Objective To investigate the characteristics of laparoscopic cholecystectomy(LC) in the elderly. Methods A retrospective analysis was made on clinical data of 118 elderly patients treated with LC in this hospital between January 2000 and January 2005. Results The LC was successfully completed in 116 patients,while conversions to open surgery were required in 2 patients due to low level of insertion of the cystic duct(1 patient) and common bile duct injury(1 patient).The operation time was(30~120 min)(mean,50 min).The postoperative recovery was uneventful in all the patients.The length of hospital stay after operation was 3~7 d(mean,4.5 d).The patient with common bile duct injury was followed for 2 years and 6 months.Transient onsets of abdominal pain and fever were noted and cured with antibiotics for 2~5 days.No biliary tract stenosis or bile duct calculus was seen.Follow-up observations in the remaining 117 patients for 6~12 months(mean,10.5 months) revealed no abdominal pain,fever,or jaundice. Conclusions Laparoscopic cholecystectomy is acceptable and safe for elderly patients.Proper peri-operative management and careful surgical performance are essential to the success of surgery.

Esophageal cancer is a malignant tumor of the digestive system that has a high incidence in China. The traditional treatment methods include surgery, radiotherapy, and chemotherapy, but the long-term efficacy is not good and the side effects are obvious. As a traditional physical therapy, hyperthermia has no significant toxic and side effects. Studies have shown that hyperthermia can increase the sensitivity of esophageal cancer to radiotherapy and chemotherapy, and its combined use in the treatment of esophageal cancer can prolong the survival and improve the quality of life. In addition, the innovation of materials and technologies brings new breakthroughs to tumor hyperthermia.

Objective:To initially investigate whether simultaneous radiochemotherapy with hyperthermia can prolong the survival of glioblastoma (GBM) patients.Methods:Clinical data of 61 GBM patients undergoing surgery in our hospital from September 2016 to June 2019 were retrospectively analyzed. According to different treatment methods, all patients were divided into the control group ( n=34) and observation group ( n=27). In the control group, three-dimensional radiotherapy with a dose of 60 Gy combined with temoazolamine chemotherapy was delivered. In the observation group, simultaneous radiochemotherapy with 15-20 cycles of hyperthermia at 40-41℃ was supplemented. The survival time was calculated by Kaplan-Meier method, and the survival time was compared with log-rank test between two groups. Results:The median progression-free survival in the observation group was significantly longer than that in the control group (14.33 months vs.9.94 months, P<0.05). The median overall survival in the observation group was also remarkably higher than that in the control group (18 months vs. 14 months, P<0.05). Conclusions:Simultaneous radiochemotherapy with hyperthermia is innovatively applied to treat GBM after surgical resection. Preliminary findings demonstrate that compared with chemoradiotherapy, simultaneous radiochemotherapy with hyperthermia can prolong the survival time of GBM patients.

Objective:To investigate the effect of long non-coding (lnc) RNA HCP5 on the radiation sensitivity of glioma cells and underlying mechanism.Methods:The glioma cells U251 and U87 were irradiated with 0, 2, 4, 6, and 8 Gy rays as different doses.si-Con, si-HCP5, pcDNA, and pcDNA-HCP5 were transfected into cells U251 and U87, recorded as si-con group, si-HCP5 group, pcDNA group, and pcDNA-HCP5 group.si-Con and si-HCP5 were transfected into cells U251 and U87, and then irradiated with 4 Gy rays, respectively, recorded as IR+ si-con group and IR+ si-HCP5 group, the cells only irradiated with 4 Gy rays were recorded as IR group.After si-HCP5 with anti-miR-con and anti-miR-508-3p was co-transfected into cell U251 and U87, respectively, irradiated with 4 Gy rays, recorded as IR+ si-HCP5+ anti-miR-con group and IR+ si-HCP5+ anti-miR-508-3p group, respectively, the transfection was performed by liposome method.RT-qPCR was used to detect the expression of miR-508-3p and HCP5.Cell clone formation assay was used to detect the radiosensitivity of glioma cells.Flow cytometry was used to detect apoptosis, dual luciferase Reporter gene detection experiments detects fluorescence activity.Results:HCP5 was highly expressed in radiation-treated glioma cells, and miR-508-3p was lowly expressed.After silenced HCP5, U251 and U87 cells had enhanced radiosensitivity and apoptotic rate((16.67±1.68) vs (3.58±0.62), t=21.929, P<0.05; (12.32±1.08) vs (4.48±0.71), t=18.198, P<0.05) was increased, and γ-H2AX( (0.45±0.04) vs (0.23±0.05), t=10.307, P<0.05; (0.38±0.04) vs (0.24±0.03), t=8.400, P<0.05), Cleaved caspase-3((0.37±0.04) vs (0.16±0.03), t=12.600, P<0.05; (0.38±0.04) vs (0.22±0.03), t=9.600, P<0.05) expressions were increased.Compared with silencing HCP5 or radiation treatment alone, silencing HCP5 and radiation treatment of U251 cells simultaneously, the apoptosis rate ((25.34±1.54) vs (16.67±1.68), t=11.413, P<0.05; (25.34±1.54) vs (11.13±1.06), t=22.802, P<0.05) was significantly increased, and γ-H2AX((0.69±0.05) vs (0.45±0.04), t=11.245, P<0.05; (0.69±0.05) vs (0.31±0.04), t=17.804, P<0.05), Cleaved caspase-3 ((0.52±0.06/0.37±0.04, t=6.240, P<0.05) (0.52±0.06/0.34±0.04, t=7.488, P<0.05) expressions were increased.The expressions of p-PI3K ((0.21±0.02) vs (0.52±0.04), t=20.795, P<0.05; (0.26±0.23 ), ( 0.67±0.07), t=5.116, P<0.05), p- AKT ((0.22±0.03) vs (0.66±0.07), t=17.332, P<0.05; (0.23±0.04) vs (0.71±0.03), t=28.800, P<0.05) in U251 and U87 cells were decreased.HCP5 can target the regulation of miR-508-3p expression; interfering with miR-508-3p reversed the effects of silent HCP5 and radiation on the radiation sensitization and apoptosis of U251 and U87 cells.It reduced the expression levels of reducing γ-H2AX and Cleaved caspase-3, while increased the expression levels of p-PI3K and p-AKT. Conclusion:Silencing lncRNA HCP5 can enhance the radiation sensitivity of glioma cells and promote apoptosis.The mechanism may be related with the miR-508-3p and PI3K/Akt signaling pathway, which will provide new targets and new ideas for glioma treatment.

Objective To explore the sensitivity of HER-2-positive BT474 breast cancer cells to trastuzumab after knockdown or overexpression of RNA binding protein 38 ( RNPC1 ) .Methods The expressions of RNPC1 and HER-2 mRNA were detected by qRT-PCR, and the expressions of RNPC1, HER-2 and PI3K/AKT proteins were detected by Western blot after transfected with RNPC1 lentiviral vector, respectively.The experimental groups were treated with different concentration of trastuzumab, and cell apoptosis rate was analyzed by 7-AAD/APC double staining flow cytometry, and cell growth inhibition rate was tested by cell counting kit 8 ( CCK-8) .The expression of apoptosis-related proteins was detected by Western blot assay.Results The results of qRT-PCR showed that overexpression of RNPC1 increased the expressions of RNPC1 and HER-2 mRNA, and the expressions of RNPC1 and HER-2 were decreased after RNPC1 knockdown.The knockdown of RNPC1 decreased the expressions of RNPC1 and HER-2.Moreover, overexpression of RNPC1 decreased and knockdown of RNPC1 increased the levels of p-PI3K and p-AKT while the total protein expressions of both were marginally changed.The results of analysis using a cell counting CCK-8 kit showed that the RNPC1 overexpressed group had a higher growth inhibition rate [(20.33± 1.25)%,(35.38±2.05)%,(50.43±2.12)%,(65 .35±2.08)%and(76.00±2.16)%, respectively] than that of the control group [(13.67±1.24)%,(27.86±2.05)%,( 39.72±1.69)%,(53.33±1.70)%and(62.68± 2.07)%] when treated with different concentrations of trastuzumab (5, 10, 15, 20 and 25 μg/ml).The cell apoptosis rates in the RNPC1-overexpressed group [ ( 19.46 ±1.06 )%, ( 30.87 ±0.98 )%, ( 50.45 ± 1.1)3%, respectively] were also increased compared with that in the control group [(14.38±0 .64)%,(21.65± 1.24)%,(38.03±0.85)%] when treated with different concentrations of trastuzumab (0, 10, 20 and 30μg/ml) ( P<0.05 for all).Reverse results were observed in the RNPC1 knockdown experiments [ experimental groups:(9.67±1.18)%, ( 21.67 ±1.23)%, ( 30.33 ±1.25)%, ( 40.33 ±1.69)%, and ( 53.00 ± 1.63)%] compared with those of control groups:[(14.00±0.82)%, (27.67±1.25)%, (39.67±1.79)%, (53.67±1.50)%, and (63.33±1.52)%];and experimental groups:[(11.64±0.68)%, (16.60±1.01)%, and (25.14±3.12)%] compared with those of the control groups: [(14.71±0.61)%, (22.65±0.96)%, and (39.03±0.85)%].The overexpression of RNPC1 increased the expression levels of Bim and Bad and decreased the level of Bcl-xl, and reverse result was observed after knockdown of RNPC1.Conclusion RNPC1 may promote the sensitivity of breast cancer cells to trastuzumab through the increased expression of HER-2 in the BT474 breast cancer cells.

Objective To investigate the regulatory mechanism of RNA binding motif protein 38 (RNPC1) on the expression of progesterone receptor (PR) in breast cancer cell line ZR?75?1. Methods Lentiviral vector was used to induce overexpression of RNPC1 in ZR?75?1 cells. qRT?PCR and Western blot were used to assess the regulatory effect of RNPC1 on PR expression. Actinomycin was used to detect the regulatory mechanism involved. Immunohistochemical ( IHC) staining was used to determine the protein expression of RNPC1 and PR in 80 breast cancer tissues. Results IHC staining showed that the expression of RNPC1 was significantly higher in the PR positive breast cancer tissues than that in the PR negative breast cancer tissues ( P<0.05) . The qRT?PCR results showed that overexpression of RNPC1 in ZR?75?1 cells significantly upregulated the mRNA level of PR (1.764±0.028 vs. 1.001±0.037, P<0.01), whereas knockdown of RNPC1 did the opposite (0.579± 0.007 vs. 1.000±0.002, P<0.01).The Western blot results also showed that overexpression of RNPC1 up?regulated PR levels, while knockdown of RNPC1 resulted in down?regulation of PR levels in the ZR?75?1 cells. The actinomycin assay showed that overexpression of RNPC1 increased the mRNA stability of PR. The half?life of PR mRNA was increased from 4. 0 h to 6. 5 h. Knockdown of RNPC1 decreased the mRNA stability of PR and the half?life of PR transcript was decreased from 4.1 h to 3.0 h. Conclusion RNPC1 plays a crucial role in regulating the expression of PR in breast cancer ZR?75?1 cells.

Objective To explore the sensitivity of HER-2-positive BT474 breast cancer cells to trastuzumab after knockdown or overexpression of RNA binding protein 38 ( RNPC1 ) .Methods The expressions of RNPC1 and HER-2 mRNA were detected by qRT-PCR, and the expressions of RNPC1, HER-2 and PI3K/AKT proteins were detected by Western blot after transfected with RNPC1 lentiviral vector, respectively.The experimental groups were treated with different concentration of trastuzumab, and cell apoptosis rate was analyzed by 7-AAD/APC double staining flow cytometry, and cell growth inhibition rate was tested by cell counting kit 8 ( CCK-8) .The expression of apoptosis-related proteins was detected by Western blot assay.Results The results of qRT-PCR showed that overexpression of RNPC1 increased the expressions of RNPC1 and HER-2 mRNA, and the expressions of RNPC1 and HER-2 were decreased after RNPC1 knockdown.The knockdown of RNPC1 decreased the expressions of RNPC1 and HER-2.Moreover, overexpression of RNPC1 decreased and knockdown of RNPC1 increased the levels of p-PI3K and p-AKT while the total protein expressions of both were marginally changed.The results of analysis using a cell counting CCK-8 kit showed that the RNPC1 overexpressed group had a higher growth inhibition rate [(20.33± 1.25)%,(35.38±2.05)%,(50.43±2.12)%,(65 .35±2.08)%and(76.00±2.16)%, respectively] than that of the control group [(13.67±1.24)%,(27.86±2.05)%,( 39.72±1.69)%,(53.33±1.70)%and(62.68± 2.07)%] when treated with different concentrations of trastuzumab (5, 10, 15, 20 and 25 μg/ml).The cell apoptosis rates in the RNPC1-overexpressed group [ ( 19.46 ±1.06 )%, ( 30.87 ±0.98 )%, ( 50.45 ± 1.1)3%, respectively] were also increased compared with that in the control group [(14.38±0 .64)%,(21.65± 1.24)%,(38.03±0.85)%] when treated with different concentrations of trastuzumab (0, 10, 20 and 30μg/ml) ( P<0.05 for all).Reverse results were observed in the RNPC1 knockdown experiments [ experimental groups:(9.67±1.18)%, ( 21.67 ±1.23)%, ( 30.33 ±1.25)%, ( 40.33 ±1.69)%, and ( 53.00 ± 1.63)%] compared with those of control groups:[(14.00±0.82)%, (27.67±1.25)%, (39.67±1.79)%, (53.67±1.50)%, and (63.33±1.52)%];and experimental groups:[(11.64±0.68)%, (16.60±1.01)%, and (25.14±3.12)%] compared with those of the control groups: [(14.71±0.61)%, (22.65±0.96)%, and (39.03±0.85)%].The overexpression of RNPC1 increased the expression levels of Bim and Bad and decreased the level of Bcl-xl, and reverse result was observed after knockdown of RNPC1.Conclusion RNPC1 may promote the sensitivity of breast cancer cells to trastuzumab through the increased expression of HER-2 in the BT474 breast cancer cells.

Objective To investigate the regulatory mechanism of RNA binding motif protein 38 (RNPC1) on the expression of progesterone receptor (PR) in breast cancer cell line ZR?75?1. Methods Lentiviral vector was used to induce overexpression of RNPC1 in ZR?75?1 cells. qRT?PCR and Western blot were used to assess the regulatory effect of RNPC1 on PR expression. Actinomycin was used to detect the regulatory mechanism involved. Immunohistochemical ( IHC) staining was used to determine the protein expression of RNPC1 and PR in 80 breast cancer tissues. Results IHC staining showed that the expression of RNPC1 was significantly higher in the PR positive breast cancer tissues than that in the PR negative breast cancer tissues ( P<0.05) . The qRT?PCR results showed that overexpression of RNPC1 in ZR?75?1 cells significantly upregulated the mRNA level of PR (1.764±0.028 vs. 1.001±0.037, P<0.01), whereas knockdown of RNPC1 did the opposite (0.579± 0.007 vs. 1.000±0.002, P<0.01).The Western blot results also showed that overexpression of RNPC1 up?regulated PR levels, while knockdown of RNPC1 resulted in down?regulation of PR levels in the ZR?75?1 cells. The actinomycin assay showed that overexpression of RNPC1 increased the mRNA stability of PR. The half?life of PR mRNA was increased from 4. 0 h to 6. 5 h. Knockdown of RNPC1 decreased the mRNA stability of PR and the half?life of PR transcript was decreased from 4.1 h to 3.0 h. Conclusion RNPC1 plays a crucial role in regulating the expression of PR in breast cancer ZR?75?1 cells.

Objective: To investigate the effect of lncRNA GIHCG on the radiosensitivity of glioma cells and its mechanism. Methods: The expression levels of GIHCG and miR-146a-3p in human brain normal glial cells HEB and glioma cell lines U251, A172, SHG139 and U87 were quantitatively measured by qRT-PCR assay. U251 and SHG139 cells were used for subsequent experiment. After silencing the expression of GIHCG or overexpressing miR-146a-3p in U251 and SHG139 cells, cell proliferation was detected by MTT assay, cell apoptosis was detected by flow cytometry, cell radiosensitivity was detected by colony formation assay and the expression levels of CDK1, CyclinD1, Bcl-2 and Bax proteins were measured by Western blot. The bioinformatics software predicted the presence of a binding site for GIHCG and miR-146a-3p. Dual luciferase reporter gene assay and qRT-PCR assay were adopted to verify the targeting relationship between GIHCG and miR-146a-3p. Results: Compared with HEB cells, the expression of GIHCG was significantly up-regulated in glioma U87, U251, A172 and SHG139 cells (all P<0.05), whereas that of miR-146a-3p was remarkably down-regulated (P<0.05). Silencing GIHCG expression or overexpression of miR-146a-3p significantly decreased the U251 and SHG139 cell survival rate, survival fraction and the expression of CDK1, CyclinD1 and Bcl-2 proteins (all P<0.05), whereas considerably increased the apoptotic rate and expression of Bax protein (both P<0.05). GIHCG performed targeted negative regulation of miR-146a-3p expression in U251 and SHG139 cells and inhibition of miR-146a-3p expression reversed the effect of silencing GIHCG on proliferation, apoptosis and radiosensitivity of glioma cells. Conclusion Silencing GIHCG expression up-regulates the expression of miR-146a-3p, thereby enhancing the radiosensitivity of glioma cells.