bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differential expression of the interleukin 5 receptor α isoforms in blood and tissue eosinophils of nasal polyp patients
Authors: Gevaert P. , Hellman C. , Lundblad L. , Lundahl J. , Holtappels G. , Van Cauwenberge P. , Tavernier J. , Bachert C. 
Published: January 2009

Background:  Given the key role of interleukin‐5 (IL‐5) in eosinophil function, we investigated the regulated expression of the membrane‐anchored (TM‐IL‐5Rα) isoform, or a secreted (SOL IL‐5Rα) isoform, on both protein and transcript level in vitro and in vivo.Methods:  A real‐time PCR, FACS and ELISA were established to determine IL‐5Rα isoform expression in peripheral blood and nasal tissue from control subjects and nasal polyp (NP) patients with or without asthma. Human peripheral blood eosinophils were incubated with IL‐5 and were analyzed for SOL‐IL‐5Rα and TM‐IL‐5Rα mRNA and protein levels in comparison with CD‐69 expression.Results:  SOL‐IL‐5Rα and TM‐IL‐5Rα mRNA and protein expression was significantly increased in NP vs controls. In polyp tissue, SOL‐IL‐5Rα expression correlated to disease severity and eosinophils counts, whereas TM‐IL‐5Rα levels were inversely correlated to eosinophils counts and SOL‐IL‐5Rα expression. FACS analysis revealed increased CD‐69 and decreased TM‐IL‐5Rα expression in NP tissue eosinophils vs blood eosinophils. Incubation of blood eosinophils with IL‐5 caused up‐regulation of CD‐69 and down‐regulation of TM‐IL‐5Rα after 2 and 24 h.Conclusion:  The expression of SOL‐IL‐5Rα and TM‐IL‐5Rα differs according to the eosinophil activation state and localization in the body (blood vs tissue) and may therefore be involved in the fine‐tuning of the eosinophil homeostasis. Exposure of eosinophils to IL‐5 reduces their responsiveness to IL‐5 by regulated expression of the IL‐5Rα isoforms. Since, TM‐IL‐5Rα is down‐regulated and SOL‐IL‐5Rα (antagonistic) is upregulated in NP tissue, our findings are important to understand the clinical trials with anti‐IL‐5 in humans.
Teamwork and patient safety in dynamic domains of healthcare: a review of the literature
Authors: MANSER T. 
Published: January 2009

Aims/Background: This review examines current research on teamwork in highly dynamic domains of healthcare such as operating rooms, intensive care, emergency medicine, or trauma and resuscitation teams with a focus on aspects relevant to the quality and safety of patient care.Results: Evidence from three main areas of research supports the relationship between teamwork and patient safety: (1) Studies investigating the factors contributing to critical incidents and adverse events have shown that teamwork plays an important role in the causation and prevention of adverse events. (2) Research focusing on healthcare providers' perceptions of teamwork demonstrated that (a) staff's perceptions of teamwork and attitudes toward safety‐relevant team behavior were related to the quality and safety of patient care and (b) perceptions of teamwork and leadership style are associated with staff well‐being, which may impact clinician' ability to provide safe patient care. (3) Observational studies on teamwork behaviors related to high clinical performance have identified patterns of communication, coordination, and leadership that support effective teamwork.Conclusion: In recent years, research using diverse methodological approaches has led to significant progress in team research in healthcare. The challenge for future research is to further develop and validate instruments for team performance assessment and to develop sound theoretical models of team performance in dynamic medical domains integrating evidence from all three areas of team research identified in this review. This will help to improve team training efforts and aid the design of clinical work systems supporting effective teamwork and safe patient care.
Beneficial effects of high positive end‐expiratory pressure in lung respiratory mechanics during laparoscopic surgery
Authors: MARACAJÁ‐NETO L. F. , VERÇOSA N. , RONCALLY A. C. , GIANNELLA A. , BOZZA F. A. , LESSA M. A. 
Published: January 2009

Background: The effect of neuromuscular blockade (NMB) and positive end‐expiratory pressure (PEEP) on the elastic properties of the respiratory system during pneumoperitoneum (PnP) remains a controversial subject. The main objective of the present study was to evaluate the effects of NMB and PEEP on respiratory mechanics.Methods: We performed a dynamic analysis of respiratory mechanics in patients subjected to PnP. Twenty‐one patients underwent cholecystectomy videolaparoscopy and total intravenous anesthesia. The respiratory system resistance (RRS), pulmonary elastance (EP), chest wall elastance (ECW), and respiratory system elastance (ERS) were computed via the least squares fit technique using an equation describing the motion of the respiratory system, which uses primary signs such as airway pressure, tidal volume, air flow, and esophageal pressures. Measurements were taken after tracheal intubation, PnP, NMB, establishment of PEEP (10 cmH2O), and PEEP withdrawal [zero end‐expiratory pressure (ZEEP)].Results: PnP significantly increased ERS by 27%; both EP and ECW increased 21.3 and 64.1%, respectively (P<0.001). NMB did not alter the respiratory mechanic properties. Setting PEEP reduced ERS by 8.6% (P<0.05), with a reduction of 10.9% in EP (P<0.01) and a significant decline of 15.7% in RRS (P<0.05). These transitory changes in elastance disappeared after ZEEP.Conclusions: We concluded that the 10 cmH2O of PEEP attenuates the effects of PnP in respiratory mechanics, lowering RRS, EP, and ERS. These effects may be useful in the ventilatory approach for patients experiencing a non‐physiological increase in IAP owing to PnP in laparoscopic procedures.
Additives in intravenous anesthesia modulates pulmonary inflammation in a model of LPS‐induced respiratory distress
Authors: HAITSMA J. J. , LACHMANN B. , PAPADAKOS P. J. 
Published: January 2009

Background: It has been suggested that propofol with ethylenediaminetetraacetic acid (EDTA) can modulate the systemic inflammatory response. Prolonged higher levels of pulmonary inflammation are associated with poor outcome of patients with acute lung injury. In the present study, we hypothesized that pulmonary inflammation could be modulated by propofol with EDTA compared with propofol with sulfite.Methods: Respiratory distress was induced in rats (n=25) by intratracheal nebulization of lipopolysaccharide (LPS). After 24 h, animals were randomized to either propofol with EDTA (PropofolEDTA), propofol with sulfite (Propofolsulfite) or ketamine/midazolam (Ket/Mid); control animals received saline (n=30). Animals were ventilated for 4 h and blood gases were measured hourly. Bronchoalveolar lavage (BAL) was performed for cytokine analysis of: tumor necrosis factor (TNF), interleukin (IL)‐6 and macrophage inflammatory protein (MIP)‐2.Results: LPS led to increased pulmonary inflammation in all groups compared with the control groups. Gas exchange deteriorated over time only in the LPS Propofolsulfite group and was significantly lower than the Ket/Mid group. Only IL‐6 was significantly higher in the LPS Propofolsulfite group compared with both the Ket/Mid group and the PropofolEDTA group.Conclusion: Pulmonary IL‐6 can be modulated by additives in systemic anesthesia.Implication Statement: This study demonstrates that pulmonary inflammation caused by direct lung injury can be modulated by intravenous anesthesia used in critically ill patients.
Microparticle sizing by dynamic light scattering in fresh‐frozen plasma
Authors: Lawrie A. S. , Albanyan A. , Cardigan R. A. , Mackie I. J. , Harrison P. 
Published: January 2009

Background   We have previously shown that fresh‐frozen plasma (FFP) contains red blood cell‐derived procoagulant microparticles (MPs) that are removable by 0·2 µm filtration. Given the limitations of current methods for accurately sizing MPs, we have applied the novel approach of dynamic light scattering (DLS) to characterize the size distributions of these MPs within FFP.Methods   Fresh‐frozen plasma was prepared from blood Group A and O donations (n = 10 of each) after an overnight hold of whole blood at 4°C. On the day of analysis, plasma was thawed to 37°C and daughter aliquots were studied pre‐ and post‐filtration (0·2 µm filtration device, Ceveron® MFU‐500, Technoclone). MP size and dispersity was assessed using a Zetasizer Nano S (Malvern Instruments Ltd), which employs a 173° backscatter detector and an N5 Submicron Particle Size Analyser (Beckman Coulter) using multi‐angle measurements (30·1°, 62·6° and 90°). The analysers presented MP size distribution graphically as intensity plots, mean size, standard deviation and polydispersity index.Results   Of the instruments used, only the N5 utilizing a 30·1° angle of measurement could detect MPs of the expected size distribution and demonstrate their removal by filtration. MPs (range of mean particle diameters: pre, 101–464 nm; post, 21–182 nm filtration) were significantly smaller post‐filtration (P < 0·0001), but polydispersity index (median: pre, 0·746, post, 0·769) exhibited no significant change. There was no significant difference between the size of MPs from blood Group O (pre, 247 nm) and Group A (pre, 289 nm) samples (P = 0·44).Conclusion   Our data demonstrates that DLS offers a novel approach to assessing MP size and distribution, a technique that could be easily adopted as a means of assessing MPs within either FFP or other blood products.
Establishment of a cell line expressing recombinant factor VII and its subsequent conversion to active form FVIIa through hepsin by genetic engineering method
Authors: Halabian R. , Roudkenar M. H. , Esmaeili N. S. , Masroori N. , Roushandeh A. M. , Najafabadi A. J. 
Published: January 2009

Background  Factor VII (FVII) is a plasma glycoprotein that participates in the coagulation process leading to generation of fibrin. It is converted to factor VIIa that plays an important role in the coagulation cascade. The aim of this study was isolating and cloning the genes of human factor VII and hepsin and subsequent co‐transfection of the constructs to Chinese hamster ovary (CHO) cell line to obtain rFVIIa.Methods  Factor VII and hepsin cDNAs were isolated from HepG2 cell line and cloned into pcDNA3·1 (+) vector. The constructs were co‐trasfected to CHO cell line. A cell line that permanently expressed recombinant factor VII (rFVII) and hepsin was established. The expression of rFVII was confirmed by reverse transcriptase–polymerase chain reaction, enzyme‐linked immunosorbent assay and Western blot analysis. Biological activity of rFVII was evaluated by prothrombin time assay.Results  The results showed that the genes of FVII and hepsin were successfully cloned and expressed. Stable CHO cells co‐transfected with pcNDA3·1‐FVII and pcNDA3·1‐hepsin expressed FVII and hepsin mRNA, but there was no expression in the CHO cells transfected with insert free pcDNA3·1. FVIIa protein was secreted to medium of CHO cells co‐transfected with pcNDA3·1‐FVII and pcNDA3·1‐hepsin. The expected band of rFVII was detected in Western blot analysis. A three‐ to fourfold decrease in clotting time was observed when human FVII‐depleted plasma was used in combination with human thromboplastin in the presence of rFVII, confirming the biological activity of rFVII.Conclusion  As we are aware, this is the first report of establishing a cell line expressing FVIIa using genetic engineering methods.
IMAGING LUNG AERATION AND LUNG LIQUID CLEARANCE AT BIRTH USING PHASE CONTRAST X‐RAY IMAGING
Authors: Hooper Stuart B , Kitchen Marcus J , Siew Melissa LL , Lewis Robert A , Fouras Andreas , B te Pas Arjan , Siu Karen KW , Yagi Naoto , Uesugi Kentaro , Wallace Megan J 
Published: January 2009

SUMMARY

The transition to extra‐uterine life at birth is critically dependent on airway liquid clearance to allow the entry of air and the onset of gaseous ventilation. We have used phase contrast X‐ray imaging to identify factors that regulate lung aeration at birth in spontaneously breathing term and mechanically ventilated preterm rabbit pups.
Phase contrast X‐ray imaging exploits the difference in refractive index between air and water to enhance image contrast, enabling the smallest air‐filled structures of the lung (alveoli; < 100 µm) to be resolved. Using this technique, the lungs become visible as they aerate, allowing the air–liquid interface to be observed as it moves distally during lung aeration.
Spontaneously breathing term rabbit pups rapidly aerate their lungs, with most fully recruiting their functional residual capacity (FRC) within the first few breaths. The increase in FRC occurs mainly during individual breaths, demonstrating that airway liquid clearance and lung aeration is closely associated with inspiration. We suggest that transpulmonary pressures generated by inspiration provide a hydrostatic pressure gradient for the movement of water out of the airways and into the surrounding lung tissue after birth.
In mechanically ventilated preterm pups, lung aeration is closely associated with lung inflation and a positive end‐expiratory pressure is required to generate and maintain FRC after birth.
In summary, phase contrast X‐ray imaging can image the air‐filled lung with high temporal and spatial resolution and is ideal for identifying factors that regulate lung aeration at birth in both spontaneously breathing term and mechanically ventilated preterm neonates.
EFFECTS OF EMULSIFIED ISOFLURANE ON HAEMODYNAMICS AND CARDIOMYOCYTE APOPTOSIS IN RATS WITH MYOCARDIAL ISCHAEMIA
Authors: Hu Zhao‐Yang , Liu Jin 
Published: January 2009

SUMMARY

It has been shown that inhaled isoflurane limits the size of myocardial infarcts. The aim of the present study was to examine the effects of emulsified isoflurane on cardiac function and myocardial apoptosis in an ischaemia model of myocardial injury.
In the first study, 48 rats were randomly allocated to six groups (n = 8 in each): control (saline); emulsified isoflurane (EIso) at 1, 2 or 4 mL/kg; 30% intralipid (vehicle for EIso); and sham operated. Rats received isovolumetric intravenous infusions for 30 min and then, 30 min after cessation of the infusion, 90 min coronary occlusion. Haemodynamics and myocardial infarct size were measured. In the second study, another 48 rats were randomized into six groups (n = 8 in each). After 90 min ischaemia, rats were killed for histopathological study, immunohistochemical evaluation and apoptosis measurement.
Pretreatment with 2 and 4 mL/kg EIso significantly attenuated decreases in left ventricular systolic pressure and dP/dtmax, and increases in left ventricular end‐diastolic pressure and –dP/dpmax, and alleviated myocardial injury compared with the control, intralipid and 1 mL/kg EIso groups (P < 0.05). Infusion of 1 mL/kg EIso and intralipid had no effect on haemodynamics, infarct size or histological variables.
Expression of Bcl‐2 was increased, whereas expression of Bax and caspase 3 was decreased, after preconditioning with 2 and 4 mL/kg EIso (P < 0.05). The apoptotic index in the 2 and 4 mL/kg Eiso‐treated groups was reduced compared with that in the control and intralipid groups (P < 0.01).
In conclusion, EIso ameliorates cardiac dysfunction, attenuates myocardial damage and inhibits apoptosis after ischaemia, which may be attributed, in part, to diminished expression of apoptosis‐related protein.
ACUTE EFFECTS OF NICOTINE ON ARTERIAL STIFFNESS AND WAVE REFLECTION IN HEALTHY YOUNG NON‐SMOKERS
Authors: Adamopoulos Dionysios , Argacha Jean‐François , Gujic Marko , Preumont Nicolas , Degaute Jean‐Paul , Van De Borne Philippe 
Published: January 2009

SUMMARYRecently, we have demonstrated that cigarette smoke exposure proportionally increases plasma nicotine levels and arterial wave reflection to the aorta. However, the exact contribution of nicotine to the smoke‐induced enhancement of wave reflection and the potential underlying mechanisms have not been fully investigated.The present study was a prospective study in 15 healthy male non‐smokers. All received a placebo and a 2 mg nicotine tablet, according to a randomized double‐blind cross‐over study design. Each subject underwent repeated measurements at baseline and for 1 h after nicotine or placebo intake, using carotid–femoral pulse wave velocity (PWV) to assess arterial compliance. Concurrently, aortic pressures and the augmentation index were evaluated using applanation tonometry.Plasma nicotine concentrations achieved 1 h after intake of the nicotine tablet reached comparable levels to those achieved after 1 h exposure to passive smoke (3.6 ± 0.4vs3.2 ± 0.4 ng/mL, respectively;P = 0.4).Nicotine enhanced arterial wave reflection to the aorta, as assessed by the augmentation index corrected for heart rate (4.2 ± 1.3vs–0.7 ± 0.8% with placebo;P = 0.001). In addition, a progressive increase in carotid–femoral PWV was noted after nicotine administration (0.3 ± 0.1vs–0.02 ± 0.1 m/s with placebo;P = 0.04). This remained significant even after adjustment for changes in mean blood pressure and heart rate (P = 0.01).Plasma nicotine concentrations comparable to those achieved after exposure to passive smoke enhance arterial wave reflection to the aorta. This is accompanied by an increase in carotid–femoral PWV, denoting a deterioration of arterial compliance by nicotine.
CILOSTAMIDE PRODUCES HYPERPOLARIZATION ASSOCIATED WITH KATP CHANNEL ACTIVATION, BUT DOES NOT AUGMENT ENDOTHELIUM‐DERIVED HYPERPOLARIZATION IN RAT MESENTERIC ARTERIES
Authors: Kansui Yasuo , Goto Kenichi , Fujii Koji , Oniki Hideyuki , Matsumura Kiyoshi , Iida Mitsuo 
Published: January 2009

SUMMARY

Non‐nitric oxide/prostaglandin‐mediated endothelium‐derived hyperpolarization (EDH) is considered to be mediated, in part, by gap junctions and it has been suggested that cAMP increases endothelium‐derived hyperpolarizing factor (EDHF)‐mediated relaxation through the modulation of gap junctions. Cilostamide, which inhibits phosphodiesterase III, has been suggested to augment EDHF‐type relaxation by increasing the concentration of cAMP.
In the present study, we investigated the effect of cilostamide on EDH per se in mesenteric arteries of Wistar rats using a conventional microelectrode technique.
The resting membrane potential of the mesenteric arteries was significantly more negative in the presence of 10−6 mol/L cilostamide compared with control conditions. Furthermore, EDH in response to 10−6 mol/L acetylcholine (ACh) in the presence of 10−5 mol/L indomethacin and 10−4 mol/L NG‐nitro‐L‐arginine was decreased in the presence of 10−6 mol/L cilostamide by approximately 5 and 3.5 mV in proximal and distal arteries, respectively.
Glibenclamide (10−5 mol/L), an ATP‐sensitive potassium channel (KATP) inhibitor, abolished the hyperpolarization to 10−6 mol/L cilostamide. Furthermore, in the presence of glibenclamide, ACh‐induced EDH was unaffected by cilostamide, suggesting that the inhibition of ACh‐induced hyperpolarization by cilostamide in the absence of glibenclamide may be due to the smaller driving force for hyperpolarization because of the more negative membrane potential under such conditions.
The findings of the present study suggest that cilostamide produces hyperpolarization by activating KATP channels, presumably by increasing cAMP. However, cilostamide alone may not directly affect EDH.
MAGNOLOL DEPRESSES UROTENSIN‐II‐INDUCED CELL PROLIFERATION IN RAT CARDIAC FIBROBLASTS
Authors: Liou Jer‐Young , Chen Yen‐Ling , Loh Shih‐Hurng , Chen Po‐Yuan , Hong Chuang‐Ye , Chen Jin‐Jer , Cheng Tzu‐Hurng , Liu Ju‐Chi 
Published: January 2009

SUMMARY

Accumulating evidence suggests that oxidative stress plays a key role in the development of cardiac fibrosis. Urotensin‐II (U‐II) has been reported to play an important role in cardiac remodelling and fibrosis. Recently, we demonstrated the involvement of reactive oxygen species (ROS) production in U‐II‐induced cardiac fibroblast proliferation. Magnolol is an anti‐oxidant compound extracted from the cortices of Magnolia officinalis. Thus, it is feasible that magnolol may attenuate cardiac fibroblast proliferation by inhibiting ROS production. Therefore, the aims of the present study were to determine whether magnolol alters U‐II‐induced cell proliferation and to identify the putative underlying signalling pathways in rat cardiac fibroblasts.
Cultured rat cardiac fibroblasts were pretreated with magnolol (1, 3 and 10 µmol/L) for 30 min, followed by exposure to U‐II (30 nmol/L) for 24 h, after which cell proliferation and endothelin‐1 (ET‐1) protein secretion was examined. The effects of magnolol on U‐II‐induced ROS formation and extracellular signal‐regulated kinase (ERK) phosphorylation were examined to elucidate the intracellular mechanisms by which magnolol affects cell proliferation and ET‐1 expression.
Urotensin‐II (30 nmol/L) stimulated cell proliferation, ET‐1 protein secretion and ERK phosphorylation, all of which were inhibited by magnolol (10 µmol/L). Pretreatment of cardiac fibroblasts with N‐acetylcysteine (5 mmol/L) for 30 min prior to exposure to U‐II resulted in inhibition of U‐II increased ROS formation. Similar effects were observed with 10 µmol/L magnolol.
In conclusion, the results suggest that magnolol inhibits cardiac fibroblast proliferation by interfering with ROS generation. Thus, the present study provides important new insights into the molecular pathways involved, which may contribute to our understanding of the effects of magnolol on the cardiovascular system.
HIGH‐CHOLESTEROL DIET AUGMENTS ENDOTHELIAL DYSFUNCTION VIA ELEVATED OXIDATIVE STRESS AND REDUCED TETRAHYDROBIOPTERIN IN INS2AKITA MICE, AN AUTOSOMAL DOMINANT MUTANT TYPE 1 DIABETIC MODEL
Authors: Yang Xiang‐Qun , Chen Alex F 
Published: January 2009

SUMMARY

Oxidative stress contributes to endothelial dysfunction and atherogenesis in diabetes. The present study tested the hypothesis that a high‐cholesterol diet accelerates endothelial dysfunction in Ins2Akita mice, a Type 1 diabetic model with a spontaneous autosomal preproinsulin gene (Ins2 gene) mutation, through further increase of superoxide production.
The Ins2Akita diabetic mice were fed a high‐cholesterol diet (1.25% cholesterol) for 4 months. Some Ins2Akita mice were also treated for 4 months with the selective NADPH oxidase inhibitor apocynin (4 mg/kg per day in drinking water). Oxidative stress markers, tetrahydrobiopterin (BH4) levels, GTP cyclohydrolase I activity and endothelial function were determined in serum or arteries afterwards.
Serum lipid peroxidation and arterial superoxide levels were increased, whereas arterial BH4 levels and GTP cyclohydrolase I activity were decreased, in Ins2Akita mice on a high‐cholesterol diet, resulting in impaired endothelium‐dependent nitric oxide‐mediated relaxation in response to acetylcholine.
In vivo treatment with apocynin not only blunted serum lipid peroxidation and arterial superoxide levels, but also increased BH4 levels and GTP cyclohydrolase I activity, resulting in improved endothelium‐dependent relaxation.
These results suggest that NADPH oxidase may play a potential role in oxidative stress‐induced arterial BH4 and GTP cyclohydrolase I deficiency, resulting in endothelial dysfunction in Ins2Akita Type 1 diabetic mice fed a high‐cholesterol diet.