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Factors influencing the regulation of change of bacteriophage lambda DNA replication mode

100%

Narajczyk M. , Baranska S. , Gabig-Ciminska M. , Wegrzyn G.

nr Supplement 1

Genistein modulates gene activity in psoriatic patients

100%

Smolinska E. , Wegrzyn G. , Gabig-Ciminska M.

Acta Biochimica Polonica

2019

tom 66

nr 1

Putative biological mechanisms of efficiency of substrate reduction therapies for mucopolysaccharidoses

88%

Banecka-Majkutewicz Z. , Jakobkiewicz-Banecka J. , Gabig-Ciminska M. , Wegrzyn A. , Wegrzyn G.

nr 6

Molecular factors involved in the development of diabetic foot syndrome

75%

Bruhn-Olszewska B. , Korzon-Burakowska A. , Gabig-Ciminska M. , Olszewski P. , Wegrzyn A. , Jakobkiewicz-Banecka J.

Acta Biochimica Polonica

2012

tom 59

nr 4

Diabetes is one of the major challenges of modern medicine, as it is considered a global epidemic of the XXI century. The disease often leads to the development of serious, health threatening complications. Diabetic foot syndrome is a characteristic set of anatomical and molecular changes. At the macroscopic level, major symptoms are neuropathy, ischemia and chronic ulceration of the lower limb. In every third patient, the neuropathy develops into Charcot neuroarthropathy characterized by bone and joints deformation. Interestingly, all these complications are a result of impaired healing processes and are characteristic for diabetes. The specificity of these symptoms comes from impaired molecular mechanisms observed in type 1 and type 2 diabetes. Decreased wound and fracture healing reflect gene expression, cellular response, cell functioning and general metabolism. Here we present a comprehensive literature update on the molecular factors contributing to diabetic foot syndrome.

Comparison of siRNA-mediated silencing of glycosaminoglycan synthesis genes and enzyme replacement therapy for mucopolysaccharidosis in cell culture studies

75%

Chmielarz I. , Gabig-Ciminska M. , Malinowska M. , Banecka-Majkutewicz Z. , Wegrzyn A. , Jakobkiewicz-Banecka J.

Acta Biochimica Polonica

2012

tom 59

nr 4

Cytotoxicity of laronidase (Aldurazyme®), employed in enzyme replacement therapy (ERT) for mucopolysaccharidosis type I (MPS I) and various siRNAs, tested previously in studies on substrate reduction therapy (SRT) for mucopolysaccharidoses, was tested. The enzyme did not cause any cytotoxic effects, and the siRNAs did not inhibit growth of most investigated cell lines. However, some cytotoxic effects of some tested siRNAs were observed in one MPS IIIA cell line. The efficacy of a combination of enzyme replacement therapy and siRNA-based substrate deprivation therapy was tested on three MPS I cell lines. Surprisingly, different results were obtained for different cell lines. The decrease of glycosaminoglycan storage in cells treated simultaneously with both methods was: (i) less pronounced than obtained with either of those methods used alone in one cell line, (ii) similar to that observed for enzyme replacement therapy in another cell line, and (iii) stronger than that obtained with either of the methods used alone in the third cell line. Therefore, it appears that the effects of various therapeutic methods may strongly depend on the features of the MPS cell line.