EGFR testing has become the consensus before epidermal growth factor-tyrosine kinase inhibitorrs (EGFR-TKIs) treatment in non-small cell lung cancer(NSCLC) patients.Malignant pleural effusion is the common clinical manifestation in NSCLC patients,and EGFR testing by using different methods in pleural effusion cells and free nucleic acids has good prospect for predicting the efficacy of EGFR-TKIs.

Objective:This study aimed to observe the curative effect and adverse reaction of docetaxel combined with intraperitoneal cisplatin chemotherapy and hyperthermia treatment of advanced ovarian cancer. Methods:A total of 83 patients with inoperable and recurrent advanced ovarian cancer were randomly divided into two groups:hyperthermia group and control group. The hyperthermia group consisted of 42 cases of docetaxel chemotherapy immediately treated with intraperitoneal cisplatin chemotherapy combined with abdominal local hyperthermia. The control group included 41 cases of docetaxel chemotherapy and intraperitoneal cisplatin chemotherapy treatment only. Results:The total efficiencies of the hyperthermia treatment group and the control group were 81%and 58.1%, respectively, which showed that the total efficiency significantly improved (P<0.05). The ascite control rates were 78.3%and 66.7%and CA125 decreased by 84.2%and 61.5%for the hyperthermia and control groups, respectively. The main adverse reactions were gastrointestinal reaction and bone marrow suppression. However, differences were not statistically significant. Conclusion:Docetaxel combined with cisplatin intraperitoneal perfusion hyperthermia significantly improved the curative effect on advanced ovarian cancer without increasing toxicity, which indicates that it is a treatment worth popularizing.

Objective To investigate the expression and mechanism of long non-coding RNA (lncRNA) GHRLOS2 in colorectal cancer tissues and cells. Methods Real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to detect the expression levels of GHRLOS2 and microRNA-33b-5p (miR-33b-5p) in colorectal cancer tissues or cells. Overexpressing of GHRLOS2 in HCT116 and SW480 colorectal cancer cell lines were constructed, and the effects of overexpression of GHRLOS2 on the migration and invasion abilities in HCT116 and SW480 cell lines were detected by wound healing assay and Transwell assay. Glucose content in cells of overexpressing GHRLOS2 and control cells was detected using a glucose detection kit. Western blot was used to detect the expression level of PCK1 protein in cells. The targeted binding relationship between miR-33b-5p and PCK1 was predicted based on bioinformatics methods. Results The qRT-PCR results showed that the expression level of GHRLOS2 in colorectal cancer tissue samples was lower than that in adjacent non-cancerous tissues, and was lower in colorectal cancer cells than that in normal colon epithelial cells (P < 0.05). The expression of GHRLOS2 was correlated with grade classification, staging, and lymph node metastasis (P < 0.05). The expression level of miR-33b-5p in colorectal cancer tissues was higher than that in corresponding adjacent non-cancerous tissues (P < 0.001). The results of wound healing assay, Transwell assay, and glucose content detection showed that overexpression of GHRLOS2 significantly inhibited the invasion, migration, and glucose metabolism of colorectal cancer cells. Overexpression of GHRLOS2 inhibited the expression level of miR-33b-5p; GHRLOS2 functioned as a molecular sponge for miR-33b-5p, and PCK1 was a target of miR-33b-5p; overexpression of GHRLOS2 competitively bound to miR-33b-5p, thereby promoting increased expression of PCK1. Conclusion The expression of GHRLOS2 is downregulated in colorectal cancer tissues and cells, and it may regulate the invasion, migration, and glucose metabolism of colorectal cancer cells through the miR-33b-5p/PCK1 pathway, making it a potential biological target for targeted therapy of colorectal cancer.

Objective: To explore the efficacy and safety of tertiary hospital guided and community-driven family self-help cardiac rehabilitation model. Methods: This study was a prospective randomized controlled study, 80 patients from Beijing Electrical Power Hospital and Beijing Jingmei Group General Hospital with acute coronary syndrome were included from June to December 2015 and divided into 2 groups. Patients in rehabilitation group (n=52) received tertiary hospital(Peiking University Peoples′ Hospital) guided and community-driven family self-help cardiac rehabilitation for 3 months, and patients in control group (n=28) received routine secondary treatment for 3 months. Following parameters including 6 minutes walk distance, score of life quality (evaluated by Short Form-12), score of anxiety (evaluated by Generalized Anxiety Disorder-7), score of depression (evaluated by Perceived Health Questionnaire-9), self-management competency (evaluated by questionnaire) were collected at baseline and after treatment for 3 months. Results: Compared with control group, 6 minutes walk distance was longer in rehabilitation group((60.2±6.8) meters vs. (24.9±10.5)meters, P<0.01). The difference values between after and before intervention of life quality scores((0.14±3.90)scores vs.(-7.44±5.85)scores, P>0.05), anxiety scores((-0.16±2.12 ) scores vs.(0.70±1.13)scores, P>0.05) and depression scores((-1.17±2.79) scores vs.(0.60±0.36)scores, P>0.05) were similar between the 2 groups. The amplification of patients with regular exercise (50.26% vs. 0, P<0.05), limit sugary foods usually and always (53.22% vs. 3.98%, P<0.05), eat 200-400 g fruits usually and always (78.61 % vs. 0, P<0.05), eat 300-500 g vegetables usually and always (9.74% vs. 0, P<0.05), and answering very confident to questions such as let the physicians know about your diseases (40.17% vs. 5.00%, P<0.05), know how to take medicines (44.52% vs. 5.00%, P<0.05), know how much exercise was right for yourself (26.43% vs.0, P<0.05) were significantly higher in rehabilitation group than in control group. There were no cardiac rehabilitation training related cardiovascular events. Conclusion Tertiary hospital guided and community-driven family self-help cardiac rehabilitation model is an effective and safe management model of cardiovascular disease in chronic phase, and it is necessary to further expand the study population to verify the efficacy of this model.

Background/Aims: Chemoresistance is a common event after cancer chemotherapy, which is associated with the deregulation of circular RNAs (circRNAs). The objective of this study was to clarify the role of circ-LDLRAD3 in cisplatin (DDP)-resistant gastric cancer (GC). Methods: The expression of circ-LDLRAD3, miR-588, and SRY-box transcription factor 5 (SOX5) mRNA was detected by quantitative real-time polymerase chain reaction. Cell viability and the half maximal inhibitory concentration (IC 50 ) value were measured by CCK8 assay. Cell proliferation was assessed by colony formation and EdU assays. Cell apoptosis and cell invasion were assessed by flow cytometry assay and transwell assay, respectively. The expression of SOX5 protein was detected by Western blotting. A xenograft model was established to verify the role of circ-LDLRAD3 in vivo. Exosomes were isolated by differential centrifugation and identified by transmission electron microscopy and the expression of exosome-related proteins. Results: circ-LDLRAD3 was overexpressed in DDP-resistant GC tissues and cells. circ-LDL-RAD3 knockdown decreased the IC 50 of DDP-resistant cells and suppressed cell proliferation, survival and invasion. miR-588 was a target of circ-LDLRAD3, and miR-588 inhibition attenuated the inhibition of DDP resistance, proliferation, survival and invasion in DDP-resistant GC cells caused by circ-LDLRAD3 knockdown. SOX5 was a target of miR-588, and the inhibition of the DDP resistance, proliferation, survival and invasion of DDP-resistant GC cells by miR-588 restoration was largely rescued SOX5 overexpression. circ-LDLRAD3 knockdown inhibited DDP resistance and tumor growth in vivo. circ-LDLRAD3 was overexpressed in exosomes isolated from DDP-resistant GC cells. Conclusions circ-LDLRAD3 knockdown reduced DDP resistance and blocked the malignant development of DDP-resistant GC by modulating the miR-588/SOX5 pathway.

Background: MicroRNA (miRNA) plays a crucial role in neuropathic pain (NP) by targeting mRNAs. This study aims to analyze the regulatory function and mechanism of miR-382-5p/dual specificity phosphatase-1 (DUSP1) axis in NP. Methods: We utilized rats with chronic constriction injury (CCI) of the sciatic nerve as the NP model. The levels of miR-382-5p and DUSP1 were reduced by intrathecal injection of lentiviral interference vectors targeting miR-382-5p and DUSP1. The mRNA levels of miR-382-5p and DUSP1 in the dorsal root ganglions (DRGs) were measured by RT-qPCR assay. The pain behavior was evaluated by mechanical nociceptive sensitivity and thermal nociceptive sensitivity. The expression levels of interleukin-6 (IL)-6, IL-1β, and tumor necrosis factor-α in the DRGs were analyzed by ELISA assay. The targeting relationship between miR-382-5p and DUSP1 was verified by DLR assay and RIP assay. Results: Compared to the Sham group, the CCI rats exhibited higher levels of miR-382-5p and lower levels of DUSP1. Overexpression of miR-382-5p significantly decreased DUSP1 levels. Reducing miR-382-5p levels can lower the mechanical nociceptive sensitivity and thermal nociceptive sensitivity of CCI rats and inhibit the over-activation of pro-inflammatory factors. Reduced miR-382-5p levels decreased NP in CCI rats. DUSP1 is the target of miR-382-5p, and down-regulation of DUSP1 reverses the inhibitory effect of reduced miR-382-5p levels on NP. Conclusions Down-regulation of miR-382-5p inhibits the over-activation of pro-inflammatory factors by targeting and regulating the expression of DUPS1, thereby alleviating NP.

Background: MicroRNA (miRNA) plays a crucial role in neuropathic pain (NP) by targeting mRNAs. This study aims to analyze the regulatory function and mechanism of miR-382-5p/dual specificity phosphatase-1 (DUSP1) axis in NP. Methods: We utilized rats with chronic constriction injury (CCI) of the sciatic nerve as the NP model. The levels of miR-382-5p and DUSP1 were reduced by intrathecal injection of lentiviral interference vectors targeting miR-382-5p and DUSP1. The mRNA levels of miR-382-5p and DUSP1 in the dorsal root ganglions (DRGs) were measured by RT-qPCR assay. The pain behavior was evaluated by mechanical nociceptive sensitivity and thermal nociceptive sensitivity. The expression levels of interleukin-6 (IL)-6, IL-1β, and tumor necrosis factor-α in the DRGs were analyzed by ELISA assay. The targeting relationship between miR-382-5p and DUSP1 was verified by DLR assay and RIP assay. Results: Compared to the Sham group, the CCI rats exhibited higher levels of miR-382-5p and lower levels of DUSP1. Overexpression of miR-382-5p significantly decreased DUSP1 levels. Reducing miR-382-5p levels can lower the mechanical nociceptive sensitivity and thermal nociceptive sensitivity of CCI rats and inhibit the over-activation of pro-inflammatory factors. Reduced miR-382-5p levels decreased NP in CCI rats. DUSP1 is the target of miR-382-5p, and down-regulation of DUSP1 reverses the inhibitory effect of reduced miR-382-5p levels on NP. Conclusions Down-regulation of miR-382-5p inhibits the over-activation of pro-inflammatory factors by targeting and regulating the expression of DUPS1, thereby alleviating NP.

Background: MicroRNA (miRNA) plays a crucial role in neuropathic pain (NP) by targeting mRNAs. This study aims to analyze the regulatory function and mechanism of miR-382-5p/dual specificity phosphatase-1 (DUSP1) axis in NP. Methods: We utilized rats with chronic constriction injury (CCI) of the sciatic nerve as the NP model. The levels of miR-382-5p and DUSP1 were reduced by intrathecal injection of lentiviral interference vectors targeting miR-382-5p and DUSP1. The mRNA levels of miR-382-5p and DUSP1 in the dorsal root ganglions (DRGs) were measured by RT-qPCR assay. The pain behavior was evaluated by mechanical nociceptive sensitivity and thermal nociceptive sensitivity. The expression levels of interleukin-6 (IL)-6, IL-1β, and tumor necrosis factor-α in the DRGs were analyzed by ELISA assay. The targeting relationship between miR-382-5p and DUSP1 was verified by DLR assay and RIP assay. Results: Compared to the Sham group, the CCI rats exhibited higher levels of miR-382-5p and lower levels of DUSP1. Overexpression of miR-382-5p significantly decreased DUSP1 levels. Reducing miR-382-5p levels can lower the mechanical nociceptive sensitivity and thermal nociceptive sensitivity of CCI rats and inhibit the over-activation of pro-inflammatory factors. Reduced miR-382-5p levels decreased NP in CCI rats. DUSP1 is the target of miR-382-5p, and down-regulation of DUSP1 reverses the inhibitory effect of reduced miR-382-5p levels on NP. Conclusions Down-regulation of miR-382-5p inhibits the over-activation of pro-inflammatory factors by targeting and regulating the expression of DUPS1, thereby alleviating NP.

Background: MicroRNA (miRNA) plays a crucial role in neuropathic pain (NP) by targeting mRNAs. This study aims to analyze the regulatory function and mechanism of miR-382-5p/dual specificity phosphatase-1 (DUSP1) axis in NP. Methods: We utilized rats with chronic constriction injury (CCI) of the sciatic nerve as the NP model. The levels of miR-382-5p and DUSP1 were reduced by intrathecal injection of lentiviral interference vectors targeting miR-382-5p and DUSP1. The mRNA levels of miR-382-5p and DUSP1 in the dorsal root ganglions (DRGs) were measured by RT-qPCR assay. The pain behavior was evaluated by mechanical nociceptive sensitivity and thermal nociceptive sensitivity. The expression levels of interleukin-6 (IL)-6, IL-1β, and tumor necrosis factor-α in the DRGs were analyzed by ELISA assay. The targeting relationship between miR-382-5p and DUSP1 was verified by DLR assay and RIP assay. Results: Compared to the Sham group, the CCI rats exhibited higher levels of miR-382-5p and lower levels of DUSP1. Overexpression of miR-382-5p significantly decreased DUSP1 levels. Reducing miR-382-5p levels can lower the mechanical nociceptive sensitivity and thermal nociceptive sensitivity of CCI rats and inhibit the over-activation of pro-inflammatory factors. Reduced miR-382-5p levels decreased NP in CCI rats. DUSP1 is the target of miR-382-5p, and down-regulation of DUSP1 reverses the inhibitory effect of reduced miR-382-5p levels on NP. Conclusions Down-regulation of miR-382-5p inhibits the over-activation of pro-inflammatory factors by targeting and regulating the expression of DUPS1, thereby alleviating NP.

Background: MicroRNA (miRNA) plays a crucial role in neuropathic pain (NP) by targeting mRNAs. This study aims to analyze the regulatory function and mechanism of miR-382-5p/dual specificity phosphatase-1 (DUSP1) axis in NP. Methods: We utilized rats with chronic constriction injury (CCI) of the sciatic nerve as the NP model. The levels of miR-382-5p and DUSP1 were reduced by intrathecal injection of lentiviral interference vectors targeting miR-382-5p and DUSP1. The mRNA levels of miR-382-5p and DUSP1 in the dorsal root ganglions (DRGs) were measured by RT-qPCR assay. The pain behavior was evaluated by mechanical nociceptive sensitivity and thermal nociceptive sensitivity. The expression levels of interleukin-6 (IL)-6, IL-1β, and tumor necrosis factor-α in the DRGs were analyzed by ELISA assay. The targeting relationship between miR-382-5p and DUSP1 was verified by DLR assay and RIP assay. Results: Compared to the Sham group, the CCI rats exhibited higher levels of miR-382-5p and lower levels of DUSP1. Overexpression of miR-382-5p significantly decreased DUSP1 levels. Reducing miR-382-5p levels can lower the mechanical nociceptive sensitivity and thermal nociceptive sensitivity of CCI rats and inhibit the over-activation of pro-inflammatory factors. Reduced miR-382-5p levels decreased NP in CCI rats. DUSP1 is the target of miR-382-5p, and down-regulation of DUSP1 reverses the inhibitory effect of reduced miR-382-5p levels on NP. Conclusions Down-regulation of miR-382-5p inhibits the over-activation of pro-inflammatory factors by targeting and regulating the expression of DUPS1, thereby alleviating NP.