Bioremediation of soil contaminated crude oil by Agaricomycetes.

BACKGROUND: One of the most important environmental problems is the decontamination of petroleum hydrocarbons polluted soil, particularly in the oil-rich country. Bioremediation is the most effective way to remove these pollutants in the soil. Spent mushroom compost has great ability to decompose lignin-like pollution. The purpose of this study was the bioremediation of soil contaminated with crude oil by an Agaricomycetes. METHODS: Soil sample amended with spent mushroom compost into 3%, 5% and 10% (w/w) with or without fertilizer. Ecotoxicity germination test was conducted with Lipidium sativa. RESULTS: The amplified fragment (18 s rDNA) sequence of this mushroom confirmed that the strain belonged to Pleurotus ostreatus species with complete homology (100% identity). All tests experiment sets were effective at supporting the degradation of petroleum hydrocarbons contaminated soil after three months. Petroleum contaminated soil amended with Spent mushroom compost 10% and fertilizer removed 64.7% of total petroleum hydrocarbons compared control. The germination index (%) in ecotoxicity tests ranged from 60.4 to 93.8%. CONCLUSIONS: This showed that the petroleum hydrocarbons contaminated soil amended with 10% Spent mushroom compost had higher bioremediation ability and reduced soil toxicity in less than three months.

Analysis of killer cell immunoglobulin-like receptors and their human leukocyte antigen-ligands gene polymorphisms in Iranian patients with systemic lupus erythematosus.

OBJECTIVE: Systemic lupus erythematosus (SLE) is an inflammatory autoimmune disease. Natural killer (NK) cells play a critical role in the pathogenesis of autoimmune disorders that mainly express killer cell immunoglobulin-like receptors (KIRs). The present study was undertaken to determine the association of the KIR alleles, genotypes, and KIR-human leukocyte antigen (HLA) ligand gene combinations with the susceptibility to SLE. METHODS: The genotyping of 17 KIR and 5 HLA loci was performed using the polymerase chain reaction-sequence specific primer (PCR-SSP) method. The study population consisted of 230 SLE patients and 273 ethnical-, age-, and sex-matched healthy controls. The association of the polymorphisms with the prevalence of 11 clinical criteria in patients was analyzed. RESULTS: The carrier frequency of HLA-A-Bw4 was modestly decreased in the SLE patients. The prevalence of hematological and renal disorders was significantly increased in patients with combination of KIR3DL1(+); HLA-B-Bw4(Thr80+) and KIR2DS1(+); HLA-C2(+) genes, respectively. Female patients with combination of KIR2DL2(+); HLA-C1(-) genes were more likely to develop serositis. In addition the prevalence of renal disorders, oral ulcer and serositis was significantly increased in male patients with KIR3DP1(+), KIR2DS1(+), and KIR2DS3(+) genotypes respectively. CONCLUSION: Our results showed that the presence of activating KIR receptors alone or in combination with their HLA ligands and the absence of inhibitory KIRs in combination with their HLA ligands may activate NK cells and are significantly correlated with the prevalence of renal disease, hematologic disorders, serositis, and oral ulcer in SLE patients.

The role of microRNAs in the resistance to colorectal cancer treatments.

Colorectal cancer (CRC) is one of the leading cancer-related causes of death in the world. Several approaches such as surgery, chemotherapy, radiotherapy, targeted therapy, or combinations thereof have been used to treat CRC patients. However, the fact that many patients develop a drug resistance during the course of the treatment is a major obstacle. Understanding the mechanisms underlying resistance is critical in order to develop more effective targeted treatments. Recently, several studies have reported on the regulatory role of microRNAs (miRNAs) in the response to anti-cancer drugs and suggested them as a source of predictive biomarkers for the purpose of patient stratification and for the prognosis of treatment success. For example, overexpressing miR-34a, a master regulator of tumor suppression attenuates chemoresistance to 5-FU by downregulating silent information regulator 1 (SIRT1) and E2F3. MRX34, a miR-34a replacement is the first synthetic miRNA mimic to enter clinical testing. MiR-34a antagonizes cancer stemness, metastasis, and chemoresistance processes that are necessary for cancer viability. This example shows that miRNAs are coming into focus for the design of enhanced cancer therapies that aim to sensitise tumor cells for anti-cancer drugs. In this review, we provide an overview on the role of miRNAs in the resistance to current colorectal cancer therapies. Furthermore, we discuss the value of miRNAs as biomarkers for predicting chemosensitivity and their potential to enhance treatment strategies.

Indirect role of microRNAs and transcription factors in the regulation of important cancer genes: A network biology approach.

Cancer is one of the leading causes of death worldwide. Although the mechanisms of gene regulation in cancer have been the subject of intense investigation during the last decades, the precise role of regulatory processes in cancer is largely unknown. More specifically, it is not completely understood how microRNAs and transcription factors regulate and influence the cancer-related processes. In the present study, using cancer-specific biological networks we examine the role of microRNAs and transcription factors (TFs) in regulation of important cancer genes. The importance measures which are used in this study consider both network structure information and biological data on miRNA- and TF-based gene regulation. By analyzing cancer-specific PPI, signaling and metabolic networks, it was shown that microRNAs and transcription factors tend to regulate those genes which are in the neighborhood of important components of cancer-specific PPI, signaling, and metabolic networks. The role of microRNAs was found to be particularly important, which confirms our previously-published results on the importance of microRNAs in detecting important network components. Moreover, we highlight that the miRNAs appear to apply their function via regulating the "neighbors" of important cancer genes, which implies their indirect role in cancer, and presumably, in fine-tuning the effect of other cancer-related genes.

IL-1A rs1800587, IL-1B rs1143634 and IL-1R1 rs2234650 polymorphisms in Iranian patients with systemic sclerosis.

Systemic Sclerosis (SSc) is a systemic autoimmune disorder, with ambiguous pathogenesis. Genetic and environmental factors were proved to be correlated with SSc aetiology. Single nucleotide polymorphisms (SNPs) in cytokine genes can alter the structure and function of the cytokines and consequently may increase the susceptibility to a specific disease. In this study, we investigated SNPs of the IL-1 gene cluster in Iranian SSc patients. We obtained blood samples from 170 SSc patients and 213 healthy individuals. Cytokine genotyping results were obtained by polymerase chain reaction with sequence-specific primers (PCR-SSP). IL-1A rs1800587, IL-1B rs1143634 and IL-1R1 rs2234650 were evaluated for SNP study. The frequency of the IL-1B rs1143634 CT genotype was significantly lower in SSc patients compared to the controls (OR = 0.584; 95% CI = 0.385-0.886; P-value = 0.023), so we propose that CT genotype of this allele might be protective. According to our haplotype analysis, CCC haplotype frequency is higher in the control group compared to SSc patients (OR = 1.575; 95% CI = 1.176-2.111; P-value = 0.008) and in contrast, CTC haplotype frequency is lower in the control group compared to SSc patients (OR = 0.152; 95% CI = 0.047-0.484; P-value = 0.002), so they might decrease and increase the susceptibility of having SSc, respectively. In addition, we reported two significant diplotypes frequency differences among SSc patients and healthy individuals. It is highly important that there is not much resemblance between the IL-1 gene cluster polymorphism in different populations, so we can indicate that SNPs may play critical roles when they are combined with other genetic and environmental factors.

Analysis of Y-chromosomal short tandem repeat (STR) polymorphism in an Iranian Sadat population.

The molecular genotyping of individuals and reconstruction of kinship through short and highly polymorphic DNA markers, so called short tandem repeats (STR), has become one of the important and efficient methods in anthropology studies and forensic science. Although many populations have been analyzed, no study has yet been carried out on Sadat populations who are putative descendents of Prophet Mohammad (peace be upon him). Polymorphisms of 6 Y-STR loci (DYS19, DYS385a/b, DYS389II, DYS390, DYS392, and DYS393) have been studied in an unrelated population of Sadat males. The aim of this study was to find possible similarities within Sadat males, resided in Iran. Among Sadat, DYS385b was proved to be the most polymorphic (GD = 0.8588), and DYS392 showed the lowest polymorphism (GD = 0.3527). In 50 samples, 45 different haplotypes were found, of which 39 haplotypes were unique. In the study, three samples had multi-allelic patterns. Haplotype diversity, in regard to these 7 markers was 0.9942.

Demography and life history of the egg parasitoid, Trichogramma brassicae, on two moths Anagasta kuehniella and Plodia interpunctella in the laboratory.

The egg parasitoid, Trichogramma brassicae Bezdenko (Hymenoptera: Trichogrammatidae) is the most important and widely distributed species of Trichogramma in Iran. It attacks eggs of several lepidopterous pests, and is a major biological control agent. Rearing parasitoids is necessary for experimental work, and, potentially, for mass release in the field. Selecting a suitable host is critical for developing a successful rearing method. If other conditions are the same, the rate of population increase will be a suitable indicator of parasitoid performance on different hosts. However, conclusions based on a single generation can be misleading because of the learning ability of parasitoids. Life history parameters of T. brassicae were studied on two hosts easily reared in the laboratory, Anagasta kuehniella Zeller, and Plodia interpunctella Hübner (Lepidoptera: Pyralidae). All the experiments were carried out at 24 +/- 1 degrees C, 65+/-10% RH, and 16:8 L:D photoperiod. Eight parameters including gross and net reproductive rates (GRR and R(0) respectively), intrinsic rate of natural increase (r(m)), finite rate of population increase (lambda), intrinsic birth and death rates (b and d respectively), cohort generation time (T), and doubling time (DT) were compared between two hosts for two generations. All parameters showed a highly significant difference (alpha = 0.01) between hosts. GRR, R(0), r(m), lambda, and b were higher, while d, T, and DT were lower in Anagasta than Plodia. The intrinsic rate of natural increase was 0.2912 and 0.2145 female/female/day and net replacement rate was 45.51 and 19.26 female/female/generation in Anagasta and Plodia respectively. Differences between generations were significant except for r(m), lambda, and d. The net replacement rate was 28.56 and 39 in the 1(st) and 2(nd) generations respectively. These results showed that A. kuehniella was a better host than P. interpunctella. Higher reproduction occurred in the second generation that may be due to increased adaptation to experimental conditions.

Sex-chromosome linked gene expression in in-vitro produced bovine embryos.

The expression of XIST, G6PD, HPRT, ZFX and ZFY were investigated in in-vitro produced bovine embryos. Transcripts of these genes were assayed by RT-PCR in pools of pre-compaction stage embryos and sexed pools of morulae and blastocysts. The expression of XIST, G6PD, HPRT and ZFX in female and male morulae and blastocysts were compared using a semi-quantitative RT-PCR. G6PD, HPRT and ZFX transcripts were noted in all pre-compaction stage embryos and in female and male blastocysts. ZFY transcripts were detected in unsexed pools of 8-16-cell stage embryos and in male blastocysts. XIST transcripts were detected in unsexed pools at the 8-16 cell stage, in male and female morulae, and in female blastocysts. The level of XIST RNA was significantly higher in female morulae than in males. Levels of G6PD and HPRT RNA were also higher in female morulae and blastocysts than in males, but only G6PD levels were significantly different between the sexes. The expression of ZFX was also significantly higher in female than in male blastocysts. These results show sexually dimorphic expression of sex chromosome linked genes prior to the blastocyst stage in in-vitro produced bovine embryos.

Sex-linked genes are not silenced in fetal bovine testes expressing X-inactive specific transcript (XIST).

X-inactive specific transcript (XIST), which is thought to be the central factor for the X-inactivation process in female mammals, is known to be expressed in males during spermatogenesis. Our studies have shown that XIST is not only expressed in adult bovine testis but is also expressed in fetal, newborn, and prepubertal testes long before spermatogenesis is established. To determine whether the XIST expressed in fetal testes is involved in silencing the genes on the X chromosome, we investigated the status of X-linked genes, including glucose-6-phosphate-dehydrogenase (G6PD), hypoxanthine phosphoribosyl transferase (HPRT), and X-linked zinc finger protein gene (ZFX), in fetal bovine gonads at the developmental stage, when meiosis is initiated in fetal ovaries in this species. Reverse transcription and a semiquantitative polymerase chain reaction based on the optical density of each gene-specific band relative to that of the co-amplified Quantum RNA 18S Internal Standard (Ambion, Austin, TX) showed that the XIST gene was expressed in the testes of approximately 90-day-old fetuses and was silent in all their nongonadal organs tested, although at a significantly lower level than that in fetal organs of female fetuses. Our observation that the expression of X-linked genes in the fetal testis was comparable to that in male nongonadal organs, in which X inactivation does not occur, indicates that the low level of XIST, or XIST-like RNA, expressed in the fetal bovine testis is not involved in silencing X-linked genes.

X-autosome translocation and low fertility in a family of crossbred cattle.

An investigation was carried out on a family of Limousin-Jersey crossbreds exhibiting low fertility in the females, to determine the impact of a previously identified X-autosome translocation (X-AT) on the reproductive performance of the carrier cows. Three of the identified translocation carriers, including a cow and two of her daughters, were maintained at our University Research Station and artificially inseminated periodically with semen from different bulls of known fertility. Attempts to breed the X-AT carriers resulted in high rates of return to estrus between days 28 and 60, abortions between days 121 and 235 after insemination, and a total of 13 live births including 4 translocation carrier calves. Results of superovulation and embryo retrieval trials on X-AT carriers revealed significantly higher proportions of unfertilized and uncleaved ova and abnormal embryos compared to those from normal cows, and no pregnancy in the recipients transferred with morphologically normal blastocysts from X-AT carriers. While the higher rates of failed fertilization and cleavage, abnormal embryos and return to estrus in X-AT carriers could be attributed to chromosome imbalance expected in their gametes, the relatively high prevalence of abortion (late in gestation) was unexpected. Our observations on the fetuses expelled by X-AT carriers after 5 months of gestation indicated that a majority (three out of four) of these fetuses were products of abnormal (3:1) segregation in meiosis I and that these chromosomally unbalanced (hyperdiploid) conceptuses were able to survive early embryogenesis and fetal life up to the end of the second trimester. We hypothesize that their relatively long in utero life and the absence of any overt birth defects may be attributable to the type of chromosomes over-represented in these fetuses and that their eventual expulsion may have been the result of selection against the clonal population of cells in which the altered X carrying a segment of chromosome 23 (Xp(+)), remained inactive.

Expression of X inactive specific transcript (Xist) and testicular morphogenesis in bovine fetuses.

Inactivation of one of the 2 X chromosomes in the somatic cells of female mammals is the process by which their X-linked gene products are equalized to those of their male counterparts. In male mammals, however, a sex vesicle representing the condensed and transcriptionally silenced sex chromosomes is detected during early meiotic prophase. Since the exact stage of development at which X inactivation is initiated in the bovine testis is not established as yet, we undertook to study fetuses ranging in age from 30 to 180 days of gestation, to determine the transcriptional status of the Xist gene currently thought to be the prerequisite component of X inactivation. Our studies using reverse transcription polymerase chain reaction (RT-PCR) approach with primers designed to amplify a 463 bp product from a conserved region of the first exon of bovine Xist gene, proved that Xist expression is evident in bovine fetal testes as early as 50 days of gestation and that it continues at least to the end of the second trimester (180 days) of gestation. Morphological studies on fetal testes during gestational stage spanning the period of Xist expression revealed the presence of large intra-tubular cells overtly resembling the prespermatogonia of postnatal bovine testes, at 50 days and preleptotene like cells as early as 90 days of gestation. We hypothesize that the expression of the Xist gene, or the recently discovered Tsix gene antisense to Xist in orientation, may be related to the presence of these cells which participate in the morphogenesis of the fetal bovine testis.