bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characterization of canine filaggrin: gene structure and protein expression in dog skin
Authors: Kanda Satoko , Sasaki Takashi , Shiohama Aiko , Nishifuji Koji , Amagai Masayuki , Iwasaki Toshiroh , Kudoh Jun 
Published: January 2013

Background –  Filaggrin (FLG) is a key protein for skin barrier formation and hydration of the stratum corneum. In humans, a strong association between FLG gene mutations and atopic dermatitis has been reported. Although similar pathogenesis and clinical manifestation have been argued in canine atopic dermatitis, our understanding of canine FLG is limited.Hypothesis/Objectives –  The aim of this study was to determine the structure of the canine FLG gene and to raise anti‐dog FLG antibodies, which will be useful to detect FLG protein in dog skin.Methods –  The structure of the canine FLG gene was determined by analysing the publicly available canine genome DNA sequence. Polyclonal anti‐dog FLG antibodies were raised based on the canine FLG sequence analysis and used for defining the FLG expression pattern in dog skin by western blotting and immunohistochemistry.Results –  Genomic DNA sequence analysis revealed that canine FLG contained four units of repeated sequences corresponding to FLG monomer protein. Western blots probed with anti‐dog FLG monomer detected two bands at 59 and 54 kDa, which were estimated sizes. The results of immunohistochemistry showed that canine FLG was expressed in the stratum granulosum of the epidermis as a granular staining pattern in the cytoplasmic region.Conclusions and clinical importance –  This study revealed the unique gene structure of canine FLG that results in production of FLG monomers larger than those of humans or mice. The anti‐dog FLG antibodies raised in this study identified FLG in dog skin. These antibodies will enable us to screen FLG‐deficient dogs with canine atopic dermatitis or ichthyosis.
Canine inflamed nonepitheliotropic cutaneous T‐cell lymphoma: a diagnostic conundrum
Authors: Moore Peter F. , Affolter Verena K. , Keller Stefan M. 
Published: January 2013

Background – Cutaneous T‐cell lymphoma (CTCL) in dogs is a heterogeneous disease complex, which consists of nonepitheliotropic (NE) and epitheliotropic forms. These lymphomas are readily recognized by the presence of dominant populations of cytologically atypical lymphocytes.Objective – The objective of this study was to introduce the key features of inflamed NE‐CTCL, which is easily confused with reactive, inflammatory histiocytic disease.Animals – Twenty‐four dogs (mean age 7.5 years) presented with inflamed NE‐CTCL. Lesions presented as nodules, plaques or masses. An initial diagnosis of cutaneous reactive histiocytosis (11 dogs) or histiocytic neoplasia (three dogs) was made by primary pathologists.Methods – Lesions were assessed by histology and immunohistochemistry to detect canine leukocyte antigens. Lesional genomic DNA was extracted and gene rearrangement analysis of the T‐cell receptor γ locus was assessed.Results – The cutaneous lesions consisted of pleocellular infiltration of the dermis with variable extension into the subcutis. The lesions often surrounded vessels and adnexae. Epitheliotropism was minimal or lacking. Small lymphocytes, plasma cells and intermediate to large, cytologically atypical lymphocytes were scattered between prominent histiocytic infiltrates. Atypical lymphocytes often had marked variation in the intensity of CD3 expression. Molecular clonality analysis of the T‐cell receptor γ locus revealed clonal expansion of T cells in 22 of 23 dogs tested.Conclusion – The recognition of inflamed NE‐CTCL and its differentiation from cutaneous reactive histiocytosis depends on careful assessment of lymphocyte morphology and immunostaining patterns. Confirmation of the diagnosis is best accomplished by T‐cell antigen receptor gene rearrangement analysis.
Advances in the management of skin cancer
Authors: Martin Pamela D. , Argyle David J. 
Published: January 2013

Skin cancer is one of the most commonly diagnosed cancers in the world today in both humans and our pet population. Advances in molecular techniques are now affording us an opportunity to develop therapeutics targeted at specific cancer‐related cellular pathways. However, despite progress in conventional treatments, such as chemotherapy and radiation, and the new targeted therapies, some cancers, such as melanoma and cutaneous lymphoma, continue to cause significant mortality and morbidity.This short synopsis is not complete but is aimed at providing an insight into current advanced treatments and horizon therapies for cutaneous malignancies in dogs and cats with comparative aspects.
Equine sarcoidosis: clinical signs, diagnosis, treatment and outcome of 22 cases
Authors: Sloet van Oldruitenborgh‐Oosterbaan Marianne M. , Grinwis Guy C. M. 
Published: January 2013

Background – Equine sarcoidosis may present as a generalized or localized exfoliative dermatitis and/or as a granulomatous inflammation of multiple organs.Objectives – To report the clinical signs, diagnosis, treatment and outcome for 22 horses with histologically confirmed sarcoidosis.Animals – Twenty‐two horses of different breeds, between 3 and 17 years of age.Methods – Diagnosis was based on clinical signs and histopathological findings.Results – The following three forms of equine sarcoidosis were identified: generalized (13.6%), partially generalized (18.2%) and localized (68.2%). High‐dose systemic corticosteroids were used as the initial treatment in all three forms, followed by lower doses for a variable number of weeks. No local treatment was prescribed. Case outcome was variable; one of three cases of generalized sarcoidosis was euthanized immediately and the remaining two were euthanized after 2–3 months of unsuccessful treatment; all four cases of partially generalized sarcoidosis deteriorated despite treatment and were euthanized after 3.5–12 months; two cases with localized disease showed no response or insufficient response to treatment and were euthanized; four cases recovered fully with or without treatment, and one showed partial recovery without treatment; and eight cases improved whilst receiving prednisolone but required continuous low doses to maintain remission.Conclusions and clinical importance – Recognition of the different forms of sarcoidosis based on history, clinical appearance and histopathology assisted in making an informed choice between treatment and euthanasia and prevented unnecessary local treatment. Equine sarcoidosis should be included in the differential diagnosis of a localized exfoliative dermatitis of unknown origin.
Serum anti‐Staphylococcus pseudintermedius IgE and IgG antibodies in dogs with atopic dermatitis and nonatopic dogs
Authors: Bexley Jennifer , Nuttall Timothy J. , Hammerberg Bruce , Fitzgerald J. Ross , Halliwell Richard E. 
Published: January 2013

Background –  Dogs and humans with atopic dermatitis (AD) are predisposed to colonization and recurrent infection with Staphylococcus spp. Studies in humans suggest that staphylococcus‐specific immunoglobulin E (IgE) plays a key role in disease pathogenesis. Few such studies have been undertaken in dogs.Hypothesis/Objectives –  The aim of this study was to compare levels of staphylococcus‐specific IgE and immunoglobulin G (IgG) in dogs with AD, nonatopic dogs with staphylococcal pyoderma, and nonatopic and noninfected control dogs.Animals –  Sera were collected from 108 dogs with AD, 39 nonatopic dogs with staphylococcal pyoderma secondary to different underlying conditions, 67 age‐matched nonatopic control dogs, and nine control dogs reared in minimal disease conditions.Methods –  Serum Staphylococcus pseudintermedius‐specific IgE and IgG antibodies were measured by enzyme‐linked immunosorbent assay.Results –  Dogs with AD had significantly higher levels of anti‐staphylococcal IgE than nonatopic dogs with staphylococcal pyoderma and the two groups of control dogs. Levels of anti‐staphylococcal IgG were significantly higher in atopic dogs and nonatopic dogs with pyoderma compared with nonatopic control dogs and control dogs reared in minimal disease conditions, but there was no significant difference in levels of anti‐staphylococcal IgG between dogs with AD and nonatopic dogs with pyoderma.Conclusions and clinical importance –  A significantly increased IgE response to S. pseudintermedius antigens in atopic dogs suggests an immunopathogenic role for anti‐staphylococcal IgE. The finding of elevated IgE and IgG in atopic dogs is also important as a prelude to studies on antigenic specificity and possible correlations with disease phenotype.
Photodynamic therapy for pythiosis
Authors: Pires Layla , Bosco Sandra de M. G. , da Silva Junior Nelson F. , Kurachi Cristina 
Published: January 2013

Background – Pythiosis is a life‐threatening disease caused by Pythium insidiosum. Photodynamic therapy (PDT) is an alternative treatment to surgery that uses the interaction of a photosensitizer, light and molecular oxygen to cause cell death.Objectives – To evaluate the effect of PDT on the in vitro growth of P. insidiosum and in an in vivo model of pythiosis.Methods – For in vitro studies, two photosensitizers were evaluated: a haematoporphyrin derivative (Photogem®) and a chlorine (Photodithazine®). Amphotericin B was also evaluated, and the control group was treated with sterile saline solution. All experiments (PDT, porphyrin, chlorine and light alone, amphotericin B and saline solution) were performed as five replicates. For in vivo studies, six rabbits were inoculated with 20,000 zoospores of P. insidiosum, and an area of 1 cm3 was treated using the same sensitizers. The PDT irradiation was performed using a laser emitting at 660 nm and a fluence of 200 J/cm2. Rabbits were clinically evaluated daily and histopathological analysis was performed 72 h after PDT.Results – For in vitro assays, inhibition rates for PDT ranged from 60 to 100% and showed better results in comparison to amphotericin B. For the in vivo assays, after PDT, histological analysis of lesions showed a lack of infection up to 1 cm in depth.Conclusions and clinical importance – In vitro and in vivo studies showed that PDT was effective in the inactivation of P. insidiosum and may represent a new approach to treating pythiosis.
Epithelial‐to‐mesenchymal transition: immunohistochemical investigation of related molecules in canine cutaneous epithelial tumours
Authors: Bongiovanni Laura , D’Andrea Alessandra , Romanucci Mariarita , Malatesta Daniela , Candolini Melissa , Salda Leonardo D. , Mechelli Luca , Sforna Monica , Brachelente Chiara 
Published: January 2013

Background – Epithelial‐to‐mesenchymal transition (EMT) is a multistep process, important in tumour invasion and metastasis, characterized by loss of epithelial markers, redistribution of β‐catenin and gain of mesenchymal markers.Hyposthesis/Objectives – Our aim was to investigate the immunohistochemical aberrant expression of cytokeratin, vimentin, survivin and heat shock protein 72 (Hsp72) in canine cutaneous epithelial tumours, to understand the association of expression of these molecules with features of malignancy and their role in the EMT phenotype.Methods – Ten canine squamous cell carcinomas (SCCs; one with lymph node metastasis), 30 canine hair follicle tumours (six pilomatricomas, eight infundibular keratinizing acanthomas, six trichoepitheliomas and 10 trichoblastomas) and five normal skin samples were investigated by immunohistochemistry using specific anti‐vimentin, ‐cytokeratin, ‐survivin and ‐Hsp72 antibodies. A semi‐quantitative method was used to analyse the results, as follows: 0 to <5%; ≥5 to <10%; ≥10 to <25%; and ≥25% of positive cells. Immunofluorescence was performed to investigate survivin–vimentin and survivin–Hsp72 colocalization in selected SCCs.Results – In malignant hair follicle tumours and SCCs, a reduced intensity of cytokeratin and increased survivin and Hsp72 expression were observed. In SCCs, loss of cytokeratin expression and vimentin immunolabelling, suggestive of the EMT phenotype, were evident in <5% of neoplastic cells in the front of tumour invasion. In the same areas, strong nuclear survivin and cytoplasmic Hsp72 staining was evident, often colocalizing. Only a few neoplastic cells in the front of tumour invasion showed vimentin–survivin colocalization.Conclusions and clinical importance – A possible simultaneous involvement of survivin and Hsp72 in tumour invasion and the multistep process of EMT of cutaneous epithelial tumours of dogs is suggested.
Non‐surgical periodontal therapy decreases serum elastase levels in aggressive but not in chronic periodontitis
Authors: Eickholz Peter , Siegelin Yasemin , Scharf Susanne , Schacher Beate , Oremek Gerhard M. , Sauer‐Eppel Hildegund , Schubert Ralf , Wohlfeil Martin 
Published: January 2013

AbstractAimAssessment of the effect of non‐surgical periodontal therapy (SRP) on serum inflammatory parameters in patients with untreated aggressive (AgP) and chronic (ChP) periodontitis.MethodsOverall, 31 ChP and 29 AgP were examined clinically prior to and 12 weeks after SRP (subgingival scaling of all pockets within 2 days) with systemic antibiotics for patients positive for Aggregatibacter actinomycetemcomitans (14 AgP, 9 ChP). Blood was sampled prior to, one day, 6, and 12 weeks after the first SRP visit. Serum elastase, C‐reactive protein (CRP), lipopolysaccharide‐binding protein (LBP), interleukin (IL) 6, 8, and leukocyte counts were assessed.ResultsAt baseline, serum elastase, CRP, and LBP were significantly (p < 0.01) higher in AgP than ChP. Serum elastase, CRP, LBP, and IL‐6 were significantly (p < 0.001) elevated one day after scaling in both groups. Both groups showed significant clinical improvement (p < 0.001). A significant difference was observed regarding change of serum elastase 12 weeks after SRP between AgP and ChP (p = 0.015). Multiple regression analysis revealed AgP, African origin, and bleeding on probing to be associated with more pronounced elastase reduction. CRP reduction was associated with African origin, systemic antibiotics, and baseline probing pocket depth.ConclusionSRP results in serum elastase reduction in AgP but not in ChP.
Biologic width dimensions – a systematic review
Authors: Schmidt Julia C. , Sahrmann Philipp , Weiger Roland , Schmidlin Patrick R. , Walter Clemens 
Published: January 2013

AbstractBackgroundConsideration of the biologic width in restorative dentistry seems to be important for maintaining periodontal health.ObjectiveTo evaluate the dimensions of the biologic width in humans.Materials and MethodsA systematic literature search was performed for publications published by 28 September 2012 using five different electronic databases; this search was complemented by a manual search. Two reviewers conducted the study selection, data collection, and validity assessment. The PRISMA criteria were applied. From 615 titles identified by the search strategy, 14 publications were included and six were suitable for meta‐analyses.ResultsIncluded studies were published from the years 1924 to 2012. They differed with regard to measurements of the biologic width. Mean values of the biologic width obtained from two meta‐analyses ranged from 2.15 to 2.30 mm, but large intra‐ and inter‐individual variances (subject sample range: 0.2 – 6.73 mm) were observed. The tooth type and site, the presence of a restoration and periodontal diseases/surgery affected the dimensions of the biologic width. Pronounced heterogeneity among studies regarding methods and outcome measures exists.ConclusionsNo universal dimension of the biologic width appears to exist. Establishment of periodontal health is suggested prior to the assessment of the biologic width within reconstructive dentistry.
Barriers and facilitators to undertaking nutritional screening of patients: a systematic review
Authors: Green S. M. , James E. P. 
Published: January 2013

AbstractBackgroundRecent reports have suggested that registered nurses may not screen patients admitted to their care for malnutrition. The objective of this integrative review was to locate and review published research investigating barriers and facilitators to nutritional screening by nurses.MethodsA systematic search for relevant English language publications was conducted through CINAHL®, Web of Science, MEDLINE® and EMBASE and an Internet search engine (completed November 2011). Reference lists of relevant publications were also searched. Search terms included nursing, dietetics, nutrition disorders and screening, as well as associated MeSH® terms and Subject Headings. Six hundred and sixteen publications were identified and 605 were excluded. Publications reporting research concerning barriers and facilitators to nutritional screening by nurses were selected using exclusion and inclusion criteria. These were reviewed and the key findings described, categorised, combined, reviewed and refined to create themes.ResultsEleven publications were reviewed. Publications primarily reported hospital‐based studies undertaken in three continents and considered barriers rather than facilitators. Five themes emerged: organisational culture, competing priorities, the value of clinical judgement, training and education, and discrepancy between attitudes and practice.ConclusionsStudies primarily involved acute care and indicated that routine screening for malnutrition will not take place unless it is considered an integral part of nursing assessment that is required by policy and resourced appropriately. Qualitative studies investigating barriers and facilitators to screening for malnutrition in community settings are needed and research is required to test interventions designed to modify or remove barriers and facilitate screening.
Systematic review of randomised controlled trials of the effects of caffeine or caffeinated drinks on blood glucose concentrations and insulin sensitivity in people with diabetes mellitus
Authors: Whitehead N. , White H. 
Published: January 2013

AbstractBackgroundCompounds other than macronutrients have been shown to influence blood glucose concentrations and insulin sensitivity in people with diabetes, with caffeine being one such substance. The present study systematically reviewed the evidence of the effects of caffeine on blood glucose concentrations and/or insulin sensitivity in people with diabetes.MethodsFour databases, including MEDLINE and EMBASE, were searched up to 1 February 2012. Randomised controlled trials (RCTs) investigating the effects of caffeine on blood glucose and/or insulin sensitivity in humans, diagnosed with type I, type II or gestational diabetes mellitus (GDM), were included. Quality assessment and data extraction were conducted and agreed by both authors.ResultsOf 253 articles retrieved, nine trials (134 participants) were identified. Trials in people with type II diabetes demonstrated that the ingestion of caffeine (approximately 200–500 mg) significantly increased blood glucose concentrations by 16–28% of the area under the curve (AUC) and insulin concentrations by 19–48% of the AUC when taken prior to a glucose load, at the same time as decreasing insulin sensitivity by 14–37%. In type I diabetes, trials indicated enhanced recognition and a reduced duration of hypoglycaemic episodes following ingestion of 400–500 mg caffeine, without altering glycated haemoglobin. In GDM, a single trial demonstrated that approximately 200 mg of caffeine induced a decrease in insulin sensitivity by 18% and a subsequent increase in blood glucose concentrations by 19% of the AUC.ConclusionsEvidence indicates a negative effect of caffeine intake on blood glucose control in individuals with type II diabetes, as replicated in a single trial in GDM. Larger‐scale RCTs of longer duration are needed to determine the effects of timing and dose. Early indications of a reduced duration and an improved awareness of hypoglycaemia in type I diabetes require further confirmation.
The transcription factor Pitx3 is expressed selectively in midbrain dopaminergic neurons susceptible to neurodegenerative stress
Authors: Luk Kelvin C. , Rymar Vladimir V. , van den Munckhof Pepijn , Nicolau Stefan , Steriade Claude , Bifsha Panojot , Drouin Jacques , Sadikot Abbas F. 
Published: January 2013

AbstractThe homeodomain transcription factor Pitx3 is critical for the survival of midbrain dopaminergic (mDA) neurons. Pitx3‐deficient mice exhibit severe but selective developmental loss of mDA neurons, with accompanying locomotor deficits resembling those seen in Parkinson's disease (PD) models. Here, we identify specific mDA cell subpopulations that are consistently spared in adult Pitx3‐hypomorphic (aphakia) mice, demonstrating that Pitx3 is not indiscriminately required by all mDA neurons for their survival. In aphakia mice, virtually all surviving mDA neurons in the substantia nigra (SN) and the majority of neurons in the adjacent ventral tegmental area (VTA) also express calbindin‐D28k, a calcium‐binding protein previously associated with resistance to injury in PD and in animal models. Cell‐mapping studies in wild‐type mice revealed that Pitx3 is primarily expressed in the ventral SN, a region particularly susceptible to MPTP and other dopaminergic neurotoxins. Furthermore, Pitx3‐expressing SN cells are preferentially lost following MPTP treatment. Finally, SN mDA neurons in Pitx3 hemizygous mice show increased sensitivity when exposed to MPTP. Thus, SN mDA neurons are represented by at least two distinct subpopulations including MPTP‐resistant Pitx3‐autonomous, calbindin‐positive neurons, and calbindin‐negative Pitx‐3‐dependent cells that display elevated vulnerability to toxic injury, and probably correspond to the subpopulation that degenerates in PD. Impairment of Pitx3‐dependent pathways therefore increases vulnerability of mDA neurons to toxic injury. Together, these data suggest a novel link between Pitx3 function and the selective pattern of mDA cell loss observed in PD.
nAChR‐induced octopamine release mediates the effect of nicotine on a startle response in Drosophila melanogaster
Authors: Fuenzalida‐Uribe Nicolás , Meza Rodrigo C. , Hoffmann Hernán A. , Varas Rodrigo , Campusano Jorge M. 
Published: January 2013

AbstractBiogenic amines (BAs) play a central role in the generation of complex behaviors in vertebrates and invertebrates, including the fly Drosophila melanogaster. The comparative advantages of Drosophila as a genetic model to study the contribution of BAs to behaviors stumble upon the difficulty to access the fly brain to ask relevant physiological questions. For instance, it is not known whether the activation of nicotinic acetylcholine receptors (nAChRs) induces the release of BAs in fly brain, a phenomenon associated to several behaviors in vertebrates. Here, we describe a new preparation to study the efflux of BAs in the adult fly brain by in vitro chronoamperometry. Using this preparation we show that nAChR agonists including nicotine induce a fast, transient, dose‐dependent efflux of endogenous BAs, an effect mediated by α‐bungarotoxin‐sensitive nAChRs. By using different genetic tools we demonstrate that the BA whose efflux is induced by nAChR activation is octopamine (Oct). Furthermore, we show that the impairment of a mechanically induced startle response after nicotine exposure is not observed in flies deficient in Oct transmission. Thus, our data show that the efflux of BAs in Drosophila brain is increased by nAChR activation as in vertebrates, and that then AChR‐induced Oct release could have implications in a nicotine‐induced behavioral response.