Increased uptake of technetium-99m methylene diphosphonate in muscles in the course of polymyositis

A case of a woman aged 46 years with signs of rhabdomyolysis and acute renal failure is presented. Coxsackie serum test was positive. Increased uptake of Technetium-99m methylene diphosphonate (99mTc-MDP) by muscles of thighs and calves was observed. After 1 year no increased accumulation of radiotracer in the muscles was found

Basic product data in e-commerce : specifications and problems of data exchange

PURPOSE: This paper summarizes and compares the types and interpretations of the basic attributes necessary to enter product data in selected e-commerce platforms.DESIGN/METHODOLOGY/APPROACH: The research methodology was based on an analysis and selection of a reference group of basic product attributes and identification of appropriate market representatives, platforms and tools commonly used in e-commerce. Furthermore, for each of the selected basic attributes of the product, an analysis was made in terms of the presence, mandatory field, and data input validators. The best practices indicated by the platform developers were also reviewed.FINDINGS: The research results indicate discrepancies in the understanding of the basic attributes of the product. A lack of commonly available, standardized, consistent data describing products for which the manufacturer would take responsibility lead to creating own solutions for the e-commerce market and development of their own meanings of some data.PRACTICAL IMPLICATIONS: It is necessary to clearly understand e-product data as e-commerce market is relatively young and for which product data has a much greater and often completely different meaning than in a traditional trade.ORIGINALITY: It provides recommendations for e-commerce platforms for managing e-product core/ basic product data while using a single standard for product master data and common product identifier.peer-reviewe

PDGF and TGF-β contribute to the natural course of human IgA glomerulonephritis

PDGF and TGF-β contribute to the natural course of human Ig-A glomerulonephritis. PDGF and TGF-β are known mediators of mesangial cell proliferation and matrix expansion. The presence of these regulatory factors was examined in 30 renal biopsies from patients with IgA glomerulonephritis (IgA-GN) at the mRNA and protein level. Normal renal tissue served as control. The mRNA expression of PDGF A/B chains, PDGF-βR and TGF-β1 was evaluated by means of RT/PCR with subsequent Southern blot hybridization and/or non-radiactive in situ hybridization. In addition, PDGF-AB/BB, PDGF-βR, TGF-β isoforms (β1, β1+2, β2+3), the small TGF-β1 latency associated peptide (TGF-β1 LAP) and the extracellular matrix proteins tenascin and decorin were analyzed by immunocytochemistry. The expression of growth factors was correlated with light microscopic and clinical features. Compared to normal control kidneys, an increased expression of PDGF-BB/PDGF-βR mRNAs and the corresponding proteins was observed in all biopsies with IgA-GN. Up-regulation was related to the degree of glomerular proliferation and the extent of fibrosing interstitial lesions. In contrast, there was a discordance between TGF-β1 mRNA and protein expression (evaluated by immunocytochemistry). In all biopsies, irrespective of the stage of the disease, abundant TGF-β1 transcripts were detected, whereas TGF-β1 immunoreactivity was expressed to a lesser degree and disclosed a more variable staining pattern. In patients with significant proliferative glomerular lesions and minor tubulointerstitial alterations, TGF-β1 positivity was confined to areas of glomerular proliferation, whereas in cases with more severe histology including sclerosing lesions TGF-β1 immunoreactivity was less prominent. The distribution and the intensity of TGF-β1 LAP staining commonly exceeded the positivity noted for TGF-β1, indicating only limited TGF-β1 activation. A decreased reactivity for tenascin accompanied the morphological features of glomerular sclerosis. The staining patterns and the fact that only very few inflammatory cells, particularly CD68 positive monocytes/macrophages, were detected in glomeruli confirm that predominantly resident glomerular cells (mesangial and endothelial cells) are the major source of up-regulated growth factor production in IgA-GN. Since the expression of PDGF-AB/BB paralleled the severity of proliferative glomerular changes, PDGF seems to represent a potential indicator of activity in this condition. It is suggested that an imbalance between PDGF and TGF-β (by restricted translation and/or activation) production contribute to the progressive nature of IgA-GN

Creativity in Engineering Education

The paper examines the creativity in engineering education. The authors substantiate the topicality of the training of creative professionals in Russia and abroad and present training of creative professionals experience at the Department of Engineering Entrepreneurship of NR TPU. The empirical basis of the paper is the definition of the algorithm and conditions of the training of creative professionals

Interleukin-10 Promoter Polymorphism is Associated with the Predisposition to the Development of IgA Nephropathy and Focal Segmental Glomerulosclerosis in Korea

The roles of interleukin-10 (IL-10) have been emphasized in several models of glomerulonephritis (GN). Three biallelic polymorphisms within the IL-10 promoter region, at positions -1,082, -819, and -592 from the transcription initiation site, were shown to affect the level of IL-10 production. To investigate the effect of IL-10 promoter polymorphisms on the predisposition to development of GN in Korea, IL-10 promoter polymorphisms were assayed by polymerase chain reaction followed by restriction fragment length polymorphism in 108 patients with IgA nephropathy (IgAN), 49 focal segmental glomerulosclerosis (FSGS), and 100 healthy controls. In comparison with the control, the frequency of -1,082*G alleles were lower in IgAN and the frequencies of -592*C and -819*C were lower in FSGS, respectively. As for the haplotype, GCC haplotype was less frequent among IgAN than the control and ATA haplotype was more frequent among FSGS than the control (p<0.05). The frequency of intermediate producer genotypes (GCC/ACC and GCC/ATA) were lower among IgAN or FSGS than the control. Our findings suggested that IL-10 promoter polymorphism predisposed to the development of IgAN and FSGS in Korean patients

Excessive activation of the TLR9/TGF-β1/PDGF-B pathway in the peripheral blood of patients with systemic lupus erythematosus

Abstract Background Our aim is to study the existence of the TLR9/TGF-β1/PDGF-B pathway in healthy humans and patients with systemic lupus erythematosus (SLE), and to explore its possible involvement in the pathogenesis of lupus nephritis (LN). Methods Protein levels of the cytokines were detected by ELISA. mRNA levels of the cytokines were analyzed by real-time PCR. MTT assay was used to test the proliferation of mesangial cells under different treatments. Results Compared to healthy controls (N Control = 56), levels of Toll-like receptor (TLR)9, transforming growth factor (TGF)-β1, and platelet-derived growth factor B (PDGF-B) were increased significantly in the peripheral blood of SLE patients (N SLE = 112). Significant correlations between the levels of TLR9, TGF-β1, and PDGF-B were observed in both healthy controls and SLE patients. The levels of TGF-β1 and PDGF-B were greatly enhanced by TLR9 activation in primary cell cultures. The proliferation of mesangial cells induced by the plasma of SLE patients was significantly higher than that induced by healthy controls; PDGF-B was involved in this process. The protein levels of PDGF-B homodimer correlated with the levels of urine protein in SLE patients with LN (N LN =38). Conclusions The TLR9/TGF-β1/PDGF-B pathway exists in humans and can be excessively activated in SLE patients. High levels of PDGF-B may result in overproliferation of mesangial cells in the kidney that are involved in the development of glomerulonephritis and LN. Further studies are necessary to identify TLR9, TGF-β1, and PDGF-B as new therapeutic targets to prevent the development of glomerulonephritis and LN

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