Quality improvement of nursing on patients with complex cerebral arteriovenous malformation undergoing hybrid surgery: a prospective single-center study.

BACKGROUND: We sought to explore an optimal clinical nursing mode following a hybrid surgery for cerebral arteriovenous malformation. METHODS: Patients with complex cerebral arteriovenous malformations seen in our neurosurgery department from January 2016 to December 2017 were prospectively enrolled. The hybrid surgery protocol included "angiographic diagnosis, surgical resection, and intraoperative angiographic evaluation" and "angiographic diagnosis and embolization, surgical resection, and intraoperative angiographic evaluation". The patients were randomly stratified into intensive care group and routine care group. After surgery, intensive or routine care was provided, and the prognosis of patients was evaluated, with a subsequent comparative analysis. RESULTS: A total of 109 cases were divided into the routine nursing group (n = 54 cases) and intensive nursing group (n = 55 cases). There were no significant differences between the two groups in baseline data before surgery. Postoperative lung infection in the intensive nursing group was significantly less frequent than those in the routine nursing group (5.5% vs. 18.5%, P=0.039) with pulmonary infection and lower extremity venous thrombosis (5.5% vs. 24.1%, P=0.006). The average hospital stay in the intensive nursing group was 14.4 ± 5.78 days, which was significantly lower than that in the routine nursing group (19.3 ± 6.38 days, P=0.013). At 3 months' follow-up after surgery, the Generic Quality of Life Inventory-74 (GQOLI-74) dimension score and GQOLI-74 total score in the enhanced group were significantly better than those in the routine nursing group (P=0.017 and 0.023, respectively). CONCLUSIONS: Intensive postoperative nursing can improve the safety of patients after hybrid surgery, reduce the postoperative complications and the average length of hospital stay, and improve the quality of life of patients.

[Total nasal reconstruction with total rib cartilage framework].

OBJECTIVE: To investigate a new technique for nasal reconstruction with total rib cartilage framework. METHODS: The expanded frontal flap was fabricated by skin expansion and flap delay to cover the reconstructed nose. The dorsal flap was reversed as the lining of reconstructed nose. The whole framework was made by rib cartilage. Secondary revision operation was also performed to make the reconstructed nose more natural. RESULTS: Total nasal reconstruction was performed successfully in 37 cases. Each patient underwent 4-7 operation during a period of 6-8 months. 32 patients were followed up for 12-24 months. The reconstructed nose had a natural skin color and symmetric appearance with good ventilation and less scar. Both doctors and patients were satisfied with the results. CONCLUSION: Satisfactory cosmetic result and ventilation function can be achieved by nasal reconstruction with total rib cartilage framework.

[Correction of secondary nasal deformity of cleft lip with autogenous costal cartilage framework].

OBJECTIVE: To investigate the correction of secondary nasal deformity of cleft lip with autogenous costal cartilage framework. METHODS: 237 cases with secondary nasal deformity of unilateral cleft lip were treated. The rib cartilage was harvested through a mini-invasive incision, and was fabricated as a C-shaped framework, as well as some cartilage fragments. Through transcolumella incision, the C-shaped framework was implanted to support the depressed alar and the cartilage fragments were used to augment the nasal base. RESULTS: Satisfactory cosmetic and functional results were achieved in all the patients with primary healing. 93 patients were followed up one year after operation with good cosmetic results. CONCLUSIONS: Autogenous costal cartilage framework can be used for the correction of secondary nasal deformity of cleft lip with satisfactory results.

[Closure of cystic cavity-type bedsore by subcutaneous undermining dissection with continuous negative pressure drainage].

OBJECTIVE: To investigate the clinical effect of subcutaneous undermining dissection with continuous negative pressure drainage for the closure of cystic cavity-type bedsore. METHODS: 12 patients with cystic cavity-type bedsore underwent surgical debridement and the wounds were closed after subcutaneous undermining dissection. The negative pressure drainage was put in the deep space. The healing process was observed. RESULTS: Completed healing was achieved in all the 12 cases. The skin wounds healed after 17-20 days and the deep spaces closed after 36-43 days. 12 cases were followed up for 1 year with no occurrence. CONCLUSIONS: It is an easy and effective method to treat cystic cavity -type bedsore by subcutaneous undermining dissection with continuous negative pressure drainage.

Polo-like kinase 1 regulates mitotic arrest after UV irradiation through dephosphorylation of p53 and inducing p53 degradation.

Ultraviolet (UV) irradiation can result in cell cycle arrest. The reactivation of Polo-like kinase 1 (Plk1) is necessary for cell cycle reentry. But the mechanism of how Plk1 regulates p53 in UV-induced mitotic arrest cells remained elusive. Here we find that UV treatment leads HEK293 cells to inverse changes of Plk1 and p53. Over-expression of Plk1 rescue UV-induced mitotic arrest cells by inhibiting p53 activation. Plk1 could also inhibit p53 phosphorylation at Ser15, thus facilitates its nuclear export and degradation. Further examination shows that Plk1, p53 and Cdc25C can form a large complex. Plk1 could bind to the sequence-specific DNA-binding domain of p53 and active Cdc25C by hyperphosphorylation. These results hypothesize that Plk1 and Cdc25C participate in recovery the mitotic arrest through binding to the different domain of p53. Cdc25C may first be actived by Plk1, and then its phosphatase activity makes p53 dephosphorylated at Ser15.

Knockdown of c-Met by adenovirus-delivered small interfering RNA inhibits hepatocellular carcinoma growth in vitro and in vivo.

c-Met is highly expressed and constitutively activated in various human tumors. We employed adenovirus-mediated RNA interference technique to knock down c-Met expression in hepatocellular carcinoma cells and observed its effects on hepatocellular carcinoma cell growth in vitro and in vivo. Among the five hepatocellular carcinoma and one normal human liver cell lines we analyzed, c-Met was highly expressed and constitutively tyrosine phosphorylated in only MHCC97-L and HCCLM3 hepatocellular carcinoma cells. Knockdown of c-Met could inhibit MHCC97-L cells proliferation by arresting cells at G0-G1 phase. Soft agar colony formation assay indicated that the colony forming ability of MHCC97-L cells decreased by approximately 70% after adenovirus AdH1-small interfering RNA (siRNA)/met infection. In vivo experiments showed that adenovirus AdH1-siRNA/met inhibited the tumorigenicity of MHCC97-L cells and significantly suppressed tumor growth when injected directly into tumors. These results suggest that knockdown of c-Met by adenovirus-delivered siRNA may be a potential therapeutic strategy for treatment of hepatocellular carcinoma in which c-Met is overexpressed.

[The study on the STAT3 labeled by GFP affecting the migration of BEL-7402 cell line].

Signal transducers and activators of transcription (STATs) are key DNA-binding proteins in JAK/STATs signal pathway. Aberrant expression and activation of STAT3 have been identified in many kinds of tumors. We report here that constitutive activation of STAT3 was present in BEL-7402 cells. We constructed the fusing genes of STAT3 (wild type/mutant) and GFP to study the function of constitutively activated STAT3 in BEL-7402 cells. By measuring the migration of the cells labeled by GFP-STAT3(WT/CYF), we proved that overexpression of STAT3(WT) could augment the migration of BEL-7402 cells, while STAT3(CYF) could decrease the migration.

The association of calmodulin with central spindle regulates the initiation of cytokinesis in HeLa cells.

Calmodulin is a major cytoplasmic calcium receptor that performs multiple functions in the cell including cytokinesis. Central spindle appears between separating chromatin masses after metaphase-anaphase transition. The interaction of microtubules from central spindle with cell cortex regulates the cleavage furrow formation. In this paper, we use green fluorescence protein (GFP)-tagged calmodulin as a living cell probe to examine the detailed dynamic redistribution and co-localization of calmodulin with central spindle during cytokinesis and the function of this distribution pattern in a tripolar HeLa cell model. We found that calmodulin is associated with spindle microtubules during mitosis and begins to aggregate with central spindle after anaphase initiation. The absence of either central spindle or central spindle-distributed calmodulin is correlated with the defect in the formation of cleavage furrow, where contractile ring-distributed CaM is also extinct. Further analysis found that both the assembly of central spindle and the formation of cleavage furrow are affected by the W7 treatment. The microtubule density of central spindle was decreased after the treatment. Only less than 10% of the synchronized cells enter cytokinesis when treated with 25 microM W7, and the completion time of furrow regression is also delayed from 10 min to at least 40 min. It is suggested that calmodulin plays a significant role in cytokinesis including furrow formation and regression, The understanding of the interaction between calmodulin and microtubules may give us insight into the mechanism through which calmodulin regulates cytokinesis.

hNRAGE, a human neurotrophin receptor interacting MAGE homologue, regulates p53 transcriptional activity and inhibits cell proliferation.

hNRAGE, a neurotrophin receptor p75 interacting MAGE homologue, is cloned from a human placenta cDNA library. hNRAGE can inhibit the colony formation of and arrest cell proliferation at the G1/S and G2/M stages in hNRAGE overexpressing cells. Interestingly, hNRAGE also increases the p53 protein level as well as its phosphorylation (Ser392). Further studies demonstrated that hNRAGE does not affect the proliferation of mouse p53-/- embryonic fibroblasts, suggesting that p53 function is required for hNRAGE induced cell cycle arrest. Moreover, the cell cycle inhibiting protein p21(WAF) is induced by hNRAGE in a p53 dependent manner. The data provide original evidence that hNRAGE arrests cell growth through a p53 dependent pathway.

Aberrant expression and function of TCF4 in the proliferation of hepatocellular carcinoma cell line BEL-7402.

Wnt signaling pathway is essential for development and tumorigenesis, however, this signaling pathway in the progress of hepatocellular carcinoma (HCC) remains unclear. In this paper, we studied the function of human T-cell transcription factor-4 (TCF4), a key factor of Wnt signaling pathway, on the proliferation of HCC cell line. We showed that the expression of TCF4 mRNA in HCC cell line BEL-7402 was higher than that in immortalized normal liver cell line L02. Blockage of Wnt pathway by Delta-NTCF4, a dominant negative TCF4, could suppress BEL-7402 cells growth and decrease the expression of cyclin D1 and c-myc, two of target genes of Wnt pathway. On the other hand, stimulating Wnt pathway by introducing a degradation-resistant -catenin S37A could increase BEL-7402 cells proliferation. But all the treatments had no effect on L02 cells. Our data indicated that TCF4 might be another key factor in Wnt pathway involved in HCC cells proliferation and TCF4 could be an effective therapeutic target for suppressing the growth of hepatocellular cancers.

[The distribution of calmodulin with midbody and its involvement in cytokinesis regulation].

Calmodulin (CaM) is a major cytoplasmic Ca2+ receptor and performs a multiplicity of functions in the cell. By using GFP-CaM fusion protein, we have studied the detailed dynamic redistribution of CaM during cytokinesis in HeLa cells. CaM associates with midbody in late cytokinesis phase. When the cells were treated with Ca2+/CaM inhibitor W7, the dissolving of the midbody was delayed. Moreover, we have found that gamma-tubulin colocalized with CaM at the midbody during cytokinesis. W7 treatment could affect the dissociation of gamma-tubulin from midbody. These results suggest that CaM may involve in the regulation of midbody microtubules disassembly and may thus affect the completion of cytokinesis.

[Study on the role of calcium signal during mature resumption of isolated mouse germinal vesicles in a cell free system].

A cell-free system including HeLa cell lysate of synchronized metaphase or G2-phase and isolated germinal vesicles (GV) from mouse oocytes was used to study the role of calcium and its downstream mediator during mature resumption. The isolated GVs could resume meiotic maturation in the lysate prepared from M phase HeLa cell, which marked by chromatin condensation. And this process was not affected by calcium chelating agent. But calcium in lysate from G2 phase cells was critical to meiotic maturation. Only in mid-G2 phase cell lysate (released from nocodazole for about 20-23h) chromatin condensation could be induced by calcium. Calcium had no effect on the cell lysate prepared from earlier (18-20h) and later (24h) G2 phase cells. Further studies showed that down stream mediator CaM and CaMKII might also involove in this process. Inhibition the function of CaM and CaMKII could block GVBD and first polar body extrusion of DOs cultured in vitro. The target of calcium signal might be MPF because MPF was existed from mid-G2 phase to metaphase and the tyrosine phosphorylation level of Cdc2 subunit was significantly dephosphorylated in M phase. Our results further confirmed that the resumption of meiosis maturation was promoted in a calcium/CaM depended pathway.