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Background: Use of antiepileptic drugs during pregnancy can be associated with an increased risk of teratogenicity as well as congenital abnormalities. However, there are numerous discrepancies to determine whether lamotrigine, as an antiepileptic drug, can significantly induce malformation in newborn infants or not. Thus, the purpose of the study was to evaluate the teratogenic effects of lamotrigine on mouse fetuses.

Colorectal cancer (CRC) is one of the most frequent causes of cancer‑related death worldwide. The prognosis of the malignancy and patient survival is commonly poor. Therefore, the discovery of pertinent biomarkers is essential to provide an accurate diagnosis and effective therapy. Newly, a group of noncoding RNAs named long noncoding RNAs (lncRNAs) has been found to involve in CRC development and progression. In this review, we highlighted the biological function of lncRNAs and reviewed their potentials as clinical tools in the CRC. A literature search of PubMed, EMBASE, MEDLINE, Web of Science, Scopus, and Cochrane Library using the MeSH terms “CRC,” “long noncoding RNA,” “lncRNA,” and relevant was completed. The review included all articles that reported on the significance and role of lncRNAs in CRC development and clinical settings. All identified articles were cross‑referenced for further articles, and any unavailable online were retrieved from hardcopy archive libraries. CRC‑related lncRNAs could regulate a number of cellular processes, and their dysregulations have been suggested as potential biomarkers. [ABSTRACT FROM AUTHOR]

Background: Hepatitis C virus (HCV) infection is one of the most important risk factors for liver failure which can lead to chronic hepatitis, cirrhosis, and hepatocellular carcinoma. Approximately 170-200 million (almost 3% of the world's population) people have been reported to have HCV infection worldwide. HCV has six genotypes and multiple subtypes. HCV genotyping and identification of subtypes are critical steps for HCV vaccine development. Materials and Methods: In this community-based study, we aimed to investigate the HCV genotypes in infected patients referring to the laboratory of Hajar Hospital of Shahrekord city (the capital of Chaharmahal and Bakhtiari Province) in Iran from November 21, 2016, to October 21, 2017. During 2016-2017, the sera were obtained from 2377 individuals referring to the laboratory of Hajar Hospital of Shahrekord, Iran. The anti-HCV antibody was tested for all sera by enzyme-linked immunosorbent assay test. Following HCV RNA isolation and cDNA synthesis, HCV genotype detection was performed by quantitative reverse transcription-polymerase chain reaction. Results: Genotypes 3, 1a, and 1b were found in 28.6% (95% confidence interval [CI]: 17.0%-40.0%), 9.5% (95% CI: 2.1%-17.0%), and 3.2% (95% CI: 0.0%-7.6%) of the patients, respectively. In 5 patients (7.9%, 95% CI: 1.1%-14.8%), however, we did not observe any genotypes. We could not find any significant difference between the plasma viral load of infected patients and different genotypes. There was no significant difference either between age groups and genotypes (P > 0.05). Conclusion: The findings of the present study determined that HCV genotype 3 was the predominant genotype followed by the genotypes 1a and 1b in Chaharmahal and Bakhtiari Province. [ABSTRACT FROM AUTHOR]

Transforming growth-interacting factors (TGIFs), as one of the main classes of three amino acid loop extension (TALE) homeodomain proteins, play important roles in key cellular processes including cell growth, proliferation, differentiation as well as apoptosis and cell fate. Currently, four members of TGIF family known in human include TGIF1, TGIF2, TGIF2LX (X-linked) and TGIF2LY (Y-linked) which expressed in many human tissues. This protein family is dys-regulated in several cancers, including prostate, ovarian and colorectal cancer. In this review, we presented the results of research on TGIFs, indicating these factors act as potential biological mediators in carcinogenesis. However, additional investigations are needed to clarify the underlying mechanisms which TGIFs involve in cancer development. [ABSTRACT FROM AUTHOR]

Retinoblastoma is the most common intraocular tumor in children resulting from genetic alterations and transformation of mature retinal cells. The objective of this study was to investigate the effects of SD-208, TGF-β-RI kinase inhibitor, on the expression of some miRNAs including a miR-17/92 cluster in retinoblastoma cells. Prior to initiate this work, the cell proliferation was studied by Methyl Thiazolyl Tetrazolium (MTT) and bromo-2'-deoxyuridine (BrdU) assays. Then, the expression patterns of four miRNAs (18a, 20a, 22, and 34a) were investigated in the treated SD-208 (0.0, 1, 2 and 3 μM) and untreated Y-79 cells. A remarkable inhibition of the cell proliferation was found in Y-79 cells treated with SD-208 versus untreated cells. Also, the expression changes were observed in miRNAs 18a, 20a, 22 and 34a in response to SD-208 treatment (P<0.05). The findings of the present study suggest that the anti-cancer effect of SD-208 may be exerted due to the regulation of specific miRNAs, at least in this particular retinoblastoma cell line. To the best of the researchers' knowledge, this is the first report demonstrating that the SD-208 could alter the expression of tumor suppressive miRNAs as well as oncomiRs in vitro. In conclusion, the present data suggest that SD-208 could be an alternative agent in retinoblastoma treatment. [ABSTRACT FROM AUTHOR]

A member of homeodomain protein namely TGIF2LX has been implicated as a tumor suppressor gene in human malignancy as well as in spermatogenesis. However, to our knowledge, dynamic functional evidence of the TGIF2LX has not yet been provided. The aim of the present study was to investigate the human TGIF2LX target gene(s) using a cDNA-AFLP as a differential display method. A pEGFP-TGIF2LX construct containing the wild-type TGIF2LX cDNA was stably transfected into SW48 cells. UV microscopic analysis and Real-time RT-PCR were used to confirm TGIF2LX expression. The mRNA expressions of TGIF2LX in transfected SW48 cells, the cells containing empty vector (pEGFP-N), and untransfected cells were compared. Also, a Real-time PCR technique was applied to validate cDNA-AFLP results. The results revealed a significant down-regulation and up-regulationby TGIF2LX of Nir1 and Nir2 genes, respectively. The genes are engaged in the cell morphogenesis process. Our findings may provide new insight into the complex molecular pathways underlying colorectal cancer development. [ABSTRACT FROM AUTHOR]

Colorectal cancer (CRC) is a notable cause of cancer-associated mortality worldwide, making it a pertinent topic for the study of cancer and its treatment. Staphylococcal enterotoxin B (SEB), an enterotoxin produced by Staphylococcus aureus, has been demonstrated to exert anticancer and antimetastatic effects due to its ability to modify cell immunity and cellular signaling pathways. In the current study, SEB was investigated, including whether it exerts its growth inhibitory effects on colon adenocarcinoma cells. This may occur through the manipulation of a key tumor growth factor, termed transforming growth factor-β (TGF-β), and its signaling pathway transducer, Smad2/3. The human colon adenocarcinoma HCT116 cell line was treated with different concentrations of SEB, and cell number was measured using MTT assay at different treatment times. Smad2/3 RNA expression level was analyzed in untreated or SEB-treated cells using quantitative polymerase chain reaction, which indicated significant differences between cell viability and Smad2/3 expression levels. SEB effectively downregulated Smad2/3 expression in the HCT116 cells at concentrations of 1 and 2 μg/ml (P=0.0021 and P=0.0017, respectively). SEB concentrations that were effective at inhibiting Smad2/3 expression were correlated with those able to inhibit the proliferation of the cancer cells. SEB inhibited Smad2/3 expression at the mRNA level in a concentration- and time-dependent manner. The present study thus proposed SEB as an agent able to significantly reduce Smad2/3 expression in colon cancer cells, provoking moderate TGF-β growth signaling and the reduction of tumor cell proliferation. [ABSTRACT FROM AUTHOR]

Background and purpose: Bacterial and fungal bioaerosols play important roles in the atmosphere and have significant effects on human health. This study aimed at investigating the concentration of bioaerosols in ambient air in Shahrekord, Iran during two warm and cold seasons at three different points in 2019. Moreover, the effect of meteorological factors such as temperature, relative humidity, UV intensity, and wind speed and direction on bioaerosols were studied. Materials and methods: In this descriptive-analytical study, sampling of bioaerosols was conducted using Andersen single-stage sampler at a flow rate of 28.3 L/min for 5 min on Sabrod dextrose agar (SDA) and Tryptic Soy agar (TSA) media for bacterial and fungal bioaerosols, respectively. Results: The study showed that the concentration of fungal bioaerosols was higher than bacterial bioaerosols in warm and cold seasons. The predominant genera of bacteria in both seasons included Micrococcus luteus (21.35%), Pseudomonas aeruginosa (12.68%), Bacillus subtilis (10.14%), and Staphylococcus aureus (9.93%). The predominant genus of fungi were Cladosporium (41%), Alternaria (16%), and Aspergillus (11%). Correlation analysis showed a significant positive correlation between the concentration of bioaerosols and wind direction and relative humidity and a significant negative correlation between temperature, wind speed and UV intensity in warm season. Conclusion: The predominant species of bioaerosols identified in this study were opportunistic pathogens and allergens which can threaten public health. So, monitoring of the concentration of airborne bioaerosols in cities is a vital key to assess the health effects of ambient air pollution. [ABSTRACT FROM AUTHOR]

Background: Breast cancer remains a significant global health challenge, with thymoquinone showing promise as a therapeutic agent, but hindered by poor solubility., Objective: This study aimed to enhance TQ delivery to MCF-7 breast cancer cells using mesitylene- mesoporous silica nanoparticles coated with liposomes, designed for controlled drug release., Methods: Nanoparticles were synthesized using the sol-gel method and coated with phosphatidylserine- cholesterol liposomes. Different nanocharacterization techniques and in vitro assays were employed to assess the drug release kinetics, cellular uptake, cytotoxicity, and apoptosis., Results: The nanoparticles exhibited favorable properties, including a large pore size of 3.6 nm, a surface area of 248.96 m2/g, and a hydrodynamic size of 171.571 ± 8.342 nm with a polydispersity index of 0.182 ± 0.017, indicating uniformity and stability. The successful lipid bilayer coating was confirmed by a zeta potential shift from +6.25 mV to -5.65 mV. The coated nanoparticles demonstrated a slow and sustained drug release profile, with cellular uptake of FITC-formulated nanoparticles being approximately 5-fold higher than free FITC (P < 0.0001). Cytotoxicity assays revealed a significant reduction in cell viability (P < 0.0001), reaching an IC50 value of 25 μM at 48 hours. Apoptosis rates were significantly higher in cells treated with the formulated TQ compared to the free drug and control at both 24 and 48 hours (P < 0.0001)., Conclusion: This nanoformulation significantly enhanced TQ delivery, offering a promising strategy for targeted breast cancer therapy. Further preclinical studies are recommended to advance this approach in cancer treatment., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: TGIF2LX (transforming growth factor beta-induced factor 2 like, X-linked) is a homeodomain (HD) protein that has been implicated in the negative regulation of cell signaling pathways. The aim of this study was to investigate the possible functions of TGIF2LX in colon adenocarcinoma cells. Methods: The human SW48 cell line was transfected with cDNA for the wild-type TGIF2LX gene and gene/protein over-expression was confirmed by microscopic analysis, real time RT-PCR and Western blotting techniques. In vitro cell proliferation was evaluated by MTT and BrdU assays. After developing a colon tumor model in nude mice, immunohistochemical (IHC) staining of tumor tissue was carried out for Ki-67 (proliferation) and CD34 (angiogenesis) markers. To predict potential protein partners of TGIF2LX, in-silico analysis was also conducted. Results: Obtained results showed over-expression of TGIF2LX as a potential transcription factor could inhibit either proliferation or angiogenesis (P<0.05) in colon tumors. In-silico results predicted interaction of TGIF2LX with other proteins considered important for cellular development. Conclusions: Our findings provided evidence of molecular mechanisms by which TGIF2LX could act as a tumor suppressor in colon adenocarcinoma cells. Thus, this gene may potentially be a promising option for colon cancer gene-based therapeutic strategies., (Creative Commons Attribution License)

Background: Transforming growth factor-β (TGF-β) pathway is involved in primary tumor progression and in promoting metastasis in a considerable proportion of human cancers such as colorectal cancer (CRC). Therefore, blockage of TGF-β pathway signaling via an inhibitor could be a valuable tool in CRC treatment., Methods: To evaluate the efficacy of systemic targeting of the TGF-β pathway for therapeutic effects on CRC, we investigated the effects of a TGβRI (TGF-β receptor 1) or TβRI kinase inhibitor, SD-208, on SW-48, colon adenocarcinoma cells. In this work, in vitro cell proliferation was studied by methyl thiazolyl tetrazolium (MTT) and bromo-2'-deoxyuridine (BrdU) assays. Also, the histopathological and immunohistochemical evaluations were conducted by hematoxylin and eosin, and Ki-67 and CD34 markers were stained, respectively., Results: Our results showed no significant reduction in cell proliferation and vessel formation (170 ± 70 and 165 ± 70, P > 0.05) in treated SW-48 cells with SD-208 compared to controls., Conclusion: Our data suggested that SD-208 could not significantly reduce tumor growth and angiogenesis in human colorectal cancer model at least using SW-48 cells.