Publications by authors named "Wernicke D"

Background/aims: Peripheral neuropathies perturbate the sensorimotor system, causing difficulties in walking-related motor tasks and, eventually, falls. Falls result in functional dependency and reliance on healthcare, especially in older persons. We investigated if peripheral neuropathy is a genuine risk factor for falls in the elderly and if quantification of postural control via posturography is helpful in identifying subjects at risk of falls.

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RNA editing is a finely tuned, dynamic mechanism for post-transcriptional gene regulation that has been thoroughly investigated in the last decade. Nevertheless, RNA editing in non-coding RNA, such as microRNA (miRNA), have caused great debate and have called for deeper investigation. Until recently, in fact, inadequate methodologies and experimental contexts have been unable to provide detailed insights for further elucidation of RNA editing affecting miRNAs, especially in cancer.

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Nucleolin (NCL) is a nucleocytoplasmic protein involved in many biological processes, such as ribosomal assembly, rRNA processing, and mRNA stabilization. NCL also regulates the biogenesis of specific microRNAs (miRNAs) involved in tumor development and aggressiveness. Interestingly, NCL is expressed on the surface of actively proliferating cancer cells, but not on their normal counterparts.

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MicroRNAs (miRNAs) are short non-coding RNAs with a length of ∼22 nucleotides, involved in posttranscriptional regulation of gene expression. Until now, over 2588 miRNAs have been identified in humans and the list is growing. MicroRNAs have an important role in all biological processes and aberrant miRNA expression is associated with many diseases including cancer.

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Recent investigations of chromosomal aberrations in chronic lymphocytic leukemia (CLL) led to a better understanding of the molecular causes of CLL. Here we report a rearrangement between MAML2 (mastermind-like protein 2) and CXCR4 (specific receptor for CXC chemokine stromal cell-derived factor-1) in CLL cells of a patient with a t(2;11)(q22.1;q21) chromosomal translocation.

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Deregulation of the miR-15a/16-1 cluster has a key role in the pathogenesis of chronic lymphocytic leukemia (CLL), a clinically heterogeneous disease with indolent and aggressive forms. The miR-15a/16-1 locus is located at 13q14, the most frequently deleted region in CLL. Starting from functional investigations of a rare SNP upstream the miR cluster, we identified a novel allele-specific mechanism that exploits a cryptic activator region to recruit the RNA polymerase III for miR-15a/16-1 transcription.

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Article Synopsis
  • *Researchers studied microRNA (miR) expression in tumor samples from 198 patients to identify a signature associated with chemoresistance, ultimately finding 23 miRs linked to treatment resistance.
  • *Three specific miRs (miR-484, -642, and -217) were validated as predictive markers for chemoresistance, with miR-484 also playing a role in tumor blood vessel regulation, suggesting that combined targeting of VEGFB and VEGFA may enhance treatment efficacy.
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MicroRNAs (miRNAs) are small noncoding RNAs, 19-24 nucleotides in length, that regulate gene expression and are expressed aberrantly in most types of cancer. MiRNAs also have been detected in the blood of cancer patients and can serve as circulating biomarkers. It has been shown that secreted miRNAs within exosomes can be transferred from cell to cell and can regulate gene expression in the receiving cells by canonical binding to their target messenger RNAs.

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Infection-driven inflammation has been implicated in the pathogenesis of ~15-20% of human tumors. Expression of microRNA-155 (miR-155) is elevated during innate immune response and autoimmune disorders as well as in various malignancies. However, the molecular mechanisms providing miR-155 with its oncogenic properties remain unclear.

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Objectives: Does experience with rituximab treatment of rheumatoid arthritis (RA) in daily clinical practice confirm the results of controlled randomized studies?

Methods: This is a retrospective data-analysis of the first 50 patients from one center with rituximab treatment for RA. The patients received at least one cycle of 2 rituximab infusions (1000 mg, respectively) within 2 weeks. Clinical assessment was performed 3-5 months after the first infusion.

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Objective: Modern ultrasound (US) equipment allows rheumatologists to directly visualize hand and finger arteries. How does US aid in diagnosis of Raynaud's phenomenon (RP)?

Methods: Color Doppler US of the proper and common palmar digital, radial, and ulnar arteries and the superficial palmar arch of both hands was performed in 135 consecutive patients who presented with suspected RP.

Results: US was pathologic in 63% of patients with secondary RP, in 6% with primary RP, and in none with pseudo-RP (p < 0.

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Objective: To investigate the association between immunohistopathological and morphological features of synovitis in rheumatoid arthritis and the amounts of collagen degradation products pyridinoline and deoxypyridinoline in the synovial tissue and in body fluids in order to discover potential markers of erosive disease.

Methods: Histopathological analysis of synovial tissue samples from 22 patients with RA was performed according to the histopathologic scoring system of RA synovitis by P. Stiehl.

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Objective: To verify ultrasonographic criteria for examination of the major salivary glands in diagnosis of primary and secondary Sjögren's syndrome (SS).

Methods: Three hundred sixteen consecutive patients with rheumatic diseases were selected according to the European Consensus Study Group diagnostic criteria for SS. Fifty-seven had primary SS, 33 had secondary SS, 78 had Sicca symptoms, and 148 patients served as asymptomatic controls.

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The objective of this article was to assess whether matrix metalloproteinase-13 (MMP-13) is produced by cells of the peri-implant interface tissues and to further characterize these cells. Tissue specimens were collected from the bone-prosthesis interface at the time of revision surgery of clinically loosened hip and knee arthroplasties (n = 27). Synovial tissues from osteoarthritic patients and young patients with mild joint deformity were used as controls (n = 6).

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Animal models of cardiovascular diseases allow to investigate relevant pathogenetic mechanisms in detail. In the present study, the mutations Asp175Asn and Glu180Gly in alpha-tropomyosin (TPM1), known cause familiar hypertrophic cardiomyopathy (FHC) were studied for changes in hemodynamic parameters and spontaneous baroreflex regulation in transgenic rats in comparison to transgenic and non-transgenic controls by telemetry. Heart rate variability (HRV) and blood pressure variability (BPV) were analyzed using time- and frequency domain, as well as non-linear measures.

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Analysis of heart rate variability (HRV) and blood pressure variability (BPV) and baroreceptor sensitivity (BRS) has become a proven tool in clinical cardiovascular diagnostics and risk stratification. In the present work, traditional and new methodological approaches for analysis of HRV, BPV, and BRS data are summarized. HRV, BPV, and BRS parameters were obtained from animal studies designed to study pathogenetic mechanisms of distinct cardiovascular diseases.

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The histopathologic analysis of the synovial tissue is important to distinguish rheumatoid arthritis (RA) from other forms of synovitis and to provide information about prognosis and therapeutic strategies at early stages of the disease. In this context, the present study was performed to investigate the correlation between immunohistopathological and morphological features of synovitis and the expression of collagenase 3 (MMP-13) known to contribute significantly to cartilage degradation in RA. In the histopathologic scoring system used in this study, type I synovitis is characterized by B lymphocyte infiltration and an intact lining, and is only mild destructive to cartilage and bone.

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Articular symptoms are frequent manifestations of hereditary haemochromatosis. The clinical signs of the arthropathy of haemochromatosis are not specific and difficult to identify in case of co-incidence of haemochromatosis with Heberden's and Bouchard's osteoarthritis or rheumatoid arthritis (RA). Here the manifestation of RA in a patient is reported who was successfully treated for haemochromatosis.

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Case Reports: Three patients-two with Wegener's granulomatosis and one with an overlap syndrome of rheumatoid vasculitis, systemic lupus erythematosus, and antiphospholipid syndrome-are described. All patients experienced a sudden onset of Raynaud's phenomenon or acrocyanosis when they had a flare of their disease.

Discussion: Ultrasonography (US) showed dark (hypoechoic) arteries without colour signals, resembling the US pattern of embolism.

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To study the mechanisms by which missense mutations in alpha-tropomyosin cause familial hypertrophic cardiomyopathy, we generated transgenic rats overexpressing alpha-tropomyosin with one of two disease-causing mutations, Asp(175)Asn or Glu(180)Gly, and analyzed phenotypic changes at molecular, morphological, and physiological levels. The transgenic proteins were stably integrated into the sarcomere, as shown by immunohistochemistry using a human-specific anti-alpha-tropomyosin antibody, ARG1. In transgenic rats with either alpha-tropomyosin mutation, molecular markers of cardiac hypertrophy were induced.

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Objective: To study the pattern and cell type-specificity of collagenase 3, membrane-type 1 matrix metalloproteinase (MT1-MMP), and gelatinase A mRNA expression in the synovial membrane in rheumatoid arthritis (RA).

Methods: The mRNA expression of collagenase 3, MT1-MMP, and gelatinase A was characterised by northern blot analysis, reverse transcriptase-polymerase chain reaction, and in situ hybridisation. In situ hybridisation was performed in combination with the immunohistochemical detection of cell type-specific antigens.

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Objective: To study the expression of collagenase 3 (matrix metalloproteinase 13 [MMP-13]) and collagenase 1 (MMP-1) in synovial fibroblasts from patients with rheumatoid arthritis (RA) when cultured within 3-dimensional collagen gels or coimplanted with normal cartilage in immunodeficient NOD/SCID mice.

Methods: Messenger RNA (mRNA) and protein expression of collagenase 3 and collagenase 1 were characterized in synovial and skin fibroblasts by Northern blot and Western blot analysis. The mRNA expression of both collagenases in cell-cartilage implants in NOD/SCID mice was investigated by in situ hybridization in combination with immunohistochemistry of human fibroblasts.

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Objective: To study the localization and cell type-specific expression of collagenase 3 messenger RNA (mRNA) in the synovial membrane, its regulation in primary synovial fibroblasts, and the correlation with systemic markers of inflammation and radiographic damage in rheumatoid arthritis (RA).

Methods: The expression of collagenase 3 mRNA was characterized by Northern blot analysis, reverse transcriptase-polymerase chain reaction, and in situ hybridization. Immunohistochemical detection of cell type-specific antigens was used in combination with in situ hybridization of collagenase 3 mRNA to characterize the cellular origin of collagenase 3 mRNA expression.

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