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1.
Chin Neurosurg J ; 7(1): 23, 2021 May 01.
Article in English | MEDLINE | ID: mdl-33931131

ABSTRACT

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.

2.
Zhonghua Zheng Xing Wai Ke Za Zhi ; 29(2): 91-3, 2013 Mar.
Article in Chinese | MEDLINE | ID: mdl-23772483

ABSTRACT

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.


Subject(s)
Nose/surgery , Rhinoplasty/methods , Ribs/transplantation , Adult , Braces , Female , Humans , Male , Treatment Outcome
3.
Zhonghua Zheng Xing Wai Ke Za Zhi ; 29(3): 167-9, 2013 May.
Article in Chinese | MEDLINE | ID: mdl-25069339

ABSTRACT

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.


Subject(s)
Cleft Lip/surgery , Costal Cartilage/transplantation , Nose Deformities, Acquired/surgery , Rhinoplasty/methods , Humans
4.
Zhonghua Zheng Xing Wai Ke Za Zhi ; 28(2): 113-5, 2012 Mar.
Article in Chinese | MEDLINE | ID: mdl-22737936

ABSTRACT

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.


Subject(s)
Debridement/methods , Drainage/methods , Negative-Pressure Wound Therapy , Pressure Ulcer/surgery , Wound Healing , Humans
5.
FEBS Lett ; 580(15): 3624-30, 2006 Jun 26.
Article in English | MEDLINE | ID: mdl-16753148

ABSTRACT

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.


Subject(s)
Cell Cycle Proteins/metabolism , Mitosis/radiation effects , Protein Serine-Threonine Kinases/metabolism , Proto-Oncogene Proteins/metabolism , Tumor Suppressor Protein p53/metabolism , Cell Cycle Proteins/genetics , Cell Line , DNA Damage/genetics , Humans , Phosphorylation/radiation effects , Phosphoserine/metabolism , Protein Binding , Protein Processing, Post-Translational , Protein Serine-Threonine Kinases/genetics , Protein Transport , Proto-Oncogene Proteins/genetics , cdc25 Phosphatases/metabolism , Polo-Like Kinase 1
6.
Mol Cancer Ther ; 4(10): 1577-84, 2005 Oct.
Article in English | MEDLINE | ID: mdl-16227408

ABSTRACT

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.


Subject(s)
Carcinoma, Hepatocellular/enzymology , Carcinoma, Hepatocellular/pathology , Liver Neoplasms/enzymology , Liver Neoplasms/pathology , Proto-Oncogene Proteins c-met/antagonists & inhibitors , RNA, Small Interfering/genetics , Adenoviridae/genetics , Animals , Carcinoma, Hepatocellular/genetics , Carcinoma, Hepatocellular/metabolism , Cell Line , Cell Line, Tumor , Flow Cytometry , Humans , Immunohistochemistry , Liver Neoplasms/genetics , Liver Neoplasms/metabolism , Mice , Mice, Inbred BALB C , Phosphorylation , Proto-Oncogene Proteins c-met/biosynthesis , Proto-Oncogene Proteins c-met/genetics , Proto-Oncogene Proteins c-met/metabolism , RNA, Messenger/genetics , Reverse Transcriptase Polymerase Chain Reaction
7.
Shi Yan Sheng Wu Xue Bao ; 38(4): 317-23, 2005 Aug.
Article in Chinese | MEDLINE | ID: mdl-16231698

ABSTRACT

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.


Subject(s)
Cell Movement/genetics , Green Fluorescent Proteins/metabolism , STAT3 Transcription Factor/physiology , Cell Line , Cell Line, Tumor , Cell Movement/drug effects , Green Fluorescent Proteins/genetics , Hep G2 Cells , Humans , Interleukin-6/pharmacology , STAT3 Transcription Factor/genetics , STAT3 Transcription Factor/metabolism
8.
Int J Biochem Cell Biol ; 36(8): 1562-72, 2004 Aug.
Article in English | MEDLINE | ID: mdl-15147735

ABSTRACT

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.


Subject(s)
Calmodulin/metabolism , Cytokinesis , Spindle Apparatus/metabolism , Anaphase , Green Fluorescent Proteins , HeLa Cells , Humans , Microtubules/metabolism , Mitosis , Protein Transport , Sulfonamides/pharmacology , Time
9.
FEBS Lett ; 564(1-2): 171-6, 2004 Apr 23.
Article in English | MEDLINE | ID: mdl-15094062

ABSTRACT

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.


Subject(s)
Interphase , Neoplasm Proteins/physiology , Transcription, Genetic , Tumor Suppressor Protein p53/physiology , Antigens, Neoplasm , Cell Division , Cell Line, Tumor , Cloning, Molecular , Cyclin-Dependent Kinase Inhibitor p21 , Cyclins/biosynthesis , Gene Expression Regulation , Humans , Neoplasm Proteins/genetics , Phosphorylation , Transfection , Tumor Suppressor Protein p53/genetics , Tumor Suppressor Protein p53/metabolism
10.
Cell Res ; 14(1): 74-80, 2004 Feb.
Article in English | MEDLINE | ID: mdl-15040893

ABSTRACT

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.


Subject(s)
Carcinoma, Hepatocellular/physiopathology , DNA-Binding Proteins/physiology , Liver Neoplasms/physiopathology , Transcription Factors/physiology , Blotting, Western , Carcinoma, Hepatocellular/genetics , Carcinoma, Hepatocellular/metabolism , Cell Division/genetics , Cell Division/physiology , Cell Line , Cell Line, Tumor , Cyclin D1/genetics , Cyclin D1/metabolism , Cytoplasm/chemistry , Cytoskeletal Proteins/analysis , Cytoskeletal Proteins/genetics , Cytoskeletal Proteins/physiology , DNA-Binding Proteins/genetics , Gene Expression/genetics , Gene Expression Regulation, Neoplastic , Genes, Reporter/genetics , Genetic Vectors/genetics , Humans , Immunohistochemistry , Liver Neoplasms/genetics , Liver Neoplasms/metabolism , Lymphoid Enhancer-Binding Factor 1 , Microscopy, Fluorescence , Mutation/genetics , Proto-Oncogene Proteins/physiology , Proto-Oncogene Proteins c-myc/genetics , Proto-Oncogene Proteins c-myc/metabolism , Reverse Transcriptase Polymerase Chain Reaction , Signal Transduction/physiology , Spectrometry, Fluorescence , TCF Transcription Factors , Trans-Activators/analysis , Trans-Activators/genetics , Trans-Activators/physiology , Transcription Factor 7-Like 2 Protein , Transcription Factors/genetics , Transfection , Wnt Proteins , beta Catenin
11.
Shi Yan Sheng Wu Xue Bao ; 36(5): 335-41, 2003 Oct.
Article in Chinese | MEDLINE | ID: mdl-14724944

ABSTRACT

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.


Subject(s)
Calmodulin/metabolism , Centrosome/physiology , Sulfonamides/pharmacology , Tubulin/metabolism , Calmodulin/antagonists & inhibitors , Cell Cycle , Cell Division/physiology , Centrosome/metabolism , Green Fluorescent Proteins , HeLa Cells , Humans , Luminescent Proteins/metabolism , Microtubules/metabolism , Recombinant Fusion Proteins/metabolism
12.
Shi Yan Sheng Wu Xue Bao ; 35(4): 249-56, 2002 Dec.
Article in Chinese | MEDLINE | ID: mdl-15346980

ABSTRACT

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.


Subject(s)
Calcium/metabolism , Animals , Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism , Calmodulin/metabolism , Cell Differentiation/physiology , Cell-Free System/metabolism , Female , HeLa Cells , Humans , Meiosis/physiology , Mesothelin , Mice , Oocytes/metabolism , Oocytes/physiology
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