157 research outputs found

    Dirac-Kronig-Penney model for strain-engineered graphene

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    Motivated by recent proposals on strain-engineering of graphene electronic circuits we calculate conductivity, shot-noise and the density of states in periodically deformed graphene. We provide the solution to the Dirac-Kronig-Penney model, which describes the phase-coherent transport in clean monolayer samples with an one-dimensional modulation of the strain and the electrostatic potentials. We compare the exact results to a qualitative band-structure analysis. We find that periodic strains induce large pseudo-gaps and suppress charge transport in the direction of strain modulation. The strain-induced minima in the gate-voltage dependence of the conductivity characterize the quality of graphene superstructures. The effect is especially strong if the variation of inter-atomic distance exceeds the value a^2/l, where a is the lattice spacing of free graphene and l is the period of the superlattice. A similar effect induced by a periodic electrostatic potential is weakened due to Klein tunnelling.Comment: 11 pages, 8 figure

    Matrix metalloproteinase-13 refines pathological staging of precancerous colorectal lesions

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    An exact classification of precancerous stages of colorectal polyps might improve therapy and patientsÂŽ outcome. Here we investigate the association between grade of dysplasia and Matrix metalloproteinase-13 (MMP-13) expression in 137 biopsies from patients with cancerous and non-cancerous colorectal adenomas. A reproducible staining procedure for histologic MMP-13 analysis in routinely fixed colorectal biopsy specimens has been established. A newly adopted immunoreactive scoring system for MMP-13 was demonstrated as reliable readout. The strength of the association between pathologic stage and immunoreactive MMP-13 scoring emphasizes its eligibility for diagnosis in precancerous colorectal lesions

    Hepatitis B virus surface proteins accelerate cholestatic injury and tumor progression in Abcb4-knockout mice

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    Understanding of the pathophysiology of cholestasis associated carcinogenesis could challenge the development of new personalized therapeutic approaches and thus improve prognosis. Simultaneous damage might aggravate hepatic injury, induce chronic liver disease and even promote carcinogenesis. We aimed to study the effect of Hepatitis B virus surface protein (HBsAg) on cholestatic liver disease and associated carcinogenesis in a mouse model combining both impairments. Hybrids of Abcb4-/- and HBsAg transgenic mice were bred on fibrosis susceptible background BALB/c. Liver injury, serum bile acid concentration, hepatic fibrosis, and carcinogenesis were enhanced by the combination of simultaneous damage in line with activation of c-Jun N-terminal kinase (JNK), proto-oncogene c-Jun, and Signal transducer and activator of transcription 3 (STAT3). Activation of Protein Kinase RNA-like Endoplasmic Reticulum Kinase (PERK) and Eukaryotic translation initiation factor 2A (eIF2a) indicated unfolded protein response (UPR) in HBsAg-expressing mice and even in Abcb4-/- without HBsAg-expression. CONCLUSION: Cholestasis-induced STAT3- and JNK-pathways may predispose HBsAg-associated tumorigenesis. Since STAT3- and JNK-activation are well characterized critical regulators for tumor promotion, the potentiation of their activation in hybrids suggests an additive mechanism enhancing tumor incidence

    Expression of CD56 isoforms in primary and relapsed adult granulosa cell tumors of the ovary

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    <p>Abstract</p> <p>Background</p> <p>Adult granulosa cell tumors of the ovary (GCTs) are sex cord stromal tumors of unpredictable behaviour. Up to now, the prediction of the relapsing/malignant potential remains difficult. CD56 (NCAM) in GCTs was previously described in only two studies. However, the expression of its isoforms was not examined.</p> <p>Methods</p> <p>30 GCTs (16 primaries, 14 relapses) were investigated immunohistochemically with antibodies against Pan-CD56 (CD56<sup>Pan</sup>) and the isoform with 140/180 kDa length (CD56<sup>140/180 kDa</sup>). The reaction was assessed with respect to percentage of positive cells and intensity of staining.</p> <p>Results</p> <p>In all GCTs, CD56<sup>Pan </sup>was expressed, but differences were found between primaries and relapses. The percentage of CD56<sup>Pan </sup>positive tumor cells was lower in relapses, whereas CD56<sup>140/180 kDa </sup>showed a higher staining intensity in the latter.</p> <p>Conclusion</p> <p>Expression of CD56 is an additional sensitive and helpful immunohistochemical tool for histopathologists diagnosing a GCT. It does not seem possible to provide a validly individual risk assessement. However, the different expression of CD56 isoforms might indicate important changes in the course to a more malignant behaviour.</p

    Chronic nonbacterial osteomyelitis in childhood: prospective follow-up during the first year of anti-inflammatory treatment

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    Introduction: Chronic nonbacterial osteomyelitis (CNO) is an inflammatory disorder of unknown etiology. In children and adolescents CNO predominantly affects the metaphyses of the long bones, but lesions can occur at any site of the skeleton. Prospectively followed cohorts using a standardized protocol in diagnosis and treatment have rarely been reported. Methods: Thirty-seven children diagnosed with CNO were treated with naproxen continuously for the first 6 months. If assessment at that time revealed progressive disease or no further improvement, sulfasalazine and short-term corticosteroids were added. The aims of our short-term follow-up study were to describe treatment response in detail and to identify potential risk factors for an unfavorable outcome. Results: Naproxen treatment was highly effective in general, inducing a symptom-free status in 43% of our patients after 6 months. However, four nonsteroidal anti-inflammatory drug (NSAID) partial-responders were additionally treated with sulfasalazine and short-term corticosteroids. The total number of clinical detectable lesions was significantly reduced. Mean disease activity estimated by the patient/physician and the physical aspect of health-related quality of life including functional ability (global assessment/childhood health assessment questionnaire and childhood health assessment questionnaire) and pain improved significantly. Forty-one percent of our patients showed radiological relapses, but 67% of them were clinically silent. Conclusions: Most children show a favorable clinical course in the first year of anti-inflammatory treatment with NSAIDs. Relapses and new radiological lesions can occur at any time and at any site in the skeleton but may not be clinically symptomatic. Whole-body magnetic resonance imaging proved to be very sensitive for initial and follow-up diagnostics

    Biologische Vielfalt fĂŒr Deinen Erfolg

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    BIOLOGISCHE VIELFALT FÜR DEINEN ERFOLG Biologische Vielfalt fĂŒr Deinen Erfolg / Gattenlöhner, Udo (Rights reserved) ( -

    Concordance of KRAS/BRAF Mutation Status in Metastatic Colorectal Cancer before and after Anti-EGFR Therapy

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    Anti-EGFR targeted therapy is a potent strategy in the treatment of metastatic colorectal cancer (mCRC) but activating mutations in the KRAS gene are associated with poor response to this treatment. Therefore, KRAS mutation analysis is employed in the selection of patients for EGFR-targeted therapy and various studies have shown a high concordance between the mutation status in primary CRC and corresponding metastases. However, although development of therapy related resistance occurs also in the context of novel drugs such as tyrosine kinase-inhibitors the effect of the anti-EGFR treatment on the KRAS/BRAF mutation status itself in recurrent mCRC has not yet been clarified. Therefore, we analyzed 21 mCRCs before/after anti-EGFR therapy and found a pre-/posttherapeutic concordance of the KRAS/BRAF mutation status in 20 of the 21 cases examined. In the one discordant case, further analyses revealed that a tumor mosaicism or multiple primary tumors were present, indicating that anti-EGFR therapy has no influence on KRAS/BRAF mutation status in mCRC. Moreover, as the preselection of patients with a KRASwt genotype for anti-EGFR therapy has become a standard procedure, sample sets such ours might be the basis for future studies addressing the identification of potential anti-EGFR therapy induced genetic alterations apart from KRAS/BRAF mutations

    Leitfaden zur Entwicklung von biodiversitÀtsfreundlichen Unternehmen

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    LEITFADEN ZUR ENTWICKLUNG VON BIODIVERSITÄTSFREUNDLICHEN UNTERNEHMEN Leitfaden zur Entwicklung von biodiversitĂ€tsfreundlichen Unternehmen / Volles, Ronja (Rights reserved) ( -
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