Summary MADS‐box transcription factor Mcm1 plays crucial roles in regulating mating processes and pathogenesis in some fungi. However, its roles are varied in fungal species, and its function remains unclear in entomopathogenic fungi. Here, Mcm1 orthologue, Bbmcm1, was characterized in a filamentous entomopathogenic fungus, Beauveria bassiana. Disruption of Bbmcm1 resulted in a distinct reduction in growth with abnormal conidiogenesis, and a significant decrease in conidial viability with abnormal germination. ΔBbmcm1 displayed impaired cell integrity, with distorted cell wall structure and altered cell wall component. Abnormal cell cycle was detected in ΔBbmcm1 with longer G2/M phase but shorter G1/G0 and S phases in unicellular blastospores, and sparser septa in multicellular hyphae, which might be responsible for defects in development and differentiation due to the regulation of cell cycle‐involved genes, as well as the corresponding cellular events‐associated genes. Dramatically decreased virulence was examined in ΔBbmcm1, with impaired ability to escape haemocyte encapsulation, which was consistent with markedly reduced cuticle‐degrading enzyme production by repressing their coding genes, and downregulated fungal effector protein‐coding genes, suggesting a novel role of Mcm1 in interaction with host insect. These data indicate that Mcm1 is a crucial regulator of development, cell integrity, cell cycle and virulence in insect fungal pathogens.

Pathogenic bacterial strains can alter the normal function of cells and induce different levels of inflammatory responses that are connected to the development of different diseases, such as tuberculosis, diarrhea, cancer etc. Chlamydia trachomatis (C. trachomatis) is an intracellular obligate gram-negative bacterium which has been connected with the cervical cancer etiology. Nevertheless, establishment of causality and the underlying mechanisms of carcinogenesis of cervical cancer associated with C. trachomatis remain unclear. Studies reveal the existence of C. trachomatis in cervical cancer patients. The DNA repair pathways including mismatch repair, nucleotide excision, and base excision are vital in the abatement of accumulated mutations that can direct to the process of carcinogenesis. C. trachomatis recruits DDR proteins away from sites of DNA damage and, in this way, impedes the DDR. Therefore, by disturbing host cell-cycle control, chromatin and DDR repair, C. trachomatis makes a situation favorable for malignant transformation. Inflammation originated due to infection directs over production of reactive oxygen species (ROS) and consequent oxidative DNA damage. This review may aid our current understanding of the etiology of cervical cancer in C. trachomatis-infected patients.

Abstract. The aim of the present study was to investigate the role of homocysteine (Hcy) in the pathogenesis of pulmonary embolism (PE) and the associated molecular mechanisms in human umbilical vein endothelial cells (HUVECs). Hcy contents were detected with high-performance liquid chromatography. Apoptosis was detected by flow cytometry using Annexin-V staining. Cytochrome c oxidase (COX) activity was assessed with an enzyme activity assay, and the expression levels of COX 17 were determined by western blot analysis. Intracellular reactive oxygen species levels were measured using a microplate reader with a fluorescence probe. The results demonstrated that, compared with the control group, the serum Hcy levels were significantly elevated in the PE group, suggesting that Hcy may be an indicator for PE. Following treatment with Hcy, the apoptosis rate was markedly elevated in HUVECs. Moreover, Hcy decreased COX activity and downregulated the expression of COX 17 in HUVECs. Furthermore, Hcy increased the ROS levels in these endothelial cells. However, all the above-mentioned physiopathological changes induced by Hcy in HUVECs could be restored by folic acid. In conclusion, the results of the present study demonstrated that Hcy inhibited COX activity, downregulated COX 17 expression, increased intracellular ROS levels and enhanced apoptosis in endothelial cells. IntroductionPulmonary embolism (PE) is a frequent clinical syndrome with abnormal pulmonary circulation, which is predominantly caused by the blockage of pulmonary and/or bronchial arteries by thrombus shedding (1). Due to the sudden disease onset, PE is difficult to treat and usually results in the patient succumbing to the disease (2,3). Homocysteine (Hcy) is an intermediate product of methionine metabolism, and is an independent risk factor for cardiovascular diseases (4,5). Previous studies reported that serum Hcy levels are markedly elevated in patients with PE, which is implicated in the disease pathogenesis (6-8).Vessel wall injury is one of the important factors for PE, as the pathological changes in endothelial cells may result in the formation of thrombosis (9,10). It has been demonstrated that high concentrations of Hcy induce apoptosis in endothelial cells (11,12), in which mitochondria are involved. Cytochrome c oxidase (COX) is a key enzyme in mitochondrial function (13)(14)(15). Enhanced COX activity may increase intracellular reactive oxygen species (ROS) levels, resulting in cellular apoptosis (16)(17)(18)(19)(20)(21). Based on these reports, it would be of interest to define the association between Hcy, COX, and ROS in apoptosis, specifically in the context of PE pathogenesis.In the present study, the effects of Hcy on endothelial cells and the associated molecular mechanisms were investigated. Materials and methods Patients.A total of 10 patients with PE, 4 males and 6 females, aged 50-67 years (with an average age of 60.4 years), were included in this study. These PE cases were diagnosed based on the clinical manifestations and the resu...

Silver selenide nanoparticles have advantages of low cytotoxicity, desirable near-infrared light response characteristics, and easy surface modification, which attract increasing attention in chemo-photothermal therapy and nursing care of cancer patients. In this contribution, we synthesized Ag 2 Se nanoparticles modified by the surfactant of cetyltrimethylammonium bromide (CTAB) using a ligand exchange strategy. Their microstructure and composition were characterized by transmission electron microscopy, X-ray diffraction, X-ray Photo-electronic Spectroscopy, and Fourier transform infrared spectroscopy. The CTAB modified Ag 2 Se nanoparticles exhibited a uniform diameter distribution centered at ~12 nm. In order to investigate the photothermal and adsorption effects of CTAB-Ag 2 Se nanocomposites, we also prepared sodium dodecyl benzene sulfonate (SDBS) modified Ag 2 Se nanoparticles to make a comparison. The CTAB-Ag 2 Se nanoparticles showed high photothermal properties, a photothermal conversion efficiency of 20.1% and a high drug adsorption performance of 48.2 μg/mg. Importantly, the CTAB-Ag 2 Se-DOX presented an MCF-7 cell activity of only 27.3% under near-infrared radiation. The results revealed that the surface-modified Ag 2 Se nanoparticles with CTAB had stronger antitumor ability.

Different drying methods, including hot air drying (HAD), freeze drying (FD), spray drying and vacuum drying (VD), were investigated to determine their influence on the chromatic coordinates, phenolics, anthocyanins and antioxidant activities of dried red raspberry (Rubus lambertianus). Pelargonidin-3-O-glucoside and catechin were found to be the main anthocyanin and non-anthocyanin phenolics, respectively, in fresh red raspberry. The most effective method for controlling browning was FD. The highest protective effects against bioactive compounds were observed in freeze-dried powders, when measuring the total anthocyanins, the scavenging of DPPH (1,1-diphenyl-2-picrylhydrazyl) and hydroxyl radicals and the inhibition effects on lard oxidation. HAD was effective for the preservation of total phenolics, while VD was useful for protecting catechin and procyanidin B1.