Wyniki wyszukiwania - Biblioteka Nauki

Nowa wersja platformy, zawierająca wyłącznie zasoby pełnotekstowe, jest już dostępna.
Przejdź na https://bibliotekanauki.pl

Ograniczanie wyników

Znaleziono wyników: 3

Liczba wyników na stronie

Wyniki wyszukiwania

Sortuj według:

Ogranicz wyniki do:

Dentinogenesis imperfecta type II: Ultrastructure of teeth in sagittal sections

100%

Wieczorek A. , Loster J.

Folia Histochemica et Cytobiologica

2013

tom 51

nr 3

Dentinogenesis imperfecta : hardness and Young’s modulus of teeth

80%

Wieczorek A. , Loster J. , Ryniewicz W. , Ryniewicz A. M.

Acta of Bioengineering and Biomechanics

2013

tom Vol. 15, no. 3

65--69

Dentinogenesis imperfecta type II (DI-II) is the most common dental genetic disease with reported incidence 1 in 8000. Elasticity and hardness of the enamel of teeth are important values which are connected with their resistance to attrition. It is hypothesized that values of physical properties for healthy teeth and teeth with DI-II are different. The aim of the study was to investigate some physical properties of teeth extracted from patients with DI-II in comparison with normal teeth. The material of the study was six teeth: three lower molars, with clinical signs of DI-II, which were extracted due to complications of pulp inflammation and three other lower molars which were extracted for orthodontic reasons – well formed, without any signs of pathology. The surfaces of DI-II and normal teeth were tested on the CSM Instruments Scratch Tester machine (producer CSEM Switzerland) by Oliver & Pharr method. The indenter used was Vicker’s VG-73 diamond indenter. Additionally, the Scanning Electron Microscopy (SEM) analysis of the surface of the teeth with DI-II was made. Vickers hardness of the teeth with dental pathology (DI-II) was seven times smaller, and Young’s modulus six times smaller than those of healthy teeth. The parameters of hardness and elasticity of enamel of teeth with clinical diagnosis of DI-II were very much smaller than in normal teeth and because of that can be responsible for attrition.

Superoxide dismutase activity and expression in human venous and arterial bypass graft vessels

41%

Guzik T. J. , Olszanecki R. , Sadowski J. , Kapelak B. , Rudzinski P. , Jopek A. , Kawczynska A. , Ryszawa N. , Loster J. , Jawien J. , Czesnikiewicz-Guzik M. , Channon K. M. , Korbut R.

Journal of Physiology and Pharmacology

2005

tom 56

nr 2

Venous bypass grafts are more prone to accelerated atherosclerosis than arterial grafts, which is partly related to increased oxidative stress and diminished nitric oxide bioavailability. In veins superoxide production is dependent primarily on nox2 NAD(P)H oxidase expression, while in arteries nox4 appears to play an important role. This may in part explain differences in susceptibility to graft failure. Net levels of oxidative stress are however determined in parallel by the production as well as by degradation of free radicals (eg. by superoxide dimutases, catalases, thioredoxins etc). The differences in superoxide dismutase (SOD) expression and activity in human bypass conduit vessels remain unclear. Accordingly, we aimed to compare SOD activity and protein levels as well as its functional effects on superoxide production in segments of human internal mammary arteries (IMA) and saphenous veins (HSV) from patients undergoing bypass graft surgery (n=24). SOD activity was assessed by inhibition of pyrogallol autoxidation, Cu-Zn SOD and Mn SOD protein levels were studied by immunoblotting. Basal superoxide release was detected by lucigenin (5µM) enhanced chemiluminescence. Total SOD activity did not differ significantly between HSV and IMA. Similarly, no difference was observed in SOD activity in the presence of KCN (Mn-SOD). Human bypass conduit vessels show amounts of Cu-Zn SOD or Mn-SOD protein levels. In both HSV and IMA segments superoxide production was more than doubled in the presence of SOD inhibitor - DETC. Conclusions: These studies suggest that the differences in oxidative stress between human arteries and veins are unlikely to be caused by SOD activity. However SOD plays and important role in amelioration of oxidative stress in both types of vessels.