retrospectively assessed the distance of these four ZRLs from computed tomography-derived right and left atrial centre levels and from one another in patients undergoing right heart catheterisation and calculated the respective differences in pressure readings. We included 196 consecutive patients. The ZRL at "1/3 thoracic diameter" was most often (98.5%) level with the right atrium, and the ZRL at "mid-thoracic level" was level with the left atrium (97.4%), revealing a median (range) pressure difference of -0.3 (-3.0-1.3) and 0.2 (-2.0-1.3) mmHg from the right and left atrial centre level, respectively. The largest differences (8.0 (2.0-15.4) mmHg) were found between the ZRLs "5 cm below anterior thorax surface" and "10 cm above table level". Accordingly, 59% versus 80% of patients would be classified with pulmonary hypertension and 7% versus 38% with elevated left heart pressures. The choice of ZRL strongly influences pulmonary pressure readings and pulmonary hypertension classification. 1/3 thoracic diameter mostly represents the right atrium while the left atrium is best represented by the mid-thoracic level.
Dietary Beta Carotene and Lung Cancer Risk in U.S. Nonsmokers
Authors: S. T. Mayne, D. T. Janerich, P. Greenwald, S. Chorost, C. Tucci, M. B. Zaman, M. R. Melamed, M. Kiely, M. F. McKneally
Journal: JNCI Journal of the National Cancer Institute (1994)

Journal Article Dietary Beta Carotene and Lung Cancer Risk in U.S. Nonsmokers Get access Susan Taylor Mayne, Susan Taylor Mayne Department of Epidemiology and Public Health, Yale University School of MedicineNew Haven, Conn. Correspondence to : Susan Taylor Mayne, Ph.D., Department of Epidemiology and Public Health, Yale University School of Medicine, P.O. Box 208034, New Haven, CT 06520. Search for other works by this author on: Oxford Academic PubMed Google Scholar Dwight T. Janerich, Dwight T. Janerich Utah Cancer CenterSalt Lake City Search for other works by this author on: Oxford Academic PubMed Google Scholar Peter Greenwald, Peter Greenwald Division of Cancer Prevention and Control, National Cancer InstituteBethesda, Md Search for other works by this author on: Oxford Academic PubMed Google Scholar Sherry Chorost, Sherry Chorost New York State Department of HealthAlbany Search for other works by this author on: Oxford Academic PubMed Google Scholar Cathy Tucci, Cathy Tucci New York State Department of HealthAlbany Search for other works by this author on: Oxford Academic PubMed Google Scholar Muhammad B. Zaman, Muhammad B. Zaman New York Medical CollegeValhala Search for other works by this author on: Oxford Academic PubMed Google Scholar Myron R. Melamed, Myron R. Melamed New York Medical CollegeValhala Search for other works by this author on: Oxford Academic PubMed Google Scholar Maureen Kiely, Maureen Kiely deceased, formerly form the New York State Departmen tof HealthAlbany Search for other works by this author on: Oxford Academic PubMed Google Scholar Martin F. McKneally Martin F. McKneally Toronto General HospitalOntario, Canada * See “Notes” section following “References.” Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 86, Issue 1, 5 January 1994, Pages 33–38, https://doi.org/10.1093/jnci/86.1.33 Published: 05 January 1994 Article history Received: 07 June 1993 Revision received: 28 September 1993 Accepted: 04 October 1993 Published: 05 January 1994
Prevention of chemotherapy-induced menopause by temporary ovarian suppression with goserelin in young, early breast cancer patients
Authors: L. Del Mastro, T. Catzeddu, L. Boni, C. Bell, M.R. Sertoli, C. Bighin, M. Clavarezza, D. Testa, M. Venturini
Journal: Annals of Oncology (2005)
Progressive ventricular remodeling in response to diffuse isoproterenol-induced myocardial necrosis in rats.
Authors: J R Teerlink, J M Pfeffer, M A Pfeffer
Journal: Circulation Research (1994)

The purpose of the present study was to gain a better understanding of the relation between ventricular remodeling and heart failure by assessing the adaptation of the heart through time to graded myocardial injury in the presence of a patent coronary circulation. Left ventricular (LV) remodeling is a dynamic response of the heart to injury and a critical component in the development of heart failure. However, most previous studies have been in the presence of an occluded coronary vessel, which may in itself effect remodeling. Male Wistar rats received two subcutaneous injections of either 0, 85, 170, or 340 mg isoproterenol per kilogram of body weight. At 2, 6, and 16 weeks after injection, LV pressure, the pressure-volume relation, and histology were assessed. The graded myocardial necrosis produced in isoproterenol-treated rats was associated with dose-dependent increases in LV end-diastolic pressure, volume indexes, and global diastolic wall stress. In the higher dose groups, the LV continued to enlarge after 2 weeks, resulting in a further reduction in the ratio of LV mass to volume and a persistent rise in diastolic wall stress. These progressive changes in LV structure were associated with an increase in long-term mortality in rats from the intermediate- and high-isoproterenol dose groups. The present study in rats demonstrates that diffuse isoproterenol-induced myocardial necrosis results in a progressive enlargement of the LV cavity that is out of proportion to mass, a finding similar to that observed in discrete myocardial infarction.
Gene expression profiling studies of aging in cardiac and skeletal muscles
Authors: S PARK, T PROLLA
Journal: Cardiovascular Research (2005)

To examine transcriptional alterations associated with aging in skeletal muscle and the heart, we and others have used DNA microarrays to compare the gene expression profile of young and old animals. Aging results in a differential gene expression pattern specific to each tissue, and most alterations can be completely or partially prevented by caloric restriction (CR) in both heart and skeletal muscle. Transcriptional patterns of tissues from calorie-restricted animals suggests that CR retards the aging process by reducing endogenous damage and by inducing metabolic shifts associated with specific transcriptional profiles. These studies demonstrate that DNA microarrays can be used in cardiovascular aging research to generate panels of hundreds of transcriptional biomarkers, providing a new tool to measure biological age of cardiac and skeletal muscles and to test interventions designed to retard aging in these tissues.