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Aflatoxin M1 (AFM1) is a 4-hydroxylated metabolite of aflatoxin B1 (AFB1). It induces various toxicological effects including immunotoxicity. In the present study, we investigated the effects of AFM1 on immune system and its modulation by MicroRNA (miR)-155. AFM1 was administered intraperitoneally at doses of 25 and 50 µg/kg for 28 days to Balb/c mice and different immune system parameters were analyzed. The levels of miR-155 and targeted proteins were evaluated in isolated T cells from spleens of mice. Spleen weight was reduced in mice exposed to AFM1 compared to negative control. Proliferation of splenocytes in response to phytohemagglutinin-A was reduced in mice exposed to AFM1. IFN-γ was decreased in mice exposed to AFM1, whereas IL-10 was increased. Concentration of IL-4 did not change different in mice exposed to AFM1 compared to negative control. Exposure to AFM1 reduced the expression of miR-155. Significant upregulation of phosphatidylinositol-3, 4, 5-trisphosphate 5-phosphatase 1 (Ship1) and suppressor of cytokine signaling 1 (Socs1) was observed in isolated T cells from spleens of mice treated with AFM1, but the transcription factor Maf (c-MAF) was not affected. These results suggest that miR-155 and targeted proteins might be involved in the immunotoxicity observed in mice exposed to AFM1. The Immunotoxic effects of AFM1 on T cell functions. Exposure to AFM1 reduced the expression of miR-155. Significant upregulation of Ship1 and Socs1 was observed in isolated T cells from spleens of mice treated with AFM1, but the c-MAF was not affected. Since Ship1 is a functional target of miR-155 that modulates production of IFN-γ, miR-155 may play a role in AFM1-induced Th1 response suppression (DTH) through targeting of this protein (↑ increase; ↓ decrease). AFM1 inhibited cell-mediated immunity. Exposure of mice to AFM1 resulted in a significant decrease in expression of miR-155. Exposure of mice to AFM1 resulted in up-regulation of Ship1 and Socs1. [ABSTRACT FROM AUTHOR]

Dicyandiamide (DCD) is a nitrogenous compound which is generally used as a fertilizer, antimicrobial and nitrogen enrichment agent in soil. Grass and drinking water contamination with DCD may lead to presence of the chemical residues in milk and infant formula. The aim of this study was to investigate a rapid, simple and accurate method for quantitation of DCD in infant formula using electromemebrane extraction with reinforced hallow fiber by graphene oxide (GO-EME). The extraction method was optimized by solvent, graphene oxide concentration, voltage, stirring speed, pH and time parameters. After extraction, DCD was analyzed by HPLC coupled with UV/Vis detector. The analytical method validation parameters including accuracy, precision, LOD and LOQ were determined to ensure the method's validity.The calibration curve with a correlation ratio of 0.999 was obtained. The recoveries were from 78.0% to 80.0%. The LOD and LOQ were 0.04 mg L-1 and 0.1 mg L-1. This study indicates that the graphen oxideelectromembrane extraction is a simple, accurate and rapid method for determination of DCD in infant formula. [ABSTRACT FROM AUTHOR]

Healthcare professionals worldwide have expressed concern over infections by extended-spectrum ß-lactamase (ESBL) and metallo-ß-lactamase (MBL)–producing bacteria. We evaluated the prevalence of ESBL- and MBL-producing Escherichia coli (E. coli) isolated from community-acquired urinary tract infections (UTIs) and their antibiotic-resistance profiles at 3 private laboratories in Tehran, Iran. E. coli isolates were mostly susceptible to meropenem (90.4%) and imipenem (90.0%), followed by amikacin (89.0%) and gentamicin (84.7%). Moreover, we detected that, of the E. coli isolates, 67 (22.3%) were ESBL producers and 21 (7.0%) of E. coli isolates were MBL positive via the imipenem-ethylenediaminetetraacetic acid (EDTA) combined disc test. This report is the first, to our knowledge, on the prevalence of MBL-producing uropathogenic E. coli (UPEC) strains in Iran. The antibiotic resistance of E. coli isolates revealed that 122 (40.7%) were multidrug resistant. The high number of antibiotic-resistant and ß-lactamase–producing UPEC strains necessitates further attention and consideration, particularly MBL-producing strains. [ABSTRACT FROM AUTHOR]

Background: Rosemary (Rosmarinus officinalis) possesses various pharmacological properties such as antioxidant, anti-tumorigenesis and anti-mutagenesis activities. In this study, we investigated the possible protective effects of ethanol and aqueous extracts of rosemary on human lymphocyte DNA damage induced by H2O2. The extent of DNA lesions was measured using comet assay. Methods: Blood samples were taken from healthy volunteers and lymphocytes were isolated. The lymphocytes were then incubated in aqueous and ethanol extract of rosemary (0.05, 0.1, 0.5, 1 and 2.5 mg/mL) and H2O2 (50, 100 and 200 mM). Lymphocytes were also incubated with a combination of H2O2 (100 mM) with either 1 or 2.5 mg/mL of both extracts for 30 min at 4°C. Results: Our findings showed that H2O2 treatment led to a significant concentrate-dependent DNA damage in human lymphocyte when compared to respective controls (p<0.001). The DNA damage which was initially occurred as the result of 100 µM H2O2 (Percentage tail DNA 55.1%) was inhibited due to the ethanol extract of rosemary at the doses tested (percentage tail DNA 4.7% and 4.03%). However, the aqueous extract has no effects on H2O2 genotoxicity. Conclusions: We suggest that antioxidant constituents in ethanol extract of rosemary can prevent human lymphocytes oxidative DNA damage which is due to its free radical scavenging activity. [ABSTRACT FROM AUTHOR]

Background: Bacterial endophthalmitis is a sight-threatening complication of ocular surgery which requires urgent medical consideration including comprehensive diagnosis. Polymerase chain reaction (PCR) as a sensitive molecular method has been extensively used for detection of microbial species in clinical specimens. Aim: The aim of this study was to identify the causative organisms of endophthalmitis in our patient population using a procedure based on PCR. Materials and Methods: Vitreous samples from 32 patients with post-operative endophthalmitis were collected. Total vitreous DNA was extracted and then assessed by agarose gel electrophoresis. Bacterial 16S rRNA gene was amplified from genomic DNA using PCR with a pair of HAD2 universal primers. Library of PCR products from 16S rRNA, cloned into the pTZ57R/T vector. The ligated products were then transformed into E. coli DH5α strain and grown in the LB-ampicillin/X-Gal/ IPTG plate. Results: From the total of 32 vitreous samples, 18 specimens were positive, illustrating the presence of bacterial infection (56.4 %). Twelve species including Escherichia coli, Enterobacter cloacae, Bacillus subtilis, Neisseria gonorrhoeae, Streptococcus pneumoniae, Haemophilus influenzae, Chlamydia trachomatis, Staphylococcus aureus, Neisseria meningitides, Staphylococcus epidermidis, Pseudomonas aeruginosa and Bacillus cereus were identified using BLAST for known 16S rRNA sequences. Conclusion: Polymerase chain reaction (PCR) accompanied with cloning and sequencing approved to be sensitive and specific. The rapid molecular technique was useful in detection of 12 major microbial species, in infectious endophthalmitis. [ABSTRACT FROM AUTHOR]

Aflatoxin M1 (AFM1) is a 4-hydroxylated metabolite of aflatoxin B1 (AFB1). It induces various toxicological effects including immunotoxicity. In the present study, we investigated the effects of AFM1 on immune system and its modulation by MicroRNA (miR)-155. AFM1 was administered intraperitoneally at doses of 25 and 50 µg/kg for 28 days to Balb/c mice and different immune system parameters were analyzed. The levels of miR-155 and targeted proteins were evaluated in isolated T cells from spleens of mice. Spleen weight was reduced in mice exposed to AFM1 compared to negative control. Proliferation of splenocytes in response to phytohemagglutinin-A was reduced in mice exposed to AFM1. IFN-γ was decreased in mice exposed to AFM1, whereas IL-10 was increased. Concentration of IL-4 did not change different in mice exposed to AFM1 compared to negative control. Exposure to AFM1 reduced the expression of miR-155. Significant upregulation of phosphatidylinositol-3, 4, 5-trisphosphate 5-phosphatase 1 (Ship1) and suppressor of cytokine signaling 1 (Socs1) was observed in isolated T cells from spleens of mice treated with AFM1, but the transcription factor Maf (c-MAF) was not affected. These results suggest that miR-155 and targeted proteins might be involved in the immunotoxicity observed in mice exposed to AFM1. The Immunotoxic effects of AFM1 on T cell functions. Exposure to AFM1 reduced the expression of miR-155. Significant upregulation of Ship1 and Socs1 was observed in isolated T cells from spleens of mice treated with AFM1, but the c-MAF was not affected. Since Ship1 is a functional target of miR-155 that modulates production of IFN-γ, miR-155 may play a role in AFM1-induced Th1 response suppression (DTH) through targeting of this protein (↑ increase; ↓ decrease). AFM1 inhibited cell-mediated immunity. Exposure of mice to AFM1 resulted in a significant decrease in expression of miR-155. Exposure of mice to AFM1 resulted in up-regulation of Ship1 and Socs1. [ABSTRACT FROM AUTHOR]

Aflatoxin M 1 (AFM 1 ) is a 4-hydroxylated metabolite of aflatoxin B 1 (AFB 1 ). It induces various toxicological effects including immunotoxicity. In the present study, we investigated the effects of AFM 1 on immune system and its modulation by MicroRNA (miR)-155. AFM 1 was administered intraperitoneally at doses of 25 and 50 µg/kg for 28 days to Balb/c mice and different immune system parameters were analyzed. The levels of miR-155 and targeted proteins were evaluated in isolated T cells from spleens of mice. Spleen weight was reduced in mice exposed to AFM 1 compared to negative control. Proliferation of splenocytes in response to phytohemagglutinin-A was reduced in mice exposed to AFM 1 . IFN-γ was decreased in mice exposed to AFM 1 , whereas IL-10 was increased. Concentration of IL-4 did not change different in mice exposed to AFM 1 compared to negative control. Exposure to AFM 1 reduced the expression of miR-155. Significant upregulation of phosphatidylinositol-3, 4, 5-trisphosphate 5-phosphatase 1 (Ship1) and suppressor of cytokine signaling 1 (Socs1) was observed in isolated T cells from spleens of mice treated with AFM 1, but the transcription factor Maf (c-MAF) was not affected. These results suggest that miR-155 and targeted proteins might be involved in the immunotoxicity observed in mice exposed to AFM 1 .

The aim of this study was to investigate the contribution of acute alcohol in sepsis-related liver damages using a Cecal Ligation and Puncture (CLP) model. Rats were divided into 7 groups (5 rats/group): control (saline-injected), sham-operated, CLP, ethanol (1.0 and 2.0 g/kg b.w) and CLP+ethanol. The CLP+ethanol group received a single dose of ethanol following sepsis induction. Sepsis induction caused early changes in lipid peroxidation products in liver, whereas ethanol alone (2.0 g/kg b.w) resulted in a significant increase (~21%) in lipid peroxidation, which was further increased (~57%) in CLP rats treated with alcohol. CLP operation and alcohol treatment exhibited additive effects on plasma catalase, liver glutathione and glutathione S-transferase (GST), which were primarily suppressed due to ethanol. Hepatic cytochrome P4501A1, which was elevated in CLP rats, was reversed in the CLP+ethanol group. Plasma tumor necrosis factor-α was markedly elevated (~85%) in septic rats, but was unaffected in septic rats having received ethanol. Histopathological observations revealed that inflammatory reactions in liver in response to CLP operation are not intensified by ethanol administration. On the basis of biochemical and histopathological results, it can be concluded that acute ethanol treatment is responsible for early changes in oxidative stress, which may lead to polymicrobial sepsis-related organ damage., (Copyright © 2012 Elsevier GmbH. All rights reserved.)