bluuebunny/crossref_metadata_2025_split huggingface dataset:
European Veterinary Renal Pathology Service: A Survey Over a 7‐Year Period (2008–2015)
Authors: Aresu L. , Martini V. , Benali S.L. , Brovida C. , Cianciolo R.E. , Dalla Riva R. , Trez D. , Van Der Lugt J.J. , Van Dongen A. , Zini E. 
Published: August 2017

BackgroundThe European Veterinary Renal Pathology Service (EVRPS) is the first Web‐based registry for canine renal biopsy specimens in Europe.Hypothesis/ObjectivesThe aim was to verify whether differences exist between the clinical and laboratory presentation of dogs with nephropathy according to renal pathological findings, as defined by light and electron microscopy of renal biopsy specimens submitted toEVRPS.AnimalsRenal biopsy specimens of dogs were collected from the archive of the service (n = 254). Cases were included if both light and electron microscopy were available (n = 162).MethodsRenal biopsy specimens were classified based on the morphological diagnoses. Thereafter, they were grouped into 3 disease categories, including immune‐complex‐mediated glomerulonephritis (ICGN), non‐immune‐complex‐mediatedGN(non‐ICGN), and renal lesions not otherwise specified (RL‐NOS). Differences among morphological diagnoses and among disease categories were investigated for clinical and laboratory variables.ResultsSerum albumin concentration was lower in dogs withICGNthan in those with non‐ICGN(P = 0.006) orRL‐NOS(P = 0.000), and the urine protein‐to‐creatinine ratio (UPC) was significantly higher inICGNthan in the other 2 disease categories. Regarding morphological diagnoses, albumin was significantly lower in amyloidosis (AMY) and membranous (MGN), membranoproliferative (MPGN) or mixed glomerulonephritis (MixGN) than in minimal change disease, primary (FSGSI) or secondary (FSGS II) focal and segmental glomerulosclerosis and juvenile nephropathies (JN). TheUPCwas higher inMPGNthan inFSGSI andFSGS II.Conclusions and clinical importanceDogs withICGN, in particularMPGN, had higher protein loss than those with non‐ICGNorRL‐NOS, leading to more severe hypoalbuminemia. Clinical and laboratory differentiation among dogs with the different morphological diagnoses and among dogs with different disease categories was difficult due to overlapping results.
F‐group bZIPs in barley—a role in Zn deficiency
Authors: Nazri Ahmad Zulhilmi , Griffin Jonathan H.C. , Peaston Kerry A. , Alexander‐Webber Douglas G.A. , Williams Lorraine E. 
Published: August 2017

AbstractZinc (Zn) deficiency negatively impacts the development and health of plants and affects crop yield. When experiencing low Zn, plants undergo an adaptive response to maintain Zn homeostasis. We provide further evidence for the role of F‐group transcription factors, AtbZIP19 and AtbZIP23, in responding to Zn deficiency in Arabidopsis and demonstrate the sensitivity and specificity of this response. Despite their economic importance, the role of F‐group bZIPs in cereal crops is largely unknown. Here, we provide new insights by functionally characterizing these in barley (Hordeum vulgare), demonstrating an expanded number of F‐group bZIPs (seven) compared to Arabidopsis. The F‐group barley bZIPs, HvbZIP56 and HvbZIP62, partially rescue the Zn‐dependent growth phenotype and ZIP‐transporter gene regulation of an Arabidopsis bzip19‐4 bzip23‐2 mutant. This supports a conserved mechanism of action in adapting to Zn deficiency. HvbZIP56 localizes to the cytoplasm and nucleus when expressed in Arabidopsis and tobacco. Promoter analysis demonstrates that the barley ZIP transporters that are upregulated under Zn deficiency contain cis Zn‐deficiency response elements (ZDREs). ZDREs are also found in particular barley bZIP promoters. This study represents a significant step forward in understanding the mechanisms controlling Zn responses in cereal crops, and will aid in developing strategies for crop improvement.
LED Phototherapy with Gelatin Sponge Promotes Wound Healing in Mice
Authors: Zhang Heng , Liu Shupeng , Yang Xiangfei , Chen Na , Pang Fufei , Chen Zhenyi , Wang Tingyun , Zhou Jianshe , Ren Fuji , Xu Xiaoyin , Li Taihao 
Published: August 2017

AbstractTiny but highly efficient, a light‐emitting diode (LED) can power a therapy device, such as a phototherapy device, and, at the same time, decrease the device's size requirements. In this study, a LED phototherapy device was designed to investigate the possible impact on wound healing using a mouse model and a cell line exposed to red and blue light. To enhance wound phototherapy, a gelatin sponge was fabricated. Results showed that the red and blue lights promoted cell growth and wound healing, while the blue light with a gelatin sponge protected the wound from infection in the early stages of wound healing. The LED phototherapy device combined with the gelatin sponge, therefore, has potential significance in clinical application for wound healing.
Physiological Doses of Red Light Induce IL‐4 Release in Cocultures between Human Keratinocytes and Immune Cells
Authors: Leong Cheryl , Bigliardi Paul L. , Sriram Gopu , Au Veonice B. , Connolly John , Bigliardi‐Qi Mei 
Published: August 2017

AbstractPhototherapy is routinely used for the treatment of various skin conditions and targeted therapy of superficial cancers. However, the molecular mechanisms behind their biological effects and the need for efficacy enhancing photosensitizers are not well addressed. Particularly, not much is known about the inherent effect of light from the visible spectrum on cytokine release and its downstream effects in keratinocytes and immune cells located in skin and therefore exposed to light. To address this, we delivered calibrated doses of well‐defined light qualities (380 to 660 nm) to cocultures of human keratinocytes and macrophage/dendritic cells in the absence or presence of the commonly used photosensitizer 8‐methoxypsoralen (8‐MOP). The experiments identified IL‐4 as a key effector cytokine released by this coculture model with need for 8‐MOP in the UVA1/blue (380 nm) and no requirement for photosensitizer in the red light spectrum (627 nm). 3D organotypic skin cultures treated with IL‐4 showed thickening of the epidermal layer and delayed differentiation. However unlike IL‐4 and UVA1/blue light treatment, red light did not reduce the expression of keratinocyte differentiation markers or increase signs of photo‐oxidative damage. This supports the application of isolated red light as a possible alternative for photo‐immunotherapy without need for additional photosensitizers.
Multi‐sited ethnography: Opportunities for the study of race
Authors: Carney Nikita 
Published: August 2017

AbstractMulti‐sited ethnography (MSE) is an underutilized research method that presents particular challenges and unique possibilities for generative research that can build upon existing theories of race and ethnicity. This review discusses the theoretical and methodological components of MSE and provides examples of both transnational and translocal ethnographic studies. These examples illustrate how MSE as a method can enrich analyses of race and ethnicity by enabling ethnographers to identify site‐specific phenomena as well as social processes that transcend a single locale. MSE, when intentionally paired with methodological framings in line with research priorities, can enable scholars to produce rigorous sociological analysis and theory building. Multi‐sited ethnographies of race can provide a set of analyses that complement a range of other sociological research tools, including single‐sited ethnography and quantitative studies, to deepen our understandings about the production and maintenance of racial and ethnic categories in the United States and transnationally.
Exploring How National Politics Influences the Outcome of Intergroup Contact among Muslim Minority Members
Authors: Thomsen Jens Peter Frølund , Rafiqi Arzoo 
Published: August 2017

This article adds to the existing research in intergroup contact among ethnic minority members by hypothesizing that national political debate has the capacity to enhance the positive outcomes of cross‐group interaction. Analyses show that the capacity of intergroup contact to reduce prejudice toward majority members is disproportionately stronger among Muslims than among non‐Muslim minority members. Specifically, at the time of data collection, the two categories—Muslims and majority members—were highly salient in the public debate, whereas the non‐Muslim minority member category was not primed as a contrast to the majority culture. The political debate most likely stimulated Muslims to generalize their positive contact experiences to the entire majority group. The analysis contributes to the theoretical refinement of the so‐called categorization model by focusing on politically induced reactions among contacted ethnic minority members toward majority members. The analysis utilizes a tailor‐made national sample (fielded during the Mohammad Cartoon Crisis in 2006) among ethnic minority members in Denmark (N = 3,272).
Modelling future impacts of urban development in Kuwait with the use of ABM and GIS
Authors: Alghais Nayef , Pullar David 
Published: August 2017

AbstractDuring the last six decades, Kuwait has experienced rapid and unprecedented population growth with only a small increase in the urban areas. The alarming rise in urban density in Kuwait has caused issues for the residents' lifestyles, the economy and the environment. These issues have been aggravated by urban planning which perpetuated a city‐centric urban form without modelling the impacts of current patterns of urban growth. A spatial model using Agent Based Modelling (ABM) and Geographical Information Systems (GIS) is proposed to model disaggregate future changes in land‐use patterns given forecast population estimates and planning policies. The two main impacts considered are housing shortage and traffic congestion, as these are the two most significant social impacts for Kuwaitis. This article discusses the design methodology and parameterization of the ABM and the agent groups. It characterizes urban growth by rules for different citizen groups, historical growth patterns and the influence of decision‐makers. The model is validated against data for the period 1995‐2015 and simulations run to 2050; the results predict that continued city‐centric growth will aggravate the problems, with more than 50% increase in housing shortage and congestion unless the government intervenes to rectify the situation.
Sex‐specific differences in cardiovascular and metabolic hormones with integrated signalling in the paraventricular nucleus of the hypothalamus
Authors: Loewen Spencer P. , Paterson Alex R. , Loh Su Yi , Rogers Mark F. , Hindmarch Charles C. T. , Murphy David , Ferguson Alastair V. 
Published: August 2017

New Findings
What is the topic of this review?
We describe roles of crucial signalling molecules in the paraventricular nucleus of the hypothalamus and highlight recent data suggesting sex‐specific changes in the expression of crucial signalling molecules and their receptors, which may underlie sex differences in both cardiovascular and metabolic function.

What advances does it highlight?
This review highlights the integrative capacity of the paraventricular nucleus in mediating cardiovascular and metabolic effects by integrating information from multiple signalling molecules. It also proposes that these signalling molecules have sex‐specific differential gene expression, indicating the importance of considering these differences in our ongoing search to understand the female–male differences in the regulation of crucial autonomic systems.

Many traditional cardiovascular hormones have been implicated in metabolic function. Conversely, many hormones traditionally involved in metabolic regulation have an effect on cardiovascular function. Many of these signalling molecules exert such effects through specific actions in the paraventricular nucleus, an integrative autonomic control centre located in the hypothalamus. Here, we focus on four cardiovascular/metabolic peptide hormones that signal within the paraventricular nucleus, namely angiotensin II, orexin, adiponectin and nesfatin‐1. Each of these hormones has specific electrophysiological effects on paraventricular nucleus neurons that can be related to its physiological actions. In addition, we introduce preliminary transcriptomic data indicating that the genes for some of these hormones and their receptors have sex‐specific differential expression.
In Vitro
Isolation and Characterization of Oxazolidinone-Resistant Mycobacterium tuberculosis
Authors: McNeil Matthew B. , Dennison Devon D. , Shelton Catherine D. , Parish Tanya 
Published: August 2017

ABSTRACT

Oxazolidinones are promising candidates for the treatment of
Mycobacterium tuberculosis
infections. We isolated linezolid-resistant strains from H37Rv (Euro-American) and HN878 (East-Asian) strains; resistance frequencies were similar in the two strains. Mutations were identified in ribosomal protein L3 (RplC) and the 23S rRNA (
rrl
). All mutant strains were cross resistant to sutezolid; a subset was cross resistant to chloramphenicol. Mutations in
rrl
led to growth impairment and decreased fitness that may limit spread in clinical settings.
Molecular Characterization of Fluoroquinolone-Resistant Moraxella catarrhalis Variants Generated
In Vitro
by Stepwise Selection
Authors: Yamada Kageto , Saito Ryoichi , Muto Saori , Kashiwa Machiko , Tamamori Yoshiko , Fujisaki Shingo 
Published: August 2017

ABSTRACT

Moraxella catarrhalis
causes respiratory infections. In this study, fluoroquinolone-resistant strains were selected
in vitro
to evaluate the mechanism of fluoroquinolone resistance. Strains with reduced fluoroquinolone susceptibility were obtained by stepwise selection in levofloxacin, and fluoroquinolone targets
gyr
and
par
were sequenced. Six novel mutations in GyrA (D84Y, T594dup, and A722dup), GyrB (E479K and D439N), and ParE (Q395R) involved in
M. catarrhalis
resistance to fluoroquinolones were revealed.
Downmodulation of Effector Functions in NK Cells upon Toxoplasma gondii Infection
Authors: Sultana M. Afifa , Du Ann , Carow Berit , Angbjär Catrine M. , Weidner Jessica M. , Kanatani Sachie , Fuks Jonas M. , Muliaditan Tamara , James Jaime , Mansfield Imogen O. , Campbell Tessa M. , Liu Lifeng , Kadri Nadir , Lambert Henrik , Barragan Antonio , Chambers Benedict J. 
Published: August 2017

ABSTRACTThe obligate intracellular parasiteToxoplasma gondiican actively infect any nucleated cell type, including cells from the immune system. The rapid transfer ofT. gondiifrom infected dendritic cells to effector natural killer (NK) cells may contribute to the parasite's sequestration and shielding from immune recognition shortly after infection. However, subversion of NK cell functions, such as cytotoxicity or production of proinflammatory cytokines, such as gamma interferon (IFN-γ), upon parasite infection might also be beneficial to the parasite. In the present study, we investigated the effects ofT. gondiiinfection on NK cells.In vitro, infected NK cells were found to be poor at killing target cells and had reduced levels of IFN-γ production. This could be attributed in part to the inability of infected cells to form conjugates with their target cells. However, even upon NK1.1 cross-linking of NK cells, the infected NK cells also exhibited poor degranulation and IFN-γ production. Similarly, NK cells infectedin vivowere also poor at killing target cells and producing IFN-γ. Increased levels of transforming growth factor β production, as well as increased levels of expression of SHP-1 in the cytosol of infected NK cells upon infection, were observed in infected NK cells. However, the phosphorylation of STAT4 was not altered in infected NK cells, suggesting that transcriptional regulation mediates the reduced IFN-γ production, which was confirmed by quantitative PCR. These data suggest that infection of NK cells byT. gondiiimpairs NK cell recognition of target cells and cytokine release, two mechanisms that independently could enhanceT. gondiisurvival.
Genetic Evidence for Erythrocyte Receptor Glycophorin B Expression Levels Defining a Dominant Plasmodium falciparum Invasion Pathway into Human Erythrocytes
Authors: Dankwa Selasi , Chaand Mudit , Kanjee Usheer , Jiang Rays H. Y. , Nobre Luis V. , Goldberg Jonathan M. , Bei Amy K. , Moechtar Mischka A. , Grüring Christof , Ahouidi Ambroise D. , Ndiaye Daouda , Dieye Tandakha N. , Mboup Souleymane , Weekes Michael P. , Duraisingh Manoj T. 
Published: August 2017

ABSTRACT

Plasmodium falciparum
, the parasite that causes the deadliest form of malaria, has evolved multiple proteins known as invasion ligands that bind to specific erythrocyte receptors to facilitate invasion of human erythrocytes. The EBA-175/glycophorin A (GPA) and Rh5/basigin ligand-receptor interactions, referred to as invasion pathways, have been the subject of intense study. In this study, we focused on the less-characterized sialic acid-containing receptors glycophorin B (GPB) and glycophorin C (GPC). Through bioinformatic analysis, we identified extensive variation in glycophorin B (GYPB) transcript levels in individuals from Benin, suggesting selection from malaria pressure. To elucidate the importance of the GPB and GPC receptors relative to the well-described EBA-175/GPA invasion pathway, we used an
ex vivo
erythrocyte culture system to decrease expression of GPA, GPB, or GPC via lentiviral short hairpin RNA transduction of erythroid progenitor cells, with global surface proteomic profiling. We assessed the efficiency of parasite invasion into knockdown cells using a panel of wild-type
P. falciparum
laboratory strains and invasion ligand knockout lines, as well as
P. falciparum
Senegalese clinical isolates and a short-term-culture-adapted strain. For this, we optimized an invasion assay suitable for use with small numbers of erythrocytes. We found that all laboratory strains and the majority of field strains tested were dependent on GPB expression level for invasion. The collective data suggest that the GPA and GPB receptors are of greater importance than the GPC receptor, supporting a hierarchy of erythrocyte receptor usage in
P. falciparum
.
Tpl2 Promotes Innate Cell Recruitment and Effector T Cell Differentiation To Limit Citrobacter rodentium Burden and Dissemination
Authors: Acuff Nicole V. , Li Xin , Latha Krishna , Nagy Tamas , Watford Wendy T. 
Published: August 2017

ABSTRACT

Tumor progression locus 2 (Tpl2) is a serine-threonine kinase that regulates Th1 differentiation, secretion of the inflammatory cytokine gamma interferon (IFN-γ), and host defense against the intracellular pathogens
Toxoplasma gondii
,
Listeria monocytogenes
, and
Mycobacterium tuberculosis
. However, relatively little is known about the contribution of Tpl2 to Th17 differentiation and immune cell function during infection with an extracellular pathogen. The goal of this study was to determine whether Tpl2 influences the immune response generated to the extracellular bacterium
Citrobacter rodentium
, which induces a mixed Th1 and Th17 response. During peak infection with
C. rodentium
,
Tpl2
−/−
mice experienced greater bacterial burdens with evidence of dissemination to the liver and spleen but ultimately cleared the bacteria within 3 weeks postinfection, similar to the findings for wild-type mice.
Tpl2
−/−
mice also recruited fewer neutrophils and monocytes to the colon during peak infection, which correlated with increased bacterial burdens. In mixed bone marrow chimeras, Tpl2 was shown to play a T cell-intrinsic role in promoting both IFN-γ and interleukin-17A production during infection with
C. rodentium
. However, upon CD4 T cell transfer into
Rag
−/−
mice,
Tpl2
−/−
CD4 T cells were as protective as wild-type CD4 T cells against the dissemination of bacteria and mortality. These data indicate that the enhanced bacterial burdens in
Tpl2
−/−
mice are not caused primarily by impairments in CD4 T cell function but result from defects in innate immune cell recruitment and function.
Overexpression of Candida albicans Secreted Aspartyl Proteinase 2 or 5 Is Not Sufficient for Exacerbation of Immunopathology in a Murine Model of Vaginitis
Authors: Willems Hubertine M. E. , Bruner Winter S. , Barker Katherine S. , Liu Junyan , Palmer Glen E. , Peters Brian M. 
Published: August 2017

ABSTRACT

The secreted aspartyl proteinases of
Candida albicans
have long been implicated in virulence at the mucosal surface, including contributions to colonization and immunopathogenesis during vulvovaginal candidiasis. In an effort to disentangle hypha-associated virulence factor regulation from morphological transition, the purpose of this study was to determine if overexpression of
SAP2
or
SAP5
in an
efg1
Δ/Δ
cph1
Δ/Δ mutant could restore the capacity to cause immunopathology during murine vaginitis to this avirulent hypofilamentous strain. Two similar yet distinct genetic approaches were used to construct expression vectors to achieve SAP overexpression, and both genetic and functional assays confirmed elevated SAP activity in transformed strains. Similar to previous findings, intravaginal challenge of C57BL/6 mice with hypha-defective strains attained high levels of mucosal colonization but failed to induce robust vaginal immunopathology (neutrophil recruitment, interleukin-1β [IL-1β] secretion, and lactate dehydrogenase release) compared to that with the hypha-competent control. Moreover, constitutive expression of
SAP2
or
SAP5
in two distinct sets of such strains did not elicit immunopathological markers at levels above those observed during challenge with isogenic empty vector controls. Therefore, these results suggest that the physiological contributions of SAPs to vaginal immunopathology require hypha formation, other hypha-associated factors, or genetic interaction with
EFG1
and/or
CPH1
to cause symptomatic infection. Additionally, the outlined expression strategy and strain sets will be useful for decoupling other downstream morphogenetic factors from hyphal growth.
Streptococcus pneumoniae Colonization Is Required To Alter the Nasal Microbiota in Cigarette Smoke-Exposed Mice
Authors: Shen Pamela , Whelan Fiona J. , Schenck L. Patrick , McGrath Joshua J. C. , Vanderstocken Gilles , Bowdish Dawn M. E. , Surette Michael G. , Stämpfli Martin R. 
Published: August 2017

ABSTRACT

Smokers have nasal microbiota dysbiosis, with an increased frequency of colonizing bacterial pathogens. It is possible that cigarette smoke increases pathogen acquisition by perturbing the microbiota and decreasing colonization resistance. However, it is difficult to disentangle microbiota dysbiosis due to cigarette smoke exposure from microbiota changes caused by increased pathogen acquisition in human smokers. Using an experimental mouse model, we investigated the impact of cigarette smoke on the nasal microbiota in the absence and presence of nasal pneumococcal colonization. We observed that cigarette smoke exposure alone did not alter the nasal microbiota composition. The microbiota composition was also unchanged at 12 h following low-dose nasal pneumococcal inoculation, suggesting that the ability of the microbiota to resist initial nasal pneumococcal acquisition was not impaired in smoke-exposed mice. However, nasal microbiota dysbiosis occurred as a consequence of established high-dose nasal pneumococcal colonization at day 3 in smoke-exposed mice. Similar to clinical reports on human smokers, an enrichment of potentially pathogenic bacterial genera such as
Fusobacterium
,
Gemella
, and
Neisseria
was observed. Our findings suggest that cigarette smoke exposure predisposes to pneumococcal colonization independent of changes to the nasal microbiota and that microbiota dysbiosis observed in smokers may occur as a consequence of established pathogen colonization.