The effect of health literacy on patient's perceived shared decision-making among Chinese cancer patients.

OBJECTIVES: To explore the relationship between patient's health literacy and perceived shared decision-making (SDM) among Chinese cancer patients. METHODS: A cross-sectional study was conducted involving a convenience sample of 458 cancer patients from four public hospitals in Guangzhou, China. Patients' self-reported data were collected using the Health Literacy Management Scale (HeLMS) and the nine-item Shared Decision-Making Questionnaire (SDM-Q-9). Hierarchical multiple regressions, controlling for patient-doctor relationship, social support, sociodemographic and clinical variables were conducted to explore the effect of health literacy on perceived SDM. RESULTS: Health literacy itself accounted for 68.0% of the variance in perceived SDM. Higher scores in domains "information acquisition ability," and "communication interaction ability" of HeLMS were significantly associated with a higher level of perceived SDM after controlling the covariates (R2  = 75.7%). CONCLUSIONS: Health literacy, especially the information acquisition ability and communication interaction ability, played a prominent role for Chinese cancer patients to be involved in treatment decision making.

BBOX1-AS1 Accelerates Nasopharyngeal Carcinoma Progression by Sponging miR-3940-3p and Enhancing KPNA2 Upregulation.

BACKGROUND: Upregulation of lncRNA BBOX1 antisense RNA 1 (BBOX1-AS1) has been examined in various tumors. However, its role in nasopharyngeal carcinoma (NPC) remains poorly understood. METHODS: RT-qPCR was performed to measure the expression of BBOX1-AS1, KPNA2, and miR-3940-3p. In vitro assays were performed to determine the alteration of cell phenotypes in NPC cells upon transfection or co-transfection with sh-BBOX1-AS1, sh-KPNA2, or miR-3940-3p inhibitor. The BBOX1-AS1-miR-3940-3p and miR-3940-3p-KPNA2 interplay was verified via luciferase reporter and RNA pull-down assays. RESULTS: High BBOX1-AS1 levels were detected in the nasopharyngeal carcinoma tissues. BBOX1-AS1 silencing considerably suppressed the proliferative, migratory, and invasive abilities of NPC cells in vitro. Interestingly, BBOX1-AS1 could specifically bind to miR-3940-3 and abrogate the inhibition of KPNA2 induced by miR-3940-3. Additionally, analysis of tissue samples showed that miR-3940-3 was inversely correlated with BBOX1-AS1 and KPNA2. CONCLUSION: Our findings revealed that the BBOX1-AS1/miR-3940-3/KPNA2 axis is pro-oncogenic in NPC progression, uncovering novel insights into targeted therapy for this disorder.

Comprehensive network analysis of different subtypes of molecular disorders in lung cancer.

Lung cancer is the leading cause of cancer-related death worldwide. In this study, we attempted to identify the common pathogenesis of lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) based on a modular and comprehensive analysis method. Data were downloaded and the differences analyzed in LUAD samples, LUSC samples, and normal samples, respectively. Co-expression analysis, enrichment analysis, and hypergeometric testing were used to predict transcription factors (TFs) and ncRNAs, as well as target genes. We obtained 4,596 differentially expressed genes which were clustered into 14 modules dysfunction. The 14 clustered genes (including DOK2, COL5A1, and TSPAN8) were identified as the core genes of the module. Module genes are substantially involved in biological processes, such as extracellular matrix, carbohydrate binding and renal system development, and signal transduction as well, including PPAR signal transduction, cGMP-PKG signal transduction, PI3K-Akt signal transduction, and Apelin signal transduction. We identified ncRNA (miR-335-5p, ANCR, TUG1) and transcription factors (RELA, SP1) to regulate dysfunction module genes essentially. The analysis showed that comprehensive co-expression analysis contributes to understanding the TF ncRNA. Moreover, it assisted in further understanding of the molecular pathogenesis of co-expression of modular genes that regulate LUAD and LUSC. It provided a precious resource and theoretical basis for further experiments.

Preference of cancer patients and family members regarding delivery of bad news and differences in clinical practice among medical staff.

OBJECTIVES: To study the preferences of cancer patients and their families in way of being informed of their condition and, by comparing their preferences with the medical staff's clinical practices, explore the factors underlying the latter's preferences. METHODS: A survey was conducted with 216 cancer patients, 242 families, and 176 clinical staff members with the Medical Status Communication questionnaire (Simplified Chinese edition). RESULTS: The clinical staff scored lower than the cancer patients and their families in terms of the total score, way of communication, emotional support, and additional information (F = 16.134, p < .001; F = 28.604, p < .001; F = 13.839, p < .001; F = 16.745, p < .001). Factors underlying the medical staff's clinical practices included, as revealed by the multiple linear regression analysis, gender (p = .03), and willingness to improve the way of communication about cancer (p = .006). CONCLUSIONS: A gap existed between the medical staff's clinical practice and the preferences of the cancer patients and their families. The medical staff should receive adequate training in cancer communication skills and techniques for improvement in this respect. When designing training for skills in delivering bad news to cancer patients, the well-being of cancer patients and their families must be thoroughly considered, and patient demands for information should be satisfied in the context of the information explosion of the current age.

Triple herbal extract DA-9805 exerts a neuroprotective effect via amelioration of mitochondrial damage in experimental models of Parkinson's disease.

Moutan cortex, Angelica Dahurica root, and Bupleurum root are traditional herbal medicines used in Asian countries to treat various diseases caused by oxidative stress or inflammation. Parkinson's disease (PD) has been associated with mitochondrial dysfunction, but no effective treatment for mitochondrial dysfunction has yet been identified. In this study we investigated the neuroprotective effects of the triple herbal extract DA-9805 in experimental models of PD. DA-9805 was prepared by extracting three dried plant materials (Moutan cortex, Angelica Dahurica root, and Bupleurum root in a 1:1:1 mixture) with 90% ethanol on a stirring plate for 24 h at room temperature and fingerprinted using high-performance liquid chromatography. 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and its active metabolite 1-methyl-4-phenylpyridinium (MPP+), which both exert neurotoxic effects on dopaminergic neurons by inhibiting mitochondrial oxidative phosphorylation (OXPHOS) complex I, were used to make experimental models of PD. In MPP+-treated SH-SY5Y cells, DA-9805 ameliorated the suppression of tyrosine hydroxylase expression and mitochondrial damage on OXPHOS complex 1 activity, mitochondrial membrane potential, reactive oxygen species (ROS) generation, and oxygen consumption rate. In the MPTP-induced subacute PD model mice, oral administration of DA-9805 recovered dopamine content as well as bradykinesia, as determined by the rotarod test. DA-9805 protected against neuronal damage in the substantia nigra pars compacta (SNpc) and striatum. In both in vitro and in vivo models of PD, DA-9805 normalized the phosphorylation of AKT at S473 and T308 on the insulin signaling pathway and the expression of mitochondria-related genes. These results demonstrate that the triple herbal extract DA-9805 showed neuroprotective effects via alleviating mitochondria damage in experimental models of PD. We propose that DA-9805 may be a suitable candidate for disease-modifying therapeutics for PD.

Overexpression of TP53 mutation-associated microRNA-182 promotes tumor cell proliferation and migration in head and neck squamous cell carcinoma.

OBJECTIVE: To investigate the functional mechanism of microRNA-182 (miR-182) in head and neck squamous cell carcinoma (HNSCC). DESIGN: HNSCC and normal samples were used to check both p53 and miR-182 expression. Two cancer cell lines with overexpression of miR-182 were used to check cell proliferation and migration. In vivo role of miR-182 was assessed using mouse xenograft tumor model. ß-TrCP2 was found to be direct target of miR-182 by luciferase reporter assay. RESULTS: Overexpression of miR-182 was closely related with overproduction of p53 in HNSCC. Overexpression of miR-182 promoted cell proliferation and migration and its oncogenic effect was also confirmed in vivo. ß-TrCP2 acted as direct target of miR-182 and its overexpression can reverse the miR-182 induced cell proliferation and migration. CONCLUSION: Overexpression of TP53 mutation-associated miR-182 may promote tumor cell proliferation and migration in HNSCC and suggest possible biomarker for the prediction of tumor recurrence.

[Mechanism of SPARC-enhanced chemosensitivity of pancreatic cancer cells to gemcitabine].

OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSION: SPARC can enhance the chemosensitivity of pancreatic cancer cells to gemcitabine via regulating the expression of apoptosis-related proteins.

[Clinical observation of placement of tympanostomy microtube to treat middle ear atelectasis].

OBJECTIVE: To investigate the treatment efficacy of tympanostomy microtube placement surgery for middle ear atelectasis. METHODS: A retrospective analysis was conducted on 26 patients (28 ears) with middle ear atelectasis, who complained fullness or pressure in the ears.Otoscope showed tympanic membrane invagination, scattered or disappeared cone of light, tympanic membrane was pale and dull. The pure tone audiometry air-bone gap >10 dB. Acoustic immittance showed tympanic negative pressure. All the ears had atelectasis of I-III grade. Patients were performed tympanic membrane microtube placement under local anesthesia, and were followed up for 6-12 months. RESULTS: Twenty-five ears recovered from the fullness after operation, in which, 23 ears reverted from type "C" to type "A" in acoustic immittance tests and the pure-tone average (PTA) of hearing thresholds were decreasing from 5 to 20 dB, while 2 ears relapse after removal of the microtube. Three ears with middle ear atelectasis of III grade were ineffectiveness. All the 26 cases had no complications including middle ear infection, tympanosclerosis, and permanent perforation after removal of the microtubes. CONCLUSIONS: The placement of tympanostomy microtube can be used to treat middle ear atelectasis, especially to the patients with middle ear atelectasis of I-II grade as it is effective on elimination of middle ear negative pressure and remission of fullness.

Preparation and characterization of Apo2L/TNF-related apoptosis-inducing ligand-loaded human serum albumin nanoparticles with improved stability and tumor distribution.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has received considerable attention as a potential anticancer agent. However, recombinant Apo2L/TRAIL has several limitations, which include a weak pharmacokinetic profile, namely, a short biological half-life and rapid renal clearance, and an inability to form a homotrimeric structure. In this research, we attempted to develop a sustained release nanoparticle (NP) formulation that stabilizes Apo2L/TRAIL and preserves its antitumor activity. Apo2L/TRAIL-loaded human serum albumin (HSA) NPs were prepared using a desolvation technique optimized by particle size, zeta-potential, and entrapment efficiency. Apo2L/TRAIL in HSA-NPs continuously released over 24 h at 37°C in phosphate buffered saline and rat plasma condition, and the biological activity of Apo2L/TRAIL-HSA-NPs was preserved (IC(50) = 67.2 ng/mL versus Apo2L/TRAIL IC(50) = 55.4 ng/mL) with negligible activity loss. Furthermore, in vivo pharmacokinetic profiles and tumor distribution demonstrated the superiority of Apo2L/TRAIL-HSA-NPs over Apo2L/TRAIL. The circulating half-life period was significantly prolonged from 9.8 to 90.7 min (9.2-fold enhancement), and drug bioavailability was clearly enhanced on the basis of area under the curve analysis (2.7-fold). And tumor distribution of Apo2L/TRAIL-HSA-NPs was also increased at 1 h after injection, which was about 14-fold (1-h point) over that of Apo2L/TRAIL. These results show that Apo2L/TRAIL-loaded HSA-NPs should be considered as potential long-acting cancer agents.