bluuebunny/crossref_metadata_2025_split huggingface dataset:
Production of a Heterozygous Mutant Cell Line by Homologous Recombination (Single Knockout)
Authors: Mortensen Richard 
Published: April 2011

AbstractGene targeting by homologous recombination is a powerful and widely used technique for introduction of specific gene mutations (frequently a gene inactivation) in transgenic animals. The basic method detailed in this unit uses sequences homologous to the endogenous gene flanking the mutation. While methods using bacterial artificial chromosomes (BACs) and recombineering may be used, in most cases simpler bacterial plasmid clones with several kb of homology are sufficient. This protocol details the strategic factors in designing the constructs for selection and screening for homologous recombination. Curr. Protoc. Neurosci. 55:4.30.1‐4.30.12. © 2011 by John Wiley & Sons, Inc.
Experimental Asexual Blood Stage Malaria Immunity
Authors: Amante Fiona H. , Engwerda Christian R. , Good Michael F. 
Published: April 2011

AbstractImmunity to asexual blood stages of malaria is complex, involving both humoral and cell‐mediated immune mechanisms. The availability of murine models of malaria has greatly facilitated the analysis of immune mechanisms involved in resistance to the asexual blood stages. This unit details the materials and methods required for inducing protective immunity toward experimental blood stage malaria parasites by vaccination, repeated infection, and drug cure, as well as adoptive transfer of antigen‐specific T cells. Curr. Protoc. Immunol. 93:19.4.1‐19.4.26. © 2011 by John Wiley & Sons, Inc.
Early social experience affects behavioral and physiological responsiveness to stressful conditions in infant rhesus macaques (Macaca mulatta)
Authors: Rommeck Ina , Capitanio John P. , Strand Sarah C. , McCowan Brenda 
Published: April 2011

AbstractStudies on early development have demonstrated the profound effects of early social experience on the behavioral development and physiology of young rhesus macaques. Given these relationships, we hypothesized that rhesus macaques exposed to different nursery‐rearing conditions may develop unique biobehavioral profiles. If this is true, the assessment of temperament may allow us to pinpoint successful rearing environments, thus improving the overall health of nonhuman primates that are raised in captive environments. We conducted biobehavioral assessments in order to examine differences in the development of infants raised under four different peer‐rearing conditions (continuous pairing (CP), intermittent pairing, CP with partner rotation, and intermittent rotational pairing) and compared these animals with data from a mother‐reared control group. Overall, continuous rotationally paired animals were most similar to mother‐reared controls on most behavioral and temperament measures, suggesting that more socially complex rearing environments (greater number of social partners) favor a more active behavioral style. Cortisol profiles of mother‐reared controls were similar to both CP groups, and these three groups had higher cortisol concentrations than the intermittent rotational‐pairing group. In addition, intermittently paired infants displayed a significantly higher frequency of self‐stroke behavior during a human intruder challenge, an abnormal behavior also known as floating limb which has been shown to be a precursor of self‐biting. Overall, the data are consistent with the idea that social complexity in the nursery, as operationalized in our continuous rotational pairing, leads to a biobehavioral profile that is most similar to that of infants raised by their mothers in large, socially complex, cages. Am. J. Primatol. 73:692–701, 2011. © 2011 Wiley‐Liss, Inc.
Benzothieno[3,2‐e][1,2,4]triazolo[4,3‐c]pyrimidines: Synthesis, Characterization, Antimicrobial Activity, and Incorporation into Solid Lipid Nanoparticles
Authors: Panchamukhi Shridhar I. , Mulla Jameel Ahmed S. , Shetty Nitinkumar S. , Khazi Mohammed Iqbal A. , Khan Ashraf Y. , Kalashetti Mallikarjun B. , Khazi Imitiyaz Ahmed M. 
Published: April 2011

AbstractFused triazolothienopyrimidines were prepared from the corresponding 2‐amino‐4,5,6,7‐tetrahydrobenzo[b]thiophene‐3‐carbonitrile. These precursors were intern prepared by employing the Gewald's reaction. All the newly synthesized compounds were characterized by spectral and analytical data. Title compounds displayed promising antibacterial and antifungal activities. Compound 3h which exhibited good antimicrobial activity was incorporated into SLN and characterized for particle size, entrapment efficiency (EE%), scanning electron microscopy (SEM), differential scanning calorimetry (DSC) and in‐vitro release studies. It showed narrow particle size distribution with high entrapment efficiency. In‐vitro release study of compound loaded SLNs in phosphate buffer of pH 7.4, exhibited a biphasic pattern with an initial burst and prolonged release over 24 h.
Randomized clinical trial of routine on-table cholangiography during laparoscopic cholecystectomy (Br J Surg 2011; 98: 362–367)
Authors: Cockbain A J , Young A L , Toogood G J 
Published: April 2011

Abstract
The Editors welcome topical correspondence from readers relating to articles published in the Journal. Responses should be sent electronically via the BJS website (www.bjs.co.uk). All letters will be reviewed and, if approved, appear on the website. A selection of these will be edited and published in the Journal. Letters must be no more than 250 words in length.
Synthesis and Structures of the C5Me4SiMe3‐Supported Polyhydride Complexes over the Full Size Range of the Rare Earth Series
Authors: Nishiura Masayoshi , Baldamus Jens , Shima Takanori , Mori Kyouichi , Hou Zhaomin 
Published: April 2011

AbstractThe acid–base reaction of [Ln(CH2SiMe3)3(thf)2] with Cp′H gave the corresponding half‐sandwich rare earth dialkyl complexes [(Cp′)Ln(CH2SiMe3)2(thf)] (1‐Ln: Ln=Sc, Y, Gd, Tb, Dy, Ho, Er, Tm, Yb, Lu; Cp′=C5Me4SiMe3) in 62–90 % isolated yields. X‐ray crystallographic studies revealed that all of these complexes adopt a similar overall structure, in spite of large difference in metal‐ion size. In most cases, the hydrogenolysis of the dialkyl complexes in toluene gave the tetranuclear octahydride complexes [{(Cp′)Ln(μ‐H)2}4(thf)x] (2‐Ln: Ln=Sc, x=0; Y, x=1; Er, x=1; Tm, x=1; Gd, x=1; Dy, x=1; Ho, x=1) as the only isolable product. However, in the case of Lu, a trinuclear pentahydride [(Cp′)2Lu3(μ‐H)5(μ‐CH2SiMe2C5Me4)(thf)2] (3), in which the CH activation of a methyl group of the Me3Si unit on a Cp′ ligand took place, was obtained as a major product (66 % yield), in addition to the tetranuclear octahydride [{(Cp′)Lu(μ‐H)2}4(thf)] (2‐Lu, 34 %). The use of hexane instead of toluene as a solvent for the hydrogenolysis of 1‐Lu led to formation of 2‐Lu as a major product (85 %), while a similar reaction in THF yielded 3 predominantly (90 %). The tetranuclear octahydride complexes of early (larger) lanthanide metals [{Cp′Ln(μ‐H)2}4(thf)2] (2, Ln=La, Ce, Pr, Nd, Sm) were obtained in 38–57 % isolated yields by hydrogenolysis of the bis(aminobenzyl) species [Cp′Ln(CH2C6H4NMe2‐o)2], which were generated in‐situ by reaction of [Ln(CH2C6H4NMe2‐o)3] with one equivalent of Cp′H. X‐ray crystallographic studies showed that the fine structures of these hydride clusters are dependent on the size of the metal ions.
Stereoselective metabolism of the herbicide fluroxypyr methylheptyl ester in rabbits
Authors: Xu Xinyuan , Shen Zhigang , Diao Jinling , Zhang Ping , Jiang Jiazhen , Zhou Zhiqiang 
Published: April 2011

AbstractWe investigated the stereoselective degradation kinetics of fluroxypyr methylheptyl ester (FPMH) in rabbits using a chiral high‐performance liquid chromatographic method. In 20% rabbit plasma, the half lives of (+)‐FPMH and (−)‐FPMH were 2.5 and 10.9 min, respectively. Thus, the enantioselective degradation was faster for (+)‐FPMH than for (−)‐FPMH in rabbit plasma in vitro, and there was no chiral conversion or transformation during incubation of the plasma. The degradation of (+)‐FPMH was also much faster than that of the (−)‐FPMH in the kidney, lung, and muscle after the intravenous administration of 50 mg/kg racemic FPMH (rac‐FPMH), whereas the concentrations of FPMH were below the limit of quantification in other tissues. Furthermore, 98% rac‐FPMH was quickly (within 10 min) hydrolyzed to fluroxypyr (FP) in rabbit liver microsomes. Therefore, we examined FP in rabbit plasma and tissues in vivo. We detected FP in all tissues; its concentration was higher in the urine than in the other tissues. FP was rapidly excreted unchanged, principally in the urine. The data presented here are important for a more thorough understanding of this pesticide and should be useful for its full environmental assessment. Chirality, 2011. © 2011 Wiley‐Liss, Inc.
Sub‐stage PCA modelling and monitoring method for uneven‐length batch processes
Authors: Chang Yu‐Qing , Lu Yun‐Song , Wang Fu‐Li , Wang Shu , Feng Shu‐Min 
Published: April 2011

AbstractFor the characteristic of multistage of batch processes, a new PCA‐based sub‐stage division algorithm is proposed. This algorithm is based on the fact that production transition can be detected by analysing the loading matrixes and principal component matrixes, which reveal objectively evolvement of underlying process behaviours. Sub‐stage PCA models for each stage are built, and then extended to monitor the batch processes with uneven‐length durations by choosing the right sub‐stage model according to the principle of minimum similarity distance of principal component matrixes. With the proposed method, multi‐stage batch processes with durations of uneven‐length can be monitored effectively.
Anomalous Origin of the Left Coronary Artery From the Pulmonary Artery in Adults: A Comprehensive Review of 151 Adult Cases and A New Diagnosis in a 53‐Year‐Old Woman
Authors: Yau James M. , Singh Rajiv , Halpern Ethan J. , Fischman David 
Published: April 2011

AbstractBackground:Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) is a rare congenital coronary abnormality associated with early infant mortality and adult sudden death. As it predominantly presents in the first year of life, diagnosis in living adults is extremely rare. Current management is based on limited case series or extrapolated from pediatric cases. Modern advances in noninvasive cardiac imaging have substantially increased the number of diagnoses, uncovering a large adult population that has not been reviewed.Hypothesis:The availability of newer diagnostic modalities correlates with an increasing incidence in an older cohort, and true association between sudden death and ALCAPA may be lower, especially among older patients.Methods:A comprehensive literature search was performed for all case reports of ALCAPA on MEDLINE and PubMed using the keywords ALCAPA, Bland‐White‐Garland, and coronary anomaly; and augmented by references from published case reports from 1908 to 2008. All adult cases, defined by age 18 years and older, were reviewed for this article.Results:One hundred fifty‐one adult cases of ALCAPA are described, in addition to the case of an asymptomatic 53‐year‐old woman. The average reported age was 41 years old with the oldest being 83. Sixty‐six percent of the patients presented with symptoms of angina, dyspnea, palpitations, or fatigue; 17% presented with ventricular arrhythmia, syncope, or sudden death; and 14% were asymptomatic. Twelve percent were diagnosed at autopsy. The majority had some form of surgical correction during their clinical course.Conclusions:ALCAPA is a rare and life‐threatening condition in adults. The availability of newer, less invasive diagnostic modalities has resulted in more frequent identification of this condition in an older cohort. © 2011 Wiley Periodicals, Inc.The authors have no funding, financial relationships, or conflicts of interest to disclose.
Pulmonary Vascular Diseases
Authors: Mélot C. , Naeije R. 
Published: April 2011

AbstractDiseases of the pulmonary vasculature are a cause of increased pulmonary vascular resistance (PVR) in pulmonary embolism, chronic thromboembolic pulmonary hypertension (CTEPH), and pulmonary arterial hypertension or decreased PVR in pulmonary arteriovenous malformations on hereditary hemorrhagic telangiectasia, portal hypertension, or cavopulmonary anastomosis. All these conditions are associated with a decrease in both arterial Po2and Pco2. Gas exchange in pulmonary vascular diseases with increased PVR is characterized by a shift of ventilation and perfusion to high ventilation‐perfusion ratios, a mild to moderate increase in perfusion to low ventilation‐perfusion ratios, and an increased physiologic dead space. Hypoxemia in these patients is essentially explained by altered ventilation‐perfusion matching amplified by a decreased mixed venous Po2caused by a low cardiac output. Hypocapnia is accounted for by hyperventilation, which is essentially related to an increased chemosensitivity. A cardiac shunt on a patent foramen ovale may be a cause of severe hypoxemia in a proportion of patients with pulmonary hypertension and an increase in right atrial pressure. Gas exchange in pulmonary arteriovenous malformations is characterized by variable degree of pulmonary shunting and/or diffusion‐perfusion imbalance. Hypocapnia is caused by an increased ventilation in relation to an increased pulmonary blood flow with direct peripheral chemoreceptor stimulation by shunted mixed venous blood flow. © 2011 American Physiological Society.Compr Physiol1:593‐619, 2011.
Experimental and Transgenic Models of Pulmonary Hypertension
Authors: West James , Hemnes Anna 
Published: April 2011

AbstractPulmonary hypertension in human patients can result from increased pulmonary vascular tone, pressure transferred from the systemic circulation, dropout of small pulmonary vessels, occlusion of vessels with thrombi or intimal lesions, or some combination of all of these. Different animal models have been designed to reflect these different mechanistic origins of disease. Pulmonary hypertension models may be roughly grouped into tone‐related models, inflammation‐related models, and genetic models with unusual or mixed mechanism. Models of tone generally use hypoxia as a base, and then modify this with either genetic modifications (SOD, NOS, and caveolin) or with drugs (Sugen), although some genetic modifications of tone‐related pathways can result in spontaneous pulmonary hypertension (Hph‐1). Inflammation‐related models can use either toxic chemicals (monocrotaline, bleomycin), live pathogens (stachybotrys, schistosomiasis), or genetic modifications (IL‐6, VIP). Additional genetic models rely on alterations in metabolism (adiponectin), cell migration (S100A4), the serotonin pathway, or the BMP pathway. While each of these shares molecular and pathologic symptoms with different classes of human pulmonary hypertension, in most cases the molecular etiology of human pulmonary hypertension is unknown, and so the relationship between any model and human disease is unclear. There is thus no best animal model of pulmonary hypertension; instead, investigators must select the model most related to the specific pathology they are studying. © 2011 American Physiological Society.Compr Physiol1:769‐782, 2011.
Ventilation‐Induced Lung Injury
Authors: Uhlig Ulrike , Uhlig Stefan 
Published: April 2011

AbstractMechanical ventilation (MV) is, by definition, the application of external forces to the lungs. Depending on their magnitude, these forces can cause a continuum of pathophysiological alterations ranging from the stimulation of inflammation to the disruption of cell‐cell contacts and cell membranes. These side effects of MV are particularly relevant for patients with inhomogeneously injured lungs such as in acute lung injury (ALI). These patients require supraphysiological ventilation pressures to guarantee even the most modest gas exchange. In this situation, ventilation causes additional strain by overdistension of the yet non‐injured region, and additional stress that forms because of the interdependence between intact and atelectatic areas. Cells are equipped with elaborate mechanotransduction machineries that respond to strain and stress by the activation of inflammation and repair mechanisms. Inflammation is the fundamental response of the host to external assaults, be they of mechanical or of microbial origin and can, if excessive, injure the parenchymal tissue leading to ALI. Here, we will discuss the forces generated by MV and how they may injure the lungs mechanically and through inflammation. We will give an overview of the mechanotransduction and how it leads to inflammation and review studies demonstrating that ventilator‐induced lung injury can be prevented by blocking pathways of mechanotransduction or inflammation. © 2011 American Physiological Society.Compr Physiol1:635‐661, 2011.
Acute Lung Injury and Pulmonary Vascular Permeability: Use of Transgenic Models
Authors: Parker James C. 
Published: April 2011

AbstractAcute lung injury is a general term that describes injurious conditions that can range from mild interstitial edema to massive inflammatory tissue destruction. This review will cover theoretical considerations and quantitative and semi‐quantitative methods for assessing edema formation and increased vascular permeability during lung injury. Pulmonary edema can be quantitated directly using gravimetric methods, or indirectly by descriptive microscopy, quantitative morphometric microscopy, altered lung mechanics, high‐resolution computed tomography, magnetic resonance imaging, positron emission tomography, or x‐ray films. Lung vascular permeability to fluid can be evaluated by measuring the filtration coefficient (Kf) and permeability to solutes evaluated from their blood to lung clearances. Albumin clearances can then be used to calculate specific permeability‐surface area products (PS) and reflection coefficients (σ). These methods as applied to a wide variety of transgenic mice subjected to acute lung injury by hyperoxic exposure, sepsis, ischemia‐reperfusion, acid aspiration, oleic acid infusion, repeated lung lavage, and bleomycin are reviewed. These commonly used animal models simulate features of the acute respiratory distress syndrome, and the preparation of genetically modified mice and their use for defining specific pathways in these disease models are outlined. Although the initiating events differ widely, many of the subsequent inflammatory processes causing lung injury and increased vascular permeability are surprisingly similar for many etiologies. © 2011 American Physiological Society.Compr Physiol1:835‐882, 2011.
Gas Mixing in the Airways and Airspaces
Authors: Verbanck Sylvia , Paiva Manuel 
Published: April 2011

AbstractBasic physical concepts of diffusion, convection, and dispersion pertaining to gas transport in the human airways are reviewed. Their incorporation into quantitative models of gas mixing is presented, also illustrating the crucial interaction of gas transport equations with the model geometry. Model simulations are confronted with the available experimental gas mixing indices such as the phase III slope obtained in normal human lungs, with some pertinent examples in laboratory animals and in human lung disease. The use of inert gases with differing diffusion coefficients and their associated phase III slope provides invaluable experimental information on gas mixing in the lungs, with the concept of the diffusion front playing a central role. Sources of inter‐ and intraregional ventilation heterogeneity can be related to the location of the diffusion front, which offers the possibility to distinguish between ventilation heterogeneity proximal to the diffusion front (driven by convection between lung units larger than acini) and more peripheral ventilation heterogeneity (driven by diffusion‐convection interaction mainly within the acinus). While specific ventilation distribution and flow asynchrony co‐act to generate convection‐dependent ventilation heterogeneity, local structural asymmetry of the acinar air spaces is sufficient to generate diffusion‐convection‐dependent ventilation heterogeneity. The remaining hiatus in our understanding of ventilation heterogeneity in the human lung is described, together with some potential perspectives for its investigation. © 2011 American Physiological Society.Compr Physiol1:809‐834, 2011.
Urea Transport in the Kidney
Authors: Klein Janet D. , Blount Mitsi A. , Sands Jeff M. 
Published: April 2011

AbstractUrea transport proteins were initially proposed to exist in the kidney in the late 1980s when studies of urea permeability revealed values in excess of those predicted by simple lipid‐phase diffusion and paracellular transport. Less than a decade later, the first urea transporter was cloned. Currently, theSLC14Afamily of urea transporters contains two major subgroups:SLC14A1, the UT‐B urea transporter originally isolated from erythrocytes; andSLC14A2, the UT‐A group with six distinct isoforms described to date. In the kidney, UT‐A1 and UT‐A3 are found in the inner medullary collecting duct; UT‐A2 is located in the thin descending limb, and UT‐B is located primarily in the descending vasa recta; all are glycoproteins. These transporters are crucial to the kidney's ability to concentrate urine. UT‐A1 and UT‐A3 are acutely regulated by vasopressin. UT‐A1 has also been shown to be regulated by hypertonicity, angiotensin II, and oxytocin. Acute regulation of these transporters is through phosphorylation. Both UT‐A1 and UT‐A3 rapidly accumulate in the plasma membrane in response to stimulation by vasopressin or hypertonicity. Long‐term regulation involves altering protein abundance in response to changes in hydration status, low protein diets, adrenal steroids, sustained diuresis, or antidiuresis. Urea transporters have been studied using animal models of disease including diabetes mellitus, lithium intoxication, hypertension, and nephrotoxic drug responses. Exciting new animal models are being developed to study these transporters and search for active urea transporters. Here we introduce urea and describe the current knowledge of the urea transporter proteins, their regulation, and their role in the kidney. © 2011 American Physiological Society.Compr Physiol1:699‐729, 2011.
Both CD62 and CD162 antibodies prevent formation of CD36‐dependent platelets, rosettes, and artefactual pseudoexpression of platelet markers on white blood cells: A study with ImageStream®
Authors: Ouk Catherine , Jayat‐Vignoles Chantal , Donnard Magali , Feuillard Jean 
Published: April 2011

AbstractFluorescent labeled monoclonal antibodies (mAbs) against CD36 are routinely used as monocyte, erythroid, or platelet markers in clinical cytometry. CD36 has recently been proposed by various authors as a valuable marker helping to enumerate leukocyte's subpopulations by flow cytometry. However, it is known that binding of CD36 may induce platelet activation and formation of platelet's rosettes on leukocytes, resulting in false expression of platelet markers on white blood cells. To study this phenomenon, we have combined classical flow cytometry and a new quantitative flow imaging technique with the ImageStream® analyzer. We show that CD36 ligation induces activation of platelets with CD62 expression and their adhesion on leukocytes due to CD62 and CD162 interactions. Preincubation of whole blood samples with either anti‐CD62 or anti‐CD162 antibodies could prevent formation of these rosettes. Our approach also emphasizes the fact that immunomorphological analysis of cell events with ImageStream technology is a useful tool to validate the specificity of marker's labeling or to elucidate incoherent results obtained with classical flow cytometry. We thus propose to prevent false platelet labeling on leukocytes by preincubation with either anti‐CD62 or anti‐CD162 antibodies when using CD36 mAbs. © 2011 International Society for Advancement of Cytometry