Plantago major L. is a perennial, wild plant that belongs to the Plantaginaceae family, and is used as a good indicator in the assessment of destructive anthropogenic impact on the environment. The ...aim of the present study was to evaluate cyto/genotoxic effects of methanol extracts of Plantago major, collected from two locations (Tetovo and Smetovi), using Allium cepa test. We demonstrated that the highest concentration of P. major extracts from both locations reduced the mitotic index, while the lowest increased mitotic index value comparing to the positive control. As for genotoxic effects of extract from Tetovo, all concentrations increased the frequency of sticky chromosomes and chromosome missegregations in comparison with both controls, and frequency of multipolar anaphases when compared to the negative control. Higher number of cells with vagrants in comparison with positive control was detected after the treatment with 0.005 and 0.02 mg/ml concentrations. P. major extract from Smetovi (0.005 and 0.01 mg/ml) induced an increase in the number of vagrants as compared to the positive control, and frequency of sticky chromosomes when compared to both controls (0.01 mg/ml). Exposure to extract (0.005 and 0.02 mg/ml) caused increased number of multipolar anaphases in comparison with negative control. Apoptosis were not detected for P. major extract from Smetovi, while its highest concentration (0.02 mg/ml) induced increase in the frequency of necrosis as compared to the positive control. Our results demonstrated that methanol extracts of P. major, collected from Tetovo and Smetovi, showed cyto/genotoxic effects on A. cepa meristem cells.
In this paper, special attention was paid to the effect of snake venom on the erythrocytes of humans and horses and on human lymphocytes. The damage caused by a certain amount of snake venom is ...ascertained. After the snake venom was added to blood, the number of erythrocytes changed. The main reason for the usage of whole blood in the experiment is getting a complete insight into the effect of the poison. Obtained results point out that
Vipera ammodytes
venom has a hemolytic effect, and that effect varies between individuals. It was observed that the hemolytic effect of the venom destroys blood elements to a certain extent. Special attention was also given to the degree of agglutination. Statistically significant hemolytic effects tend to occur in horses (
Equus caballus)
(p < 0.5), while lower are observed in human blood. In the present study, experiments were carried out to evaluate the strong mutagenic and cytotoxic potential and genotoxic effects of
Vipera ammodytes
venom and its isolated toxins on human lymphocytes using cell culture as a method. We detected cells that have micronuclei, two or more nuclei, nuclear bridges, unregular cell divisions, full lysis of the cells (depending on the concentration), etc. Some cells aborted the nucleus and part of the cytoplasm. There is still just a small number of studies regarding the cytogenetic toxicology of snake venoms and their isolated protein compounds. Our work may contribute to a better understanding of snake venom’s effects on human cells, which could be useful for therapeutic purposes.
Glioblastoma multiforme (GBM) is the most frequent type of primary astrocytomas. We examined the association between single nucleotide polymorphisms (SNPs) in Aurora kinase A (AURKA), Aurora kinase B ...(AURKB), Aurora kinase C (AURKC) and Polo-like kinase 1 (PLK1) mitotic checkpoint genes and GBM risk by qPCR genotyping. In silico analysis was performed to evaluate effects of polymorphic biological sequences on protein binding motifs. Chi-square and Fisher statistics revealed a significant difference in genotypes frequencies between GBM patients and controls for AURKB rs2289590 variant (p = 0.038). Association with decreased GBM risk was demonstrated for AURKB rs2289590 AC genotype (OR = 0.54; 95% CI = 0.33-0.88; p = 0.015). Furthermore, AURKC rs11084490 CG genotype was associated with lower GBM risk (OR = 0.57; 95% CI = 0.34-0.95; p = 0.031). Bioinformatic analysis of rs2289590 polymorphic region identified additional binding site for the Yin-Yang 1 (YY1) transcription factor in the presence of C allele. Our results indicated that rs2289590 in AURKB and rs11084490 in AURKC were associated with a reduced GBM risk. The present study was performed on a less numerous but ethnically homogeneous population. Hence, future investigations in larger and multiethnic groups are needed to strengthen these results.
To present a compendium of off-ladder alleles and other genotyping irregularities relating to rare/unexpected population genetic variation, observed in a large short tandem repeat (STR) database from ...Bosnia and Serbia.
DNA was extracted from blood stain cards relating to reference samples from a population of 32800 individuals from Bosnia and Serbia, and typed using Promega's PowerPlex16 STR kit.
There were 31 distinct off-ladder alleles were observed in 10 of the 15 STR loci amplified from the PowerPlex16 STR kit. Of these 31, 3 have not been previously reported. Furthermore, 16 instances of triallelic patterns were observed in 9 of the 15 loci. Primer binding site mismatches that affected amplification were observed in two loci, D5S818 and D8S1179.
Instances of deviations from manufacturer's allelic ladders should be expected and caution taken to properly designate the correct alleles in large DNA databases. Particular care should be taken in kinship matching or paternity cases as incorrect designation of any of these deviations from allelic ladders could lead to false exclusions.
Single nucleotide polymorphisms (SNPs) in genes encoding mitotic kinases could influence development and progression of gastric cancer (GC).
Case-control study of nine SNPs in mitotic genes was ...conducted using qPCR. The study included 116 GC patients and 203 controls. In silico analysis was performed to evaluate the effects of polymorphisms on transcription factors binding sites.
The AURKA rs1047972 genotypes (CT vs. CC: OR, 1.96; 95% CI, 1.05-3.65; p = 0.033; CC + TT vs. CT: OR, 1.94; 95% CI, 1.04-3.60; p = 0.036) and rs911160 (CC vs. GG: OR, 5.56; 95% CI, 1.24-24.81; p = 0.025; GG + CG vs. CC: OR, 5.26; 95% CI, 1.19-23.22; p = 0.028), were associated with increased GC risk, whereas certain rs8173 genotypes (CG vs. CC: OR, 0.60; 95% CI, 0.36-0.99; p = 0.049; GG vs. CC: OR, 0.38; 95% CI, 0.18-0.79; p = 0.010; CC + CG vs. GG: OR, 0.49; 95% CI, 0.25-0.98; p = 0.043) were protective. Association with increased GC risk was demonstrated for AURKB rs2241909 (GG + AG vs. AA: OR, 1.61; 95% CI, 1.01-2.56; p = 0.041) and rs2289590 (AC vs. AA: OR, 2.41; 95% CI, 1.47-3.98; p = 0.001; CC vs. AA: OR, 6.77; 95% CI, 2.24-20.47; p = 0.001; AA+AC vs. CC: OR, 4.23; 95% CI, 1.44-12.40; p = 0.009). Furthermore, AURKC rs11084490 (GG + CG vs. CC: OR, 1.71; 95% CI, 1.04-2.81; p = 0.033) was associated with increased GC risk. A combined analysis of five SNPs, associated with an increased GC risk, detected polymorphism profiles where all the combinations contribute to the higher GC risk, with an OR increased 1.51-fold for the rs1047972(CT)/rs11084490(CG + GG) to 2.29-fold for the rs1047972(CT)/rs911160(CC) combinations. In silico analysis for rs911160 and rs2289590 demonstrated that different transcription factors preferentially bind to polymorphic sites, indicating that AURKA and AURKB could be regulated differently depending on the presence of particular allele.
Our results revealed that AURKA (rs1047972 and rs911160), AURKB (rs2241909 and rs2289590) and AURKC (rs11084490) are associated with a higher risk of GC susceptibility. Our findings also showed that the combined effect of these SNPs may influence GC risk, thus indicating the significance of assessing multiple polymorphisms, jointly. The study was conducted on a less numerous but ethnically homogeneous Bosnian population, therefore further investigations in larger and multiethnic groups and the assessment of functional impact of the results are needed to strengthen the findings.
Familial adenomatous polyposis (FAP) is an autosomal dominant illness with the highest risk for appearance of colorectal cancer's disease. In our study, we have used Bethesda criteria that define ...colorectal cancers which can be tested on microsatellite instability. The aim of our study is make an analysis of microsatellite instability (MSI), appearance of RER+ phenotype, genetic alteration of tumor suppressor genes as like as one of responsible factor for genesis of adenomatous polyposis. The base for this study were shown families with clinical diagnosed FAP. In this study two families with clinical diagnosed adenomatous polyposis were involved. Our study of both families showed that three tumor tissues belonged to RER negative phenotype, but only one belonged to RER positive phenotype. Microsatellite analysis showed instability of mononucleotide marker Bat 40 at 4 samples and Bat 26 at 2 samples, but Bat 25 and in 1 sample. Dinucleotide marker TP 53 did no show any microsatellite alterations. Genetic alteration of tumor suppressor gene APC appeared at 4 samples, p53 at 3 samples, RB1 at 2 samples and NM23 only at 1 sample, but tumor suppressor genes DCC1 and DCC2 were homozygote. Our results are agree with results of earlier studies and also the got results confirm the fact that loss of heterozygosity of tumor suppressor gene APC and p53 are responsible for genesis of adenomatous polypose and it also represents the characteristic of genetic changes FAP's patients in our region.
HNPCC (Hereditary non-polyposis colorectal cancer) development is caused by mutation of genes included in system of mismatch repair genes. The mutation exists at 60% of patients in hMSH2 gene, 30% in ...hMLH1 and 10% both in hPMS1and hPMS2 genes. RER+ exists in about 90% in hereditary non-polyposis colorectal cancer and about 15-28% in sporadic cancers.The purpose of the study was to determine highly sensitive microsatellite markers which can be fast and efficient way of microsatellite screening for detection of HNPCC patients. Moreover, we have analysed the loss of heterozygosity of tumour suppressor genes which could have the diagnostic value in detection of HPNCC patients.
Considering its frequency, high mortality rate as well as many etiological mysteries colorectal cancer is a challenge to contemporary science. In our study we analyzed RER + and RER--phenotypes and ...their relations with clinical-pathological characteristics of sporadic colorectal cancers. We also analyzed genetic alterations of tumor suppressor genes as well as their relation with microsatellite instability. The study was based on 54 tumor samples and 54 samples of the surrounding healthy tissue of patients with colorectal cancer. According to Amsterdam Criteria and Bethesda Criteria 35/54 or 64,81% belonged in the group of sporadic colorectal cancer. Mononucleotide marker Bat 25 showed instability in 48,57%; Bat 26 in 45,71% and Bat 40 in 29/35 82,86% of tumor samples. Considering dinucleotide markers, TP 53 showed instability in 54,29% and DS123 in 37,14% of tumor samples. Genetic alterations in tumor suppressor genes were found in tumor tissue: NM 23 in 54,29% samples, p53 in 51,43%, APC in 51,43%, DCC2 in 34,29%, RB1 in 22, 86% and DCC 1 in 28,57%. Our studies confirmed that genetic instability had an important role in the development of tumor type. Our results showed that mononucleotide marker Bat 40 might be used for an easy and fast screening procedure in Bosnian population, because it exhibited high percent of microsatellite instability and was in relation with RER+ phenotype. This investigation showed that different genetic alterations may occur during cancer development in each individual patient's tumor. These changes result in MMR inactivation, which causes RER+ phenotype. Our results suggest a connection between alteration in some tumor suppressor genes and MSI phenotype of sporadic colorectal cancer in Bosnian population.
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