ABSTRACT
Objective To study the effect of nursing intervention on the catheter prolapse of the powerpPICC (high pressure injection type PICC catheter). Methods A total of 140 patients with powerpPICC were divided into observation group and control group by the catheter inserting time, with 70 cases in each group. The observation group received conventional nursing care, and the control group the targeted care measures based on analysis of catheter prolapse in the observation group. Result The rate of catheter prolapse in the observation group was significantly higher than that of the control group (P<0.05). Conclusions The prolapse of powerpPICC is related to catheter material, exposed length, fixed method, patient's compliance, catheter caring method. The care measures based on the different causes can decrease the rate of catheter prolapse and extend its duration.
ABSTRACT
<p><b>OBJECTIVE</b>The aim of this study was to explore the effect of SPARC on the anti-cancer effect of gemcitabine and underlying mechanism in pancreatic cancer.</p><p><b>METHODS</b>After treating with gemcitabine, the proliferation rate of MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells was detected by MTT assay. The cell cycle distribution and cell apoptosis in each group were examined by flow cytometry, and the capability of clone formation was tested by adhesion-dependent clone formation assay. The apoptosis-related proteins were analyzed by Western blot.</p><p><b>RESULTS</b>The growth of pancreatic cancer cells was inhibited by gemcitabine in a time-dependent and dose-dependent manner. Its IC50 at 24, 48, and 72-h was (40.1 ± 2.5) µmol/L, (15.0 ± 0.5) µmol/L and (6.6 ± 0.1) µmol/L, respectively. The overexpression of SPARC increased the inhibitory effect of gemcitabine on growth of pancreatic cancer MIA PaCa2/SPARC69 cells, presenting a dose- and time- dependent manner. Its IC50 at 24, 48, 72 h was (24.3 ± 1.5) µmol/L, (7.7 ± 0.3) µmol/L and (4.8 ± 0.2) µmol/L, respectively. The clone formation assay showed that before gemcitabine treatment, the clone numbers of MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were (2350 ± 125), (2130 ± 120) and (1567 ± 11), respectively. After gemcitabine treatment, the clone numbers of MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were ( 1674 ± 79) , (1587 ± 94) and (557 ± 61), respectively. The overexpression of SPARC enhanced the chemosensitivity of MIA PaCa2 cells to gemcitabine chemotherapy. After treating with 10 µmol/L gemcitabine for 48 h, the ratio of G0/G1 cells in MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were (56.0 ± 5.5)%, (55.0 ± 4.5)% and (68.0 ± 7.0)%, respectively. The cells arrested at G0/G1 phase were significantly increased in the MIA PaCa2/SPARC69 cells. The apoptosis rates of MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were (22.4 ± 2.5)%, (19.9 ± 2.0)% and (37.7 ± 3.9)%, respectively, indicating that overexpression of SPARC enhanced the gemcitabine-induced apoptosis in MIA PaCa2 cells. The Western blot analysis showed that, compared with MIA PaCa2 and MIA PaCa2/V cells, the expression of caspase-2, -8, -9 and cleaved PARP protein was significantly increased, while the expression of Bcl-2 was not changed significantly in the MIA PaCa2/SPARC69 cells.</p><p><b>CONCLUSION</b>SPARC can enhance the chemosensitivity of pancreatic cancer cells to gemcitabine via regulating the expression of apoptosis-related proteins.</p>
Subject(s)
Humans , Antimetabolites, Antineoplastic , Pharmacology , Apoptosis , Caspase 2 , Metabolism , Caspase 8 , Metabolism , Caspase 9 , Metabolism , Cell Cycle , Cell Cycle Checkpoints , Cell Line, Tumor , Cell Proliferation , Cysteine Endopeptidases , Metabolism , Deoxycytidine , Pharmacology , Dose-Response Relationship, Drug , Drug Resistance, Neoplasm , Osteonectin , Metabolism , Pancreatic Neoplasms , Metabolism , Pathology , Poly(ADP-ribose) Polymerases , Metabolism , Time FactorsABSTRACT
Objective To compare sleep electroencephalogram-modulated repetitive transcranial magnetic stimulation (SEM-rTMS) with routine repetitive transcranial magnetic stimulation (R-rTMS) in the treatment of primary insomnia. Methods One hundred and twenty six patients with insomnia were divided randomly into a SEM-rTMS group (44 cases) , a R-rTMS group (42 cases) and a sham rTMS group (40 cases). Each case was treated with rTMS for 30 min once a day for 10 d under double blinding of the patient and therapist. The clinical effect was observed along with Krakow sleep scores, electroencephalograms and blood pressure before and after a 10-day course of therapy and 30 days later. Results During rTMS treatment, some patients reported feeling sleepy, and this was confirmed by their EEGs at the time. After the entire course of therapy, 80% of the SEM-rTMS group and 45% of the R-rTMS group showed improvements, a significant difference. At the 30th day after therapy, the effect in the SEM-rTMS group was still significantly better than in the R-rTMS group. There were no obvious side effects in any group throughout the whole observation period. Conclusions SEM-rTMS is more effective and more reliable than R-rTMS. SEM-rTMS is safe to use with primary insomnia patients.