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All fields of industry are applying nanotechnologies for the development of advanced materials, there¬fore at present the number of workers exposed to nanosized materials are significantly increasing. Unfortunately, protective equipment for nanoparticles (NPs) is of uncertain efficacy so the risk of noxious effects, in particular allergic sensitization, on workers gives many concerns. At the same time, studies of allergic physiopathology demonstrated that the lack of prevention and treatment could result in invalidating dis¬eases that, in case of professional etiology, might imply removal from the job and compensation. Therefore, a deeper knowledge of the role of NPs in inducing allergic diseases is mandatory to implement the risk assessment and preventive measures for nanosafety in the workplace. The possibility that NPs favor, ex¬acerbate or directly induce allergy is being suggested by recent experimental investigations in cellular and animal models. Unfortunately, studies are heterogeneous and few data have received experimental confir¬mation, lacking reproducibility. What comes to attention is the uncertainty about the real plausibility of the observed experimental effects, as there are only a few reported cases of allergy onset or exacerbation for workers exposed to NPs. However, the potential for NPs to induce, favor or exacerbate allergies seems possible even though not completely demonstrated. This should be a greater incentive to carry out appro¬priate epidemiological studies that are lacking and really needed.
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Endometrial cells undergo very specific changes associated with reproductive processes. Cells prepare for embryo development by increasing their volume. Then, if fertilization fails, endometrial cells are liable for apoptosis, preparing new cells that are ready for subsequent processes related to the possibility of embryo implantation and the development of pregnancy. PTX3 and TNFAIP6 are absent or reduced in cultured COCs, resulting in a functional change in COC in vitro. In this work, we want to check how PTX3, HAS2 and TNFAIP6 behave in luminal epithelium primary cell culture. Cells obtained during slaughter from porcine specimens were cultured primarily in vitro for 7 days. Their proliferation patterns were then analysed using RTCA, with the expression of genes of interest evaluated with the use of immunofluorescence and RT-qPCR. The results of these changes in the expression of the genes of interest were analysed on each of the seven days of the porcine luminal primary cell culture. Our study showed the increased level of PTX3, HAS2 and TN¬FAIP6 expression at the same hours of primary culture. Rt-qPCR showed a higher level of expression of the PTX3 gene in the first 72 h, at the end of the lag phase (in the phase of stasis in which the cells adapt to the new environment and often die). In contrast, TNFAIP6 expression increases about 96 hours when the cells are in the full log phase (logarithmic phase growth) and continue this trend in the plateau phase. We did not observe such drastic changes in the HAS2 expression pattern, which leads us to hypothesize that PTX3 and TNFAIP6 are designed to maintain a constant level of HAS2 in the cell throughout its lifetime. The obtained results could become a point of reference for further in vivo and clinical research.
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To investigate the effect of exogenous insulin-like growth factor-1 (IGF-1) on the healing of skin ulcers in diabetic rats, male Sprague Dawleys (SD) rats with back skin ulcers were selected and divided into control group, model group and IGF-1 treatment group which received different doses of IGF-1 (0.5, 1.0, 1.5, and 2.0mg/L). The results showed that the healing speed of the skin ulcers was significantly affected by IGF-1, which reduced the size of wound (P less than 0.05). The expression of MMP-9 was enhanced while the expression of TIMP-1 was decreased in diabetic rats with skin ulcers. The IGF-1 treatment helped to re¬store the normal expression of both MMP-9 and TIMP-1 in diabetic rats with skin ulcers, and diabetic skin ulcers in the 1.5 mg/L IGF-1 group showed the best healing. Histological examination showed that after 20 days, fibroblasts in the IGF-1 experimental group with an appropriate concentration increased and the numbers of fibroblasts and capillaries were significantly higher than those of the other groups. Moreover, there were obvious wound surface contractions and re-epithelialization, and the new epithelium moved to the center of the wound faster. Therefore, it is concluded that an appropriate concentration of IGF-1 can significantly promote the healing of skin ulcers in diabetic rats.
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Lipids are an alternative energy source for cells and provide structural integrity in cell membrane and their metabolism is regulated with the use of different pathways, such as integrin signalling, oxidative stress, mechanical stress, and pH changes. All of those processes take place in the oral mucosa which is subject to different environmental impacts. In this study, porcine buccal pouch mucosal cells (pBPMCs) were used during long-term primary in vitro culture. The cultured cells were collected at 7, 15 and 30 days of IVC and subsequently transferred to RNA isolation. In the results of the following microarray analysis, we analyzed the genes detected, belonging to ontology groups, such as "cellular lipid metabolic process", "response to lipid" and "response to lipopolysaccharides. All of the genes involved in these ontological groups were expressed at higher levels at 7 days of IVC and substantially decreased in expression at days 15 and 30 of primary culture. We observed new genes, which may be recognized as markers in regulation of lipid metabolism in mucosal cells in vitro. The results suggested that the biochemical mechanism-involved lipids were accompanied by increased enzymatic activation and synthesis of crucial growth factors reaching high activity at day 7 of culture, which is also well documented as a stage of tissue regeneration period within oral mucosa. Therefore, this "biochemical fingerprint" may be an additional checkpoint of the integrity, resistance and easy adaptability of oral tissues, which are important conditions of success in tissue engineering and grafting for tissue reconstruction.
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The familiar glitazone anti-diabetics are thiazolidinedione derivatives, known to elicit action through full agonistic activity on PPAR-γ receptors. Full agonists are known for the side effect of weight gain, while partial agonists are weak to non-adipogenic compounds possessing anti-diabetic property. This work identified a new synthetic oxadiazolyl thiazolidinedione (OXTZD) as a ligand for PPAR-γ receptor with partial agonist activity and less transactivation potential compared to rosiglitazone through in-vitro PPAR-γ competitive binding assay and PPAR-γ transactivation-based luciferase reporter assay, respectively. OXTZD did not induce significant lipid accumulation when compared to differentiation control which contained insulin in PPAR-γ-dependent adipogenesis assay. In-vivo studies have proved that OXTZD effectively reduced blood glucose level in type 2 diabetic rats and also improved glucose tolerance and insulin sensitivity. After 15 days of oral treatment with OXTZD, rats did not gain weight, suggesting that OXTZD was effective in suppressing the weight gain. Molecular docking of OXTZD to PPAR-γ, predicted hydrogen bonds with SER342, ARG288, and CYS285 residues in arm III of the ligand binding domain which are unique to the partial agonists. Results of in-vitro, in-vivo, and docking studies were in good correlation to the fact that OXTZD is a PPAR-γ partial agonist having glucose-lowering property and lacks the side effect of weight gain. In conclusion, OXTZD could be developed as a therapeutic agent for diabetes and/or serve as a lead compound for further drug design studies targeting PPAR-γ for effective management of type 2 diabetes without inducing weight gain.
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This study aimed to investigate the mechanism underlying the inhibitory effect of tumor suppressor gene miR-186 and zinc finger protein 545 (ZNF545) on the proliferation of multiple myeloma (MM) cells. CD138 magnetic beads were used to isolate different types of myeloma cell lines (KM3, U266, RPMI-8226, and H929), which were then infected by lentivirus carrying the miR-186 gene. Using uninfected myeloma cells as the control, MTT [3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide, Thiazolyl Blue Tetrazolium Bromide] assay was performed to calculate the rate of cell proliferation at different time points. In addition, the correlation between the expression of Jagged 1 and miR-186 was analyzed by real-time Polymerase Chain Reaction (PCR). Furthermore, the effect of 5-Aza-2-deoxycytidine and acetylase inhibitor Trichomycin A (TSA) on the expression of ZNF545 and proliferation/apoptosis of MM cells was investigated using Reverse Transcription-Polymerase Chain Reaction (RT-PCR), Western blotting (WB), MTS [3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium] cell proliferation assay, and Annexin V-FITC/PI staining. Compared with the control group, the proliferation of miR-186-overexpressing U266 and RPMI-8226 cells was significantly decreased. In cell cloning experiments, miR-186 decreased the number of U266 and RPMI-8226 clones while reducing the protein expression of Jagged 1. The expression level of ZNF545 in myeloma patients was also reduced to some extent. ZNF545 protein also promoted the apoptosis of myeloma cells. By inhibiting the proliferation of myeloma cells, miR-186 gene and ZNF protein may be used as tumor suppressors in the treatment of myeloma.
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Arsenic acts as a human carcinogen and contributes to skin cancer via mechanisms that remain largely unknown. Recent evidence implicates the perturbation of Wnt, Shh and BMP signals as a potential mechanism. We initiated studies to examine gene expression changes in these signaling pathways. Meanwhile, the antagonistic effect of retinoic acid was explored. In this study, HaCaT and NHEK cells were treated with arsenic trioxide (As2O3) alone or in combination with arotinoid trometamol (retinoic acid receptor agonist). Flow cytometric analysis, PCR array and Western blot were used to determine the potential mechanism and signaling pathways associated with arsenic carcinogenesis. The results showed that low concentration As2O3 could stimulate keratinocyte proliferation, and arotinoid trometamol inhibited the process via regulating the expression of about 20 genes. These genes included components of Wnt signaling (CSNK1A1L, CTNNB1, SFRP1, Wnt10B, Wnt11, Wnt16, Wnt5A, Wnt8A), Shh signaling (C6orf138, HHIP, PTCHD1) and BMP signaling pathway (BMP2, BMP7). The changes of some differentially expressed genes of these signaling pathways in As2O3 treatment group were counteracted by the subsequent arotinoid trometamol treatment. Our data suggest that dysregulation and cross-talk of Wnt, Shh and BMP signals play great roles in the process of arsenic-induced carcinogenesis, which could be antagonized by arotinoid trometamol.
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This study aimed to explore the effect of Sca-1+ bone marrow stromal stem cells (BMSCs) on lung ischemia reperfusion injury in mice. Five healthy Sprague-Dawley rats were selected to isolate and purify their Sca-1+ BMSCs using a Sca-1+ magnetic sorting kit in conjunction with whole bone marrow culture. In addition, 21 male C57BL/6J mice were divided into 3 groups (7 mice in each group), namely sham group (group A), I/R group (group B) and BMSCs group (group C). A pulmonary ischemia reperfusion injury model was established by ligating the left pulmonary portal vessel for 60 min and reperfusion for 240 min, after which the right pulmonary portal vessel was blocked to measure arterial partial pressure of oxygen (PaO2) and arterial partial pressure of carbon dioxide (PaCO2). Subsequently, the mice were sacrificed to determine their superoxide dismutase (SOD) activity, malondialdehyde (MDA) content and myeloperoxidase (MPO) activity in the lung tissue. The histological changes were observed by light microscopy, while an enzyme-linked immunosorbent assay (ELISA) was used to detect the changes in plasma expressions of tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10) in the mice. In addition, plasma expressions of TNF-α and B-cell lymphoma-2 (bcl-2) in the mice were detected by immunohistochemistry, while the apoptosis of transplanted lung cells was detected by a TdT-mediated dUTP Nick-End Labeling (TUNEL) method. Compared with group A, group B showed a decreased level of PaO2 and SOD activity but an increased level of MDA content and MPO activity (P less than 0.01), indicating that group B had significant ischemia reperfusion injury compared to group A. In conclusion, BMSCs significantly reduced lung ischemia-reperfusion injury and improved lung function through their anti-oxidation, anti-inflammatory and anti-apoptosis properties.
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The root cause of obstructive sleep apnea-hypopnea syndrome (OSAHS) is repeated hypoxia during sleep. The genioglossus is one of the most important upper airway dilatation muscles and is important for maintaining normal oxygen supply during sleep. Hypoxia can directly affect the energy metabolism level of the genioglossus muscle, thereby weakening muscle function. MicroRNAs (miRNAs) can regulate mitochondrial function at the post-transcriptional level and achieve recovery or even enhancement of genioglossus function, but the specific mechanism is still unclear. In this study, an intermittent hypoxic cell model was established to detect the effects of hypoxia on the proliferation and apoptosis of Genioglossus muscle satellite cells (GG MuSCs), and the damage to the mitochondrial structure and function was assessed by transmission electron microscopy and mitochondrial membrane potential. Then, miR-17-5p was upregulated and downregulated by miRNA mimics and inhibitors, respectively, and bioinformatics analysis was used to predict and validate the target genes of miR-17-5p. The results showed that the hypoxic environment affected the proliferation of GG MuSCs and mitochondrial membrane potential, which promoted the occurrence of apoptosis and mitochondrial edema. After upregulation of miR-17-5p, cell proliferative capacity and mitochondrial function were restored. Bioinformatics prediction and gene and protein level analyses found that Mfn2 may be a target gene of miR-17-5p.
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Melatonin plays an important role in various gut functions through melatonin receptors. The gut microbiota/gut hormone axis has recently received increasing attention. However, the relationship between the gut microbiota and melatonin receptors has not yet been evaluated. We aimed to determine the effect of the gut microbiota on colonic melatonin receptor expression in germ-free (GF) rats and to further explore the potential mechanism in Caco-2 cells. In this study, GF rats were transplanted with fecal samples from a healthy human donor. Subsequently, 16S rRNA sequencing was performed to analyze the microbial communities. Colon tissue was collected for immunohistochemical analysis. The correlations between melatonin receptor expression and the gut microbiota were assessed. Melatonin receptor expression in Caco-2 cells was detected by Western blot. We found that fecal microbiota transplantation significantly increased the expression of colonic melatonin receptors in GF rats. The amount of fecal Short chain fatty acids (SCFAs) was significantly higher in fecal microbiota transplantation (FMT) rats than in GF rats. SCFA-producing bacteria, such as Alistipes and Blautia, were positively correlated with colonic melatonin receptor expression in FMT rats. Additionally, acetate and propionate significantly increased melatonin receptor-1 expression in Caco-2 cells. Therefore, the gut microbiota may promote melatonin receptor expression, and the mechanism may involve the action of SCFAs. This finding may facilitate the development of new therapeutic treatments for various gastrointestinal disorders.
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This study aimed to investigate the role of long-chain non-coding RNA CTBP1-AS in breast cancer progression and cell invasion as well as migration. Clinical data of breast cancer patients (N = 155) in our hospital was collected for further analysis. qRT-PCR was used to detect LncRNA CTBP1-AS expression levels in human normal breast epithelial cell (MCF-10A) and breast cancer cells (MCF-7, BT- 549, MDA-MB-231 and MDA-MB-435). LncRNA CTBP1-AS knock-down and overexpressed lentivirus vectors were constructed to transfect breast cancer cells. Colony formation assay was employed to detect cell proliferative abilities. Flow cytometry was performed to detect cell apoptosis ratio. Wound healing scratch assay was used to detect cell migration, and Transwell matrigel assay was used to detect cell invasion. Bioinformatics analysis was performed to predict the downstream targets of LncRNA CTBP1-AS, which were further validated by dual-luciferase reporter gene system. The results showed that LncRNA CTBP1-AS was aberrantly overexpressed in breast cancer tissues and breast cancer cells compared to the control group. Moreover, the expression levels of LncRNA CTBP1-AS were positively related with tumor size, histological grade and the expression levels of Ki-67 and Her2. Further analysis showed that LncRNA CTBP1-AS expression levels negatively correlated with patient survival time and clinical prognosis. Of note, overexpressed LncRNA CTBP1-AS promoted breast cancer cell proliferation and invasion as well as migration, and decreased cell apoptosis ratio. Bioinformatics analysis and dual-luciferase reporter gene system results validated that microRNA-940 was the downstream target of LncRNA CTBP1-AS. Interestingly, overexpressed microRNA-940 abrogated the effects of LncRNA CTBP1-AS on cell proliferation, apoptosis, and invasion. In conclusion, overexpressed LncRNA CTBP1- AS promoted breast cancer cell proliferation, invasion as well as migration, inhibited cell apoptosis and accelerated breast cancer development by sponging microRNA-940.
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The aim of this 10-year retrospective study was to evaluate the long-term reliability, survival rate and mechanical and biological complications of single-crown implant rehabilitations with two different types of fixture-abutment connections: screw-retained abutments (SRAs) with internal hexagonal connection, and cemented retained abutments (CRAs). A total of 300 single implant-supported crowns were analysed, which had been inserted between 2004 and 2007. Patients were classified according to two groups: the SRA group (n = 150) and the CRA group (n = 150). The primary outcome was marginal bone loss (MBL) on peri-apical radiographs. Bleeding on probing (BOP) and probing depth (PD) were also evaluated. Moreover, prosthetic complications were recorded. Analysis of variance (ANOVA) was used to evaluate the differences between the groups. The overall implant failure rate was 4.2%. The overall positive BOP index was 81.9% of the sites under investigation, as 83.4% for SRA and 80.4% for CRA. Moreover, >5 mm PD demonstrated a rate of 21.0% for CRA, and 13.8% for SRA. The primary outcome of mean MBL was 2.09±1.07 mm for SRA and 1.54±1.20 mm for CRA. Analysis of variance of MBL showed statistical significance for the difference between these two groups (P less than 0.001). For the mechanical aspects, an overall 12.5% of complications occurred. No implant or abutment fractures were recorded. Although complications occurred, the results from this 10-year retrospective study show that these two methods have positive long-term follow-up. With MBL significantly greater for the SRA group than the CRA group, the clinical use of CRA is encouraged in terms of the lower bone resorption rate.
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Prostate cancer continues to be a major cause of morbidity and mortality in men around the world. The data concerning the antioxidant status and the degree of lipid peroxidation at the moment of the initiation of cancer is limited. The aim of this research is to assess the effect of selected minerals (zinc, selenium, iron, copper and calcium) on the growth of the neoplastic process and the concentrations of selected biomarkers of the oxidative damage in rats with implanted prostate cancer cells. It was found that the diet supplementation with selected minerals (zinc, selenium, iron, copper and calcium) affect the occurrence of prostate tumor growth in the examined rats. The intraperitoneal implantation of prostate cancer cells resulted in the occurrence of prostatic adenoma in 71% of the examined rats. In the rats that were additionally supplemented with selenium and with copper, the cancer cell aggregates constituted, respectively, 25% and 38% of the cases. As a result of implantation of cancer cells, the level of biomarkers of lipid peroxidation increased both in the urine and in tissues of the examined animals (rat group without supplementation). No relationship was found between the process of lipid peroxidation due to the supplementation with selenium and copper, and the lower incidence of cancer and the induction of apoptosis. The reduced activity of antioxidative enzymes (catalase, superoxide dismutase and glutathione peroxidase) creates favorable conditions for the formation of cancer cell aggregates, which was shown in the rats whose diet was supplemented with iron. In summary, we conclude that lipid peroxidation represents a fruitful approach to early stage cancer prevention. Supplementation of rats with trace elements correlated with the risk of developing cancer, but the mechanisms of this action is complicated and dose-dependent.
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Children with severe pneumonia often have heart failure. This study explored the clinical effect of highquality nursing intervention on children with pneumonia complicated with heart failure. In the study,96 children with pneumonia complicated with heart failure were selected and randomly divided into aconventional nursing group (n=48) and a high quality nursing group (n=48). Based on the conventionalnursing, the children in one group were given high quality nursing, and comprehensive nursing wascarried out in aspects such as respiratory tract, medication, psychology and diet. Then, the heart rate,respiratory rate, heart failure correction time, hospitalization time, cost and nursing satisfaction werecompared between the two groups. The results showed that the heart rate of the high quality nursinggroup was 145.37±8.72 times/min and the respiratory rate was 45.65±6.08 times/min, which weresignificantly lower than those of the conventional nursing group (P<0.05). The correction time of heartfailure was about 32 h in the high quality nursing group, and the length and cost of hospitalization weresignificantly lower than those in the conventional nursing group (P<0.05). The nursing satisfaction of thepatients’ family members in the high quality nursing group was also higher (P<0.05). This study showsthat high quality nursing can promote the recovery of children with pneumonia complicated with heartfailure, and is worth popularizing widely in clinics.a
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