bluuebunny/crossref_metadata_2025_split huggingface dataset:
Photosensitive atopic dermatitis – a neglected subset: Clinical, laboratory, histological and photobiological workup
Authors: Ellenbogen E. , Wesselmann U. , Hofmann S.C. , Lehmann P. 
Published: November 2015

AbstractBackgroundPhotosensitive atopic dermatitis (PhAD) is a scarcely reported entity characterized clinically by a photodistributed rash in patients who fulfil the criteria for atopic dermatitis (AD).ObjectivesThe aim of this retrospective study is to define significant clinical, laboratory and immunological parameters as well as photobiological features for diagnosing PhAD.MethodsWe conducted a single‐centre retrospective analysis of 17 patients with long‐standing AD who in the disease course suddenly developed photosensitivity. All patients with suspected PhAD treated in our department between 2009 and 2014 were included in the study. Diagnostic methods were immunological parameters, prick and patch testing, histology and phototesting procedures.ResultsOnset of photosensitivity was observed during spring, summer and during exposure to artificial UVR (Ultraviolet radiation) as part of the patients' treatment regimen. Symptoms appeared 31.5 months on average after AD diagnosis was established. Although the MED (Minimal erythematous dose) was normal compared to a control group, all patients tested with photoprovocation methods exhibited a positive reaction. Two types of reactions were observed: papular and eczematous reactions, both types having similar histology. The wavelength spectrum most commonly involved was UVA. The disease seems to affect women more often than men. Predilection sites included face, neck, exposed trunk areas and arms. Patients with PhAD had coexistent eczematous lesions in non‐sun‐exposed skin. IgE levels were elevated in 11/17 patients (65%), with a median value of 269 kU/L.ConclusionPhAD is an underreported subset of atopic dermatitis, which is rarely diagnosed. This study suggests that several features including atopic diathesis, eczematous lesions in UVR exposed body regions and positive photoprovocation reaction are suggestive of PhAD as the likely diagnosis. Typically, the atopic eczema starts without a sign of photosensitivity, however, in a subgroup of AD patients after a few months to years, a switch occurs leading to PhAD.
Comparative genomic study of arachnid immune systems indicates loss of beta‐1,3‐glucanase‐related proteins and the immune deficiency pathway
Authors: Bechsgaard J. , Vanthournout B. , Funch P. , Vestbo S. , Gibbs R. A. , Richards S. , Sanggaard K. W. , Enghild J. J. , Bilde T. 
Published: November 2015

AbstractAnalyses of arthropod genomes have shown that the genes in the different innate humoral immune responses are conserved. These genes encode proteins that are involved in immune signalling pathways that recognize pathogens and activate immune responses. These immune responses include phagocytosis, encapsulation of the pathogen and production of effector molecules for pathogen elimination. So far, most studies have focused on insects leaving other major arthropod groups largely unexplored. Here, we annotate the immune‐related genes of six arachnid genomes and present evidence for a conserved pattern of some immune genes, but also evolutionary changes in the arachnid immune system. Specifically, our results suggest that the family of recognition molecules of beta‐1,3‐glucanase‐related proteins (βGRPs) and the genes from the immune deficiency (IMD) signalling pathway have been lost in a common ancestor of arachnids. These findings are consistent with previous work suggesting that the humoral immune effector proteins are constitutively produced in arachnids in contrast to insects, where these have to be induced. Further functional studies are needed to verify this. We further show that the full haemolymph clotting cascade found in the horseshoe crab is retrieved in most arachnid genomes. Tetranychus lacks at least one major component, although it is possible that this cascade could still function through recruitment of a different protein. The gel‐forming protein in horseshoe crabs, coagulogen, was not recovered in any of the arachnid genomes; however, it is possible that the arachnid clot consists of a related protein, spätzle, that is present in all of the genomes.
Pharmacokinetics of florfenicol and behaviour of its metabolite florfenicol amine in orange‐spotted grouper (Epinephelus coioides) after oral administration
Authors: Feng J‐B , Huang D‐R , Zhong M , Liu P , Dong J‐D 
Published: November 2015

AbstractPharmacokinetics and elimination of florfenicol and florfenicol amine in grouper held in sea water at 23.3 ± 0.8 °C were studied using HPLC method after they were given a single peroral dose of florfenicol at 24 mg kg−1 body weight. Florfenicol was rapidly absorbed from intestine and distributed extensively to all the tissues examined. The maximum concentrations (Cmax, μg g−1 or μg mL−1) in plasma and tissues were observed at 2–6 h (the time to reach maximum concentration, Tmax) except for bile (Tmax = 24 h) and were in the order of intestine (52.02 ± 25.07) > bile (49.41 ± 28.16) > gill (45.12 ± 11.10) > plasma (28.28 ± 5.43) > liver (21.97 ± 12.08) > muscle (21.63 ± 6.12) > kidney (20.88 ± 11.28) > skin (19.10 ± 5.88). The drug distribution level was higher in plasma than in extravascular tissues except for bile, based on the ratios of the area under concentration–time curve between tissue and plasma (AUCtissue/plasma). The elimination of florfenicol was rapid in fish, and the corresponding half‐lives (T1/2β) in the order of magnitude were bile (13.92 h) > muscle or liver (12.31 h) > skin (11.77 h) > plasma (11.57) > gill (11.04 h) > intestine (10.55 h) > kidney (10.05 h). The delayed Tmax, lower Cmax and longer T1/2β for florfenicol amine compared with florfenicol were measured in grouper.
Cutaneous myxidiosis in European eel, Anguilla anguilla (Linnaeus, 1758): histopathology, histochemistry and laminin immunohistochemistry
Authors: Manera M , Borreca C , Dezfuli B S 
Published: November 2015

AbstractHistopathology, histochemistry and immunohistochemistry of the integument of European eel, Anguilla anguilla (Linnaeus, 1758), infected by Myxidium sp. are reported. Skin samples from affected and unaffected eels were dissected, formalin fixed, paraffin embedded, sectioned and stained with H&E, Periodic acid–Schiff's staining method, Alcian Blue 8 GX pH 2.5/Periodic acid–Schiff's and McCallum‐Goodpasture's Gram stain. Moreover, immunohistochemistry was performed using a primary polyclonal laminin antibody. Histologically, cysts (diameter 2–3 mm) were observed mainly under the scale pockets, encircled by a thin collagen layer, lined by elongated, flattened fibroblasts and containing bipolar, PAS‐ and Gram‐positive spores with opposite polar capsules. The epidermis stretched by the underlying cyst appeared dysplastic, thinned with a significant reduction in mucous cells number. Only inconsistent and aspecific inflammatory reaction was noted around the cysts at the dermis/epidermis interface. Intense laminin‐like protein immunolabel was documented in the plasmodial ectoplasm and related to host anergia. This was the first report of laminin immunolabel in a member of the Myxozoa. Epidermal dysplasia represents likely an aspecific response against the underlying tensile force exerted by the developing parasite cyst, while fibroblast and collagen encapsulation denote a parasite‐driven host response protecting, rather than harming, the encircled parasite.
Apolipoprotein E4 reduces evoked hippocampal acetylcholine release in adult mice
Authors: Dolejší Eva , Liraz Ori , Rudajev Vladimír , Zimčík Pavel , Doležal Vladimír , Michaelson Daniel M. 
Published: November 2015

AbstractApolipoprotein E4 (apoE4) is the most prevalent genetic risk factor for Alzheimer's disease. We utilized apoE4‐targeted replacement mice (approved by the Tel Aviv University Animal Care Committee) to investigate whether cholinergic dysfunction, which increases during aging and is a hallmark of Alzheimer's disease, is accentuated by apoE4. This revealed that levels of the pre‐synaptic cholinergic marker, vesicular acetylcholine transporter in the hippocampus and the corresponding electrically evoked release of acetylcholine, are similar in 4‐month‐old apoE4 and apolipoprotein E3 (apoE3) mice. Both parameters decrease with age. This decrease is, however, significantly more pronounced in the apoE4 mice. The levels of cholinacetyltransferase (ChAT), acetylcholinesterase (AChE), and butyrylcholinesterase (BuChE) were similar in the hippocampus of young apoE4 and apoE3 mice and decreased during aging. For ChAT, this decrease was similar in the apoE4 and apoE3 mice, whereas it was more pronounced in the apoE4 mice, regarding their corresponding AChE and BuChE levels. The level of muscarinic receptors was higher in the apoE4 than in the apoE3 mice at 4 months and increased to similar levels with age. However, the relative representation of the M1 receptor subtype decreased during aging in apoE4 mice. These results demonstrate impairment of the evoked release of acetylcholine in hippocampus by apoE4 in 12‐month‐old mice but not in 4‐month‐old mice. The levels of ChAT and the extent of the M2 receptor‐mediated autoregulation of ACh release were similar in the adult mice, suggesting that the apoE4‐related inhibition of hippocampal ACh release in these mice is not driven by these parameters.
image
Evoked ACh release from hippocampal and cortical slices is similar in 4‐month‐old apoE4 and apoE3 mice but is specifically and significantly reduced in hippocampus, but not cortex, of 12‐month‐old apoE4 mice. This effect is accompanied by decreased VAChT levels. These findings show that the hipocampal cholinergic nerve terminals are specifically affected by apoE4 and that this effect is age dependent.
Plasmatic retinol‐binding protein 4 and glial fibrillary acidic protein as biomarkers to differentiate ischemic stroke and intracerebral hemorrhage
Authors: Llombart Víctor , García‐Berrocoso Teresa , Bustamante Alejandro , Giralt Dolors , Rodriguez‐Luna David , Muchada Marian , Penalba Anna , Boada Cristina , Hernández‐Guillamon Mar , Montaner Joan 
Published: November 2015

AbstractA rapid differentiation of acute ischemic stroke and intracerebral hemorrhage (ICH) is essential for an adequate treatment and to promote a better outcome. Our aim was to identify new plasma biomarkers to differentiate stroke subtypes and to combine their diagnostic ability with other biomarkers already described for this clinical indication.Plasma samples of ischemic stroke patients (36) and ICH patients (10) were screened using a 177 antibodies library, and 11 showed different concentrations among stroke subtypes (p < 0.05), mainly chemokines, growth factors and angiogenic factors. Five proteins were selected for replication in 16 ischemic stroke patients and 16 ICH patients, and retinol‐binding protein 4 (RPB4), apolipoprotein B100 and pigment epithelial–derived factor were replicated (p < 0.05). These proteins, together with glial fibrillary acidic protein (GFAP) and receptor for advanced glycation end product, were tested in 38 ischemic stroke and 28 ICH samples. Finally, RBP4 >61 μg/mL and GFAP <0.07 ng/mL showed a specificity of 100% for both subtypes. Moreover, after multivariate logistic regression analysis, RBP4 >48.75 μg/mL (ORadj: 6.09 (1.3–28.57), p = 0.02) and GFAP <0.07 ng/mL (ORadj: 0.03 (0.003–0.31), p = 0.003) resulted in independent predictors of stroke subtype, improving discrimination by 29% (p < 0.0001). Both biomarkers might be useful as diagnostic biomarkers to differentiate ischemic stroke and ICH.
imageA rapid differentiation of ischemic stroke from intracerebral hemorrhage is essential to provide the appropriate treatment. We describe the discovery and subsequent replications of RBP4 and its combination with circulating GFAP as plasmatic biomarkers for hyperacute stroke subtype differentiation. The combination of these biomarkers and others might aid to speed up the discrimination of both stroke subtypes improving the outcome of patients.
Enjoyment in nursing – experiences from the clinical milieu
Authors: Wilkes Lesley , Doull Michelle , Ng Chok Harrison , Mashingaidze Gladys 
Published: November 2015

Aims and objectivesTo present findings from a qualitative study which aimed to explore and describe experiences of enjoyment in nursing.BackgroundThe topic of ‘enjoying nursing’ is often part of job satisfaction surveys conducted in the workplace and in some studies it has been found to be the prime reason that nurses stay in the workforce. However, there is little research which explores the concept fully.DesignQualitative in‐depth interviews.MethodSemi‐structured individual interviews were conducted with 17 nurses in a local health district in Sydney, Australia. Data from digitally recorded individual interviews were transcribed and the content was analysed for themes relating to aspects of nursing that were enjoyable and others that were not.ResultsThe major themes to emerge from the data describing enjoyment of nursing were: doing for others, supporting others and educating others. Themes that identified not enjoying nursing were related to the aggression of others, i.e. patients/clients, families or other staff in the workplace, as well as system issues. System issues referred mainly to the need for support from other nurses and management.ConclusionNurses still enjoy caring for patients and teaching others to care. This is the reason they remain in nursing even though the system and people are not always supportive or encouraging.Relevance to clinical practiceManagers and educators can use these results to assist them to understand the importance of giving support to nursing staff to optimise their enjoyment of caring for their patients/clients.
Nursing assessment of continuous vital sign surveillance to improve patient safety on the medical/surgical unit
Authors: Watkins Terri , Whisman Lynn , Booker Pamela 
Published: November 2015

Aims and objectivesEvaluate continuous vital sign surveillance as a tool to improve patient safety in the medical/surgical unit.BackgroundFailure‐to‐rescue is an important measure of hospital quality. Patient deterioration is often preceded by changes in vital signs. However, continuous multi‐parameter vital sign monitoring may decrease patient safety with an abundance of unnecessary alarms.DesignProspective observational study at two geographically disperse hospitals in a single hospital system.MethodsA multi‐parameter vital sign monitoring system was installed in a medical/surgical unit in Utah and one in Alabama providing continuous display of SpO2, heart rate, blood pressure and respiration rate on a central station. Alarm thresholds and time to alert annunciations were set based on prior analysis of the distribution of each vital sign. At the end of 4 weeks, nurses completed a survey on their experience. An average alert per patient, per day was determined retrospectively from the saved vital signs data and knowledge of the alarm settings.ResultsNinety‐two per cent of the nurses agreed that the number of alarms and alerts were appropriate; 54% strongly agreed. On average, both units experienced 10·8 alarms per patient, per day. One hundred per cent agreed the monitor provided valuable patient data that increased patient safety; 79% strongly agreed.ConclusionsContinuous, multi‐parameter patient monitoring could be performed on medical/surgical units with a small and appropriate level of alarms. Continuous vital sign assessment may have initiated nursing interventions that prevented failure‐to‐rescue events. Nurses surveyed unanimously agreed that continuous vital sign surveillance will help enhance patient safety.Relevance to clinical practiceNursing response to abnormal vital signs is one of the most important levers in patient safety, by providing timely recognition of early clinical deterioration. This occurs through diligent nursing surveillance, involving assessment, interpretation of data, recognition of a problem and meaningful response.
The Porphyromonas gingivalis O antigen is required for inhibition of apoptosis in gingival epithelial cells following bacterial infection
Authors: Soto C. , Bugueño I. , Hoare A. , Gonzalez S. , Venegas D. , Salinas D. , Melgar‐Rodríguez S. , Vernal R. , Gamonal J. , Quest A. F. G. , Pérez‐Donoso J. M. , Bravo D. 
Published: November 2015

Background and ObjectivePorphyromonas gingivalis infection induces apoptosis inhibition in gingival epithelial cells; however, it is not fully understood which bacterial effectors are involved in this process. The aim of this study is to evaluate whether the P. gingivalis lipopolysaccharide (LPS), specifically the O‐antigen region, affects adherence, invasion, viability and apoptosis of gingival epithelial cells.Material and MethodsGingival epithelial cells (OKF6/TERT2 line) were infected by different freshly prepared P. gingivalis clinical isolates, obtained from subjects with chronic periodontitis (CP3 and CP4) and healthy individuals (H1 and H3). Periodontitis and healthy isolates show differences in O‐antigen production, as healthy isolates lack the O‐antigen region. In addition, cells were infected by a site‐specific mutant lacking the O‐antigen portion. After 24 h postinfection, cell proliferation, viability and apoptosis were evaluated by Trypan blue, MTS and annexin V assays, respectively. Bacterial invasion, adhesion and proliferation were measured by gentamicin/metronidazole protection assays. Finally, toll‐like receptor (TLR)2 and TLR4 mRNA expression was evaluated by quantitative reverse transcription–polymerase chain reaction. Statistical analysis was performed using ANOVA, Tukey's or Dunnett's tests (p < 0.05).ResultsAt 24 h postinfection, strains lacking the O‐antigen region (healthy isolates and O‐antigen ligase‐deficient strain) were unable to increase proliferation and viability, or decrease apoptosis as compared with strains producing intact LPS (periodontitis isolates and reference strain). However, the presence of the O‐antigen neither contributed to changes in the ability of the bacteria to adhere to or invade cells, nor to intracellular survival. The presence of O‐antigen also increased the expression of TLR4 (nearly sixfold), which correlated with inhibition of apoptosis.ConclusionThe O‐antigen region of P. gingivalis LPS is required to increase gingival epithelial cell viability upon infection by bacteria and this increase is attributable to a reduction in apoptosis. Moreover, although bacterial internalization is required, the effects observed are not due to alterations in P. gingivalis adherence, invasion or intracellular survival. Interestingly, inhibition of apoptosis correlates with increased TLR4 expression, suggesting a role for TLR4 in this process.
14,15‐epoxyeicosatrienoic acid promotes production of brain derived neurotrophic factor from astrocytes and exerts neuroprotective effects during ischaemic injury
Authors: Yuan L. , Liu J. , Dong R. , Zhu J. , Tao C. , Zheng R. , Zhu S. 
Published: November 2015

Aims14,15‐Epoxyeicosatrienoic acid (14,15‐EET) is abundantly expressed in brain and exerts protective effects against ischaemia. 14,15‐EET is hydrolysed by soluble epoxide hydrolase (sEH). sEH−/− mice show a higher level of 14,15‐EET in the brain. Astrocytes play a pivotal role in neuronal survival under ischaemic conditions. However, it is unclear whether the neuroprotective effect of 14,15‐EET is associated with astrocytes.MethodsA mouse model of focal cerebral ischaemia was induced by middle cerebral artery occlusion. Oxygen–glucose deprivation/reoxygenation (OGD/R) was performed on cultured murine astrocytes, neurons and a human cell line. Cell viabilities were measured by 3‐(4, 5‐dimethyl‐2‐thiazolyl)‐2, 5‐diphenyl‐2H‐tetrazolium bromide (MTT) assay. The mRNA expressions were quantified by real‐time PCR. Brain derived neurotrophic factor (BDNF) concentration was measured by ELISA. Protein expressions were quantified by Western blotting. BDNF and peroxisome proliferators‐activated receptor gamma (PPAR‐γ) expressions were analysed by confocal microscopy.ResultsDecreased infarct volumes, elevated BDNF expression and increased numbers of BDNF/GFAP Glial Fibrillary Acidic Protein double‐positive cells were observed in the ischaemic penumbra of sEH−/− mice. The decreased infarct volumes of sEH−/− mice were diminished by intracerebroventricular injection of a blocker of BDNF receptor. 14,15‐EET increases BDNF expression and cell viability of murine astrocytes and U251 cells by BDNF‐TrkB Tyrosine receptor kinase‐B‐extracellular signal‐regulated kinase 1/2 signalling during OGD/R. 14,15‐EET protects neurons from OGD/R by stimulating the production of astrocyte‐derived BDNF. 14,15‐EET stimulates the production of astrocyte‐derived BDNF through PPAR‐γ/p‐cAMP‐response element binding protein signal pathways.ConclusionsOur study demonstrates the importance of 14,15‐EET‐mediated production of astrocyte‐derived BDNF for enhancing viability of astrocytes and protecting neurons from the ischaemic injury and provides insights into the mechanism by which 14,15‐EET is involved in neuroprotection.
Cortical Lewy bodies and Aβ burden are associated with prevalence and timing of dementia in Lewy body diseases
Authors: Ruffmann C. , Calboli F. C. F. , Bravi I. , Gveric D. , Curry L. K. , de Smith A. , Pavlou S. , Buxton J. L. , Blakemore A. I. F. , Takousis P. , Molloy S. , Piccini P. , Dexter D. T. , Roncaroli F. , Gentleman S. M. , Middleton L. T. 
Published: November 2015

AimsOur main objective was to determine the neuropathological correlates of dementia in patients with Lewy body disease (LBD). Furthermore, we used data derived from clinical, neuropathological and genetic studies to investigate boundary issues between Dementia with Lewy bodies (DLB) and Parkinson's disease with (PDD) and without (PDND) dementia.MethodsOne hundred and twenty‐one cases with a neuropathological diagnosis of LBD and clinical information on dementia status were included in the analysis (55 PDD, 17 DLB and 49 PDND). We carried out topographical and semi‐quantitative assessment of Lewy bodies (LB), Aβ plaques and tau‐positive neuropil threads (NT). The APOE genotype and MAPT haplotype status were also determined.ResultsThe cortical LB (CLB) burden was the only independent predictor of dementia (OR: 4.12, P < 0.001). The total cortical Aβ plaque burden was an independent predictor of a shorter latency to dementia from onset of motor signs (P = 0.001). DLB cases had a higher LB burden in the parietal and temporal cortex, compared to PDD. Carrying at least one APOE ϵ4 allele was associated with a higher cortical LB burden (P = 0.02), particularly in the neocortical frontal, parietal and temporal regions.ConclusionsHigh CLB burden is a key neuropathological substrate of dementia in LBD. Elevated cortical LB pathology and Aβ plaque deposition are both correlated with a faster progression to dementia. The higher CLB load in the temporal and parietal regions, which seems to be a distinguishing feature of DLB, may account for the shorter latency to dementia and could be mediated by the APOE ϵ4 allele.