bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cancer incidence among persons with fragile X syndrome in Finland: a population‐based study
Authors: Sund R. , Pukkala E. , Patja K. 
Published: August 2008

AbstractBackground  Fragile X syndrome is a common inheritable cause of intellectual disability (ID) and is characterised by a large number of CGG repeats at the gene FMR1 located on the X‐chromosome. It has been reported that this genetic mechanism may protect against malignant transformations.Methods  We extracted from the Finnish registry on persons with ID a cohort of 302 persons with a fragile X diagnosis during 1982–1986. Follow‐up for cancer incidence was performed in the Finnish Cancer Registry until the end of the year 2005.Results  There were 11 reported cancers during the mean follow‐up of 21.4 years per person. The expected number of cancers based on the average Finnish population was 13.8 and no statistically significant protective effect was detected [standardised incidence ratios (SIR) 0.80, confidence interval (CI) 95% 0.40–1.4]. An increased risk for lip cancer was found (SIR 23, CI 95% 2.8–85).Conclusions  Confirmation of hypotheses about the mechanisms linking FXS and cancer needs further research.
Acquired Glanzmann's thrombasthenia caused by glycoprotein IIb/IIIa autoantibodies of the immunoglobulin G1 (IgG1), IgG2 or IgG4 subclass: a study in six cases
Authors: Porcelijn L. , Huiskes E. , Maatman R. , De Kreuk A. , De Haas M. 
Published: August 2008

Background  Acquired Glanzmann's thrombasthenia (GT) is an uncommon bleeding disorder caused by glycoprotein (GP) IIb/IIIa‐specific autoantibodies. Covering of the fibrinogen binding site of GPIIb/IIIa results in a moderate‐to‐severe bleeding tendency.Materials and Methods  We performed a diagnostic evaluation and evaluated the underlying risk factors in six patients with a bleeding tendency caused by acquired GT.Results  One patient, with GPIIb/IIIa autoantibodies of the immunoglobulin G2 (IgG2) subclass, used diclophenac and recovered after discontinuation of this drug. A second patient was primarily diagnosed with multiple angiodysplastic lesions. In this patient, the acquired GT was caused by GPIIb/IIIa autoantibodies of the IgG4 subclass that was treated with DDAVP and platelet transfusions. A third patient with Hodgkin's lymphoma and anti‐GPIIb/IIIa of the IgG2 subclass was treated for haemorrhagic diathesis with corticosteroids and azathioprin. A fourth patient, with IgG2 anti‐GPIIb/IIIa autoantibodies, diagnosed with mantle cell lymphoma, responded well to treatment of an axillary mass with local radiotherapy. The fifth and sixth patients, with IgG1 anti‐GPIIb/IIIa autoantibodies, appeared to have GT after splenectomy because of autoimmune thrombocytopenia. They were treated with corticosteroids, intravenous immunoglobulin and Rituximab.Conclusion  Although it might be a rare event, one should be aware of acquired GT as a cause of an unexpected primary disorder of haemostasis in patients with lymphoma or autoimmune disease. The lack of platelet destruction in these cases of acquired GT can be explained, either by the subclass of the autoantibodies (i.e. IgG2 or IgG4) or by the arrested platelet destruction by IgG1 (or IgG3) autoantibodies after splenectomy.
Role of anti‐Naka antibody, monocytes and platelets in the development of transfusion‐related acute lung injury
Authors: Nakajima F. , Nishimura M. , Hashimoto S. , Okazaki H. , Tadokoro K. 
Published: August 2008

Background and Objectives  Transfusion‐related acute lung injury (TRALI) is one of the most serious side‐effects of transfusion. We report here the first two cases of TRALI caused by anti‐Naka (anti‐CD36) antibody from a single blood donor. The aim of this study was to clarify the role of the anti‐Naka antibody in TRALI development.Materials and Methods  Human lung microvascular endothelial cells were co‐cultured with Naka‐positive monocytes and Naka‐positive platelets together with serum prepared from blood products of a TRALI‐caused anti‐Naka antibody‐carrying donor. Expressions of leukotriene B4 (LTB4) and tumour necrosis factor α (TNF‐α) in the co‐culture supernatants were determined.Results  The expressions of LTB4 and TNF‐α were found to be markedly increased, particularly in the presence of both Naka‐positive monocytes and platelets. The expressions of these mediators were almost completed within 4 h after the initiation of co‐culture. Monocyte contribution seemed to be stronger than that of platelets. In the absence of human lung microvascular endothelial, no significant LTB4 or TNF‐α release was observed.Conclusion  Anti‐Naka antibody may be strongly implicated in lung microvascular endothelial dysfunctions that lead to TRALI in a monocyte‐ and platelet‐dependent manner.
Resistance in pepper plants induced by Fusarium oxysporum f. sp. lycopersici involves different defence‐related genes
Authors: Silvar C. , Merino F. , Díaz J. 
Published: August 2008

AbstractInoculation with Fusarium oxysporum f. sp. lycopersici (FOL) protects pepper plants from subsequent infection with Phytophthora capsici. In the present paper, the level of local and systemic protection achieved by plants induced with FOL was evaluated by quantifying the pathogen biomass and using real‐time PCR. Differences in the amount of pathogen were found in stems and roots between FOL‐treated and untreated plants, while pathogen biomass could not be detected in leaves of induced plants. Five defence‐related genes coding for a PR‐1 protein, a β‐1,3‐glucanase, a chitinase, a peroxidase and a sesquiterpene cyclase were up‐regulated 48 h after treatment in all the tissues studied, and maximal mRNAs levels were found in leaves.
An RNA Probe for the Detection of Grapevine virus A
Authors: Komínek Petr , Komínková‐Bryxiová Marcela , Jandurová Olga Mercedes , Holleinová Věra 
Published: August 2008

AbstractA specific dot‐blot hybridization assay was developed using an in vitro‐transcribed non‐radioactive RNA probe for the routine detection of Grapevine virus A (GVA) for use as an alternative diagnostic tool for large‐scale surveys. GVA was detected in RNA isolated from infected vine plants, plant extracts and tissue prints using this probe however no reaction was observed with healthy plants of genus Vitis.
A fatal case of cutaneous zygomycosis in a patient with severe metabolic acidosis
Authors: Kosmidis C. , Katsogianni K. , Matsoukas S. , Tsagarakis M. , Georgiou P. , Giannopoulou P. , Liapi G. , Antonopoulos A. 
Published: August 2008

SummaryWe present a case of cutaneous zygomycosis in a patient with an ureteroileostomy and severe metabolic acidosis, but without diabetes. The patient died despite multiple aggressive surgical interventions and antifungal therapy with liposomal amphotericin B. Ureteroileostomy‐related acidosis can be a predisposing factor for zygomycosis. Metabolic acidosis can have a role in the severity of cutaneous disease.
Complement and fungal pathogens: an update
Authors: Speth Cornelia , Rambach Günter , Würzner Reinhard , Lass‐Flörl Cornelia 
Published: August 2008

SummaryFungal infections are a serious complication in immunocompromised patients such as human immunodeficiency virus‐infected individuals, patients with organ transplantations or with haematological neoplasia. The lethality of opportunistic fungal infection is high despite a growing arsenal of antimycotic drugs, implying the urgent need for supportive immunological therapies to strengthen the current inefficient antimicrobial defences of the immunocompromised host. Therefore, increasing effort has been directed to investigating the interplay between fungi and the host immunity and thus to find starting points for additional therapeutic approaches. In this article, we review the actual state of the art concerning the role of complement in the pathogenesis of fungal infections. Important aspects include the activation of the complement system by the fungal pathogen, the efficiency of the complement‐associated antimicrobial functions and the arsenal of immune evasion strategies applied by the fungi. The twin functions of complement as an interactive player of the innate immunity and at the same time as a modulator of the adaptive immunity make this defence weapon a particularly interesting therapeutic candidate to mobilise a more effective immune response and to strengthen in one fell swoop a broad spectrum of different immune reactions. However, we also mention the ‘Yin‐Yang’ nature of the complement system in fungal infections, as growing evidence assigns to complement a contributory part in the pathogenesis of fungus‐induced allergic manifestations.
Evaluation of Candida albicans allergens reactive with specific IgE in asthma and atopic eczema patients
Authors: Khosravi A. R. , Bandghorai A. Naseri , Moazzeni M. , Shokri H. , Mansouri P. , Mahmoudi M. 
Published: August 2008

Summary Candida albicans (C. albicans) produces important allergenic components which can induce allergic reactions in sensitised patients. The purpose of this study was to extract the C. albicans antigens for evaluating the specific anti‐Candida IgE in sera of atopic eczema (AE) and asthmatic patients (AS). 95 AE, 85 AS, and 70 non‐atopic cases were selected with sequential trials. Candida albicans antigens were prepared and then skin prick test (SPT), ELISA and IgE‐immunoblotting tests were performed for all patients. Positive SPT reactions were obtained on 52.6% of AE and 54.1% of AS patients and 4.3% of healthy controls (P < 0.05). Using ELISA, specific anti‐C. albicans IgE antibody was detected in 32.6% and 41.2% of patients with AE and AS, respectively. No specific IgE antibody was detected in healthy controls (P < 0.05). In SDS‐PAGE, protein bands with molecular weights between 13 and 135 kDa were detected, and some of them reacted with specific IgE in immunoblotting. In AE patients, the most important allergenic components were 25, 34, and 57 kDa protein bands, whereas in AS, 22, 25, and 34 kDa protein bands were observed as major allergens. Candida albicans produces different allergenic components that can induce allergic reactions and may be pathogenetically important in patients with AE and AS.
A real‐time polymerase chain reaction assay for quantitative detection of the human‐specific enterococci surface protein marker in sewage and environmental waters
Authors: Ahmed W. , Stewart J. , Gardner T. , Powell D. 
Published: August 2008

SummaryA real‐time polymerase chain reaction (PCR) assay using SYBR Green I dye was developed to quantify the Enterococcus faecium enterococci surface protein (esp) marker in sewage (n = 16) and environmental waters (n = 16). The concentration of culturable enterococci in raw sewage samples ranged between 1.3 × 105 and 5.6 × 105 colony‐forming units (cfu) per 100 ml. The real‐time PCR detected 9.8 × 103−3.8 × 104 gene copies of the esp marker per 100 ml of sewage. However, the concentration of culturable enterococci and the esp marker in secondary effluent was two orders of magnitude lower than raw sewage. Surface water samples were collected from a non‐sewered catchment after storm events and the real‐time PCR was applied to quantify the esp marker. Of the 16 samples tested, 6 (38%) were PCR‐positive and the concentration of the esp marker ranged between 1.1 × 102 and 5.3 × 102 gene copies per 100 ml of water samples. The newly developed real‐time PCR method was successfully used to quantify the esp marker in samples collected from sewage and environmental waters. The presence of the esp marker in water samples immediately after storm events not only indicated human faecal pollution but also provided evidence of the degree of human faecal pollution. To our knowledge, this is the first study that reports the use of a real‐time PCR assay to quantify the esp marker in sewage and surface waters. Such study would provide valuable information for managers for the improved management of water quality.
Systematic evaluation of single mismatch stability predictors for fluorescence in situ hybridization
Authors: Yilmaz L. Safak , Bergsven Lindsey I. , Noguera Daniel R. 
Published: August 2008

SummaryThe mismatch discrimination potential of probes in fluorescence in situ hybridization can be defined as the difference between the melting formamide points of perfect complementary and mismatched duplexes (Δ[FA]m). Using a combined experimental and theoretical approach, Δ[FA]m was determined for a set of 35 mismatched probes targeting seven locations in the 16S rRNA of Escherichia coli. The mismatches were created by changing single nucleotides on the probes, while maintaining the target unmodified. Estimated Δ[FA]m values were used to systematically evaluate four predictors of mismatch stability: weighted mismatch (WM) scores from the software arb, published statistical summary of microarray hybridizations, free energy of mismatch stability (ΔΔG°1) and theoretical Δ[FA]m estimations obtained with a thermodynamic model. Based on the predictors' ability to explain variability in Δ[FA]m and to discriminate weak mismatches from strong ones, ΔΔG°1 and WM scores from arb (with an updated set of relative strength parameters) were demonstrated to be adequate estimators of mismatch stability, with ΔΔG°1 offering the benefit of capturing the variability associated with nearest‐neighbour effects and being compatible with thermodynamic models of in situ hybridization. The use of ΔΔG°1 and WM in probe design was illustrated as a tool that complements experimental design approaches.
Predominance of Gram‐positive bacteria in house dust in the low‐allergy risk Russian Karelia
Authors: Pakarinen Jaakko , Hyvärinen Anne , Salkinoja‐Salonen Mirja , Laitinen Sirpa , Nevalainen Aino , Mäkelä Mika J. , Haahtela Tari , Von Hertzen Leena 
Published: August 2008

SummarySimple living conditions and farming environment have been associated with reduced risk for allergic diseases such as atopy and asthma but the factors responsible for this effect remain unresolved. We examined the bacterial composition of house dusts obtained from Finnish and Russian Karelia, two adjacent areas with high and low occurrence of atopic diseases respectively. Two dust mixes, both composed of 10 randomly selected dust samples from 349 Finnish and 417 Russian Karelian households were studied for bacterial biomarkers (DNA, Limulus‐active endotoxin, 3‐OH fatty acids, muramic acid) and for 16S rRNA gene sequences. Overall, the DNA cloning revealed more taxons (94 different genera) of dustborne bacteria than seen in any previous study on residential environments. Majority (67%) of the bacterial DNA clones in house dust from the low‐allergy Russian Kareliarepresented Gram‐positive bacteria (Firmicutes and Actinobacteria), predominantly Staphylococcaceae and Corynebacteriaceae. Russian Karelian dust showed up to 20‐fold higher contents of muramic acid (marker of Gram‐positive bacteria) and a sevenfold higher number of clones of animal‐associated species, whereas in Finnish Karelian dust Gram‐negatives (mainly Proteobacteria) predominated. Clones of plant‐associated bacterial species and of chloroplast, indicating plant biomass, were more numerous in Finnish than in Russian Karelian dust. In conclusion, this study revealed major disparities between Finnish and Russian house dusts. The higher bacterial content and the predominance of Gram‐positive bacteria in Russian dust may have implications for occurrence of atopy.
The come back kid
Authors: Cresswell Amanda , Tuffrey‐Wijne Irene 
Published: August 2008

Accessible summary

I had cancer, but I got better. This story is about what happened in my life, and about having cancer.
I was born with cerebral palsy and learning disabilities. My mum died of cancer when I was 14. It was difficult because she never told me that she was ill. It would have been better to know.
I went to my GP when my cancer started, but he kept saying there was nothing wrong. In the end, I was taken to hospital because I collapsed.
The first hospital never explained anything to me. I didn’t know what was going on, and I was very scared.
My doctor in the second hospital told me I had cancer. He explained everything. My doctor and carers helped me to decide what to do. I had chemotherapy (strong cancer medicine in a drip) and radiotherapy (a cancer treatment which is a bit like having an X‐ray). It was hard but I knew I didn’t want to die.
My life is wonderful now. Having cancer made me stronger.
Doctors and nurses should know that it is really important people are told about their cancer. They should tell people in a way that they can understand.
Hospitalisation for cancer and co‐morbidities among people with learning disability in Australia
Authors: Sullivan Sheena G. , Hussain Rafat 
Published: August 2008

Accessible summary

People with learning disability are just as likely as people in the general population to get cancer.
In this study we have looked at how often clients who get cancer are admitted to hospital.
We found that clients who get cancer are admitted to hospital much more often than clients who do not get cancer.
We also looked at the experiences of two clients to show what clients have to go through when they get cancer.
This research could help parents/carers and clients to know what to expect when people with learning disability need treatment and care for cancer.

SummaryIn Australia, general health and medical services are subsidised by the government. This includes care for people with disabilities, screening and diagnostic services for common diseases, including cancer, and care and treatment for various medical conditions. In Western Australia, the majority of state‐provided health services are well documented in linkable databases. We have examined data from a large cohort of people receiving services for learning disability from the state and linked this with the state cancer registry and hospital records. While people with learning disability appear to be at similar risk for cancer, they may have poorer treatment outcomes as they already experience a range of health conditions which can exacerbate medical complications associated with treatment and/or other primary or secondary co‐morbid conditions. Our results show that the mean number of hospital admissions were higher for the cancer group, even when adjustments were made for conditions such as childhood leukaemia and renal dialysis both of which often require frequent hospitalisations. Multivariate regression analyses showed that younger age, female sex and severe or unspecified level of disability were significant contributors to the frequency of hospital admissions. Qualitative information gleaned from detailed chart reviews showed that in addition to considerable morbidity, some patients were admitted repeatedly either because of lack of supportive environments and/or lack of compliance with treatment. Issues in providing appropriate support services for individuals and their carers are discussed.
Everolimus‐ and Zotarolimus‐Eluting Stents for Bare Metal Stent In‐Stent Restenosis Treatment: A Prospective Study
Authors: TOUTOUZAS KONSTANTINOS , PATSA CHRYSOULA , TSIAMIS ELEFTHERIOS , TSIOUFIS COSTAS , SPANOS ANASTASIOS , STEFANADI ELLI , TENTOLOURIS COSTAS , STEFANADIS CHRISTODOULOS 
Published: August 2008

Background: Treatment of in‐stent restenosis (ISR) is a challenging clinical problem. Recent studies have verified the safety and efficacy of first‐generation DES for the treatment of ISR. The safety and effectiveness of new‐generation drug‐eluting stents (nDES) for ISR has not been previously investigated. The aim of the present study was to prospectively evaluate the clinical outcomes after treatment with nDES implantation in patients with bare metal stent (BMS) ISR.
Methods: Consecutive patients with ISR after BMS implantation were included. Primary end‐point was a major adverse cardiac event (MACE), defined as death, myocardial infarction (MI), or target vessel revascularization (TVR). The incidence of stent thrombosis was also evaluated.
Results: A total of 46 consecutive patients were enrolled for the treatment of ISR, 23 patients from ZES and 23 from EES group. There were two (8.7%) cases of TVR in ZES cohort due to proliferative ISR at 6 and 7 months after DES implantation, and none in EES. One (4.3%) patient underwent percutaneous coronary intervention and the other (4.3%) was treated surgically. Neither acute nor subacute thrombosis was observed during the 13.3±6.3 months follow‐up period. In all other patients, stress test was negative for ischemia at 6 months.
Conclusions: In this prospective study, we showed that direct nDES implantation is highly effective for ISR and seems to be a promising management for the treatment of ISR.
Mycobacteria‐induced granuloma necrosis depends on IRF‐1
Authors: Aly Sahar , Mages Jörg , Reiling Norbert , Kalinke Ulrich , Decker Thomas , Lang Roland , Ehlers Stefan 
Published: August 2008

AbstractIn a mouse model of mycobacteria‐induced immunopathology, wild‐type C57BL/6 (WT), IL‐18‐knockout (KO) and IFN‐αβ receptor‐KO mice developed circumscript, centrally necrotizing granulomatous lesions in response to aerosol infection with M. avium, whereas mice deficient in the IFN‐γ receptor, STAT‐1 or IRF‐1 did not exhibit granuloma necrosis. Comparative, microarray‐based gene expression analysis in the lungs of infected WT and IRF‐1‐KO mice identified a set of genes whose differential regulation was closely associated with granuloma necrosis, among them cathepsin K, cystatin F and matrix metalloprotease 10. Further microarray‐based comparison of gene expression in the lungs of infected WT, IFN‐γ‐KO and IRF‐1‐KO mice revealed four distinct clusters of genes with variable dependence on the presence of IFN‐γ, IRF‐1 or both. In particular, IRF‐1 appeared to be directly involved in the differentiation of a type I immune response to mycobacterial infection. In summary, IRF‐1, rather than being a mere transcription factor downstream of IFN‐γ, may be a master regulator of mycobacteria‐induced immunopathology.
Induction of hepatic differentiation of mouse bone marrow stromal stem cells by the histone deacetylase inhibitor VPA
Authors: Chen Ye , Pan Ruo‐Lang , Zhang Xiao‐Lei , Shao Jian‐Zhong , Xiang Li‐Xin , Dong Xue‐Jun , Zhang Guo‐Rong 
Published: August 2008

AbstractBone marrow stromal stem cells (BMSSCs) may have potential to differentiate in vitro and in vivo into hepatocytes. Here, we investigated the effects of valproic acid (VPA) involved in epigenetic modification, a direct inhibitor of histone deacetylase, on hepatic differentiation of mouse BMSSCs. Following the treatment of 2.5 mM VPA for 72 hrs, the in vitro expanded, highly purified and functionally active mouse BMSSCs from bone marrow were either exposed to some well‐defined cytokines and growth factors in a sequential way (fibroblast growth factor‐4 [FGF‐4], followed by HGF, and HGF + OSM + ITS + dexamethasone, resembling the order of secretion during liver embryogenesis) or transplanted (caudal vein) in mice submitted to a protocol of chronic injury (chronic i.p. injection of CCl4). Additional exposure of the cells to VPA considerably improved the in vitro differentiation, as demonstrated by a more homogeneous cell population exhibited epithelial morphology, increasing expression of hepatic special genes and enhanced hepatic functions. Further more, in vivo results indicate that the pre‐treatment of VPA significantly increased the homing efficiency of BMSSCs to the site of liver injury and, additionally, for supporting hepatic differentiation as well as in vitro. We have demonstrated the usefulness of VPA in the transdifferentiation of BMSSCs into hepatocytes both in vitro and in vivo, and regulation of fibroblast growth factor receptors (FGFRs) and c‐Met gene expression through post‐translational modification of core histones might be the primary initiating event for these effects. This mode could be helpful for liver engineering and clinical therapy.