Patients' caring experience during procedures under regional anesthesia in Mainland China: A phenomenology study.

Background: Although regional anesthesia is common, the procedure results in feelings of uncertainty and anxiety in some patients. Increased care is needed for these patients under general anesthesia. Few studies have focused on the intraoperative caring experience of patients during regional anesthesia. This study focused on the caring experience of patients during procedures involving regional anesthesia. Methods: The descriptive phenomenology method of Husserl was employed. Semi-structured interviews were conducted with a purposive sample in five Grade III-A hospitals in Zhengzhou City, Henan Province. The seven-step analysis method of Colaizzi was applied for the analysis, summation, and theme refinement of the interview data. Results: A total of 14 patients from five hospitals participated in the interviews. Four domains and 16 themes emerged during analysis: be informed (about the operation site, progression of the operation, informed in advance, receive explanation for abnormal experience); take care of my body (painless, gentle movements, special care); be protected (work seriously, favorable atmosphere, skilled, authority); and treated as an individual (pay attention, accompany, ask for opinions, encourage patient expression, humorous). Conclusion: Patients during procedure under regional anesthesia had specific caring experiences relative to other patients. Medical staff should recognize the importance of regional anesthesia patients' intraoperative caring experience. Hospital administrators should offer support to allow healthcare staff to provide targeted caring for patients during procedure under regional anesthesia.

TAZ inhibits osteoclastogenesis by attenuating TAK1/NF-κB signaling.

Osteoporosis is an osteolytic disorder commonly associated with excessive osteoclast formation. Transcriptional coactivator with PDZ-binding motif (TAZ) is a key downstream effector of the Hippo signaling pathway; it was suggested to be involved in the regulation of bone homeostasis. However, the exact role of TAZ in osteoclasts has not yet been established. In this study, we demonstrated that global knockout and osteoclast-specific knockout of TAZ led to a low-bone mass phenotype due to elevated osteoclast formation, which was further evidenced by in vitro osteoclast formation assays. Moreover, the overexpression of TAZ inhibited RANKL-induced osteoclast formation, whereas silencing of TAZ reduced it. Mechanistically, TAZ bound to TGF-activated kinase 1 (TAK1) and reciprocally inhibited NF-κB signaling, suppressing osteoclast differentiation. Collectively, our findings highlight an essential role of TAZ in the regulation of osteoclastogenesis in osteoporosis and its underlying mechanism.

Effect of Vitamin E Supplementation on Deposition and Gene Expression Profiling of Abdominal Fat in Broiler Chickens.

The aim of this study was to study the regulation of abdominal fat deposition by DL-α-tocopherol acetate (vitamin E) in broilers. Diets supplemented with 50 IU vitamin E significantly diminished abdominal fat deposition in broilers at day 35. Transcriptome sequencing results for abdominal fat tissues of the control (FC) and 50 IU vitamin E-supplemented (FT) groups identified 602 differentially expressed genes (DEGs), which were enriched in cellular process, cell and cell part, and binding Gene Ontology terms. Pathway functional analysis revealed that the DEGs were enriched in 42 metabolic pathways. Notably, the most enriched pathway, fatty acid biosynthesis, was found to play a key role in lipid metabolism. Further, the key regulators of lipid metabolism, including fatty acid synthase, acetyl-CoA carboxylase alpha, and acyl-CoA synthetase long-chain family member 1, demonstrated decreased expression following vitamin E supplementation. Herein, we have identified pathways and genes regulated by vitamin E, thereby providing novel insights into the nutrients regulating abdominal fat deposition in broilers.

Dual effects of baicalin on osteoclast differentiation and bone resorption.

Osteoclasts (OC) are critical cells responsible for many bone diseases such as osteoporosis. It is of great interest to identify agents that can regulate the activity of OC to treat osteolytic bone diseases. In this study, we found that baicalin exerted a two-way regulatory effect on OC in a concentration-dependent manner in vitro and in vivo. In detail, baicalin at a low concentration (below 1 µmol/L) enhanced OC differentiation and bone resorption, but baicalin at a high concentration (above 2 µmol/L) exhibited inhibitory effects on OC. We demonstrated that baicalin at low concentrations enhanced the mitogen-activated protein kinase (MAPK) (ERK) signalling pathway and activated c-Fos and NFATc1 expression, and thus enhanced gene expression, OC differentiation and bone resorption. However, baicalin at higher levels not only suppressed ERK phosphorylation and c-fos and NFATc1 expression, but also altered the expression of apoptosis-related proteins, and therefore inhibiting OC function. This dual effect was further verified in an LPS-induced mouse calvarial osteolysis model, evidenced by enhanced osteolysis at a lower concentration but reduced bone loss at a higher concentration. Overall, our findings indicate that baicalin exerts dose-dependent effects on OC formation and function. Therefore, caution should be applied when using baicalin to treating OC-related bone diseases.

SPIDR significantly suppressed in tissues of small cell lung cancer promotes NCI-H446 cells proliferation by reducing serum dependence / 中国肿瘤生物治疗杂志

@# Objective: The present study was aimed to explore the role and distinctive mechanism of SPIDR, the key regulatory protein of homologous recombination pathway, in progression of small cell lung cancer (SCLC). Methods: 60 SCLC specimens and 44 normal lung tissues were collected from the patients undergoing tumor resection and bronchoscopic puncture in Shanghai Pulmonary Hospital Affiliated to Tongji University from January 2013 to January 2015. The expression of SPIDR in clinical samples and NCIH446 (SCLC cell line) and MRC-5 (normal cell line) were assayed by Real-time PCR. The role of SPIDR in SCLC was investigated in vivo and in vitro by the expression of SPIDR were artificially modified in NCI-H446. Results: Smoking was significantly associated with the occurrence of SCLC (P<0.01). The expression of SPIDR mRNAin SCLC tissues was lower than that of normal lung tissues (P <0.01), and the SPIDR transcriptional and translational levels of NCI-H446 cells were also lower than that of MRC-5.Although there is no significant changes of cell growth rate and susceptibility to cisplatin and etoposide in the NCI-H446 cells overexpressing SPIDR. However, the volume of xenograft tumors of overexpressed SPIDR group decreased by 58.99% (P<0.01) and 61.84% (P<0.01) than that of the original NCI-H446 cells and the NCI-H446 cells transfected with vector (pMSCV) and the average tumor mass decreased by 61.70% (P<0.01) and 70.25% (P<0.01) respectively. When the fetal bovine serum content in the medium was reduced to 3%, the growth rate of NCI-H446 cells overexpressing SPIDR was 22.33% (P<0.01) and 20.24% (P<0.05) lower than that of the original NCIH446 cells and control group, the similar results were obtained from the 1% serum concentration experiment as well. Conclusion: The expression of SPIDR, the key regulatory protein in the DNAdouble strand break homologous recombination repair pathway, was significantly suppressed in SCLC tissues, which markedly accelerated the growth of NCI-H446 cells in vivo and reduced the reliance of NCIH446 cells to the serum. The detailed mechanism is worthy of further investigation.

Fangchinoline suppresses the proliferation, invasion and tumorigenesis of human osteosarcoma cells through the inhibition of PI3K and downstream signaling pathways.

Osteosarcoma is the most common malignant bone tumor. Most patients diagnosed with osteosarcoma are less than 20 years of age. Osteosarcoma cells proliferate rapidly and invade other tissues. At present, neoadjuvant chemotherapy is the primary pharmacodynamic strategy to prevent the progression of osteosarcoma. However, adverse effects of this strategy limit its long­term application. Previous research has shown that fangchinoline exerts antitumor effects on several types of tumor cells; however, its effect on osteosarcoma cells remains unknown. The present study evaluated the effects of fangchinoline on the proliferation, apoptosis, migration and invasion of osteosarcoma cells in vitro and on their tumorigenesis in vivo and determined the possible underlying mechanism of action. Fangchinoline­treated MG63 and U20S cells showed significantly decreased proliferation and significantly increased apoptosis. Fangchinoline markedly suppressed the migration and invasion of the MG63 cells. Fangchinoline­treated MG63 cells showed significantly decreased expression of phosphoinositide 3­kinase (PI3K) and Aktp­Thr308. Moreover, fangchinoline­treated MG63 cells showed downregulated expression of cyclin D1 and matrix metalloproteinase 2 and 9, which act downstream of PI3K, and upregulated expression of caspase­3 and caspase­8. Furthermore, fangchinoline suppressed the growth of subcutaneous osteosarcoma tumors in Balb/c mice subcutaneously injected with osteosarcoma cells. These findings suggest that fangchinoline inhibits the progression of osteosarcoma by suppressing the proliferation, migration and invasion and by accelerating the apoptosis of osteosarcoma cells. In addition, our results suggest that the mechanism underlying the antitumor effects of fangchinoline involve the inhibition of PI3K and its downstream signaling pathways.

FIGNL1 is overexpressed in small cell lung cancer patients and enhances NCI-H446 cell resistance to cisplatin and etoposide.

Abnormal DNA repair plays an important role in tumor occurrence, progression and resistance to therapy. Fidgetin-like 1 (FIGNL1) expression was assayed in 42 small cell lung cancer (SCLC) and 45 normal lung specimens from Chinese patients by qRT-PCR. Notably, FIGNL1 was upregulated by 1.5-fold in the SCLC specimens compared to that noted in the normal counterparts. The SCLC cell line NCI-H446 that overexpresses FIGNL1 was adopted to explore the biological significance of FIGNL1 in SCLC. Even when FIGNL1 expression was suppressed by up to 48.6%, H446 cell growth was increased by only 10-16%. Although no significant changes in cell cycle distribution were observed in the H446 cells, the levels of cyclin E1 and CDK2, key cell cycle regulators, were significantly reduced. After downregulation of FIGNL1 expression by 13.5% in the H446 cells, the cells were 61.8% (24 h) to 29.1% (48 h) more sensitive to etoposide and cisplatin, respectively, consistent with the FIGNL1 function of DNA double-strand repair. The sensitivity of H446 cells to etoposide and cisplatin was negatively correlated with FIGNL1 expression. Meanwhile, an obvious positive correlation between DNA damage severity and the sensitization effect of FIGNL1 knockdown was observed. Since FIGNL1 is essential in the homologous recombination (HR) pathway, these findings suggest that abnormal activation of the HR pathway featured by FIGNL1 overexpression contributes to rapid progression and relapse of SCLC in addition to chemotherapy resistance. Further research assessing the functions and mechanisms of FIGNL1, and other HR pathway genes may disclose unique pathological characteristics of SCLC, and help identify potential therapeutic targets and biomarkers.

Galangin suppresses human osteosarcoma cells: An exploration of its underlying mechanism.

Osteosarcoma is the most common malignant bone tumor that frequently affects adolescents. Osteosarcoma cells tend to proliferate and invade other tissues such as those of the lungs. Currently, neoadjuvant chemotherapy is the primary strategy to prevent tumor progression. However, its adverse effects result in poor long-term outcomes. Previous research has shown that galangin exhibits antitumor properties on several types of cancer cells; however its effect on osteosarcoma cells is yet unknown. The aims of this study were to evaluate the effects of galangin on the proliferation, apoptosis, migration, and invasion of osteosarcoma cells and to explore the underlying mechanisms. We found that the proliferation of MG63 and U20S osteosarcoma cells decreased significantly, while the apoptosis of MG63 cells accelerated significantly after exposure to galangin. In addition, the migration and invasion of MG63 cells were significantly inhibited by galangin. Moreover, phosphoinositide 3-kinase (PI3K) and Aktp-Thr308 expression levels were found to be significantly lower in galangin-treated MG63 cells than in the control cells, and the protein expression levels of their downstream regulators cyclin D1 and matrix metalloproteinase 2/9 were also downregulated in galangin-treated groups, while those of p27Kip1, caspase-3, and caspase-8 were upregulated. These findings suggest that galangin suppresses osteosarcoma cells by inhibiting their proliferation and invasion and accelerating their apoptosis, and the mechanism may be associated with the inhibition of PI3K and its downstream signaling pathway.

The osteogenic potential of human bone callus.

Bone callus, generated during fracture healing, is commonly discarded during surgical procedures. The aim of this study was to investigate the osteogenic potential of bone callus and its possible use as autograft material for patients needing bone grafts. Histology, immunohistochemistry, micro-computed tomography, and biomechanics were performed to examine osteogenic cells, osteoinductive factors, and the osteoconductive structure of bone callus. Alkaline phosphatase-positive osteoblasts, osteoinductive factors (including BMP2, FGF2, TGFB1, and IGF1), and a porous structure were found in bone callus. Early-stage callus (within 3 months after fracture) presented significantly improved osteogenic properties compared to medium- (3-9 months) and late-stage (longer than 9 months) callus. The results revealed that bone callus induced new bone formation in a nude mouse model. Early-stage callus showed better performance to medium- and late-stage callus in the induction of new bone formation at both 8 and 12 weeks. These findings indicated that bone callus, especially early-stage callus, possesses osteogenic potential and can potentially serve as an alternative source of material for bone grafts.

Surface topography of hydroxyapatite promotes osteogenic differentiation of human bone marrow mesenchymal stem cells.

Effective and safe induction of osteogenic differentiation is one of the key elements of bone tissue engineering. Surface topography of scaffold materials was recently found to promote osteogenic differentiation. Utilization of this topography may be a safer approach than traditional induction by growth factors or chemicals. The aim of this study is to investigate the enhancement of osteogenic differentiation by surface topography and its mechanism of action. Hydroxyapatite (HA) discs with average roughness (Ra) of surface topography ranging from 0.2 to 1.65 µm and mean distance between peaks (RSm) ranging from 89.7 to 18.6 µm were prepared, and human bone-marrow mesenchymal stem cells (hBMSCs) were cultured on these discs. Optimal osteogenic differentiation was observed on discs with surface topography characterized by Ra ranging from 0.77 to 1.09 µm and RSm ranging from 53.9 to 39.3 µm. On this surface configuration of HA, hBMSCs showed oriented attachment, F-actin arrangement, and a peak in the expression of Yes-associated protein (YAP) and PDZ binding motif (TAZ) (YAP/TAZ). These results indicated that the surface topography of HA promoted osteogenic differentiation of hBMSCs, possibly by increasing cell attachment and promoting the YAP/TAZ signaling pathway.