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Wyszukujesz frazę ""resistance"" wg kryterium: Temat


Tytuł:
Influenza viruses resistant to neuraminidase inhibitors
Autorzy:
Nitsch-Osuch, Aneta
Brydak, Lidia
Powiązania:
https://bibliotekanauki.pl/articles/1039255.pdf
Data publikacji:
2014
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
influenza
resistance
neuraminidase inhibitors
Opis:
Neuraminidase inhibitors (NAIs) are antiviral drugs for treatment and prophylaxis of influenza. By blocking the activity of the enzyme neuraminidase, NAIs prevent new viral particles from being released. The increasing use of NAIs brings into focus the risk of drug resistance arising to the class. There are three levels of antiviral resistance according to the way that resistance can be detected or inferred: genotypic, phenotypic and clinical resistance. For many years seasonal influenza viruses resistance to NAIs was low (0.33%). Recently, there has been described an increasing number of resistant seasonal influenza strains to oseltamivir (2% in adults, 5-18% in children). In 2007 there were published data describing 14% resistant to oseltamivir strains of influenza A/H1N1/ in Europe. Approximately 0.5-1.0% of influenza A/H1N1/pdm09 isolates are currently resistant to oseltamivir. The established markers of the resistance to oseltamivir were found in 2.4% of human and 0.8% of avian isolates of influenza A/H5N1/. It has been not observed a cross resistance among oseltamivir and zanamivir. NAIs resistance in influenza viruses is relative and despite its presence patients with resistant viruses may still benefit from receiving these antivirals. The response to treatment with antivirals remains the most important proof of antiviral effectiveness. The rational use of NAIs is essential to preserve the best choice for treatment and prophylaxis of seasonal, avian and pandemic influenza.
Źródło:
Acta Biochimica Polonica; 2014, 61, 3; 505-508
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Comparison of antibiotic resistance and virulence between biofilm-producing and non-producing clinical isolates of Enterococcus faecium
Autorzy:
Sieńko, Anna
Wieczorek, Piotr
Majewski, Piotr
Ojdana, Dominika
Wieczorek, Anna
Olszańska, Dorota
Tryniszewska, Elżbieta
Powiązania:
https://bibliotekanauki.pl/articles/1038933.pdf
Data publikacji:
2015
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
Enterococcus
biofilm
virulence
resistance
Opis:
An increase in the antibiotic resistance among Enterococcus faecium strains has been observed worldwide. Moreover, this bacteria has the ability to produce several virulence factors and to form biofilm that plays an important role in human infections. This study was designed to compare the antibiotic resistance and the prevalence of genes encoding surface protein (esp), aggregation substance (as), surface adhesin (efaA), collagen adhesin (ace), gelatinase (gelE), and hialuronidase (hyl) between biofilm-producing and non-producing E. faecium strains. Therefore, ninety E. faecium clinical isolates were tested for biofilm-forming ability, and then were assigned to two groups: biofilm-positive (BIO+, n =70) and biofilm-negative (BIO-, n = 20). Comparison of these groups showed that BIO+ isolates were resistant to β-lactams, whereas 10% of BIO- strains were susceptible to ampicillin (statistically significant difference, p = 0.007) and 5% to imipenem. Linezolid and tigecycline were the only antibiotics active against all tested isolates. Analysis of the virulence factors revealed that ace, efaA, and gelE genes occurred more frequently in BIO- strains (ace in 50% BIO+ vs. 75% BIO-; efaA 44.3% vs. 85%; gelE 2.9% vs. 15%, respectively), while hyl gene appeared more frequently in BIO+ isolates (87.1% BIO+ vs. 65% BIO-). These differences were significant (p < 0.05). We concluded that BIO+ strains were more resistant to antibiotics than BIO- strains, but interestingly, BIO- isolates were characterized by possession of higher virulence capabilities.
Źródło:
Acta Biochimica Polonica; 2015, 62, 4; 859-866
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Cross-resistance to five glucocorticoids in childhood acute lymphoblastic and non-lymphoblastic leukemia samples tested by the MTT assay: Preliminary report.
Autorzy:
Styczyński, Jan
Wysocki, Mariusz
Dębski, Robert
Balwierz, Walentyna
Rokicka-Milewska, Roma
Matysiak, Michał
Balcerska, Anna
Kowalczyk, Jerzy
Wachowiak, Jacek
Sońta-Jakimczyk, Danuta
Chybicka, Alicja
Powiązania:
https://bibliotekanauki.pl/articles/1043813.pdf
Data publikacji:
2002
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
cross-resistance
ALL
sensitivity
acute leukemia
MTT assay
AML
glucocorticoid resistance
Opis:
In vitro antileukemic activity of five glucocorticoids and their cross-resistance pattern in childhood acute lymphoblastic and non-lymphoblastic leukemia were determined by means of the MTT assay in 25 leukemia cell samples of childhood acute leukemias. The equivalent antileukemic concentrations of the drugs tested were: 34 μM hydrocortisone (HC), 8 μM prednisolone (PRE), 1.5 μM methylprednisolone (MPR), 0.44 μM dexamethasone (DX) and 0.22 μM betamethasone (BET). In comparison with initial ALL cell samples, the relapsed ALL group was more resistant to PRE (38-fold, p = 0.044), DX (> 34-fold, p = 0.04), MPR (38-fold), BET (45-fold) and HC (33-fold). The AML cell samples were even more resistant to: PRE (>85-fold, p=0.001), DX (> 34-fold, p = 0.004), MPR (> 69-fold, p = 0.036), BET (> 69-fold, p = 0.038) and HC (54-fold, p = 0.059) when compared with ALL on initial diagnosis. A significant cross-resistance among all the glucocorticoids used was found. Only in some individual cases the cross-resistance was less pronounced.
Źródło:
Acta Biochimica Polonica; 2002, 49, 1; 93-98
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Plastoquinone: possible involvement in plant disease resistance.
Autorzy:
Maciejewska, Urszula
Polkowska-Kowalczyk, Lidia
Swiezewska, Ewa
Szkopinska, Anna
Powiązania:
https://bibliotekanauki.pl/articles/1043748.pdf
Data publikacji:
2002
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
plastoquinone
pathogen resistance
plants
Opis:
The plant Solanum nigrum treated with the pathogen Phytophthora infestans-derived elicitor responded by elevated reactive oxygen species (ROS) production, lipid peroxidation and lipoxygenase (EC 1.13.11.12) activity in comparison with control plants indicating that oxidative stress took place. We demonstrate that these events are accompanied by a significant increase in plastoquinone (PQ) level. It is postulated that PQ may be associated with mechanisms maintaining a tightly controlled balance between the accumulation of ROS and antioxidant activity that determines the full expression of effective defence.
Źródło:
Acta Biochimica Polonica; 2002, 49, 3; 775-780
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Immune response gene polymorphisms in tuberculosis
Autorzy:
Fol, Marek
Druszczynska, Magdalena
Wlodarczyk, Marcin
Ograczyk, Elzbieta
Rudnicka, Wieslawa
Powiązania:
https://bibliotekanauki.pl/articles/1038871.pdf
Data publikacji:
2015
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
tuberculosis
susceptibility/resistance genes
Opis:
Tuberculosis (TB), an infectious disease caused by Mycobacterium tuberculosis (M.tb), remains a leading public health problem in most parts of the world. Despite the discovery of the bacilli over 100 years ago, there are still many unanswered questions about the host resistance to TB. Although one third of the world's population is infected with virulent M.tb, no more than 5-10% develop active disease within their lifetime. A lot of studies suggest that host genetic factors determine the outcome of M.tb-host interactions, however, specific genes and polymorphisms that govern the development of TB are not completely understood. Strong evidence exists for genes encoding pattern recognition receptors (TLR, CD14), C-type lectins, cytokines/chemokines and their receptors (IFN-γ, TNF-α, IL-12, IL-10, MCP-1, MMP-1), major histocompatibility complex (MHC) molecules, vitamin D receptor (VDR), and proton-coupled divalent metal ion transporters (SLC11A1). Polymorphisms in these genes have a diverse influence on the susceptibility to or protection against TB among particular families, ethnicities and races. In this paper, we review recent discoveries in genetic studies and correlate these findings with their influence on TB susceptibility.
Źródło:
Acta Biochimica Polonica; 2015, 62, 4; 633-640
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Induction of the multixenobiotic/multidrug resistance system in various cell lines in response to perfluorinated carboxylic acids
Autorzy:
Rusiecka, Izabela
Składanowski, Andrzej
Powiązania:
https://bibliotekanauki.pl/articles/1040751.pdf
Data publikacji:
2008
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
multixenobiotic resistance
multidrug resistance
perfluorinated carboxylic acids
flow cytometry
ABCB1
ABCC1
Opis:
The multixenobiotic resistance (closely related to multidrug resistance) system controls transport across the plasma membrane as a defense against toxic molecules. Multixenobiotic resistance system consists of an efflux pump, ABCB1 (also named P-glycoprotein, P-gp), and/or a molecule of the ABCC family (also named multiple resistance associated protein, MRP). ABCB1 is able to increase efflux of many low-molecular foreign molecules. Measuring system induction may be used as a biomarker of cell/organism exposure to foreign substances. Various established cell lines were tested for constitutive and induced multixenobiotic resistance proteins by Western blotting immunodetection. The pumping function was indirectly assayed with Rhodamine B by visualization of cell fluorescence in the presence of verapamil. Changes in ABC proteins were measured by flow cytometry after exposition to various perfluorinated carboxylic acids. MCF7 and HeLa cells were found to contain the highest constitutive level of both ABCB1 and ABCC1. HEK293 exhibited much less ABCB1 and no activity of pumping out Rhodamine B. The pumping activity was found to be related to the amount of the cell-type specific 170 kDa ABCB1 protein. An 8-day exposure to 10-4 M perfluorononanoic acid resulted in about 2-2.5-fold increase of ABCB1 level. That was confirmed also for short times by flow cytometry of cells exposed to perfluorinated acids and its natural congeners. Both ABCB1- and ABCC1-related fluorescence increased along with the carbon chain in acids from C6 up to C9 and decreased for C10. Measuring of multixenobiotic resistance changes in vitro induced by chemicals may be a convenient test for screening for their potential toxicity.
Źródło:
Acta Biochimica Polonica; 2008, 55, 2; 329-337
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Selected mechanisms of molecular resistance of Candida albicans to azole drugs
Autorzy:
Gołąbek, Karolina
Strzelczyk, Joanna
Owczarek, Aleksander
Cuber, Piotr
Ślemp-Migiel, Anna
Wiczkowski, Andrzej
Powiązania:
https://bibliotekanauki.pl/articles/1039099.pdf
Data publikacji:
2015
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
Candida albicans
drug resistance
azoles
Opis:
A phenomenon of increasing resistance of Candida spp. to azoles has been observed for several years now. One of the mechanisms of lack of sensitivity to azoles is associated with CDR1, CDR2, MRD1 genes (their products are active transport pumps conditioning drug efflux from pathogen's cell), and ERG11 gene (encoding lanosterol 14α-demethylase). Test material was 120 strains of Candida albicans (60 resistant and 60 susceptible to azole drugs) obtained from clinical samples. The first stage of experiment assessed the expression of CDR1, CDR2, MDR1 and ERG11 genes by Q-PCR. The impact of ERG11 gene's mutations on the expression of this gene was analysed. The final stage of the experiment assessed the level of genome methylation of Candida albicans strains. An increase in the expression of CDR2, MDR1 and ERG11 was observed in azole-resistant strains of Candida albicans in comparison to strains sensitive to this class of drugs. Furthermore, 19 changes in the sequence of ERG11 were detected in tested strains. Four of the discovered mutations: T495A, A530C, G622A and A945C led to the following amino acid substitutions: D116E, K128T, V159I and E266D, respectively. It has also been found that statistically five mutations: T462C, G1309A, C216T, C1257T and A945C affected the expression of ERG11. The applied method of assessing the level of methylation of Candida albicans genome did not confirm its role in the development of resistance to azoles. The results indicate however, that resistance of Candida albicans strains to azole drugs is multifactorial.
Źródło:
Acta Biochimica Polonica; 2015, 62, 2; 247-251
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Induction of the multixenobiotic/multidrug resistance system in HeLa cells in response to imidazolium ionic liquids
Autorzy:
Rusiecka, Izabela
Składanowski, Andrzej
Powiązania:
https://bibliotekanauki.pl/articles/1039912.pdf
Data publikacji:
2011
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
multidrug resistance
multixenobiotic resistance
imidazolium ionic liquids
flow cytometry
ABCB1
ABCC1
Opis:
The multixenobiotic/multidrug resistance (MXR/MDR) system controls transport of foreign molecules across the plasma membrane as a preventive measure before toxicity becomes apparent. The system consists of an efflux pump, ABCB1, and/or a member of the ABCC family. Ionic liquids are broadly used solvents with several unique properties such as wide liquid range, negligible vapor pressure, good thermal and chemical stability and extraordinary dissolution properties for organic and inorganic compounds. Ionic liquids containing imidazolium ring are frequently used as solvents in drug synthesis. Constitutive and induced amounts of ABCB1 and ABCC1 proteins were estimated here by Western blotting and quantified by flow cytometry in HeLa cells exposed to three homologous 1-alkyl-3-methylimidazolium and one benzyl ring substituted salts. Aliphatic substituents in position 1 of the salts caused a weak toxicity but 1-benzyl ring was strongly toxic. An 8-day long treatment with 10-4 M 1-hexyl-3-methylimidazolium chloride resulted in an about 1.5-fold increase of ABCB1 level and over 2-fold increase of ABCC1 level. The amounts of both investigated ABC-proteins were linearly dependent on the length of the imidazolium ring side chain. Such distinctive changes of the amount of MXR/MDR proteins measured in cultured cells may be a useful marker when screening for potential toxicity of various chemicals.
Źródło:
Acta Biochimica Polonica; 2011, 58, 2; 187-192
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
In vitro activity of oxazaphosphorines in childhood acute leukemia: Preliminary report.
Autorzy:
Styczyński, Jan
Wysocki, Mariusz
Dębski, Robert
Balwierz, Walentyna
Rokicka-Milewska, Roma
Matysiak, Michał
Balcerska, Anna
Kowalczyk, Jerzy
Wachowiak, Jacek
Sońta-Jakimczyk, Danuta
Chybicka, Alicja
Powiązania:
https://bibliotekanauki.pl/articles/1043830.pdf
Data publikacji:
2002
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
ALL
leukemia
sensitivity
glufosfamide
resistance
Opis:
Glufosfamide (β-D-glucosyl-ifosfamide mustard) is a new agent for cancer chemotherapy. Its pharmacology is similar to commonly used oxazaphosphorines, but it does not require activation by hepatic cytochrome P-450 and preclinically demonstrates lower nephrotoxicity and myelosuppression than ifosfamide. The aim of the study was a comparison of the drug resistance profiles of glufosfamide and other oxazaphosphorines in childhood acute leukemias. Leukemic cells, taken from children with ALL on diagnosis (n = 41), ALL on relapse (n = 12) and AML on diagnosis (n= 13) were analyzed by means of the MTT assay. The following drugs were tested: glufosfamide (GLU), 4-HOO-ifosfamide (IFO), 4-HOO-cyclophosphamide (CYC) and mafosfamide cyclohexylamine salt (MAF). In the group of initial ALL samples median cytotoxicity values for GLU, IFO, CYC and MAF were 15.5, 33.8, 15.7 and 7.8 μM, respectively. In comparison with initial ALL samples, the relative resistance for GLU and IFO in relapsed ALL samples was 1.9 (p = 0.049) and 1.3 (ns), and in initial AML samples 31 (p < 0.001) and 5 (p = 0.001), respectively. All oxazaphosphorines presented highly significant cross-resistance. Glufosfamide presented high activity against lymphoblasts both on diagnosis and on relapse.
Źródło:
Acta Biochimica Polonica; 2002, 49, 1; 221-225
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Multidrug resistance-associated protein - reduction of expression in human leukaemia cells by antisense phosphorothioate olignucleotides.
Autorzy:
Niewiarowski, Wojciech
Gendaszewska, Edyta
Rębowski, Grzegorz
Wójcik, Marzena
>Mikołajczyk, Barbara
Soszyński, Mirosław
Bartosz, Grzegorz
Powiązania:
https://bibliotekanauki.pl/articles/1044273.pdf
Data publikacji:
2000
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
antisense oligonucleotides
MRP
multidrug resistance
Opis:
Multidrug resistance-associated protein (MRP1) causes cellular drug resistance in several cancer cell lines. In this paper we show that antisense oligonucleotides decrease MRP1 expression in human leukaemia cells. We investigated biological activity of a series of 12 linear phosphorothioate oligonucleotides, complementary to several regions of MRP1 mRNA. The oligonucleotides were administered to leukaemia HL60/ADR cells overexpressing MRP1 protein. Then, the level of MRP1 mRNA was determined by means of semiquantitative RT-PCR and the protein level by reaction with specific monoclonal antibodies. Some of the investigated antisense oligonucleotides decrease the expression level of the MRP1 protein by 46% and its mRNA level by 76%.
Źródło:
Acta Biochimica Polonica; 2000, 47, 4; 1183-1188
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Myocardial remodeling in rats with metabolic syndrome: role of Rho-kinase mediated insulin resistance
Autorzy:
Li, Chuan-Bao
Li, Xiao-Xing
Chen, Yu-Guo
Gao, Hai-Qing
Bao, Cheng-Mei
Liu, Xiang-Qun
Bu, Pei-Li
Zhang, Juan
Zhang, Yun
Ji, Xiao-Ping
Powiązania:
https://bibliotekanauki.pl/articles/1039743.pdf
Data publikacji:
2012
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
Rat
Metabolism
Myocardium
Phosphorylation
Insulin resistance
Opis:
Insulin resistance (IR) plays a critical role in metabolic syndrome (MS). Previous studies have demonstrated that activated ROCK is increased in MS patients. However, the effect of Rho-kinase (ROCK) on IR has not been definitely determined. Thus, the aims of the present study were to determine whether ROCK activation induces IR or affects myocardial structure and function, as well as the possible mechanisms underlying this process. Wistar rats fed high fat, high glucose and high salt diet sewed as model of MS and we used transmission electron microscopy, echocardiogram technology, and terminal deoxynucleotidyl transferase-mediated DNA nick-end labeling staining to identify any myocardial damage. The protein levels of MYPT-1 (characteristic of ROCK activation), IRS-1 and AKT were analyzed by immunohistochemistry and Western blotting. In hearts from MS rats, we found increased protein levels of phospho-MYPT-1 and phospho-IRS-1 (Ser307) and decreased phospho-AKT compared to levels in normal rats. In conclusion, the results suggest that ROCK-mediated IR is involved in the development of myocardial impairments in MS rats and that this effect is mediated probably via the IRS-1/PI3-kinase/AKT pathway.
Źródło:
Acta Biochimica Polonica; 2012, 59, 2; 249-254
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Strategies for overcoming ABC-transporters-mediated multidrug resistance (MDR) of tumor cells
Autorzy:
Borowski, Edward
Bontemps-Gracz, Maria
Piwkowska, Agnieszka
Powiązania:
https://bibliotekanauki.pl/articles/1041364.pdf
Data publikacji:
2005
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
antitumor cytostatics
antimetabolites
multidrug resistance
modulators
Opis:
The development of multidrug resistance (MDR) of tumors is a major cause of failure in antitumor chemotherapy. This type of crossresistance is due to the expression of ABC transporter glycoproteins actively effluxing the drug from the cells against the concentration gradient at the expense of metabolic energy, thus preventing the accumulation in cells of therapeutic concentration of active agents. In this review strategies for overcoming this adverse phenomenon are discussed. They comprise the control of expression of MDR glycoprotein transporters and control of the functioning of the expressed transporter proteins. The latter approach is discussed in more detail, comprising the following general strategies: (i) development of compounds that are not substrates of efflux pump(s), (ii) use of agents that inactivate (inhibit) MDR proteins, (iii) design of cytostatics characterized by fast cellular uptake, surpassing their mediated efflux, (iv) use of compounds competing with the drug for the MDR protein-mediated efflux. Positive and negative aspects of these strategies are analysed, with special attention put on strategy based on the use of MDR modulators in combination therapy, allowing the restoration of cytotoxic activity of clinical cytostatics towards resistant tumor cells.
Źródło:
Acta Biochimica Polonica; 2005, 52, 3; 609-627
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Molecular basis of mechanisms of steroid resistance in children with nephrotic syndrome
Autorzy:
Świerczewska, Monika
Ostalska-Nowicka, Danuta
Kempisty, Bartosz
Nowicki, Michał
Zabel, Maciej
Powiązania:
https://bibliotekanauki.pl/articles/1039528.pdf
Data publikacji:
2013
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
nephrotic syndrome
glucocorticoid receptor
steroid resistance
polymorphisms
Opis:
Steroid therapy, due to a wide range of anti-inflammatory properties of steroids, is a basic field of treatment in many human diseases including the nephrotic syndrome in children. However, not all patients respond positively to therapy which divides them into steroid sensitive (SS) and steroid resistance (SR) individuals. Many potential factors associated with steroid resistance have been identified so far. It seems that genetic factors associated with glucocorticoid receptor α (GRα), the structure of heterocomplex of GR as well as glycoprotein P or cytochrome P450 may play a role in the induction of glucocorticoid resistance. Here we described several of the molecular mechanisms, which can regulate glucocorticoid sensitivity and resistance. Moreover, we presented genetic defects, which can lead to various effects of treatment and, in a longer perspective, enable clinicians to individualize therapies.
Źródło:
Acta Biochimica Polonica; 2013, 60, 3; 339-344
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Inhibitors of N-glycosylation as a potential tool for analysis of the mechanism of action and cellular localisation of glycoprotein P
Autorzy:
Wojtowicz, Karolina
Szaflarski, Witold
Januchowski, Radosław
Zawierucha, Piotr
Nowicki, Michał
Zabel, Maciej
Powiązania:
https://bibliotekanauki.pl/articles/1039626.pdf
Data publikacji:
2012
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
N-glycosylation
glycoprotein P
multidrug resistance
inhibitors
Opis:
Multidrug resistance has for many years attracted attention of numerous investigators. Attempts have also been made to increase efficiency of anti-neoplastic therapy. For this reason, most of efforts have been devoted to analysing proteins engaged in the mechanism of multidrug resistance such as the N-glycosylated membrane protein glycoprotein P. Interestingly, glycosylation probably plays a significant role in the intracellular location and activity of modified proteins. Inhibitors of glycosylation have been demonstrated to alter the activity of glycoprotein P in various ways, depending on the cell line examined. These inhibitors markedly reduce multidrug resistance of cancer cells, thus promoting success of anti-neoplastic therapy. Here, we review the basic knowledge on N-glycosylation inhibitors, their effect on glycoprotein P and their therapeutic potential.
Źródło:
Acta Biochimica Polonica; 2012, 59, 4; 445-450
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Raised plasma insulin level and homeostasis model assessment (HOMA) score in cerebral malaria: evidence for insulin resistance and marker of virulence
Autorzy:
Eltahir, Elrashid
ElGhazali, Gehad
A-Elgadir, Thoraya
A-Elbasit, Ishraga
Elbashir, Mustafa
Giha, Hayder
Powiązania:
https://bibliotekanauki.pl/articles/1040314.pdf
Data publikacji:
2010
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
insulin resistance
virulence
hyperglycaemia
HOMA
cerebral malaria
Opis:
Objective: To study the glycaemic profile of patients with severe malaria (SM). Methods: For this purpose, 110 SM patients were recruited. Pre-treatment random blood glucose and plasma insulin were measured in a subset of donors. An ex-vivo experiment was developed for estimation of glucose consumption by parasitized erythrocytes. Results: Hyperglycaemia was frequent in SM but more commonly associated with cerebral malaria (CM), while hyperinsulinaemia was recognized in severe-malarial-hypotension (median, 25 %-75 %, 188.2, 93.8-336.8 pmol/L). The plasma insulin level was positively correlated with age (CC = 0.457, p < 0.001) and negatively with parasitaemia (CC = -0.368, p = 0.045). Importantly, fatal-CM was associated with hyperglycaemia (12.22, 6.5-14.6 mmol/L), hyperinsulinaemia (141.0, 54.0-186.8 pmol/L) and elevated homeostasis model assessment (HOMA) values. However, there was a trend of higher glucose consumption by parasites in CM compared with that in uncomplicated malaria (UM). Conclusion: Hyperglycaemia, hyperinsulinaemia and elevated HOMA are evidence for insulin resistance and possibly pancreatic B-cell dysfunction in fatal-CM.
Źródło:
Acta Biochimica Polonica; 2010, 57, 4; 513-520
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł

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