tbuckley/cabot-search huggingface dataset:
Prevalence of polar dyspnea in inhabitants of Gydan peninsula, Far North of Russia
Authors: Andrey Lobanov, Sergey Andronov, Andrey Popov, Alexandr Emelyanov
Journal: European Respiratory Journal (2014)

The harsh climate of the Arctic may have negative effect on respiratory system and induce polar dyspnea in its inhabitants. The aim of this study was to assess the prevalence of polar dyspnea in the population of the Gydan Peninsula, which is located on Far North of Russia.

We examined 405 healthy inhabitants (144 men) of the Gydan Peninsula aged 18-60 yrs (mean age 43.2 yr), including 117 nenets from tundra population. Hyperventilation syndrome was diagnosed by using Nijmegen questionnaire (1984). Family history was analyzed by study of three generation pedigree. Pulmonary function was measured by dry spirometry (SpiroUSB ML 2525 CareFusion, UK).

Syndrome of polar dyspnea was diagnosed in 29.4% inhabitans. It was more common in women (35.4% vs 18.7% in men, χ2-11.6; p<0.001), immigrants (33.6% vs 20.8% in aborigines, χ2-4.6; p=0.03) and residents with positive family history (60.0% vs 36.5% in residents with negative history, p=0.01). FEV1 was normal in all groups.

We conclude that polar dyspnea is a functional disorder affecting some inhabitants of Far North. Its mechanism is not clear and may reflect a dysfunction of central nervous system in cold climate.
Traumatic brain stem haematoma without prolonged loss of consciousness.
Authors: R A Shakir, R A Khan
Journal: BMJ (1984)

Une observation assez rare. Un jeune homme de 18 ans, apres un coup sur la tete, presente une perte de conscience de courte duree, moins de 2 h. Examen neurologique et radiologique negatif. 2 j plus tard, cephalees, vertiges, troubles de coordination des mouvements des membres, ataxie trunculaire. La tomographie du crâne montre un petit hematome au niveau du tronc cerebral, qui se resorbe spontanement en quelques semaines. Recuperation totale
Effects of Ramadan on physical performance: chronobiological considerations
Authors: Jim Waterhouse
Journal: British Journal of Sports Medicine (2010)

This article focuses on changes in Ramadan during the course of the waking day in physical performance, mental performance and gastrointestinal function. Possible explanations of the changes are considered by reference to the roles of the body clock and external factors such as the environment and the individual's lifestyle. The effects of these factors upon training schedules and upon changing the times of training are then discussed in terms of physiology and biochemistry. Delaying the time of training until after sunset has advantages and disadvantages, but it is a regimen that is unlikely to be widely accepted in non-Muslim countries. It is clear that the detailed nature of the problems involved and dealing with them in a manner based upon a firm body of knowledge requires far more experimental investigation.
Unexpected longevity in patients with severe kyphoscoliosis.
Authors: W N Rom, A Miller
Journal: Thorax (1978)

The threat of premature death in the fourth or fifth decades of life from cardiorespiratory failure in kyphoscoliosis is well known. Ten patients with severe kyphoscoliosis (curves greater than 100 degrees), who had survived into their seventh decade free of cardiorespiratory failure, were encountered over a four-year period. Pulmonary function studies on five patients showed impaired chest bellows function. Four patients died of acute respiratory failure at ages 65, 73, 79, and 85. These patients illustrate that severe deformity is not incompatible with a long and active life.
The Effect of Moderate Changes in Blood Volume on Left and Right Atrial Pressures
Authors: JAMES P. HENRY, OTTO H. GAUER, HERBERT O. SIEKER
Journal: Circulation Research (1956)

The blood volume of 15 dogs was progressively increased an estimated 30 per cent by repeated blood infusions and decreased 30 per cent by stepwise hemorrhage. The pressures in the venous system, both atria and the pulmonary artery, rose and fell in unison with these moderate changes in blood volume and the new levels remained stable for at least 10 to 20 minutes. Although the right ventricle anatomically separates the systemic venous bed from the pulmonary circulation, small hemorrhages and transfusions have so little effect on its activity that, from the point of view of pressure volume relationships, the systemic veins and the left atrium are parts of the same functional unit.
Breast Cancer and Use of Nonsteroidal Anti-inflammatory Drugs: A Meta-analysis
Authors: B. Takkouche, C. Regueira-Mendez, M. Etminan
Journal: JNCI Journal of the National Cancer Institute (2008)

Breast cancer is one of the leading causes of mortality among women. The use of nonsteroidal anti-inflammatory drugs (NSAIDs) may be associated with reduced risk for breast cancer, but results from these studies of the association have been inconsistent.Studies that examined the association between risk of breast cancer and use of NSAIDs, including aspirin and ibuprofen, that were published between January 1, 1966, and July 1, 2008, were identified using Medline, EMBASE, and other databases. We performed meta-analysis by pooling studies according to the inverse of their variances and performed separate analyses of studies pooled according to aspirin use and ibuprofen use. We evaluated publication bias and study quality.A total of 38 studies (16 case-control studies, 18 cohort studies, 3 case-control studies nested in well-defined cohorts, and 1 clinical trial) that included 2 788 715 subjects were identified. The results of these studies suggest that overall, NSAID use was associated with reduced risk for breast cancer (relative risk [RR] = 0.88, 95% confidence interval [CI] = 0.84 to 0.93). Specific analyses for aspirin (RR = 0.87, 95% CI = 0.82 to 0.92) and ibuprofen (RR = 0.79, 95% CI = 0.64 to 0.97) yielded similar results.This meta-analysis provides evidence that NSAID use is associated with reduced risk for breast cancer. Future research should include careful evaluation of the biologic mechanisms involved in the relationship between NSAIDs and breast cancer.
Sinusoidal endothelial cell and hepatocyte death following cold ischemia-warm reperfusion of the rat liver
Authors: Pierre-Michel Huet, Marcia R. Nagaoka, Geneviève Desbiens, Esther Tarrab, Antoine Brault, Marie-Pierre Bralet, Marc Bilodeau
Journal: Hepatology (2004)

Cold ischemia-warm reperfusion (CI-WR) injury of the liver is characterized by marked alterations of sinusoidal endothelial cells (SECs), whereas hepatocytes appear to be relatively unscathed. However, the time course and mechanism of cell death remain controversial: early versus late phenomenon, necrosis versus apoptosis? We describe the occurrence and nature of cell death after different periods of CI with University of Wisconsin (UW) solution and after different periods of WR in the isolated perfused rat liver model. After 24- and 42-hour CI (viable and nonviable livers, respectively), similar patterns of liver cell death were seen: SEC necrosis appeared early after WR (10 minutes) and remained stable for up to 120 minutes. After 30 minutes of WR, apoptosis increased progressively with WR length. Based on morphological criteria, apoptotic cells were mainly hepatocytes within liver plates or extruded in the sinusoidal lumen. In addition, only after 42-hour CI were large clusters of necrotic hepatocytes found in areas of congested sinusoids. In these same livers, the hepatic microcirculation, evaluated by means of the multiple-indicator dilution technique, revealed extracellular matrix disappearance with no-flow areas. In conclusion, different time courses and mechanisms of cell death occur in rat livers after CI-WR, with early SEC necrosis followed by delayed hepatocyte apoptosis. These processes do not appear to be of major importance in the mechanism of graft failure because they are similar under both nonlethal and lethal conditions; this is not the case for the loss of the extracellular matrix found only under lethal conditions and associated with hepatocyte necrosis.
Radioimmunotherapy of Breast Cancer Metastases with α-Particle Emitter 225Ac: Comparing Efficacy with 213Bi and 90Y
Authors: Hong Song, Robert F. Hobbs, Ravy Vajravelu, David L. Huso, Caroline Esaias, Christos Apostolidis, Alfred Morgenstern, George Sgouros
Journal: Cancer Research (2009)

alpha-Particles are suitable to treat cancer micrometastases because of their short range and very high linear energy transfer. alpha-Particle emitter (213)Bi-based radioimmunotherapy has shown efficacy in a variety of metastatic animal cancer models, such as breast, ovarian, and prostate cancers. Its clinical implementation, however, is challenging due to the limited supply of (225)Ac, high technical requirement to prepare radioimmunoconjugate with very short half-life (T(1/2) = 45.6 min) on site, and prohibitive cost. In this study, we investigated the efficacy of the alpha-particle emitter (225)Ac, parent of (213)Bi, in a mouse model of breast cancer metastases. A single administration of (225)Ac (400 nCi)-labeled anti-rat HER-2/neu monoclonal antibody (7.16.4) completely eradicated breast cancer lung micrometastases in approximately 67% of HER-2/neu transgenic mice and led to long-term survival of these mice for up to 1 year. Treatment with (225)Ac-7.16.4 is significantly more effective than (213)Bi-7.16.4 (120 microCi; median survival, 61 days; P = 0.001) and (90)Y-7.16.4 (120 microCi; median survival, 50 days; P < 0.001) as well as untreated control (median survival, 41 days; P < 0.0001). Dosimetric analysis showed that (225)Ac-treated metastases received a total dose of 9.6 Gy, significantly higher than 2.0 Gy from (213)Bi and 2.4 Gy from (90)Y. Biodistribution studies revealed that (225)Ac daughters, (221)Fr and (213)Bi, accumulated in kidneys and probably contributed to the long-term renal toxicity observed in surviving mice. These data suggest (225)Ac-labeled anti-HER-2/neu monoclonal antibody could significantly prolong survival in HER-2/neu-positive metastatic breast cancer patients.
The impact of the Factor V Leiden mutation on pregnancy
Authors: V. Spina
Journal: Human Reproduction Update (2000)

A resistance to the anticoagulant activity of activated protein C (APC), most frequently due to a point mutation in the Factor V gene (the Leiden mutation), represents the most common genetic cause of thrombophilia. The Leiden mutation has been significantly related to pregnancy complications associated with hypercoagulation, e.g. deep vein thrombosis during pregnancy (8-fold increased risk), pre-eclampsia (prevalence of the mutation up to 26%), placental infarction extending to >10% of the placenta (10-fold increased risk), abruptio placentae (prevalence of the mutation up to 29.6%), and second- and third-trimester pregnancy failure (prevalence of the mutation up to 31.3%). An association of the maternal mutation with recurrent first-trimester miscarriage does not emerge from the literature, although fetal mutation (frequency higher than twice compared with that of the general population) has been related to early spontaneous miscarriage. Although some evidence suggests an association between APC resistance and intrauterine growth retardation, no significant relationship emerges currently from the literature. Screening for the Leiden mutation would seem advisable in women with previous pregnancy complications amongst those associated with APC resistance. Carriers of the mutation should be given appropriate counselling. The screening of asymptomatic women is not recommended at present.
Indium 111-monoclonal antimyosin antibody imaging in the diagnosis of acute myocarditis.
Authors: T Yasuda, I F Palacios, G W Dec, J T Fallon, H K Gold, R C Leinbach, H W Strauss, B A Khaw, E Haber
Journal: Circulation (1987)

A definitive diagnosis of myocarditis requires right ventricular biopsy. Despite its specificity, however, right ventricular biopsy may lack sensitivity due to the focal nature of the disease. Because indium 111-monoclonal antimyosin antibody imaging can be used to detect myocardial necrosis, this procedure was performed on 28 patients clinically suspected of having myocarditis, 25 of whom had left ventricular ejection fractions of less than 45%, and the results were compared with those of right ventricular biopsy performed within 48 hr of the scan. Antimyosin scans were positive in nine patients who had evidence of myocarditis on right ventricular biopsy, and negative in 11 who had no evidence of myocarditis by biopsy. The remaining eight had positive antimyosin scans but showed no evidence of myocarditis on right ventricular biopsy. On the basis of a right ventricular biopsy standard, the sensitivity of this method was 100%, the specificity 58%. We conclude that antimyosin antibody imaging is a reliable screening method for the evaluation of patients suspected of having myocarditis, and that a positive antimyosin scan indicates the need for right ventricular biopsy to establish the histologic diagnosis.
SEROLOGICAL DIAGNOSIS OF HAEMORRHAGIC FEVER WITH RENAL SYNDROME IN EUROPEAN REGION OF U.S.S.R.
Authors: E.A. Tkachenko, T.K. Dzagurova, E.V. Leshchinskaya, I.M. Zagidulin, I.M. Ustjugova, T.A. Gasanova, G.V. Rezapkin, J.A. Miasnikov
Journal: The Lancet (1982)
Stunned and Hibernating Myocardium
Authors: Robert A. Kloner, Karin Przyklenk
Journal: Annual Review of Medicine (1991)

Myocardium that is not functioning may be dead (infarct or scar), viable but stunned (postischemic ventricular dysfunction), viable but hibernating (chronic low flow state), or acutely ischemic. Stunned myocardium has clearly been documented (a) in experimental studies of brief coronary artery occlusion followed by reperfusion, and (b) in myocardial infarct models in which early reperfusion salvages viable tissue. Recent clinical studies have confirmed the existence of stunned myocardium in humans. Evidence supporting the concept of hibernating myocardium comes from clinical studies in which patients with chronic low flow ischemia exhibit improvement in left ventricular function (sometimes immediately) following revascularization.
Cloning and expression of class I major histocompatibility complex genes of the rat.
Authors: S C Jameson, W D Tope, E M Tredgett, J M Windle, A G Diamond, J C Howard
Journal: The Journal of Experimental Medicine (1992)

Little is known about the organization of class I genes in the rat although there is prima facie evidence that it is distinct from that of the mouse. We report the cloning of 61 nonclassical rat class I genes into cosmid clusters with a total mapped length of 1,264 kb. It is certain that the total number of class I genes in the rat must exceed this number. From restriction maps it is possible to identify substantial regions of duplication. By transfection of cosmids into mouse L cells, it has been possible to demonstrate at least seven different nonclassical rat class I genes that are expressible on the cell surface. Crossreaction of a single mouse monoclonal antibody with all of these class I molecules is consistent with sequence homogenization within the rat nonclassical system. Attempts to find rat homologues of the mouse Tla genes by crosshybridization of rat cosmids with a range of different TLa-specific probes were unsuccessful, suggesting that this large group of divergent class I genes is absent or nearly so from the rat. The large number of class I genes in the rat appears to have arisen by expansion of genes more closely related to the classical sequence.
Induction of APOBEC3 family proteins, a defensive maneuver underlying interferon-induced anti–HIV-1 activity
Authors: Gang Peng, Ke Jian Lei, Wenwen Jin, Teresa Greenwell-Wild, Sharon M. Wahl
Journal: The Journal of Experimental Medicine (2006)

Apolipoprotein B mRNA-editing enzyme-catalytic polypeptide-like 3G (APOBEC3G), a cytidine deaminase, is a recently recognized innate intracellular protein with lethal activity against human immunodeficiency virus (HIV). Packaged into progeny virions, APOBEC3G enzymatic activity leads to HIV DNA degradation. As a counterattack, HIV virion infectivity factor (Vif) targets APOBEC3G for proteasomal proteolysis to exclude it from budding virions. Based on the ability of APOBEC3G to antagonize HIV infection, considerable interest hinges on elucidating its mechanism(s) of regulation. In this study, we provide the first evidence that an innate, endogenous host defense factor has the potential to promote APOBEC3G and rebuke the virus-mediated attempt to control its cellular host. We identify interferon (IFN)-α as a potent inducer of APOBEC3G to override HIV Vif neutralization of APOBEC3 proteins that pose a threat to efficient macrophage HIV replication. Our data provide a new dimension by which IFN-α mediates its antiviral activity and suggest a means to render the host nonpermissive for viral replication.
Biomarkers Unbound — The Supreme Court's Ruling on Diagnostic-Test Patents
Authors: Aaron S. Kesselheim, Jason Karlawish
Journal: New England Journal of Medicine (2012)

Interview with Dr. Aaron Kesselheim on a recent Supreme Court ruling on patents for diagnostic tests. (16:28)Download In Mayo Collaborative Services v. Prometheus Laboratories, the Supreme Court has proscribed patents from covering correlations used in making biomarker-based diagnoses when those patents simply describe “steps that must be taken in order to apply” a natural law.
Acute liver failure is associated with elevated liver stiffness and hepatic stellate cell activation
Authors: Alexander Dechêne, Jan-Peter Sowa, Robert K. Gieseler, Christoph Jochum, Lars P. Bechmann, Amr El Fouly, Martin Schlattjan, Fuat Saner, Hideo A. Baba, Andreas Paul, Volker Dries, Margarethe Odenthal, Guido Gerken, Scott L. Friedman, Ali Canbay
Journal: Hepatology (2010)

Abstract Acute liver failure (ALF) is associated with massive short-term cell death, whereas chronic liver injury is accompanied by continuous cell death. Hepatic stellate cells (HSCs) contribute to tissue repair and liver fibrosis in chronic liver injury, although their role in ALF remains unexplained. Twenty-nine patients (median age = 43 years, 17 females and 12 males) with ALF according to the Acute Liver Failure Study Group criteria were included. Upon the diagnosis of ALF and after 7 days, we determined liver stiffness (LS) with FibroScan, standard laboratory parameters, and serum levels of matrix metalloproteinase 1 (MMP-1), MMP-2, MMP-9, tissue inhibitor of metalloproteinases 1 (TIMP-1), TIMP-2, hyaluronic acid, and markers of overall cell death (M65) and apoptosis (M30). Stellate cell activation and progenitor response were analyzed immunohistochemically in biopsy samples of 12 patients with α-smooth muscle actin (α-SMA), keratin-17, and keratin-19 staining, respectively. Cell death markers (M30 level = 2243 ± 559.6 U/L, M65 level = 3732 ± 839.9 U/L) and fibrosis markers (TIMP-1 level = 629.9 ± 69.4 U/mL, MMP-2 level = 264 ± 32.5 U/mL, hyaluronic acid level = 438.5 ± 69.3 μg/mL) were significantly increased in patients versus healthy controls. This was paralleled by collagen deposition, elevated α-SMA expression, and higher LS (25.6 ± 3.0 kPa). ALF was associated with ductular progenitor proliferation. Conclusion: Our results demonstrate HSC activation and a progenitor response in ALF. Positive correlations between LS, the degree of liver cell damage, and the intensity of HSC activation suggest that fibrosis is a response to ALF in an attempt to repair damaged tissue.
What is the optimal type of physical activity to enhance health?
Authors: R J Shephard
Journal: British Journal of Sports Medicine (1997)

This review examines the potential of active daily living as a means of gaining the cardiovascular and health rewards previously sought through vigorous aerobic fitness programmes. Cross-sectional studies of occupational and leisure activity show encouraging associations between such activity and good health; in workers, the gross intensity of effort needed for health benefits has seemed to be 20 kJ/min. There has been less unanimity on the threshold intensity needed in leisure activities, but various recent "position statements" have decreased the recommendation to 50% of an individual's maximal oxygen intake, sustained for one hour three to five times per week. Life-style activities such as walking seem likely to reach this intensity in older individuals, but are unlikely to do so in young adults. A growing number of controlled longitudinal studies of walking programmes have demonstrated gains in aerobic fitness, modest reductions in blood pressure, improvements in lipid profile, increased bone density, and enhanced mood state, with less consistent reductions of body fat. However, gains have been greatest in the elderly, sedentary, and obese populations. The main component of active living, fast walking, seems likely to enhance health in such populations, but it is unlikely to be effective in young adults who are in good initial health.
CD23 bridges the gap
Authors: Heather L. Van Epps
Journal: The Journal of Experimental Medicine (2005)

Vessel-building mast cellsIrradiation instructs mast cells to rebuild blood vessels in oxygen-deprived tissues, according to Heissig and colleagues on page 739.Low-dose irradiation mobilized adult and precursor mast cells, which traveled to the ischemic tissue and produced the vesselbuilding growth factor VEGF (vascular endothelial growth factor).Ionizing irradiation has been shown to promote the growth of new blood vessels through the induction of VEGF and inhibition of endothelial cell death.However, the primary source of irradiation-induced VEGF and the precise mechanism that triggers its production were not clear.Mast cells-well-known for their production of histamine in allergic responses-had been found in tissues undergoing angiogenesis.Mast cells are also capable of producing VEGF, but whether these cells play a leading or supporting role in angiogenesis had not been explored.Heissig et al. now show that mast cells are essential for irradiation-induced vessel growth in a mouse model of ischemic limb injury.Irradiation-induced cellular damage triggers the production of the degradative enzyme matrix metalloprotease-9 (MMP-9) by largely unknown mechanisms.In this model, local irradiation of the damaged limb increased MMP-9 production in the ischemic tissue, which liberated the cytokine Kit ligand (KitL), likely from stromal cells.KitL then attracted VEGFproducing mast cells into the injured tissue.At the same time, irradiation mobilized mast cell precursors and endothelial cell progenitors from the bone marrow, and some of these cells became incorporated into the growing vessels.Without mast cells, the vessel-building benefits of irradiation were lost.The authors thus speculate that localized irradiation might improve upon