tbuckley/cabot-search huggingface dataset:
Changes in lung volumes and airway responsiveness following haematopoietic stem cell transplantation
Authors: G. Barisione, A. Bacigalupo, E. Crimi, M. T. Van Lint, T. Lamparelli, V. Brusasco
Journal: European Respiratory Journal (2008)

Changes in lung volume occur following haematopoietic stem cell transplantation (HSCT); airway hyperresponsiveness was occasionally reported, without mechanistic explanation. The present authors studied 17 patients by standard methacholine (MCh) challenge before and then 3 and 12 months after HSCT (n = 16 and n = 13, respectively). Another 6 patients were challenged before and 3 months after HSCT using a modified challenge to investigate the effect of deep inhalations. No patient developed bronchiolitis obliterans or bronchiolitis obliterans organising pneumonia. At 3 months, forced vital capacity (FVC) was significantly reduced by 0.33+/-0.55 L, forced expiratory volume in one second (FEV(1)) by 0.31+/-0.50 L, total lung capacity (TLC) by 0.39+/-0.37 L and single-breath diffusing capacity of the lung for carbon monoxide (D(L,CO)) by 15+/-12%. At 12 months, TLC decreased by 0.43+/-0.36 L and D(L,CO )by 8+/-8%. With standard challenge, no significant changes in FEV(1) response to MCh were observed after HSCT but FVC decreased significantly less after HSCT compared with prior to HSCT, suggesting less air trapping. With modified challenge, deep inhalations reversed the MCh-induced decrease in partial expiratory flow more after HSCT compared with before HSCT and this correlated with TLC decrements. In conclusion, an increase in airway responsiveness is unlikely after haematopoietic stem cell transplantation, at least in patients without pulmonary complications, and mechanisms opposing airway narrowing may blunt the bronchoconstrictor response.
Two Distinct Pathways Mediated by PA28 and hsp90 in Major Histocompatibility Complex Class I Antigen Processing
Authors: Taketoshi Yamano, Shigeo Murata, Naoki Shimbara, Noriaki Tanaka, Tomoki Chiba, Keiji Tanaka, Katsuyuki Yui, Heiichiro Udono
Journal: The Journal of Experimental Medicine (2002)

Major histocompatibility complex (MHC) class I ligands are mainly produced by the proteasome. Herein, we show that the processing of antigens is regulated by two distinct pathways, one requiring PA28 and the other hsp90. Both hsp90 and PA28 enhanced the antigen processing of ovalbumin (OVA). Geldanamycin, an inhibitor of hsp90, almost completely suppressed OVA antigen presentation in PA28α−/−/β−/− lipopolysaccharide blasts, but not in wild-type cells, indicating that hsp90 compensates for the loss of PA28 and is essential in the PA28-independent pathway. In contrast, treatment of cells with interferon (IFN)-γ, which induces PA28 expression, abrogated the requirement of hsp90, suggesting that IFN-γ enhances the PA28-dependent pathway, whereas it diminishes hsp90-dependent pathway. Importantly, IFN-γ did not induce MHC class I expressions in PA28-deficient cells, indicating a prominent role for PA28 in IFN-γ–stimulated peptide supply. Thus, these two pathways operate either redundantly or specifically, depending on antigen species and cell type.
Bismuth subsalicylate reduces peptic injury of the oesophagus in rabbits.
Authors: H P Tay, R C Chaparala, J W Harmon, J Huesken, N Saini, F Z Hakki, E J Schweitzer
Journal: Gut (1990)

Bismuth subsalicylate was tested in an in vivo perfused rabbit model of oesophagitis for its ability to prevent the mucosal injury caused by pepsin. Treatment efficacy was assessed under both a treatment-before-injury protocol and a treatment-after-injury protocol. Oesophageal mucosal barrier function was evaluated by measuring flux rates of H+, K+, and glucose. The degree of oesophagitis was determined by gross and microscopic examination of the mucosa by several independent observers. Results showed that under both treatment protocols, bismuth subsalicylate significantly reduced the pepsin induced disruption of the mucosal barrier, as well as the morphologic changes. Bismuth subsalicylate when given after exposure to pepsin was also found to protect against the morphologic injury in a dose dependent manner. Experiments in vitro suggested that bismuth subsalicylate inhibits the proteolytic action of pepsin by interacting with pepsin, rather than with the pepsin substrate. We conclude that bismuth subsalicylate can protect the oesophageal mucosa against peptic injury, probably through inactivation of pepsin.
Pikachurin, a dystroglycan ligand, is essential for photoreceptor ribbon synapse formation
Authors: Shigeru Sato, Yoshihiro Omori, Kimiko Katoh, Mineo Kondo, Motoi Kanagawa, Kentaro Miyata, Kazuo Funabiki, Toshiyuki Koyasu, Naoko Kajimura, Tomomitsu Miyoshi, Hajime Sawai, Kazuhiro Kobayashi, Akiko Tani, Tatsushi Toda, Jiro Usukura, Yasuo Tano, Takashi Fujikado, Takahisa Furukawa
Journal: Nature Neuroscience (2008)
Weekly docetaxel (Taxotere®) in patients with metastatic breast cancer
Authors: H.J. Stemmler, K. Gutschow, H. Sommer, M. Malekmohammadi, Ch. Kentenich, R. Forstpointner, S. Geuenich, J. Bischoff, W. Hiddemann, V. Heinemann
Journal: Annals of Oncology (2001)
James Angus Doull and the well-controlled common cold
Authors: Harry M Marks
Journal: Journal of the Royal Society of Medicine (2008)

In 1931, James Angus Doull (1889–1963) and his colleagues at the Johns Hopkins School of Hygiene and Public Health reported a study evaluating ‘the prophylactic value of ultra-violet light in acute upper respiratory disease’. Three hundred and seventy three medical and public health students were divided ‘at random’ into three unequal-sized groups. The first group was to receive one ultraviolet treatment per week; the second group received two treatments; and the remaining group served as controls.1
Classification of pediatric acute lymphoblastic leukemia by gene expression profiling
Authors: Mary E. Ross, Xiaodong Zhou, Guangchun Song, Sheila A. Shurtleff, Kevin Girtman, W. Kent Williams, Hsi-Che Liu, Rami Mahfouz, Susana C. Raimondi, Noel Lenny, Anami Patel, James R. Downing
Journal: Blood (2003)
Fasting plasma caffeine level in cirrhotic patients: Relation to plasma levels of catecholamines and renin activity
Authors: Mayumi Hasegawa, Sadako Yamada, Chisato Hirayama
Journal: Hepatology (1989)

Fasting plasma caffeine concentrations, plasma levels of catecholamines and plasma renin activity were measured in patients with cirrhosis and control patients without hepatic dysfunction. A careful dietary history showed no significant difference in caffeine consumption (mean +/- S.E.) among 46 cirrhotics (86 +/- 7 mg per day) vs. 34 control patients (91 +/- 8 mg per day). Fasting plasma caffeine concentrations, however, were significantly higher (7.68 +/- 1.42 micrograms per ml) in cirrhotics than in controls (1.01 +/- 0.20 micrograms per ml) (p less than 0.01). Fasting plasma caffeine concentrations in cirrhotics varied significantly with Child's criteria, namely Child's A patients (2.06 +/- 0.38 micrograms per ml); Child's B patients (6.92 +/- 1.86 micrograms per ml), and Child's C patients (17.70 +/- 3.65 micrograms per ml) (p less than 0.001). In 44 cirrhotics, fasting plasma caffeine concentrations were compared with plasma levels of catecholamines and plasma renin activity. Plasma epinephrine concentrations were normal; however, plasma norepinephrine concentrations were increased in six cirrhotics, and plasma renin activities were increased in 28 cirrhotics. After a 3-day caffeine abstinence, plasma caffeine concentration and renin activity were significantly decreased (p less than 0.01), and high plasma norepinephrine levels were also decreased in 12 cirrhotics. Plasma caffeine concentration, renin activity and norepinephrine level did not change in a control group of cirrhotics who continued to receive caffeine for 3 days (n = 6). After abstinence from caffeine, the decrease of fasting plasma caffeine concentration correlated well with the decrease of plasma renin activity (r = +0.746, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Shotgun proteomics: Identification of unique protein profiles of apoptotic bodies from biliary epithelial cells
Authors: Ana Lleo, Weici Zhang, Hayes W. McDonald, Erin H. Seeley, Patrick S.C. Leung, Ross L. Coppel, Aftab A. Ansari, David H. Adams, Simon Afford, Pietro Invernizzi, Eric M. Gershwin
Journal: Hepatology (2014)

Shotgun proteomics is a powerful analytic method to characterize complex protein mixtures in combination with multidimensional liquid chromatography-tandem mass spectrometry (LC-MS/MS). We used this platform for proteomic characterization of apoptotic bodies in an effort to define the complex protein mixtures found in primary cultures of human intrahepatic biliary epithelial cells (HiBEC), human renal proximal tubular epithelial cells, human bronchial epithelial cells, isolated intrahepatic biliary epithelial cells from explanted primary biliary cirrhosis (PBC), and control liver using a total of 24 individual samples. Further, as additional controls and for purposes of comparison, proteomic signatures were also obtained from intact cells and apoptotic bodies. The data obtained from LC-MS/MS, combined with database searches and protein assembly algorithms, allowed us to address significant differences in protein spectral counts and identify unique pathways that may be a component of the induction of the signature inflammatory cytokine response against BECs, including the Notch signaling pathway, interleukin (IL)8, IL6, CXCR2, and integrin signaling. Indeed, there are 11 proteins that localize specifically to apoptotic bodies of HiBEC and eight proteins that were specifically absent in HiBEC apoptotic bodies. Conclusion : Proteomic analysis of BECs from PBC liver compared to normal liver are significantly different, suggesting that an immunological attack affects the repertoire of proteins expressed and that such cells should be thought of as living in an environment undergoing continuous selection secondary to an innate and adaptive immune response, reflecting an almost “Darwinian” bias. (Hepatology 2014;60:1314–1323)
Fifty Years of Human Space Travel: Implications for Bone and Calcium Research
Authors: S.M. Smith, S.A. Abrams, J.E. Davis-Street, M. Heer, K.O. O'Brien, M.E. Wastney, S.R. Zwart
Journal: Annual Review of Nutrition (2014)

Calcium and bone metabolism remain key concerns for space travelers, and ground-based models of space flight have provided a vast literature to complement the smaller set of reports from flight studies. Increased bone resorption and largely unchanged bone formation result in the loss of calcium and bone mineral during space flight, which alters the endocrine regulation of calcium metabolism. Physical, pharmacologic, and nutritional means have been used to counteract these changes. In 2012, heavy resistance exercise plus good nutritional and vitamin D status were demonstrated to reduce loss of bone mineral density on long-duration International Space Station missions. Uncertainty continues to exist, however, as to whether the bone is as strong after flight as it was before flight and whether nutritional and exercise prescriptions can be optimized during space flight. Findings from these studies not only will help future space explorers but also will broaden our understanding of the regulation of bone and calcium homeostasis on Earth.
Regulation of cultured human mesangial cell growth by ionized macromolecules.
Authors: F Pugliese, G A Cinotti, P Menè
Journal: Journal of the American Society of Nephrology (1992)

We evaluated the importance of the net charge of polyionic macromolecules in the regulation of cultured human mesangial cell growth. Structurally unrelated polyanionic compounds, i.e., heparin, suramin, poly-L-aspartic acid, and poly-L-glutamic acid, strongly inhibited 10% fetal bovine serum-stimulated cell proliferation. On the other hand, two polycations, protamin sulfate and poly-L-lysine, were equally effective in inhibiting cell growth. The antiproliferative activity of each compound was neutralized by molecules with opposite net charge. These data indicate that both anionic and cationic macromolecules exert an antimitogenic effect on cultured human mesangial cells. This inhibitory effect is dependent upon charge density rather than on the net electric charge of each compound.
REGULATION OF AUTOSENSITIZATION
Authors: Irun R. Cohen, Hartmut Wekerle
Journal: The Journal of Experimental Medicine (1973)

We studied the mechanisms underlying the natural tolerance of thymus-derived (T) lymphocytes for self-antigens. Lymphocytes from the thymus or lymph nodes of inbred rats were autosensitized in vitro against monolayers of autochthonous thymus reticulum cells or syngeneic fibroblasts. Receptors for self-antigens were detected by the specific adherence of normal lymphocytes to syngeneic cells. The achievement of active cell-mediated autosensitization was assayed by measuring the immunospecific lysis of syngeneic target cells in vitro, or graft-versus-host (GvH) reactions in vivo. The following observations were made using these systems. (a) A fraction of normal lymphocytes was found to have specific surface receptors that are able to recognize self-antigens which seem to be accessible in vivo. These potentially self-reactive lymphocytes were activated by incubation with syngeneic or autochthonous cells in vitro. Hence, the elimination of potentially self-reactive lymphocytes cannot be the only basis for natural self-tolerance. Therefore, the maintenance of self-tolerance in vivo appears to involve suppression of the immune reactivity of such self-tolerant lymphocytes. (b) We found that control of autosensitization depends upon the inhibition of the recognition of self-antigens. A GvH reaction in vivo could not be suppressed once recognition of self-antigens had occurred in vitro. Moreover, studies of the kinetics of antigen recognition indicated that several hours of incubation in vitro were needed for the inactivation of factors specifically inhibiting self-recognition. (c) We found that factors which inhibit self-recognition are present in fresh autologous serum. Treatment of the lymphocytes, but not syngeneic adsorbing cells, with autologous serum prevented recognition of syngeneic antigens. Allogeneic serum did not prevent self-recognition, and autologous serum did not inhibit the recognition of foreign antigens. These findings indicate that natural tolerance of T lymphocytes to self-antigens can be regulated by serum factors which act on the lymphocytes. The immunospecificity of the inhibitory effect suggests that these factors may be soluble self-antigens in a tolerogenic form.
Lysophosphatidic acid inhibits cholera toxin-induced secretory diarrhea through CFTR-dependent protein interactions
Authors: Chunying Li, Keanna S. Dandridge, Anke Di, Kevin L. Marrs, Erica L. Harris, Koushik Roy, John S. Jackson, Natalia V. Makarova, Yuko Fujiwara, Patricia L. Farrar, Deborah J. Nelson, Gabor J. Tigyi, Anjaparavanda P. Naren
Journal: The Journal of Experimental Medicine (2005)

The cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP-regulated chloride channel localized primarily at the apical or luminal surfaces of epithelial cells that line the airway, gut, and exocrine glands; it is well established that CFTR plays a pivotal role in cholera toxin (CTX)-induced secretory diarrhea. Lysophosphatidic acid (LPA), a naturally occurring phospholipid present in blood and foods, has been reported to play a vital role in a variety of conditions involving gastrointestinal wound repair, apoptosis, inflammatory bowel disease, and diarrhea. Here we show, for the first time, that type 2 LPA receptors (LPA2) are expressed at the apical surface of intestinal epithelial cells, where they form a macromolecular complex with Na+/H+ exchanger regulatory factor–2 and CFTR through a PSD95/Dlg/ZO-1–based interaction. LPA inhibited CFTR-dependent iodide efflux through LPA2-mediated Gi pathway, and LPA inhibited CFTR-mediated short-circuit currents in a compartmentalized fashion. CFTR-dependent intestinal fluid secretion induced by CTX in mice was reduced substantially by LPA administration; disruption of this complex using a cell-permeant LPA2-specific peptide reversed LPA2-mediated inhibition. Thus, LPA-rich foods may represent an alternative method of treating certain forms of diarrhea.
Local Continuity of Myocardial Blood Flow Studied by Monochromatic Synchrotron Radiation–Excited X-ray Fluorescence Spectrometry
Authors: Hidezo Mori, Mitsuaki Chujo, Shuichi Haruyama, Hiroyasu Sakamoto, Yoshiro Shinozaki, Minhaz Uddin-Mohammed, Atsuo Iida, Hiroe Nakazawa
Journal: Circulation Research (1995)

Abstract We have developed a monochromatic synchrotron radiation–excited system for two-dimensional mapping of x-ray fluorescence evoked from heavy element–loaded microspheres, which can evaluate myocardial blood flow in small contiguous regions with a small methodological error: 10.8±2.4% of the average of difference of the dual flow for 7- to 10-mg myocardial tissue (4 dogs). The fractal D value obtained from the slope of the log relative dispersion–log mass plot was 1.21±0.08 for a voxel size of 7 to 1260 mg (5 dogs) and that for a voxel size of 2.5 to 40 mg (1.12±0.06) was smaller than that for a voxel size of 40 to 1280 mg (1.25±0.14, P &lt;.05, ANOVA, 4 dogs). The distance–correlation coefficient relation for paired myocardial regions was attenuated (correlation analysis), and the correlation coefficients between the original grouping and the two aggregates of the adjacent regions were dissociated (extended correlation analysis) under reduction of coronary perfusion pressure (6 dogs). Suppression of myocardial contraction with lidocaine (3 dogs) and vasodilation with adenosine partly improved the distance–correlation coefficient relation under reduced coronary perfusion pressure. Thus, an x-ray fluorescence system designed for precise flow measurement shows that the fractal nature of local flow distribution can be extended into regions smaller than previously reported, that in these regions the flow becomes more homogeneous, and that the self similarity and continuity of local flow are attenuated by the reduction of coronary perfusion pressure and improved by contractile suppression and coronary vasodilation.
MANAGED CARE AND PUBLIC HEALTH DEPARTMENTS: Who is Responsible for the Health of the Population?
Authors: Bruce W. Goldberg
Journal: Annual Review of Public Health (1998)

▪ Abstract This review examines changes over the past decade in the delivery of health care in the United States, specifically the move toward managed care and capitation. Over 77 million Americans are now enrolled in health maintenance organizations, and the health care delivery system is reorganizing into large group practices and integrated health systems. Examined here are the implications of this shift on the interaction between managed care and public health agencies. How will a population-based system of health care be achieved in light of managed care organizations' responsibility only for their enrolled population, in contrast to the responsibility of the public health service for the entire population? Where does the responsibility of MCOs end and that of public health begin? Should certain public health functions be absorbed by managed care organizations? What are the prospects for partnership between these two systems?
Selective inhibition of intra-alveolar p55 TNF receptor attenuates ventilator-induced lung injury
Authors: Szabolcs Bertok, Michael R Wilson, Peter J Morley, Ruud de Wildt, Andrew Bayliffe, Masao Takata
Journal: Thorax (2011)

<h3>Background</h3> Tumour necrosis factor (TNF) is upregulated in the alveolar space early in the course of ventilator-induced lung injury (VILI). Studies in genetically modified mice indicate that the two TNF receptors play opposing roles during injurious high-stretch mechanical ventilation, with p55 promoting but p75 preventing pulmonary oedema. <h3>Aim</h3> To investigate the effects of selective inhibition of intra-alveolar p55 TNF receptor on pulmonary oedema and inflammation during ventilator-induced lung injury using a newly developed domain antibody. <h3>Methods</h3> Anaesthetised mice were ventilated with high tidal volume and given an intratracheal bolus of p55-specific domain antibody or anti-TNF monoclonal antibody ('pure' VILI model). As a model of enhanced inflammation, a subclinical dose of lipopolysaccharide (LPS) was included in the intratracheal antibody bolus (LPS+VILI model). Development of lung injury was assessed by respiratory mechanics and blood gases and protein levels in lavage fluid. Flow cytometry was used to determine leucocyte recruitment and alveolar macrophage activation, while lavage fluid cytokines were assessed by ELISA. <h3>Results</h3> The ventilation protocol produced deteriorations in respiratory mechanics and gas exchange with increased lavage fluid protein levels in the two models. The p55-specific domain antibody substantially attenuated all of these changes in the 'pure' VILI model, while anti-TNF antibody was ineffective. In the LPS+VILI model, p55 blockade prevented deteriorations in respiratory mechanics and oxygenation and significantly decreased neutrophil recruitment, expression of intercellular adhesion molecule 1 on alveolar macrophages, and interleukin 6 and monocyte chemotactic protein 1 levels in lavage fluid. <h3>Conclusions</h3> Selective inhibition of intra-alveolar p55 TNF receptor signalling by domain antibodies may open new therapeutic approaches for ventilated patients with acute lung injury.
Running in a minimalist and lightweight shoe is not the same as running barefoot: a biomechanical study
Authors: Jason Bonacci, Philo U Saunders, Amy Hicks, Timo Rantalainen, Bill (Guglielmo) T Vicenzino, Wayne Spratford
Journal: British Journal of Sports Medicine (2013)

The purpose of this study was to determine the changes in running mechanics that occur when highly trained runners run barefoot and in a minimalist shoe, and specifically if running in a minimalist shoe replicates barefoot running.Ground reaction force data and kinematics were collected from 22 highly trained runners during overground running while barefoot and in three shod conditions (minimalist shoe, racing flat and the athlete's regular shoe). Three-dimensional net joint moments and subsequent net powers and work were computed using Newton-Euler inverse dynamics. Joint kinematic and kinetic variables were statistically compared between barefoot and shod conditions using a multivariate analysis of variance for repeated measures and standardised mean differences calculated.There were significant differences between barefoot and shod conditions for kinematic and kinetic variables at the knee and ankle, with no differences between shod conditions. Barefoot running demonstrated less knee flexion during midstance, an 11% decrease in the peak internal knee extension and abduction moments and a 24% decrease in negative work done at the knee compared with shod conditions. The ankle demonstrated less dorsiflexion at initial contact, a 14% increase in peak power generation and a 19% increase in the positive work done during barefoot running compared with shod conditions.Barefoot running was different to all shod conditions. Barefoot running changes the amount of work done at the knee and ankle joints and this may have therapeutic and performance implications for runners.