ObjectiveTo explore the best interventions and working patterns of clinical pharmacists in pediatrics and to determine the effectiveness of clinical pharmacists in pediatrics.MethodsWe conducted a randomized controlled trial of 160 pediatric patients with nerve system disease, respiratory system disease or digestive system disease, who were randomly allocated into two groups, with 80 in each group. Interventions by clinical pharmacists in the experimental group included answering questions of physicians and nurses, giving advice on treating patients, checking prescriptions and patient counseling at discharge. In the control group, patients were treated without clinical pharmacist interventions.ResultsOf the 109 interventions provided by clinical pharmacists during 4 months, 47 were consultations for physicians and nurses, 31 were suggestions of treatment, with 30 accepted by physicians (96.77%) and 31 were medical errors found in 641 prescriptions. Five adverse drug reactions were submitted to the adverse drug reaction monitoring network, with three in the experimental group and two in the control group. The average length of stay (LOS) for patients with respiratory system diseases in the experimental group was 6.45 days, in comparison with 10.83 days in the control group, which was statistically different (p value<0.05); Average drug compliance rate in the experimental group was 81.41%, in comparison with 70.17% of the control group, which was statistically different (p value<0.05). Cost of drugs and hospitalization and rate of readmission in two weeks after discharge in the two groups were not statistically different.ConclusionParticipation by clinical pharmacists in the pharmacotherapy of pediatric patients can reduce LOS of patients with respiratory system disease and improve compliance rate through discharge education, showing no significant effects on prevention of ADR, reduction of cost of drugs and hospitalization and readmission rate in two weeks.Trial RegistrationChinese Clinical Trial Registry ChiCTR-TRC-10001081

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PurposeColorectal cancer (CRC) is one of the most common malignant tumors worldwide. This study aimed to explore the prognostic value of lncRNAs in CRC.Material and methodsWe performed gene expression profiling to identify differentially expressed lncRNAs between 51 normal and 646 tumor tissues from The Cancer Genome Atlas database. Cox regression and robust likelihood-based survival models were used to find prognosis-related lncRNAs. A lncRNA signature was developed to predict the overall survival of patients with CRC. In addition, a receiver operating characteristic curve analysis was performed to identify the optimal cutoff with the best Youden index to divide patients into different groups based on risk level.ResultsEighty survival-related lncRNAs were identified and a 15-lncRNA signature was developed on the basis of a risk score to comprehensively predict the overall survival of patients with CRC. The prognostic value of the 15-lncRNA risk score was validated using the internal testing set and total set. The risk indicator was shown to be an independent prognostic factor (hazard ratio =2.92; 95% CI: 1.73–4.94; P<0.001). Notably, all 15 lncRNAs (AC024581.1, FOXD3-AS1, AC012531.1, AC003101.2, LINC01219, AC083967.1, AL590483.1, AC105118.1, AC010789.1, AC067930.5, AC105219.2, LINC01354, LINC02474, LINC02257, and AC079612.1) were newly found to correlate with the prognosis of patients with CRC. Furthermore, the function of 15 lncRNAs was explored through the ceRNA network. These lncRNAs regulated coding genes that were involved in many key cancer pathways.ConclusionA 15-lncRNA expression signature was discovered as a prognostic indicator for patients with CRC, which may act as competing endogenous RNA (ceRNAs) to play a crucial role in the modulation of cancer-related pathways. These findings may allow a better understanding of the prognostic value of lncRNAs.

Glioblastoma (GBM) is a highly infiltrative and malignant primary brain tumor. Despite aggressive therapy, patients with GBM have a dismal prognosis with median survival of approximately 1 year. Tamoxifen (TAM), a selective estrogen receptor modulator (SERM), has been used to treat GBM for many years. ER‐α36 is a novel variant of estrogen receptor‐alpha66 (ER‐α66) and can mediate cell proliferation through estrogen or anti‐estrogen signaling in different cancer cells. Previously, we found that ER‐α36 was highly expressed in GBM and was involved in the tamoxifen sensitivity of glioblastoma cells. However, the molecular mechanism responsible has not been well established. Here, we found that ER‐α36 is highly expressed in glioblastoma specimens. We further found that ER‐α36 knockdown increased sensitivity of glioblastoma U87 cells to TAM and decreased autophagy in these cells. However, ER‐α36 overexpression decreased TAM sensitivity and induced autophagy. We also established TAM‐resistant glioblastoma U251 cells by a long‐term culture in TAM‐containing medium and found that TAM‐resistant cells showed a six‐fold increase of ER‐α36 mRNA expression and elevated basal autophagy. ER‐α36 knockdown in these TAM‐resistant cells restored TAM sensitivity. In addition, we recapitulated the physiologically relevant tumor microenvironment in an integrated microfluidic device, and U87 cells were treated with a gradient of TAM. We found that ER‐α36 expression is consistent with autophagy protein P62 in a three‐dimensional microenvironment. In summary, these results indicate that ER‐α36 contributes to tamoxifen resistance in glioblastoma cells presumably through regulation of autophagy.

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