bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nickel Elicits Concomitant and Correlated in vitro Production of Th1‐, Th2‐Type and Regulatory Cytokines in Subjects with Contact Allergy to Nickel
Authors: Minang J. T. , Troye‐Blomberg M. , Lundeberg L. , Ahlborg N. 
Published: September 2005

AbstractNickel (Ni2+) elicits production of functionally distinct cytokines in vitro, but the relation between the cytokine profile and the degree of the allergic reaction in vivo needs to be better defined in order to improve the understanding of the immunological mechanisms involved in contact allergy and to facilitate development of in vitro diagnostics. The aim of the study was to define Th1‐type [interferon‐γ (IFN‐γ)], Th2‐type [interleukin‐4 (IL‐4), IL‐5 and IL‐13] and regulatory (IL‐10) cytokine responses to Ni2+ in peripheral blood mononuclear cells (PBMC) from subjects with varying patch test reactivity to Ni2+. The study included subjects with strong (+3), moderate (+2), weak (+1) or negative (controls) patch test reactivity to Ni2+ (n = 10 per group). All +3 and +2 subjects but only three +1 subjects had a clinical history of contact allergy to Ni2+. Cytokine production of PBMC stimulated with Ni2+ was determined by enzyme‐linked immunospot and/or enzyme‐linked immunosorbent assay. Ni2+ elicited significant production of all cytokines in PBMC from patch‐test‐positive subjects versus controls with a positive correlation between each cytokine and the patch test reactivity as well as with other cytokines. More subjects responded to Ni2+ above cut‐off values with Th2‐type cytokines as compared with IFN‐γ or IL‐10; 100% of +3, 80% of +2, 50% of +1 and 0% of control subjects displayed reactivity to Ni2+ based on IL‐4 and IL‐13 assays. Despite the prevailing view of Ni2+ allergy as a type‐1‐mediated condition, the in vivo reactivity to Ni2+ correlated with a mixed Th1‐type, Th2‐type and regulatory cytokine response to Ni2+in vitro. The results accentuate the importance of type 2 responses in contact allergy and also demonstrate that IL‐4 and IL‐13 are reliable markers for Ni2+ allergy.
Ultrastructural findings in feline corneal sequestra
Authors: Cullen Cheryl L. , Wadowska Dorota W. , Singh Amreek , Melekhovets Yuri 
Published: September 2005

AbstractObjectives (1) To describe the ultrastructural features of corneal sequestra in cats; and (2) to enhance our understanding regarding the pathogenesis of feline corneal sequestration.Methods Nine corneal sequestra were harvested via keratectomy from globes of nine cats. The sequestra were routinely fixed then postfixed for high resolution light and transmission electron microscopy (HR‐LM and TEM, respectively). The tissues were embedded in Epon/Araldite. Sections of 0.5‐µm thickness were cut and stained with 1% toluidine blue in 1% sodium tetraborate solution for HR‐LM. Ultrathin sections were collected on copper grids and stained with uranyl acetate and Sato's lead stain for TEM. Ultrathin sections were examined and the images were captured on an Advantage HR CCD camera using a Hitachi 7500 electron microscope operated at 80 kV. Two healthy corneas from two cats were harvested immediately following euthanasia. These corneal tissues (control samples) were processed in the same manner as the corneal sequestra for HR‐LM and TEM. A portion of each sequestrum was also submitted for polymerase chain reaction (PCR) testing for infectious agents including feline herpesvirus‐1 (FHV‐1),Toxoplasma gondii,Chlamydophila felisandMycoplasmaspp.Results Ultrastructure of healthy corneal tissues revealed basal corneal epithelial cells aligned adjacent to a thin acellular layer similar to Bowman's layer with underlying tightly packed, regularly arranged, collagen fibrils oriented in different planes. Keratocytes were elongated and had long and irregularly shaped nuclei, and cytoplasm contained rough endoplasmic reticulum and abundant membrane‐bound vesicles. In contrast, corneal sequestra contained varying amounts of an amorphous, electron‐dense substance, continuous with intact basal epithelial basement membranes peripherally, and overlying corneal ulceration and loosely packed collagen fibrils. Remnants of necrotic keratocytes were seen in spaces between disarranged collagen layers. In all samples, occasional keratocytes exhibited morphology indicative of apoptosis including clumping and margination of chromatin, and shrunken cytoplasm. Varying degrees of inflammation were noted on HR‐LM and TEM of affected corneas including peri‐ and intralesional neutrophils, lymphocytes, plasma cells, and macrophages. Corneal sequestra were FHV‐1‐positive (n = 3), FHV‐1‐ andT. gondii‐positive (n = 1),T. gondii‐positive (n = 3), or negative for DNA of these infectious agents (n = 2) using PCR. All corneal sequestra were negative for DNA ofChlamydophila felisandMycoplasmaspp. using PCR.Conclusions Apoptosis may play a role in the pathogenesis of feline corneal sequestration independent of the presence of DNA of these infectious organisms. Prospective clinical studies are warranted to further understand the significance ofT. gondiiin relation to feline corneal sequestration.
Schirmer tear test values and tear film break‐up times in cats with conjunctivitis
Authors: Lim Christine C. , Cullen Cheryl L. 
Published: September 2005

AbstractObjectives (1) To document tear film break‐up time (TFBUT) in a group of cats with conjunctivitis; (2) to determine if TFBUTs from cats with conjunctivitis vary significantly from previously established normal values for TFBUT in young cats without ocular disease; (3) to determine if a correlation exists between Schirmer tear test (STT) values and TFBUTs in cats with conjunctivitis; (4) to determine if the TFBUTs in cats with conjunctivitis are influenced by the detection of DNA from feline herpes virus‐type 1 (FHV‐1),Chlamydophila felis,Mycoplasmaspp., and feline calicivirus.Animals studied Fourteen cats between the ages of 0.8 years to 12 years with active, untreated conjunctivitis and without active keratitis or other ocular or systemic abnormalities were included in this study.Procedures Complete ophthalmic examinations, including TFBUT, were performed on all cats. Polymerase chain reaction (PCR) screening for FHV‐1,Chlamydophila felis,Mycoplasmaspp., and feline calicivirus was performed on conjunctival swabs from affected eyes and blood samples from all cats.Results Mean TFBUT for cats in this study was 8.9 (± 4.8) s in the right eye (OD) and 8.1 (± 4.6) s in the left eye (OS). No correlation existed between mean TFBUTs and mean STT values OD or OS. Conjunctival swabs from seven cats (n = 9 eyes) tested positive via PCR for one of the above infectious agents. Blood samples from nine cats tested positive for FHV‐1. Mean TFBUTs for cats from which the DNA from FHV‐1 was isolated from the blood were significantly lower than mean TFBUTs for cats from which no such DNA was isolated from the blood.Conclusions In this study, the mean TFBUT in cats with conjunctivitis was significantly lower than previously established values for clinically healthy cats. This supports the theory that qualitative tear film deficiency, and thus tear film instability, may play a role in the pathogenesis of feline conjunctivitis. Qualitative tear film deficiency may predispose to the development of conjunctivitis or may occur secondarily to this condition.
Oral doxycycline, niacinamide and prednisolone used to treat bilateral nodular granulomatous conjunctivitis of the third eyelid in an Australian Kelpie dog
Authors: Hurn Simon , Mc Cowan Christina , Turner Andrew 
Published: September 2005

AbstractA 5‐year‐old, female neutered, Australian Kelpie presented with a 2‐month history of dramatic bilateral erythematous thickening of the third eyelids. Ophthalmic examination demonstrated raised, pink to red, irregular thickening of the entire palpebral surface of both third eyelids. There were no other ocular abnormalities. A surgical biopsy was taken from each third eyelid. Histopathologic examination revealed sheets of macrophages, plasma cells, lymphocytes, and occasional fibroblasts and neutrophils infiltrating the third eyelid stroma. A diagnosis of chronic granulomatous conjunctivitis was made. Grossly and histopathologically this case closely resembles previously described cases of nodular granulomatous conjunctivitis involving the third eyelids of Collie dogs. This report describes an unusual case of nodular granulomatous conjunctivitis isolated to the third eyelids in an Australian Kelpie. Resolution of the condition was achieved with a combination of oral doxycycline, niacinamide and prednisolone.
Surgical management of cicatricial ectropion following scarring dermatopathies in two dogs
Authors: Donaldson David , Smith Kerry M. , Shaw Stephen C. , Sansom Jane , Hartley Claudia 
Published: September 2005

AbstractTwo dogs were presented with severe dermatopathies leading to cicatricial ectropion and severe surface ocular pathology. In one case, idiopathic sterile pyogranuloma was diagnosed on histopathology and managed with systemic immunosuppressive therapy. In the second case, demodicosis was diagnosed on skin scrapings and successfully treated with acaricidal medication. Following control of the underlying dermatopathies, both cases developed cicatricial ectropion as a result of scarring and contracture of eyelid tissue. Wharton–Jones (V–Y) blepharoplasties were performed on the affected eyelids and resulted in improved eyelid function and reduced corneal exposure in both cases.
The α1D‐adrenoceptor antagonist BMY 7378 is also an α2C‐adrenoceptor antagonist
Authors: Cleary L. , Murad K. , Bexis S. , Docherty J. R. 
Published: September 2005

Summary 1 We have investigated the actions of the α1D‐adrenoceptor selective antagonist BMY 7378 in comparison with yohimbine at α1‐ and α2‐adrenoceptors. 2 In rat aorta (α1D‐adrenoceptor), BMY 7378 (pA2 of 8.67) was about 100 times more potent than yohimbine (pA2 of 6.62) at antagonizing the contractile response to noradrenaline. 3 In human saphenous vein (α2C‐adrenoceptor), BMY 7378 (pA2 of 6.48) was approximately 10 times less potent than yohimbine (pA2 of 7.56) at antagonizing the contractile response to noradrenaline. 4 In prostatic portions of rat vas deferens, BMY 7378 (10 μm) did not significantly affect the concentration‐dependent inhibition of single pulse nerve stimulation‐evoked contractions by xylazine (an action at prejunctional α2D‐adrenoceptors). 5 In ligand‐binding studies, BMY 7378 showed 10‐fold selectivity for α2C‐adrenoceptors (pKi of 6.54) over other α2‐adrenoceptors. 6 It is concluded that BMY 7378, in addition to α1D‐adrenoceptor selectivity in terms of α1‐adrenoceptors, shows selectivity for α2C‐adrenoceptors in terms of α2‐adrenoceptors.
A novel mechanism prevents the development of hypertension during chronic cold stress
Authors: Westfall T. C. , Yang C.‐L. , Chen X. , Naes L. , Vickery L. , Macarthur H. , Han S. 
Published: September 2005

Summary 1 Chronic cold exposure of rats (7 days in a cold room at 4 °C) attenuated the sympathetic nerve stimulation (NS)‐induced overflow of noradrenaline (NE) (measured by high‐performance liquid chromatography, coupled to electrochemical detection) appearing in the perfusate/superfusate of the perfused mesenteric arterial bed as well as the increase in the perfusion pressure. 2 The same type of cold exposure resulted in an increase in tyrosine hydroxylase (TH) gene expression measured in the superior cervical ganglion and NE content measured in the mesenteric artery obtained from cold‐exposed rats. 3 Addition of sodium nitroprusside, a nitric oxide (NO) donor, to the buffer perfusing the mesenteric arterial bed obtained from rats maintained at room temperature also resulted in an attenuation of the NS‐induced overflow of NE and increase in perfusion pressure. 4
N
c‐nitro‐l‐arginine methyl ester (l‐NAME), an NO synthase inhibitor, placed in the drinking water prevented the attenuation of the pre‐ and post‐junctional responses to NS of the mesenteric arterial bed obtained from cold‐exposed rats. 5
l‐NAME treatment also increased the cold‐induced elevation of blood pressure seen in whole animals. 6 The present results are consistent with the idea that cold exposure leads to a concomitant increase in sympathetic nerve activity and production of NO. We hypothesize that the increase in production and release of NO results in a decrease in the biologically active form of NE despite increased synthesis and release of the catecholamine. 7 It is concluded that the above‐mentioned interactions serve as a protective mechanism offsetting the increased release and action of NE from sympathetic nerves and thus preventing the development of hypertension.
Deception and Fear in Politically Oppressive Contexts: Its Trickle‐Down Effect on Families
Authors: Sluzki Carlos E. 
Published: September 2005

AbstractThe mystified reality, restricted options, and inherent risks of living in countries under a repressive political regime trigger survival tactics that reduce individual's reliance on social support, as well as semantic and cognitive restrictions and alternative codes, and silences that translate into symptoms. While this is the case for the average citizen, it is even more pronounced in individuals and families directly touched by the repressive apparatus. These processes are discussed and two clinical examples are provided to illustrate them.
Absence of Evidence for the Participation of the Macrophage Cellular Prion Protein in Infection with
Brucella suis
Authors: Fontes Pascaline , Alvarez-Martinez Maria-Teresa , Gross Antoine , Carnaud Claude , Köhler Stephan , Liautard Jean-Pierre 
Published: September 2005

ABSTRACT

Brucella
spp. are stealthy bacteria that enter host cells without major perturbation. The molecular mechanism involved is still poorly understood, although numerous studies have been published on this subject. Recently, it was reported that
Brucella abortus
utilizes cellular prion protein (PrP
C
) to enter the cells and to reach its replicative niche. The molecular mechanisms involved were not clearly defined, prompting us to analyze this process using blocking antibodies against PrP
C
. However, the behavior of
Brucella
during cellular infection under these conditions was not modified. In a next step, the behavior of
Brucella
in macrophages lacking the prion gene and the infection of mice knocked out for the prion gene were studied. We observed no difference from results obtained with the wild-type control. Although some contacts between PrP
C
and
Brucella
were observed on the surface of the cells by using confocal microscopy, we could not show that
Brucella
specifically bound recombinant PrP
C
. Therefore, we concluded from our results that prion protein (PrP
C
) was not involved in
Brucella
infection.
Characterization of
Legionella pneumophila pmiA
, a Gene Essential for Infectivity of Protozoa and Macrophages
Authors: Miyake Masaki , Watanabe Takurou , Koike Hitomi , Molmeret Maëlle , Imai Yasuyuki , Abu Kwaik Yousef 
Published: September 2005

ABSTRACT

The ability of
Legionella pneumophila
to cause pneumonia is dependent on intracellular replication within alveolar macrophages. The Icm/Dot secretion apparatus is essential for the ability of
L. pneumophila
to evade endocytic fusion, to remodel the phagosome by the endoplasmic reticulum (ER), and to replicate intracellularly. Protozoan and macrophage infectivity (
pmi
) mutants of
L. pneumophila
, which include 11
dot/icm
mutants, exhibit defects in intracellular growth and replication within both protozoa and macrophages. In this study we characterized one of the
pmi
loci,
pmiA
. In contrast to the parental strain, the
pmiA
mutant is defective in cytopathogenicity for protozoa and macrophages. This is a novel mutant that exhibits a partial defect in survival within U937 human macrophage-like cells but exhibits a severe growth defect within
Acanthamoeba polyphaga
, which results in elimination from this host. The intracellular defects of this mutant are complemented by the wild-type
pmiA
gene on a plasmid. In contrast to phagosomes harboring the wild-type strain, which exclude endosomal-lysosomal markers, the
pmiA
mutant-containing phagosomes acquire the late endosomal-lysosomal markers LAMP-1 and LAMP-2. In contrast to the parental strain-containing phagosomes that are remodeled by the ER, there was a decrease in the number of ER-remodeled phagosomes harboring the
pmiA
mutant. Among several
Legionella
species examined, the
pmiA
gene is specific for
L. pneumophila
. The predicted amino acid sequence of the PmiA protein suggests that it is a transmembrane protein with three membrane-spanning regions. PmiA is similar to several hypothetical proteins produced by bacteria with a type IV secretion apparatus. Importantly, the defect in
pmiA
abolishes the pore-forming activity, which has been attributed to the Icm/Dot type IV secretion system. However, the mutant is sensitive to NaCl, and this sensitivity is abrogated in the
icm/dot
mutants. These results suggest that PmiA is a novel virulence factor that is involved in intracellular survival and replication of
L. pneumophila
in macrophages and protozoan cells.
Requirement for Intercellular Adhesion Molecule 1 and Caveolae in Invasion of Human Oral Epithelial Cells by
Porphyromonas gingivalis
Authors: Tamai Riyoko , Asai Yasuyuki , Ogawa Tomohiko 
Published: September 2005

ABSTRACT

Porphyromonas gingivalis
, a periodontopathic bacterium, is known to invade oral epithelial cells in periodontal lesions, although the mechanism is unclear. In the present study, goat polyclonal anti-intercellular adhesion molecule 1 (anti-ICAM-1) antibody inhibited the invasion of
P. gingivalis
into KB cells (human oral epithelial cells). Further, the
P. gingivalis
fimbria, a pathogenic adhesion molecule, bound to recombinant human ICAM-1, as shown by enzyme-linked immunosorbent assay.
P. gingivalis
was also found to colocalize with ICAM-1 on KB cells, as seen with an immunofluorescence microscope, and the knockdown of ICAM-1 in KB cells resulted in the inhibition of
P. gingivalis
invasion by RNA interference. In addition, methyl-β-cyclodextrin, a cholesterol-binding agent, inhibited the colocalization of
P. gingivalis
with ICAM-1 and invasion by the microorganism. The colocalization of caveolin-1, a caveolar marker protein, on KB cells with
P. gingivalis
was also shown, and the knockdown of caveolin-1 in KB cells caused a reduced level of
P. gingivalis
invasion. These results suggest that ICAM-1 and caveolae are required for the invasion of
P. gingivalis
into human oral epithelial cells, and these molecules appear to be associated with the primary stages of the development and progression of chronic periodontitis.
Infection withMycobacterium ulceransInduces Persistent Inflammatory Responses in Mice
Authors: Oliveira Martinha S. , Fraga Alexandra G. , Torrado Egídio , Castro António G. , Pereira João P. , Filho Adhemar Longatto , Milanezi Fernanda , Schmitt Fernando C. , Meyers Wayne M. , Portaels Françoise , Silva Manuel T. , Pedrosa Jorge 
Published: September 2005

ABSTRACTBuruli ulcer (BU) is a devastating, necrotizing, tropical skin disease caused by infections withMycobacterium ulcerans. In contrast to other mycobacterioses, BU has been associated with minimal or absent inflammation. However, here we show that in the mouseM. ulceransinduces persistent inflammatory responses with virulence-dependent patterns. Mycolactone-positive, cytotoxic strains are virulent for mice and multiply progressively, inducing both early and persistent acute inflammatory responses. The cytotoxicity of these strains leads to progressive destruction of the inflammatory infiltrates by postapoptotic secondary necrosis, generating necrotic acellular areas with extracellular bacilli released by the lysis of infected phagocytes. The necrotic areas, always surrounded by acute inflammatory infiltrates, expand through the progressive invasion of healthy tissues around the initial necrotic lesions by bacteria and by newly recruited acute inflammatory cells. Our observations show that the lack of inflammatory infiltrates in the extensive areas of necrosis seen in advanced infections results from the destruction of continuously produced inflammatory infiltrates and not fromM. ulcerans-induced local or systemic immunosuppression. Whether this is the mechanism behind the predominance of minimal or absent inflammatory responses in BU biopsies remains to be elucidated.
Alteration in Host Cell Tropism Limits the Efficacy of Immunization with a Surface Protein of Malaria Merozoites
Authors: Shi Qifang , Cernetich Amy , Daly Thomas M. , Galvan Gina , Vaidya Akhil B. , Bergman Lawrence W. , Burns James M. 
Published: September 2005

ABSTRACTImmunization withPlasmodium yoeliimerozoite surface protein-8 (PyMSP-8) has been shown to protect mice against lethalP. yoelii17XL malaria. Here we demonstrate that PyMSP-8-specific antibodies preferentially suppressP. yoelii17XL growth in mature erythrocytes compared to growth in reticulocytes and do not suppress the growth of nonlethalP. yoelii17X, a parasite that primarily replicates in reticulocytes. The protection against normocyte-associatedP. yoeliimalaria parasites is mediated by antibodies that recognize conformational epitopes of PyMSP-8 that are nonpolymorphic. We examined changes in gene expression in reticulocyte-restrictedP. yoelii17XL parasites that escaped neutralization by PyMSP-8-specific antibodies usingP. yoeliiDNA microarrays. Of interest,Pymsp-8gene expression decreased, while the expression ofmsp-1,msp-7, and several rhoptry protein genes increased. Breakthrough parasites also exhibited increases in the expression of a subset ofyirandPyst-agenes that are predicted to encode polymorphic antigens expressed on the surface of infected erythrocytes. These data suggest that changes in the expression of parasite proteins expressed on the merozoite surface, as well as the surface of infected erythrocytes, may alter host cell tropism and contribute to the ability of malaria parasites to evade merozoite-specific, neutralizing antibodies.
Doubly Branched Hexasaccharide Epitope on the Cell Wall Polysaccharide of Group A Streptococci Recognized by Human and Rabbit Antisera
Authors: Michon Francis , Moore Samuel L. , Kim John , Blake Milan S. , Auzanneau France-Isabelle , Johnston Blair D. , Johnson Margaret A. , Pinto B. Mario 
Published: September 2005

ABSTRACTA number of epitope specificities associated with the cell wall polysaccharide antigen of group A streptococci were identified in a polyclonal rabbit antiserum induced in rabbits by whole group A streptococci and in polyclonal convalescent human antisera from children that had recovered from streptococcal A infections. The identification was achieved by using a series of synthetic oligosaccharides, glycoconjugates, and bacterial polysaccharide inhibitors to inhibit the binding of the group A helical polysaccharide to the polyclonal antisera. The exclusively dominant epitope expressed in the convalescent human antisera was the doubly branched extended helical hexasaccharide with the structure α-l-Rhap(1→2)[β-d-GlcpNAc(1→3)]α-l-Rhap(1→3)α-l-Rhap(1→2)[β-d-GlcpNAc(1→3)]α-l-Rhap. The hexasaccharide epitope also bound with the highest immunoreactivity to the rabbit antiserum. In contrast, the human antisera did not show significant binding to the singly branched pentasaccharide with the structure α-l-Rhap(1→2)α-l-Rhap(1→3)α-l-Rhap(1→2)[β-d-GlcpNAc(1→3)]α-l-Rhapor the branched trisaccharide α-l-Rhap(1→2)[β-d-GlcpNAc(1→3)]α-l-Rhap, although both these haptens bound significantly to the same rabbit antiserum, albeit with less immunoreactivity than the hexasaccharide. Inhibition studies using streptococcal group A and B rabbit antisera and the inhibitors indicated above also suggested that the group A carbohydrate, unlike the group B streptococcal polysaccharide, does not contain the disaccharide α-l-Rhap(1→2)α-l-Rhapmotif at its nonreducing chain terminus, stressing the importance of mapping the determinant specificities of these two important streptococcal subcapsular group polysaccharides to fully understand the serological relationships between group A and group B streptococci.