Informacja

Drogi użytkowniku, aplikacja do prawidłowego działania wymaga obsługi JavaScript. Proszę włącz obsługę JavaScript w Twojej przeglądarce.

Wyszukujesz frazę "Szumiel, I." wg kryterium: Autor


Tytuł:
The importance of the nuclear and cytoplasmic signalling in the cellular response to ionizing radiation
Autorzy:
Szumiel, I.
Powiązania:
https://bibliotekanauki.pl/articles/146716.pdf
Data publikacji:
2000
Wydawca:
Instytut Chemii i Techniki Jądrowej
Tematy:
cellular signalling pathways
ionizing radiation
radiation sensitivity
Opis:
DNA is the universal primary target for ionizing radiation; however, the cellular response is highly diversified not only by differential DNA repair ability. The monitoring system for the ionizing radiation-inflicted DNA damage consists of 3 apparently independently acting enzymes which are activated by DNA breaks: two protein kinases, Atm (ataxia telangiectasia mutated) and DNA-PK (DNA-dependent protein kinase) and a poly(ADP-ribose) polymerase, PARP-1. These 3 enzymes are the source of alarm signals, which affect to various extents DNA repair, progression through the cell cycle and eventually the pathway to cell death. Their functions probably are partly over-lapping. On the side of DNA repair their role consists in recruiting and/or activating the repair enzymes, as well as preventing illegitimate recombination of the damaged sites. A large part of the nuclear signalling pathway, including the integrating role of Tp53 has been revealed. Two main signalling pathways start at the plasma membrane: the MAPK/ERK (mitogen and extracellular signal regulated protein kinase family) "survival pathway" and the SAPK/JNK (stress-activated protein kinase/c-Jun N-terminal kinase) "cell death pathway". The balance between them is likely to determine the cell’s fate. When DNA break rejoining is impaired, the cell is unconditionally radiation sensitive. The fate of a repair-competent cell is determined by the time factor: the cell cycle arrest should be long enough to ensure the completion of repair. Incomplete repair or misrepair may be tolerated, when generation of the death signal is prevented. So, the character and timing of the signals are, to a large part, responsible for the cellular intrinsic radiation sensitivity and depend on the characteristics of the cellular signalling web.
Źródło:
Nukleonika; 2000, 45, 4; 215-220
0029-5922
1508-5791
Pojawia się w:
Nukleonika
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
The bystander effect: is reactive oxygen species the driver?
Autorzy:
Szumiel, I.
Powiązania:
https://bibliotekanauki.pl/articles/148463.pdf
Data publikacji:
2003
Wydawca:
Instytut Chemii i Techniki Jądrowej
Tematy:
bystander effect
reactive oxygen species
ionising radiation
DNA repair
signalling pathways
Opis:
The paper reviews selected examples of the bystander effect, such as clonogenic survival decrease, chromosomal aberrations and mutations. The similarities and differences between the biological effects in directly targeted and bystander cells are briefly discussed. Also reviewed are the experimental data which support the role of reactive oxygen species (ROS), especially *O2-, as mediators of the bystander effect. Endogenously generated ROS, due to activation of NAD(P)H oxidases, play a key role in the induction of DNA damage in bystander cells. All the observed effects in bystander cells, such as alterations in gene expression patterns, chromosomal aberrations, sister chromatid exchanges, mutations, genome instability, and neoplastic transformation are the consequence of DNA damage.
Źródło:
Nukleonika; 2003, 48, 3; 113-120
0029-5922
1508-5791
Pojawia się w:
Nukleonika
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Wolno rosnące klony komórek białaczki L5178Y i zagadka wewnątrzklonalnej odnowy popromiennej
Autorzy:
Szumiel, I.
Powiązania:
https://bibliotekanauki.pl/articles/214333.pdf
Data publikacji:
2014
Wydawca:
Instytut Chemii i Techniki Jądrowej
Tematy:
komórki białaczki
wolno rosnące klony
odnowa popromienna
odnowa wewnątrzklonalna
Źródło:
Postępy Techniki Jądrowej; 2014, 1; 37-40
0551-6846
Pojawia się w:
Postępy Techniki Jądrowej
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Concerted control of DNA double strand break repair and cell cycle progression in X-irradiated mammalian cells
Autorzy:
Sochanowicz, B.
Szumiel, I.
Powiązania:
https://bibliotekanauki.pl/articles/148697.pdf
Data publikacji:
2005
Wydawca:
Instytut Chemii i Techniki Jądrowej
Tematy:
ATM kinase
DNA double strand break repair
RAD50
cell cycle arrest
repair foci
BRCT domain
Opis:
Upon examination of cell cycle regulation in a damaged cell, relations were discovered of the cell cycle control mechanisms with a complicated web of signalling pathways, eventually called the genome surveillance system. After infliction of DNA double strand breaks (DSB), the signalling is initiated by sensor proteins and transducer protein kinase ATM. This kinase phosphorylates downstream effector proteins, such as checkpoint kinases CHK1 and CHK2, which initiate the pathways leading to cell cycle arrest. In contrast with the older model of linear transmission of signals in a certain sequence, it is now accepted that the damage signalling system is branched and contains feedback loops. DSB's presence is signalled by sensor proteins (MRE11-RAD50-nibrin complex, MRN) to ATM and the signal is amplified through adaptor proteins, MDC1/NFBD1 or 53BP1 (Tp53 binding protein). MRN contains a forkheadassociated (FHA) domain and BRCA1 carboxyl-terminal (BRCT) domain. The combination of the FHA/BRCT domains has a crucial role for the binding of nibrin to the H2AX histone, assembling the components of repair foci. These domains also are important for interaction of other proteins localised in the foci. For example, MDC1/NFBD1 contains a FHA domain and two BRCT domains which are involved in protein interactions. The signal generated at DSBs is amplified and transduced to recruit components of DNA repair systems. In a concerted way with the sequential recruitment of components of repair foci, activation of transcription of genes takes place, that is necessary for blocking progression through the cell cycle, for DNA repair or apoptosis.
Źródło:
Nukleonika; 2005, 50, 4; 129-138
0029-5922
1508-5791
Pojawia się w:
Nukleonika
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Charge transfer in DNA and repair of oxidative damage
Autorzy:
Męczyńska, S.
Szumiel, I.
Powiązania:
https://bibliotekanauki.pl/articles/146454.pdf
Data publikacji:
2009
Wydawca:
Instytut Chemii i Techniki Jądrowej
Tematy:
charge transfer in DNA
DNA repair
oxidative base damage
base damage excision
4Fe-4S cluster
MutY glycosylase
photolyase
Opis:
The possibility of a biological role of an unusual function of DNA sequences is discussed, namely, signaling by charge transfer within chromatin. Although a general conclusion on its biological significance is premature, the idea of charge transfer accompanying repair of some types of oxidative DNA damage is based on sound experimental data. Both physical and chemical experiments reviewed here provided results indicating that DNA duplex under certain conditions (among them – hydration) – can behave as narrow band gap semiconductor. With the use of model molecules it was shown that charge transfer most probably occurs by hopping between guanine residues and tunneling through thymine-adenine (TA) base pairs. Charge transfer is nucleotide sequence and distance dependent. Furthermore, the pi-stacked base pairs must be perfectly matched to mediate charge transfer and in a damaged double helix this condition is not fulfilled. Hence, the possibility that charge transfer takes place in oxidatively damaged DNA after UV or X-irradiation and it becomes interrupted by mismatched base pairs, thus signaling the mismatch or strand break to the repair machinery. Function of base damage repair enzymes which contain [4Fe-4S] clusters is discussed in this context.
Źródło:
Nukleonika; 2009, 54, 1; 11-16
0029-5922
1508-5791
Pojawia się w:
Nukleonika
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Histone H2AX in DNA repair
Autorzy:
Lewandowska, H.
Szumiel, I.
Powiązania:
https://bibliotekanauki.pl/articles/147030.pdf
Data publikacji:
2002
Wydawca:
Instytut Chemii i Techniki Jądrowej
Tematy:
DNA double strand breaks
DNA repair
histone gamma-H2AX
ionising radiation
Opis:
The paper reviews the recent reports on the role of the phosphorylated histone H2AX (gamma-H2AX). The modification of this histone is an important part of the cellular response to the induction of DNA double strand breaks (DSB) by ionising radiation and other DSB-generating factors. In irradiated cell the modification is carried out mainly by ATM (ataxia- -telangiectasia mutated) kinase, the enzyme that starts the alarm signalling upon induction of DSB. gamma-H2AX molecules are formed within 1 3 min after irradiation and form foci at the sites of DSB. This seems to be necessary for the recruitment of repair factors that are later present in foci of damaged nuclei. Modification of a constant percentage of H2AX molecules per DSB takes place, corresponding to chromatin domains of megabase pairs of DNA.
Źródło:
Nukleonika; 2002, 47, 4; 127-131
0029-5922
1508-5791
Pojawia się w:
Nukleonika
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Relationships between EGFR-initiated signalling, DNA double-strand break rejoining and survival in X-irradiated human glioma M059 cells
Autorzy:
Grądzka, I.
Buraczewska, I.
Szumiel, I.
Powiązania:
https://bibliotekanauki.pl/articles/146764.pdf
Data publikacji:
2008
Wydawca:
Instytut Chemii i Techniki Jądrowej
Tematy:
human glioma M059 K and J cells
DNA-dependent protein kinase (DNA-PK)
radiosensitivity
DNA double-strand break (DSB) rejoining
epidermal-growth-factor-receptor (EGFR)
signalling inhibitors: tyrphostin
Opis:
The aim of this study was to investigate the effect of signalling inhibition on survival and double-strand break (DSB) rejoining in cells differing in sensitivity to inhibitors, X-rays and bleomycin. Human glioma M059 cells, K (relatively radioresistant) and J (radiosensitive, defective in DSB rejoining for lack of DNA-dependent protein kinase catalytic subunit, DNA-PKcs) were pretreated with signalling inhibitors: tyrphostin AG 1478, specific for epidermalgrowth- factor-receptor (EGFR) kinase or PD 98059, specific for kinase MEK 1/2 (mitogen-activated, extracellular signal-activated kinases 1 and 2). Subsequently, the cells were X-irradiated or treated with bleomycin. Cell survival was determined by clonogenicity test. DSB rejoining was monitored with the use of pulsed-field gel electrophoresis (PFGE). We found that in X-irradiated M059 K cells EGFR kinase activity was necessary for efficient DSB rejoining and the kinase inhibitor, tyrphostin AG 1478, acted as radiosensitizer in the dose range that reduced cell survival to 0.7-0.8. Inhibition of EGFR kinase, however, did not decrease survival or affect DSB rejoining in DNA-PKcs-deficient M059 J cells. These results indicated that the decrease in cell survival was due to a disturbed DSB rejoining by the DNA-PK dependent system. In contrast, inhibition of MEK 1/2 kinase on EGFR downstream signalling pathway by PD 98059 did not affect DSB rejoining in either cell line and exerted a radioprotective effect.
Źródło:
Nukleonika; 2008, 53, 2; 37-44
0029-5922
1508-5791
Pojawia się w:
Nukleonika
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Silver nanoparticles – allies or adversaries?
Autorzy:
Bartlomiejczyk, T.
Lankoff, A.
Kruszewski, M.
Szumiel, I.
Powiązania:
https://bibliotekanauki.pl/articles/51400.pdf
Data publikacji:
2013
Wydawca:
Instytut Medycyny Wsi
Opis:
Nanoparticles (NP) are structures with at least one dimension of less than 100 nanometers (nm) and unique properties. Silver nanoparticles (AgNP), due to their bactericidal action, have found practical applications in medicine, cosmetics, textiles, electronics, and other fields. Nevertheless, their less advantageous properties which make AgNP potentially harmful to public health or the environment should also be taken into consideration. These nanoparticles are cyto- and genotoxic and accumulate in the environment, where their antibacterial properties may be disadvantageous for agriculture and waste management. The presented study reviews data concerning the biological effects of AgNP in mammalian cells in vitro: cellular uptake and excretion, localization in cellular compartments, cytotoxicity and genotoxicity. The mechanism of nanoparticle action consists on induction of the oxidative stress resulting in a further ROS generation, DNA damage and activation of signaling leading to various, cell type-specific pathways to inflammation, apoptotic or necrotic death. In order to assure a safe application of AgNP, further detailed studies are needed on the mechanisms of the action of AgNP on mammalian cells at the molecular level.
Źródło:
Annals of Agricultural and Environmental Medicine; 2013, 20, 1
1232-1966
Pojawia się w:
Annals of Agricultural and Environmental Medicine
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
DNA double-strand break rejoining in radioadapted human lymphocytes: evaluation by neutral comet assay and pulse-field gel electrophoresis
Autorzy:
Wojewódzka, M.
Buraczewska, I.
Szumiel, I.
Grądzka, I.
Powiązania:
https://bibliotekanauki.pl/articles/146153.pdf
Data publikacji:
2006
Wydawca:
Instytut Chemii i Techniki Jądrowej
Tematy:
human lymphocytes
radioadaptation
DNA double-strand break rejoining
neutral comet assay
pulsefield gel electrophoresis
Opis:
Adaptive response (AR), an enhanced resistance to a high dose of ionising radiation acquired after pretreatment with a very low dose, was estimated in normal human lymphocytes. The question posed was whether the extent of radioadaptation, assessed by micronucleus test, would be related to the rate of DNA double-strand break (DSB) rejoining. Phytohemagglutinin-stimulated G1-lymphocytes from 5 healthy male volunteers were pre-treated (or not) with an adaptive (5 cGy) dose of X-rays, followed by a higher (5 or 10 Gy) challenge dose after 20-22 h. DSB rejoining after the challenge dose was monitored with the use of two methods: neutral comet assay, modified to reduce the contribution of single-strand breaks (SSBs) and thermolabile sites, and pulse-field gel electrophoresis (PFGE), specific for DSBs. At the level of micronuclei, an AR was observed in lymphocytes of 3 of 5 donors. Up to 60 min, comet assay showed no statistically significant differences in DNA break rejoining between adapted and non-adapted lymphocytes, independently of AR appearance. PFGE gave similar results, although in three donors it revealed secondary increases in DSBs levels at 30 min and/or 60 min post-irradiation in the adapted vs. the non-adapted samples. Failure to demonstrate changes in DSBs rejoining rate in the adapted lymphocytes could be due to diversity of AR intensity/timing at the level of DNA repair in not fully homogenous cell populations. Also, “rare” DNA cuts characteristic of early apoptosis/necrosis could overlap the process of DNA break rejoining.
Źródło:
Nukleonika; 2006, 51, 4; 185-191
0029-5922
1508-5791
Pojawia się w:
Nukleonika
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Comparison of the effects of bleomycin and ionizing radiation in two sublines of murine lymphoma L5178Y
Autorzy:
Kruszewski, M.
Zaim, J.
Grądzka, I.
Szumiel, I.
Powiązania:
https://bibliotekanauki.pl/articles/147561.pdf
Data publikacji:
2001
Wydawca:
Instytut Chemii i Techniki Jądrowej
Tematy:
bleomycin
comet assay
DNA damage
gamma radiation
single cell gel electrophoresis
Opis:
We compared the effects of bleomycin (BLM) and ionizing radiation on two sublines of murine lymphoma L5178Y (LY): LY-R, radiation resistant and LY-S, radiation sensitive. This radiosensitivity difference is related to the ability to rejoin DNA double strand breaks. LY-S cells were about two times more sensitive to BLM than LY-R, similarly as in the case of sensitivity to X rays. Since there was no difference in the P-glycoprotein-related drug transport system between the sublines, it could be expected that the enhanced sensitivity of LY-S cells to BLM was caused by the DNA repair defect. Growth disturbances in BLM treated cell populations were proportional to the lethal effect and their duration was observed until elimination of dead cells (3-6 days after 50 ěM BLM, 1 h at 37oC). There was no slow growth phase accompanied by normal viability, as previously described for X-irradiated LY-S cells. Initial DNA damage, estimated with the single cell gel electrophoresis method was linearly related to BLM dose in LY-S cells; in LY-R cells - in the low dose range (up to 10 ěM) - there was more damage than in LY-S cells, however, at higher doses the dose - effect curves became identical. The doseeffect relationship for ă rays was linear and identical in both cell sublines. DNA damage distribution in BLM treated cells was much less uniform as compared to that in irradiated cells and indicated the presence of cells with severely damaged DNA, a feature typical for BLM action in vitro.
Źródło:
Nukleonika; 2001, 46, 3; 81-86
0029-5922
1508-5791
Pojawia się w:
Nukleonika
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
The rapid interphase chromosome assay (RICA) implementation : comparison with other PCC methods
Autorzy:
Sommer, S.
Buraczewska, I.
Sikorska, K.
Bartłomiejczyk, T.
Szumiel, I.
Kruszewski, M.
Powiązania:
https://bibliotekanauki.pl/articles/147263.pdf
Data publikacji:
2015
Wydawca:
Instytut Chemii i Techniki Jądrowej
Tematy:
biodosimetry
ionizing radiation
premature chromosome condensation (PCC)
human lymphocytes
Opis:
A report is presented on the advantages of the rapid interphase chromosome assay (RICA) and the difficulties that may be met while implementing this method for application in biological dosimetry. The RICA test can be applied on unstimulated human lymphocytes; this is an advantage in comparison with the dicentric chromosomes or micronucleus tests. In the former two tests, stimulated lymphocytes are examined and hence, 48 h more are needed to obtain cells traversing the cell cycle. Due to the use of unstimulated nondividing cells, higher numbers of cells are available for RICA analysis than for dicentric chromosomes or micronuclei tests. Moreover, the method can be applied after exposure to ionizing radiation doses in excess of 5 Gy. Such doses cause a signifi cant cell cycle delay or result in the loss of G2 phase and mitotic cells because of apoptosis. Therefore, the traditional biodosimetry based on the evaluation of the incidence of damage to chromosomes is very difficult to carry out. This is due to the lack of an adequate number of mitotic cells for analysis. RICA is free of this disadvantage. An automatic microscope can be used to retrieve cell images; automatic image analysis can also be used.
Źródło:
Nukleonika; 2015, 60, No. 4, part 2; 933-941
0029-5922
1508-5791
Pojawia się w:
Nukleonika
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Effects of an antimutagen of 1,4-dihydropyridine series on cell survival and DNA damage in L5178Y murine sublines
Autorzy:
Dalivelya, O.
Savina, N.
Kuzhir, T.
Buraczewska, I.
Wojewódzka, M.
Szumiel, I.
Powiązania:
https://bibliotekanauki.pl/articles/146264.pdf
Data publikacji:
2006
Wydawca:
Instytut Chemii i Techniki Jądrowej
Tematy:
1,4-dihydropyridine
DNA repair
neutral comet assay
L5178Y cells
cytotoxicity
radioprotective effect
Opis:
In a series of studies it was shown that 1,4-dihydropyridine derivatives (1,4-DHP) show antimutagenic and anticlastogenic properties and accelerate repair of oxidant and ionising radiation generated DNA damage. Here, effects of one of 1,4-DHP compounds (sodium 3,5-bis-ethoxycarbonyl-2,6-dimethyl-1,4-dihydropyridine-4-carboxylate denoted as DHP) in X-irradiated L5178Y cells (murine lymphoma sublines, LY-R and LY-S) are reported. DHP treatment 1 h before, during and after X-irradiation gave a radioprotective effect in double strand break (DSB) repair competent LY-R cells: there was an increase in post-irradiation proliferation and cell viability as well as a slight acceleration of break rejoining as measured by the neutral comet assay. In the radiosensitive LY-S cells with impaired non-homologous end-joining system, the radioprotective effect was seen as enhanced growth and viability. There was, however, no effect on the DSB repair rate. Notably, there was no dependence of the biological effects on DHP concentration in the range of concentrations studied (1 nM - 100 mM), suggesting an all-or-none effect, as in cellular signaling induction observed in radioadaptation or bystander effect. We assume that DHP acts by decreasing fixation of radiation inflicted DNA damage, among others, by increasing the rate of DNA repair and enhancing the efficiency of checkpoint control. Direct confirmation of this assumption is necessary.
Źródło:
Nukleonika; 2006, 51, 3; 141-146
0029-5922
1508-5791
Pojawia się w:
Nukleonika
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Treatment with silver nanoparticles delays repair of X-ray induced DNA damage in HepG2 cells
Autorzy:
Wojewódzka, M.
Lankoff, A.
Dusińska, M.
Brunborg, G.
Czerwińska, J.
Iwaneńko, T.
Stępkowski, T.
Szumiel, I.
Kruszewski, M.
Powiązania:
https://bibliotekanauki.pl/articles/147061.pdf
Data publikacji:
2011
Wydawca:
Instytut Chemii i Techniki Jądrowej
Tematy:
silver nanoparticles (Ag NP)
titanium dioxide nanoparticles (TiO2 NP)
DNA break rejoining
alkaline comet assay
ionizing radiation
combined treatment with nanoparticles + X-rays
Opis:
Nanoparticles (NPs) defined as particles having at least one dimension below 100 nm have been applied in the last decade in industry and medicine. Recently, there is an increased concern about the biohazard aspect of the presence of NP in consumer goods and in the environment. Silver NP (Ag NP) cause oxidative stress in mammalian cells in result of generation of reactive oxygen species (ROS). This results in genotoxicity and mutagenicity, disturbed mitochondrial respiration, slowed proliferation and cell death. Using the alkaline comet assay, we examined the effect of combined treatment with Ag NP 20 nm or 200 nm and X-rays (2 Gy) in HepG2 cells. In addition, combined treatment with X-rays and titanium dioxide NP (TiO2 NP) 21 nm was also studied. No effect of NP pre-treatment on X-ray induced initial deoxyribonucleic acid (DNA) damage levels was observed for all three NP. In contrast, Ag NP treatment preceding exposure to X-rays caused a marked decrease in the rate of single strand break rejoining. The effect was particularly strong for Ag NP 20 nm. TiO2 NP pre-treatment had no effect on DNA repair.
Źródło:
Nukleonika; 2011, 56, 1; 29-33
0029-5922
1508-5791
Pojawia się w:
Nukleonika
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Effect of polylactide modification with β-TCP and lecithin on the properties of the material as a substrate for osteoblasts
Autorzy:
Olkowski, R.
Stefanek, A.
Kaszczewski, P.
Ciach, T.
Lewandowska-Szumieł, M.
Kalaszczyńska, I.
Powiązania:
https://bibliotekanauki.pl/articles/285423.pdf
Data publikacji:
2015
Wydawca:
Akademia Górniczo-Hutnicza im. Stanisława Staszica w Krakowie. Polskie Towarzystwo Biominerałów
Tematy:
polylactide
lecithin
osteoblasts
scaffold
bone tissue engineering
Opis:
Polylactide (PLLA) containing β-TCP is biodegradable composite and an attractive biomaterial for bone tissue engineering, however, hydrophobicity of PLLA based composites is major limitation for their use as scaffolds for cell culture. In our study lecithin was used to improve hydrophilicity and cytocompatibility of PLLA/ β-TCP composite. Thin films of PLLA, PLLA/ β-TCP and PLLA/β-TCP/lecithin were manufactured by solvent-casting technique. Comparative analysis of all types of films was performed. Addition of β-TCP did not change hydrophilicity of PLLA. The hydrophilicity of PLLA/β-TCP/lecithin increased in comparison to PLLA and PLLA/β-TCP. Degradation of PLLA/β-TCP composite surpassed the degradation of PLLA while addition of lecithin diminished the degradation of composite. The cytocompatibility of composites were studied in 7 day long in vitro assay. Human bone derived cells were seeded on all tested surfaces. Cell viability was estimated by Live/Dead fluorescent staining and Alamar Blue test. Surprisingly, although lecithin addition improved hydrophilicity of the PLLA-based composite, adhesion and proliferation of human bone derived cells were markedly hampered on PLLA/β-TCP/lecithin in comparison to PLLA and PLLA/β-TCP. Despite positive effect we found of lecithin addition on hydrophilicity and stability of PLLA-based composite, its effect on cell attachment and proliferation is negative. Hence, incorporation of lecithin did not improve properties of PLLA/β-TCP/lecithin composite intended for bone tissue regeneration.
Źródło:
Engineering of Biomaterials; 2015, 18, 131; 8-11
1429-7248
Pojawia się w:
Engineering of Biomaterials
Dostawca treści:
Biblioteka Nauki
Artykuł

Ta witryna wykorzystuje pliki cookies do przechowywania informacji na Twoim komputerze. Pliki cookies stosujemy w celu świadczenia usług na najwyższym poziomie, w tym w sposób dostosowany do indywidualnych potrzeb. Korzystanie z witryny bez zmiany ustawień dotyczących cookies oznacza, że będą one zamieszczane w Twoim komputerze. W każdym momencie możesz dokonać zmiany ustawień dotyczących cookies