Three-Dimensional Arterial Distribution Over the Midline of the Nasal Bone.

BACKGROUND: A comprehensive understanding of arterial variations around the midline of the nose is of great importance for the safety of filler injection. OBJECTIVES: The aim of the study was to clearly define the 3-dimensional location of the arteries along the midline of the nasal bone. METHODS: The arterial structures overlapping the nasal bone along the midline were observed in 79 cadavers. RESULTS: The present study found that 0 to 3 named arteries per nose segment could be identified. All the arterial structures were located in or above the superficial musculoaponeurotic system layer overlapping the nasal bone. The probability of encountering named arteries at 5 defined points, P1 to P5, was 5/79 (6.3%), 4/79 (5.1%), 1/79 (1.3%), 6/79 (7.6%), and 9/79 (11.4%), respectively. The depth of the main arterial trunk was 1.2 ± 0.4 mm, 1.6 ± 0.6 mm, 1.8 ± 0 mm, 1.0 ± 0.4 mm, and 0.9 ± 0.5 mm below the skin at P1 to P5, respectively. CONCLUSIONS: The authors confirmed that sub-superficial musculoaponeurotic system injection along the midline through a needle is anatomically reliable and that a technique with 1 entry point through the rhinion via a cannula can easily keep the needle sufficiently deep for safe nasal filler injection.

MicroRNA-647 promotes the therapeutic effectiveness of argon-helium cryoablation and inhibits cell proliferation through targeting TRAF2 via the NF-κB signaling pathway in non-small cell lung cancer.

BACKGROUND: MicroRNA-647 (miR-647) has been reported to repress cell tumorigenic phenotype, while the function of miR-647 in non-small cell lung cancer was obscure. METHODS: The effect of miR-647 and TRAF2 on A549 and H1299 cells was explored through Methyl thiazolyl tetrazolium (MTT) assay, colony formation and cell cycle assays. Luciferase reporter assays, reverse transcription quantitative PCR (RT-qPCR) and Western blot assay were carried out to determine that TRAF2 is directly regulated by miR-647. The effect of miR-647/TRAF2 axis on p65 protein level in nucleus or total was detected by Western blot assay. RESULTS: Here, we found that miR-647 was high expression in tumor that under argon-helium cryoablation treatment in contrast to the tumor under non argon-helium cryoablation treatment and inhibited cell proliferation of A549 and H1299 cells by inducing G1-S transition. TRAF2 was confirmed as a target of miR-647. TRAF2 overexpression partially rescued the suppressive function of miR-647 in A549 and H1299 cells. Moreover, we found that miR-647 repressed lung carcinogenesis by attenuating NF-κB pathway. CONCLUSION: In all, our study demonstrates that miR-647 functions as tumor suppressor via targeting and down-regulating the expression of TRAF2 and NF-κB signaling pathway in non-small cell lung cancer.

Killing effect of Ad5/F35-APE1 siRNA recombinant adenovirus in combination with hematoporphrphyrin derivative-mediated photodynamic therapy on human nonsmall cell lung cancer.

The main goal of this work is to investigate the killing effects and molecular mechanism of photodynamic therapy (PDT) mediated by the Ad5/F35-APE1 siRNA recombinant adenovirus in combination with a hematoporphrphyrin derivative (HpD) in the A549 human lung adenocarcinoma cell line in vitro to provide a theoretical reference for treating lung cancer by HpD-PDT. By using the technologies of MTT, flow cytometry, ELISA, and western blot, we observed that the proliferation inhibition and apoptosis of the A549 cells were significantly higher than the control group (P < 0.05) after HpD-PDT was performed. The inhibitory efficiency is dependent on the HpD concentration and laser intensity dose. The inhibitory effect on the proliferation of A549 cells of Ad5/F35-APE1 siRNA is more significant after combining with PDT, as indicated by a significant elevation of the intracellular ROS level and the expression of inflammatory factors (P < 0.05). The HpD-PDT-induced expression of the APE1 protein reached the peak after 24 h in A549 cells. The inhibition of APE1 expression in A549 cells was most significant after 48 hours of infection by Ad5/F35-APE1 siRNA recombinant adenovirus (10 MOI). In conclusion, the Ad5/F35-APE1 siRNA recombinant adenovirus could efficiently inhibit the HpD-PDT-induced APE1 expression hence could significantly enhance the killing effect of HpD-PDT in lung cancer cells.

[Effect of platelet-rich plasma on the proliferation and adipogenic differentiation of human adipose-derived stem cells in vitro].

OBJECTIVE: To observe the effect of platelet-rich plasma (PRP) on the proliferation and adipogenic differentiation of human adipose-derived stem cells in vitro. METHODS: Human adipose-derived stem cells were obtained by enzymatic digestion and PRP was prepared by dual centrifugal method. The ADSCS were interfused with 5%, 10%, and 20% PRP in conditioned culture media, using the untreated cells as the control group. The morphology of the cells were observed and their proliferative ability was detected using XTT colorimetric assay. The adipogenic differentiation ability of the cells was evaluated using oil Red O staining. RESULTS: The ADSCS treated with PRP showed better morphology with higher density than the control cells. XTT colorimetric assay demonstrated obviously stronger proliferative activity of PRP-treated cells than the control group (P<0.01). Interfusion with PRP caused a significant increase in adipogenic differentiation of the cells as compared to the control cells (P<0.01). CONCLUSION: PRP treatment produces obvious effects on the proliferation and adipogenic differentiation of human adipose-derived stem cells in vitro.

Polymorphisms of TP53 codon 72 with prostate carcinoma risk: a meta-analysis.

Previous published data indicated TP53 codon 72 polymorphisms as risk factors for various cancers. A large number of studies have been conducted on the association of TP53 codon 72 polymorphisms with susceptibility to prostate carcinoma and have yielded inconclusive results. The aim of the present study is to derive a more precise estimation of the relationship. We conducted a search in the Medline, EMBASE, OVID, Sciencedirect, and Chinese National Knowledge Infrastructure (CNKI) without a language limitation, covering all papers published up to Feb 2009. The associated literature was acquired through deliberate searching and selected based on the established inclusion criteria for publications. A total of six case-control studies, including 582 cases and 1075 controls, met the included criteria and thus were selected. Consequently, the relevant data were extracted and further analyzed using systematic meta-analyses. For the overall data, no associations of TP53 codon 72 polymorphisms with prostate carcinoma were observed (for Arg/Arg versus Pro/Pro: OR = 0.88; 95%CI = 0.62-1.25; for dominant model: OR = 1.05; 95%CI = 0.78-1.43; for recessive model: OR = 0.85; 95%CI = 0.67-1.06). In the subgroup analysis by ethnicity, individuals carrying Arg allele may have an increased susceptibility to prostate cancer compared with those carrying Pro allele in Caucasians. While for Asians, TP53 codon 72 polymorphism was unlikely to be a risk factor for prostate cancer. Moreover, TP53 codon 72 polymorphism seems to exert little effect on the metastasis and differentiation status of developing prostate carcinoma. Collectively, the results of the present study suggest that TP53 codon 72 polymorphism might be a low-penetrant risk factor for developing prostate carcinoma in Caucasians but not in Asians.

Knock down of the dual functional protein apurinic /apyrimidinic endonuclease 1 enhances the killing effect of hematoporphrphyrin derivative-mediated photodynamic therapy on non-small cell lung cancer cells in vitro and in a xenograft model.

Photodynamic therapy (PDT) is considered to be effective treatment for many cancers including lung cancer, head and neck cancers, and prostate cancer. It uses the combination of nontoxic photosensitizers and harmless visible light to generate reactive oxygen species and kill cells. However, DNA repair and reactive oxygen species-induced signaling pathway activation play crucial roles in cellular response to PDT and may also result in therapeutic limitation of PDT. To improve the cancer therapeutic efficacy of PDT, we targeted apurinic/apyrimidinic endonuclease (APE1), which is essential for both DNA repair and redox regulation of gene transcription, as a potential candidate for PDT combined gene therapy. In our study, an adenovirus-mediated APE1 silencing strategy was introduced to test its therapeutic enhancement for the non-small cell lung cancer cell line A549 both in vitro and in vivo after hematoporphrphyrin derivative (HpD)-mediated PDT. The adenovirus vector Ad5/F35-shAPE1 was validated to significantly suppress the protein expression of APE1 in cultured A549 cell and in its xenograft of nude mice. Ad5/F35-shAPE1 effectively inhibited APE1 protein upregulation induced by PDT and resulted in an increase in A549 cell killing by photoirradiation compared with the hematoporphrphyrin derivative-PDT alone group. Ad5/F35-shAPE1 suppressed the DNA repair capacity for single-strand breaks and abolished the activation of some stress-related transcription factors such as hypoxia-induced factor (HIF)-1 that consequently lead to increased cell apoptosis after PDT. Additionally, knock down of APE1 enhanced the tumor suppression efficacy of PDT on the A549 xenograft. Our study indicated that APE1-targeted gene therapy combined with PDT is a promising strategy for enhancement of the efficacy of PDT in treatment of non-small cell lung cancer.

Association studies of CYP1A1 and GSTM1 polymorphisms with esophageal cancer risk: evidence-based meta-analyses.

BACKGROUND AND AIMS: Previous studies have implicated cytochrome P450 1A1 (CYP1A1) and glutathione S-transferase M1 (GSTM1) polymorphisms as risk factors for various cancers. A number of studies have been devoted to the association of CYP1A1 or GSTM1 polymorphism with susceptibility to esophageal carcinoma and have yielded conflicting results. We undertook this study to assess possible associations of esophageal cancer risk with CYP1A1 genetic variation and GSTM1 null genotype, respectively. METHODS: We conducted a search in MEDLINE, EMBASE and Chinese National Knowledge Infrastructure (CNKI) without a language limitation, covering all papers published until May 2008. The associated literature was acquired through deliberate searching and selected based on the established inclusion criteria for publications. RESULTS: Ultimately, 26 studies met the included criteria and thus were selected. Relevant data were extracted and further analyzed using systematic meta-analyses. Results showed that the overall OR for CYP1A1 Msp1 polymorphism was 1.24 (95% CI = 0.84-1.83). Restricting analyses to ethnic groups and histological groups, data failed to show a correlation between CYP1A1 Msp1 polymorphism and esophageal cancer risk. Overall OR for CYP1A1 exon7 polymorphism was 1.37 (95% CI = 1.06-1.77), and subgroup analyses showed that CYP1A1 exon7 polymorphism increases esophageal cancer risk in Asians but not in Caucasians. As for GSTM1 deficiency, the overall OR was 1.20 (95% CI = 0.96-1.49), and further subgroup analyses failed to show a marked association of GSTM1 deletion with esophageal cancer. CONCLUSIONS: Results of the present study suggest that CYP1A1 exon7 polymorphisms may be a risk factor for esophageal cancer in Asians but not in Caucasians, whereas neither CYP1A1 Msp1 nor GSTM1 polymorphism was associated with increased susceptibility to esophageal cancer.

APE1 overexpression is associated with cisplatin resistance in non-small cell lung cancer and targeted inhibition of APE1 enhances the activity of cisplatin in A549 cells.

PURPOSE: Apurinic/apyrimidinic endonuclease (APE1), a bifunctional AP endonuclease/redox factor, is important in DNA repair and redox signaling, may be associated with chemoresistance. In this study, we first investigated APE1 expression and its correlation with cisplatin resistance and prognosis in non-small cell lung cancer (NSCLC) patients. Then, we investigated the effect of chimeric adenoviral vector Ad5/F35 carrying human APE1 siRNA (Ad5/F35-APE1 siRNA) on the sensitivity of cisplatin in A549 human lung adenocarcinoma cells. METHODS: Tumor specimens from 103 patients with operable NSCLC were obtained from 1999 to 2001. Among these patients, 72 patients have been treated with at least three cycles of cisplatin-based chemotherapy. APE1 protein expression was examined by immunohistochemistry and Western blot on the tumor samples and a cultured A549 cell line, respectively. Cell survival and apoptosis were determined by MTT and TUNEL, respectively. RESULTS: 83.3% (20/24) cisplatin-resistant tumors showed high APE1 expression levels, while 8.3% (4/48) cisplatin-sensitive tumors showed high APE1 expression levels (p<0.01). Univariate analysis indicated that overall survival and disease-free survival were significantly better in NSCLC patients with low vs those with high APE1 expression levels (p<0.01). Treatment with cisplatin resulted in a dose-dependent increase in APE1 protein expression in A549 cells, and Ad5/F35-APE1 siRNA effectively inhibited APE1 expression. Ad5/F35-APE1 siRNA significantly enhanced sensitivity of A549 cells to cisplatin, associated with increased cell apoptosis. CONCLUSIONS: Our results indicate that APE1 is a new promising target for the combination of cisplatin-based chemotherapy in NCSLC patients.

[Adipose tissue engineering with human adipose-derived stem cells and fibrin glue injectable scaffold].

OBJECTIVE: To explore the possibility of building tissue-engineered adipose tissue and find a new approach for repairing soft tissue defects. METHODS: Using enzymatic digestion, adipose tissue-derived stem cells (ASCs) were extracted from the lipid part of human liposuction aspirate, cultured, and underwent adipogenic induction or not. The adipogenic-induced and non-adipogenic-induced ASCs were labeled with 3, 3, 3', 3'-tetramethylindo-carbocyanine perchlorate (DiI), a fluorescent marker, in vitro to be used as seed cells. Then, they were combined with injectable fibrin glue scaffold at 1 x 10(7)/ml cell density. Six athymic BALB/C mice underwent subcutaneous injection of adipogenic-induced ASCs with fibrin glue scaffold at the density of 1 x 10(7) cells/ml into the left side of the low back (induced group), subcutaneous injection of non-adipogenic-induced ASCs into the right side of the low back (non-induced group), and subcutaneous injection of injectable fibrin glue scaffold into the middle part of the neck (blank control group), with 0.2 ml per injection. Twelve weeks later the mice were killed and the implants were taken out. The wet weight was measured. HE and oil red O staining and light and fluorescence microscopy were used for morphological observation. RESULTS: Adipose tissue-like new-born tissues were found in the injection sites of the induced and un-induced groups. The average wet-weight of the induced group new-born tissue was (28 +/- 15) mg, significantly heavier than that of the un-induced group [(22 +/- 16) mg, P < 0.01]. HE staining and oil red O staining confirmed that the new-born tissue of the induced group was mature adipose tissue and DiI fluorescent staining approved its exogenousness. Most part of the new-born tissues of the un-induced group was fibroid tissue with only a few mature adipose tissues. CONCLUSION: ASCs extracted from the lipid part after liposuction can be used as seed cells, mixed, after adipose-induction, with injectable scaffold of fibrin glue, and injected into the body to build mature adipose tissue.

Adenoviral-mediated up-regulation of Otos, a novel specific cochlear gene, decreases cisplatin-induced apoptosis of cultured spiral ligament fibrocytes via MAPK/mitochondrial pathway.

Previous reports have implicated Otos, a novel specific gene expressed by spiral ligament fibrocytes (SLFs) with unclear functions, as a protective gene for cochlea. However, whether Otos gene could protect SLFs against cisplatin (DDP)-induced apoptosis remains largely unknown. In the present study, we utilized Adenoviral-mediated gene transfection to up-regulate Otos expression in cultured SLFs and further assessed the cell viability and apoptosis as well as possible MAPK and mitochondrial pathways. As expected, the data showed that Otos up-regulation significantly decreased apoptosis of SLFs induced by DDP possibly through activation of ERK and partial inhibition of JNK and mitochondrial pathway but not p-38 pathway, suggesting Otos as a potential protective gene for cochlea and raising the possibility of Otos up-regulation as a promising approach to DDP-induced deafness therapy.

Short interfering RNA directed against TWIST, a novel zinc finger transcription factor, increases A549 cell sensitivity to cisplatin via MAPK/mitochondrial pathway.

Previous reports have implicated epithelial-mesenchymal transition (EMT) as a major cause of cancer. TWIST, a novel zinc finger transcription factor, was suggested to be an important inducer of EMT and therefore be involved in different phases of tumorigenicity. However, whether TWIST suppression could increase chemosensitivity of cancer cells to chemotherapeutic agent remains unclear. In the present study, we utilized RNA interference to knockdown TWIST expression in A549 cells and further assessed the cell viability and apoptosis as well as possible MAPKs and mitochondrial pathways. The data showed that TWIST depletion significantly sensitized A549 cells to cisplatin by inducing activation of JNK/mitochondrial pathway but not ERK and p-38 pathways, suggesting critical roles of TWIST in A549 cell chemoresistance to cisplatin and raising the possibility of TWIST depletion as a promising approach to lung cancer therapy.

[Study of adipose tissue engineering with human adipose-derived stem cells and collagen type I scaffold].

OBJECTIVE: To explore the possibility of building tissue-engineered adipose tissue and looking for a new approach for the repair of soft tissue defects. METHODS: The cells using enzymatic digestion from human liposuction part of the lipid extract were used as adipose tissue-derived cells and labeled with DiI fluorescent marker, the induced group using I collagen scaffold material as a carrier, the induced cell were planted into left back subcutaneously in nude mice at 1 x 10(7)/ml cell density, in the uninduced group cells were not induced by any, in the same cell density and type I collagen scaffold composite inoculated in nude right mouse back skin, the blank control group I collagen scaffold gaps in nude mice inoculated subcutaneously center of the neck, each of the six mice; Remove implants after 12 weeks and judge the adipogenic capacity through general and fluorescence microscopy, wet - determination, histological detection and oil red O staining qualitative. RESULTS: The primary source of fat cultured stem cells, similar to the fibroblast morphology, and has a strong proliferative capacity. In the role of adipose differentiation medium, it can be the mature fat cells in which cytoplasmic lipid droplets gather, oil red O staining was positive. In the induced group, newborn tissue were found in the experimental groups of nude mice and its average weight is about 0.020 g. Conventional pathological slices and oil red O staining confirmed it is mature adipose tissue, the fluorescence staining positive confirm them are exogenous. Uninduced group newborn tissue are found in the experimental groups of nude mice and its average weight is about 0.014 g. Conventional pathological slices and oil red O staining confirmed it include some mature adipose tissue, the fluorescence staining positive confirm them are exogenous. Two groups of the new wet weight with have statistical significance (P < 0.01); gaps in the control group no new organization formed. CONCLUSIONS: The cells using enzymatic digestion from human liposuction part of the lipid extract are adipose tissue-derived cells. The cells can be as seed cells and with solid scaffold of collagen type I it can become fat tissue in vivo successfully.

[Effects of 5F from Pteris semipinnate L on growth of human pathological scars in nude mice].

OBJECTIVE: To investigate the effect of 5F from Pteris semipinnate L on the growth of human pathological scar in nude mice. METHODS: 5F from Pteris semipinnate L was administered at different doses in nude mouse models bearing human pathological scars. The morphology, histology, tumor growth factor-beta1 and type I collagen content of the scar tissues were examined after the administration. RESULTS: Administration of 5F significantly reduced the volume of the implanted pathological scars in the nude mouse models, and histologically, the scar tissue exhibited a transition to the normal scar architecture with decreased TGF-beta1 and type I collagen content. CONCLUSION: 5F could effectively inhibit the growth of pathological scars in nude mice.

[Cellular compatibility of type collagen I scaffold and human adipose-derived stem cells].

OBJECTIVE: To study the cellular compatibility of type I collagen scaffold and human adipose-derived stem cells (ADSC(S)) in order to explore appropriate scaffold materials for adipose tissue engineering. METHODS: The morphology and function of the ADSC(S) were observed by inverted phase contrast microscope, scanning electron microscope and XTT assay when cocultured type I collagen scaffold with ADSC(S) in vitro. Cells adhesive rates were also calculated. RESULT: ADSC(S) were able to attach, grow and proliferate well on the scaffolds. CONCLUSION: collagen I scaffold exhibits excellent cellular compatibility and can be used as a vehicle for adipose tissue engineering.