I am trying to create on cluster in which i am trying to send multiple configuration file. I have installed four Redhat OS in VMWARE which is connected through IP. when i run script at host server with ssh-keygen, it always ask me for password. To resolved it i have also used sshpass and passing password from one temp file but same issue. each time it ask for password. I have follow all three steps of SSH-KEYGEN. Could you please help me, where could be a mistake.
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Hepatocellular carcinoma (HCC) is the second leading cause of cancer death in Asia; however, the molecular mechanism in its tumorigenesis remains unclear. Abnormal expression of claudins (CLDNs), a family of tight junction (TJ) proteins, plays an important role in the metastatic phenotype of epithelial-derived tumors by affecting tight junction structure, function and related cellular signaling pathways. In a previous study, we used a tissue chip assay to identify CLDN17 as an upregulated gene in HCC. Here we aimed to use molecular biology technology to explore the effect of CLDN17 on the malignant phenotype of HCC and the underlying molecular mechanism, with the objective of identifying a new target for HCC treatment and the control of HCC metastasis.
Additionally, CLDNs have been shown to participate in the transduction of intracellular/extracellular signals and may be related to tumorigenesis and cancer progression in human various carcinomas [8, 9]. For instance, genetic and pharmacological studies confirmed that the expression of CLDN3 was downregulated in colon cancer and that the loss of CLDN3 induced Wnt/β-catenin activation in a transducer and activator of transcription 3 (Stat3)-dependent manner to promote colon cancer malignancy [10]. Besides, a recent study revealed that enhanced CLDN18 expression activated ERK1/2 to contributed to the malignant potentials of bile duct cancer [11]. Our preliminary work showed that CLDN17 was strongly expressed in HCC tissues and cell lines and weakly expressed in non-neoplastic tissues and hepatocyte lines, which revealed that upregulated CLDN17 expression may play a role in the development of HCC. Furthermore, gene chip screening revealed that CLDN17 overexpression activated the tyrosine kinase 2 (Tyk2)/Stat3 pathway signaling pathway. To date, there has been no report on the impact of CLDN17 on the malignant phenotype of hepatocytes. In this study, we utilized molecular biology and other techniques to study the role and mechanisms of CLDN17 in malignant phenotype of hepatocytes and to identify novel targets for HCC treatment and the control of early metastasis.
MDR is the main cause of chemotherapy failure ingastric cancer treatment. Thus, in this study, to assess theassociation between TSPAN8 and MDR, the siRNA-transfectedSCG7901/DDP cells were treated with cisplatin, 5-Fu and adriamycin(the most commonly used drugs in clinical practice for thechemotherapeutic treatment of gastric cancer), for 2 days and theIC50 values were determined. The IC50 valuesof cisplatin, 5-Fu and adriamycin were significantly decreased inthe TSPAN8-silenced SGC7901/DDP cells compared with the negativecontrols (Table II). This resultsuggested that the silencing of TSPAN8 reduced the resistance ofthe SGC7901/DDP cells to the aforementioned drugs, which, in turn,indicated that TSPAN8 may contribute to the MDR of this cell line.In the following experiments, only cisplatin was used to maintainthe drug resistance of the SGC7901/DDP cells.
Furthermore, compared with the negative controlSGC7901/DDP cells, apoptosis was increased in the TSPAN8-silencedcells (Fig. 4C). Moreover, thelevels of apoptosis-related proteins (caspase-3, Bax and Bcl-2)were examined by western blot analysis. The results (Fig. 4D) revealed that the levels ofcaspase-3 and Bax were upregulated, while those of Bcl-2, ananti-apoptotic protein, were downregulated in the TSPAN8-silencedSGC7901/DDP cells. These results indicated that the silencing ofTSPAN8 promoted SGC7901/DDP cell apoptosis.
Thus far, our findings suggested that TSPAN8 plays acritical role in the drug resistance of SGC7901/DDP cells. It isbelieved that metastasis is the persistence of cancer stem cells(CSCs), which are highly resistant to chemotherapy (28). The Wnt/β-catenin signaling pathwayhas been reported to increase gastric cancer cell migration andinvasion (29). Therefore, in thisstudy, we investigated whether TSPAN8-mediated gastric cancer celldrug resistance is also related to the Wnt/β-catenin pathway. TheWnt/β-catenin pathway activity was detected using a TOP-flashluciferase reporter. The silencing of TSPAN8 in the SGC7901/DDPcells significantly decreased TOP-flash luciferase activity(Fig. 5A). The TSPAN8-silencedcells displayed a decreased expression of β-catenin at both themRNA (Fig. 5B) and protein level(Fig. 5C), compared to negativecontrol (NC)-infected SGC7901/DDP cells. Additionally, theaccumulation of β-catenin in the nucleus was impaired in theTSPAN8-silenced SGC7901/DDP cells (Fig. 5D). The cells were treated withCCT036477 (CCT) and XAV939 (inhibitors of the Wnt-β-cateninpathway) (30). The reducedIC50 value caused by TSPAN8 silencing was partiallyreversed when the Wnt-β-catenin pathway inhibitors were added(Table III). These dataindicated that TSPAN8 enhanced the resistance of the SGC7901/DDPcells to chemotherapy through the activation of the Wnt/β-cateninpathway and by increasing β-catenin expression and accumulation inthe nucleus. However, compared to the NC group, the inhibitors ofthe Wnt pathway still decreased the IC50 values(Table III).
Compared to the control group, erastin could significantly induce the SCD1 knockdown pancreatic cancer cell death under H/NS condition (Figure 3(c)). Also, the cell viability of SCD1-knockdown cells under H/NS condition was decreased upon erastin treatment, which was reversed in the presence of oleic acid (OA) or Fer-1 (Figure 3(d)). Furthermore, knockdown of SCD1 significantly increased MDA production in H/NS cultured PANC1 and Patu8988 in the presence of erastin (Figure 3(e)). Given that MUFAs, products of SCD1-catalyzed reaction, negatively regulate ferroptosis, we therefore asked whether MUFA concentration was altered in SCD1 shRNA groups. ELISA assay results showed a marked decrease in MUFA concentration occurred in SCD1 shRNA groups under H/NS condition (Figure 3(f)).
In the present study, the percentage of apoptotic sperm cells in the exposure group was significantly increased by 91.42 % compared with the control group. Moreover, the ROS concentration in exposure group was increased by 46.21 %, while the TAC was decreased by 28.01 %. Radiation also dramatically decreased the protein and mRNA expression of bcl-2 and increased that of bax, cytochrome c, and capase-3.
Despite the continued advances in science, the infertility rate is currently increasing because of increased stress factors. Approximately 14 % of couples in developed countries experience conception difficulties [15]. The decreased reproductive capacity of men is an important factor contributing to infertility, and RF-EMR may contribute to this condition [16]. However, whether RF-EMR affects the human reproductive system remains controversial [17]. Seze et al. found that exposure to EMR at a frequency of 900 MHz for 2 h/d exerted no significant effects on the concentrations of serum luteinizing hormone and follicle stimulating hormone [18]. Agarwal et al. reported no significant difference on total antioxidant capacity (TAC) and damage of DNA in ejaculated semen between the pilots who often use mobile phones and the control group [19]. Nevertheless, more studies have indicated that radiation intensity and duration of RF-EMR will influence the parameters of male reproduction capacity; these parameters include the concentration [20], mobility, morphology [21], viability of sperm cells [16, 20, 22] and sperm apoptosis [23]. Moreover, RF-EMR also affects or destroys leydig cells, which are adjacent to the seminiferous tubules [24], and decreases the diameter of seminiferous tubule [25] and the weight of testicular organs [26].
No significant difference in the epididymal weights was observed between the control and exposure groups after 50 d of exposure to RF-EMR at 900 MHz. However, the body weights were significantly higher in the exposure group than the control. The ratio between the epididymal and body was significantly lower in the exposure group than in the control group (Table 2). The sperm count in the exposure group was significantly lower than that in the control group (Table 3). As shown in Table 3, no statistical differences in head, tail, and total malformation percentages were found between the exposure and control groups. However, the total number of malformed sperm was higher in the exposure group than in the control group. The percentages of malformed head were also higher in the exposure group than in the control group.
Optical micrographs showed five types of sperm deformities in the heads and tails of the exposure group. In type 1, one sperm cell had two tails (Fig. 2). In type 2, one sperm cell had two heads (Fig. 2). Cuspidal sperm (type 3, Fig. 2), sperm with no head (type 4, Fig. 2), and sperm with abnormal head (type 5, Fig. 2) were also found in the exposure group. TEM was applied to observe the ultrastructural deformities in sperm (Fig. 3). The outer dense fibers (ODF) were absent (Fig. 3) in the sperm of the exposure group compared with the control (Fig. 3), and distension in the necks of sperm was observed in the exposure group (Fig. 3).
Electron micrographs of sperm necks and tails. a The cross section of sperm tail from control group. b The ODF was lost in the sperm tail of exposure group mouse as the arrow pointing. c The normal linked structure between the head and tail in the sperm of control group. d the linked structure of the sperm in exposure group was swollen as arrow pointing 2ff7e9595c
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