Relevance between Cassava Starch Liquefied by Phenol and Modification of Phenol-Formaldehyde Resin Wood Adhesive.

A novel type of phenol-formaldehyde (PF) resin was prepared by utilizing the liquefaction products liquefied by phenol under acidic conditions and then reacted with formaldehyde under alkaline conditions. The relationship between the liquefaction behavior of cassava starch and the properties of modified PF resin wood adhesive was studied. The effects of the liquid-solid ratio of phenol to cassava starch, sulfuric acid usage, and liquefaction time on the liquefaction residue rate and relative crystallinity of cassava starch were determined. The results showed that the bonding strength of modified PF resin decreased gradually with the decrease of the liquid-solid ratio. It was a great surprise that bonding strength still met the requirement of the national standard of 0.7 MPa when the liquid-solid ratio was 1.0. The detailed contents were analyzed through FT-IR, SEM, and XRD. In terms of the utilization of bio-materials for liquefaction to synthesize wood adhesive, cassava starch may be superior to the others.

lncRNA FOXP4­AS1 predicts poor prognosis and accelerates the progression of mantle cell lymphoma through the miR­423­5p/NACC1 pathway.

Long non­coding RNA (lncRNA) forkhead box P4 antisense RNA 1 (FOXP4­AS1) has been determined to function as an oncogene in various types of cancer. However, the biological function and the underlying mechanisms of FOXP4­AS1 in mantle cell lymphoma (MCL) remain to be uncovered. The expression and the associated clinicopathological characteristics and prognostic significance of FOXP4­AS1 were explored in MCL clinical samples. The effects of FOXP4­AS1 on MCL cellular behaviors, including proliferation, migration and invasion were analyzed using CCK­8, crystal violet and Transwell assays. The downstream molecules of FOXP4­AS1 were explored using bioinformatics analysis and dual luciferase assay. Our results showed that FOXP4­AS1 expression was upregulated in MCL patients, and that the high expression of FOXP4­AS1 was correlated with the unfavorable prognosis of patients. Functionally, while FOXP4­AS1 downregulation inhibited proliferation, migration and invasion of MCL cells, FOXP4­AS1 overexpression had promotive effects on these cellular processes. Mechanistically, FOXP4­AS1 was found to act as a competing endogenous (ce)RNA for miR­423­5p to regulate the expression of nucleus accumbens­associated 1 (NACC1). The negative regulation of FOXP4­AS1 on miR­423­5p compared to that of miR­423­5p on NACC1 was determined at the mRNA or protein levels in MCL cells. Moreover, an inverse expression correlation between FOXP4­AS1 and miR­423­5p, and that between miR­423­5p and NACC1 was confirmed in MCL clinical samples. In addition, rescue assay showed that miR­423­5p upregulation or NACC1 knockdown abolished the promoting effects of FOXP4­AS1 on MCL cell proliferation, migration and invasion. In conclusion, FOXP4­AS1 promotes MCL progression through the upregulation of NACC1 expression by inhibiting miR­423­5p. FOXP4­AS1 may serve as a novel therapeutic target for patients with MCL.

[Experimental studies of rAd-p53 injection by interventional approach for the treatment of rabbit VX2 liver cancer].

OBJECTIVES: To evaluate the efficacy of recombinant human adenovirus p53 gene therapy (rAd-p53) in the rabbit VX2 liver cancer model using different interventional therapy approach. METHODS: Thirty New Zealand rabbits implanted with VX2 tumor in the liver were randomized into five groups with six of each. The tumor volumes (V1) were measured by MRI and CT scan 11 days after tumors implanted. The interventional therapy scheme performed as below: intraarterial 0.9% saline solution perfusion in group A, transcatheter arterial embolization with 0.5 ml ultrafluid lipiodol in group B, intraarterial rAd-p53 gene perfusion in group C (1 x 10(6)/VP); intraarterial rAd-p53 gene perfusion (1 x 10(6)/VP) in combination with transcatheter arterial embolization (ultrofluid lipiodol, 0.5 ml) in group D and intratumoral rAd-p53 gene (1 x 10(6)/VP) injection in group E. The tumor volumes (V2) were measured by MRI and CT scan, and the tumor growth ratios were calculated 14 days after interventional procedures. Then all animals were sacrificed. RESULTS: The tumor tissues were explanted for immunohistochemistry to observe the expressions of vascular endothelial cell growth factor (VEGF) and factor VIII. Microvessel density (MVD) of the tumor tissues was assessed by factor VIII immunohistochemical analysis. In addition, apoptotic index was assessed by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. The tumor volumes before therapy were (79.4+/-8.2), (75.3+/-7.8), (74.6+/-6.6), (78.7+/-9.1), (75.8+/-8.4) mm(3) respectively, without differences found among them (F = 12.248, P = 0.0636). But the tumor volumes after therapy were (564.7+/-96.7), (176.5+/-83.2), (239.6+/-42.8), (159.8+/-58.6), (334.7+/-32.6) mm(3) respectively (F = 24.537, P = 0.0218). The tumor growth ratios were 6.9, 2.6, 3.1, 1.6 and 4.1 respectively. The mean apoptosis index were 12.0%+/-1.1%, 14.5%+/-2.1%, 17.6%+/-2.3%, 18.6%+/-2.3% and 19.6%+/-2.5% respectively. with significant differences in group E in comparison with the other four groups. Mean positive ratio of VEGF was 50.0%, 83.3%, 83.3%, 50.0% and 50.0% respectively, with significant differences observed in group B and group C compared with the other three groups (F = 7.84, P = 0.019). The differences of VIII factor positive expression ratio among each group were significant (F = 0.854, P = 0.018). Statistical analysis showed a positive correlation between the expression of VEGF and MVD (r = 2.400, P = 0.0233). CONCLUSION: The rAd-p53 has effective treatment outcomes in VX2 rabbit liver cancer, and intra-arterial rAd-p53 gene perfusion in combination with transcatheter arterial embolization is the best approach in comparison with intra-arterial rAd-p53 gene perfusion, transcatheter arterial embolization and intratumoral rAd-p53 gene injection alone.

Therapeutic effects of all trans-retinoic acid combined with transarterial chemoembolization on Walker-256 hepatoma in rats.

In order to investigate the inhibitory effects of all trans-retinoic acid (ATRA) on differentiation and apoptosis of Walker-256 hepatocellular carcinoma cells and the therapeutic effects of ATRA combined with transarterial chemoembolization (TACE) on rat Walker-256 transplanted hepatocarcinoma, Walker-256 hepatocarcinoma cell lines were treated with ATRA at different concentrations. After culture for 48 h, the inhibitory rate of cell proliferation was determined by MTT assay; the changes of Fas and Bcl-2 mRNA expression were determined by RT-PCR, and the expression levels of Caspase3 and Caspase8 proteins were detected by Western blot. Twenty-seven Wistar rat models of hepatocarcinoma were set up successfully by implanting Walker-256 cell lines. The tumor volume at the 11th day after implantation (V(preoperation)) was measured by magnetic resonance imaging (MRI). The 27 rats were randomly and equally divided into three groups, and the therapy scheme was performed as follows: group A (ATRA 0.1 mg+mitomycin 0.05 mL+lipiodol 0.05 mL+gelfoam powder 0.025 mg); group B (mitomycin 0.05 mg+lipiodol 0.05 ml+gelfoam 0.025 mg; group C (0.9% NaCl 0.2 mL). After another 11 days, MRI was performed once again to measure the tumor volume (V(postoperation)). The expression of factor and Ki VIII -67 in the tumor tissues was detected by immunohistochemistry. The results showed that ATRA could suppress proliferation of Walker-256 cell lines. After treatment of Walker-256 cell lines with ATRA, the expression of Fas mRNA was significantly up-regulated and the Bcl-2 mRNA was significantly down-regulated by ATRA at the concentration of 10 mumol/L as compared with the control group (P<0.05). After treatment with 10 mumol/L ATRA for 48 h, the Caspase3 and Caspase8 were significantly activated as compared with the control group (P<0.05). Significant difference existed in growth rate among the three groups (P<0.01) and between either two groups (P<0.05). The expression rate of factor VIII and Ki-67 was gradually increased from group A, group B to group C. The study suggests that ATRA could inhibit the proliferation of Walker-256 cells and the effectiveness of the combined therapy (ATRA+TACE) for treating transplanted hepatoma of rats is superior to that of TACE alone.

Therapeutic Effects of All Trans-retinoitc Acid Combined with Transarterial Chemoembolization on Walker-256 Hepatoma in Rats / 华中科技大学学报（医学）（英德文版）

In order to investigate the inhibitory effects of all trans-retinoitc acid (ATRA) on differentiation and apoptosis of Walker-256 hepatocellular carcinoma cells and the therapeutic effects of ATRA combined with transarterial chemoembolization (TACE) on rat Walker-256 transplanted hepa-tocarcinoma, Walker-256 hepatocarcinoma cell lines were treated with ATRA at different concentrations. After culture for 48 h, the inhibitory rate of cell proliferation was determined by MTT assay; the changes of Fas and Bcl-2 mRNA expression were determined by RT-PCR, and the expression levels of Caspase3 and Caspase8 proteins were detected by Western blot. Twenty-seven Wistar rat models of hepatocarcinoma were set up successfully by implanting Walker-256 cell lines. The tumor volume at the 11th day after implantation (Vpreoperatioi) was measured by magnetic resonance imaging (MRI). The 27 rats were randomly and equally divided into three groups, and the therapy scheme was performed as follows: group A (ATRA 0.1 mg+mitomycin 0.05 mL+lipiodol 0.05 mL+gelfoam powder 0.025 mg); group B (mitomycin 0.05 mg+lipiodol 0.05 ml+gelfoam 0.025 mg; group C (0.9% NaCl 0.2 mL). After another 11 days, MRI was performed once again to measure the tumor volume (Vpostoperation)- The expression of factor VIII and Ki-67 in the tumor tissues was detected by immuno-histochemistry. The results showed that ATRA could suppress proliferation of Walker-256 cell lines. After treatment of Walker-256 cell lines with ATRA, the expression of Fas mRNA was significantly up-regulated and the Bcl-2 mRNA was significantly down-regulated by ATRA at the concentration of 10 umol/L as compared with the control group (P<0.05). After treatment with 10 umol/L ATRA for 48 h, the Caspase3 and Caspase8 were significantly activated as compared with the control group (P<0.05). Significant difference existed in growth rate among the three groups (P<0.01) and between either two groups (P<0.05). The expression rate of factor VIII and Ki-67 was gradually increased from group A, group B to group C. The study suggests that ATRA could inhibit the proliferation of Walker-256 cells and the effectiveness of the combined therapy (ATRA+TACE) for treating transplanted hepatoma of rats is superior to that of TACE alone.

Inhibitory effect of extract of fungi of Huaier on hepatocellular carcinoma cells.

This study investigated the inhibitory effect of the extract of fungi of Huaier (EFH) on the growth of hepatocellular carcinoma (HCC) cells. Hep-G2 cells, a human HCC cell line, were cultured in DMEM containing 10% fetal bovine serum and treated with EFH of different concentrations (1, 2, 4, 8 mg/mL) for 24, 48 and 72 h respectively. The apoptosis rate of the cells was flow cytometrically measured. Thirty-six tumor-bearing New Zealand rabbits were randomly divided into 3 groups: group A (control group), in which the rabbits were infused with 0.2 mL/kg normal saline via the hepatic artery; group B (transhepatic artery chemoembolization [TACE] group), in which the rabbits were given lipiodol at 0.2 mL/kg plus MMC at 0.5 mg/kg via the hepatic artery; group C (TACE+EFH group), in which EFH (500 mg/kg) were orally administered after TACE. Two weeks after TACE, the rabbits were sacrificed and the implanted tumors were sampled. The tumor volume and the necrosis rate were determined. The tumor tissues were immunohistochemically detected for the expressions of factor VIII, VEGF, P53, Bax and Bcl-2. The microvessel density (MVD) was calculated by counting the factor VIII-positive endothelial cells. Our results showed that after treatment with EFH, the apoptosis rate of Hep-G2 cells was enhanced in a concentration- and time-dependent manner. Two weeks after the treatment, the average tumor volume, the necrosis rate and the growth rate of the implanted tumor in group C were significantly different from those in groups A and B (P<0.05). MVD and VEGF expressions were significantly decreased in the group C when compared with those in groups B (P<0.05 for all). The Bax expression was weakest in group A and strongest in group C. The expressions of P53 and Bcl-2 were minimal in group C and maximal in group A. There were significant differences in the expressions of P53, Bax and Bcl-2 among the 3 groups (P<0.05 for all) and there was significant difference between group B and group C (P<0.05). It was concluded that EFH could suppress not only the growth of HCC cells but also tumor angiogenesis and it can induce the apoptosis of HCC cells. EFH serves as an alternative for the treatment of HCC.

Ultralong pedicled superficial temporal fascia island flaps for lower nasal defect.

To explore the method of repairing nose defects of apex, ala, septum, and even opposite ala nasi with ultralong pedicled superficial temporal fascia (STF) island flaps. There were 29 cases with defects of apex nasi, ala nasi, and nasal columella, of which 12 cases were repaired with frontal-branched STF island flaps, 14 cases with apical-branched STF postauricular island flaps, and 3 cases with prefabricated apical-branched STF postauricular island flaps. The flap areas were arranged from 1.2 x 2.3 to 2.0 x 2.8 cm2; the length was more than 15 cm on average. Liners were reconstructed at the stage of prefabricating flaps with free skin graft in the cases of ala nasi defects. The surfaces of wound after flap prefabrications were covered by skin graft as well. Twenty-seven cases were successfully taken without blood circulation blocks; the color, texture, and figure were good, and the outcomes were satisfying. Seven nonprefabricated flap cases have epidermis necrosis because of the lack of artery perfusion pressure and venous return handicap, and the epidermis fell off after 1 month, 2 cases of which required secondary surgery because of partial necrosis. Ultralong pedicled STF island flap is an available way to repair defects of apex nasi, ala nasi, and nasal columella. Prefabricated flaps are with benefits of good blood circulation, primary-made liner, and minute injury of the donor site. It is a good method to repair defects of apex nasi, ala nasi, nasal septum, and opposite ala nasi simultaneously.

Inhibitory Effect of Extract of Fungi of Huaier on Hepatocellular Carcinoma Cells / 华中科技大学学报（医学）（英德文版）

This study investigated the inhibitory effect of the extract of fungi of Huaier (EFH) on the growth of hepatocellular carcinoma (HCC) cells.Hep-G2 cells,a human HCC cell line,were cultured in DMEM containing 10% fetal bovine serum and treated with EFH of different concentrations (1,2,4,8 mg/mL) for 24,48 and 72 h respectively.The apoptosis rate of the cells was flow cytometrically measured.Thirty-six tumor-bearing New Zealand rabbits were randomly divided into 3 groups:group A (control group),in which the rabbits were infused with 0.2 mL/kg normal saline via the hepatic artery;group B (transhepatic artery chemoembolization [TACE] group),in which the rabbits were given lipiodol at 0.2 mL/kg plus MMC at 0.5 mg/kg via the hepatic artery;group C (TACE +EFH group),in which EFH (500 mg/kg) were orally administered after TACE.Two weeks after TACE,the rabbits were sacrificed and the implanted tumors were sampled.The tumor volume and the necrosis rate were determined.The tumor tissues were immunohistochemically detected for the expressions of factor Ⅷ,VEGF,P53,Bax and Bcl-2.The microvessel density (MVD) was calculated by counting the factor Ⅷ-positive endothelial cells.Our results showed that after treatment with EFH,the apoptosis rate of Hep-G2 cells was enhanced in a concentration- and time-dependent manner.Two weeks after the treatment,the average tumor volume,the necrosis rate and the growth rate of the implanted tumor in group C were significantly different from those in groups A and B (P<0.05).MVD and VEGF expressions were significantly decreased in the group C when compared with those in groups B (P<0.05 for all).The Bax expression was weakest in group A and strongest in group C.The expressions of P53 and Bcl-2 were minimal in group C and maximal in group A.There were significant differences in the expressions of P53,Bax and Bcl-2 among the 3 groups (P<0.05 for all) and there was significant difference between group B and group C (P<0.05).It was concluded that EFH could suppress not only the growth of HCC cells but also tumor angiogenesis and it can induce the apoptosis of HCC cells.EFH serves as an alternative for the treatment of HCC.

[Monobloc distraction osteogenesis and cranial vault remodeling in a pediatric patient with severe Crouzon's syndrome].

OBJECTIVE: To report the treatment of a case of severe Crouzon's syndrome using monobloc distraction osteogenesis and cranial vault remodeling. METHODS: Through intra-and extra-cranial approach, monobloc osteotomy was performed and external distractor was placed. Distraction began on the 7th postoperative day at a rate of 1 mm a day, two times a day. The distractor removed after consolidation for 4 months. RESULTS: The distraction distance attained 20 mm. The exophthalmos and cross bite were corrected completely. The severe obstructive apnea improved markedly. CONCLUSIONS: Monbloc distraction osteogenesis and cranial vault remodeling are effective and safe procedure for Crouzon's syndrome.

[Effects of SODD and survivin on leukemia cell apoptosis induced by chemotherapeutic drugs].

This study was aimed to investigate the changes of silencer of death domains (SODD), survivin, caspase 3, caspase 8 and caspase 9 in the apoptotic process of human leukemia cells induced by chemotherapeutic drugs in order to explore the molecular mechanism of apoptotic modulatory genes and to search for the new target of chemotherapeutic drugs. After Jurkat cells were induced by chemotherapeutic drugs, the translocated phosphatidylserine was labeled with annexin V/PI, and the apoptosis incidence was measured by FCM; The expression changes of SODD, caspase 3, caspase 8 and caspase 9 were determined by Western blot; the changes of survivin mRNA and protein were determined by RT-PCR and immunohistochemistry SABC method respectively. The results indicated that high expressions of SODD and survivin could inhibit apoptotic signaling pathway; VCR down-regulated the function of SODD protein and effectively induced the apoptosis of Jurkat cells in a time-dependent manner and activates caspase 3 through the death receptor-mediated activation of caspase 8, in which caspase 9 and survivin were not degraded. It is concluded that SODD participates in the apoptotic process induced by VCR which induces the Jurkat cell apoptosis by downregulating expression of SODD protein and priming death receptor pathway. In the apoptotic process, the mitochondrion apoptotic pathway is not trigged.

Expression of SODD and P65 in ALL of children and its relationship with chemotherapeutic drugs.

The expression of silence of death domains (SODD) and its clinical significance and relationship with phospho-NF-kappaB-p65 proteins in bone marrow cells of childhood acute lymphoblastic leukaemia (ALL) were explored, and the expression of SODD and phospho-NF-kappaB-p65 in Jurkat cells treated with chemotherapeutic drugs was detected in order to find a new chemotherapeutic target. The expression of SODD and phospho-NF-kappaB-p65 proteins in bone marrow cells was detected by immunohistochemistry in 25 children with ALL. The apoptosis rate was measured by Annexin-V-Fluorescence/PI double-labeling flow cytometry and the expression of SODD and phospho-NF-kappaB-p65 proteins determined by Western blotting in the Jurkat cells. It was found that the expression of SODD and active P65 in ALL was significantly higher than that in normal control group (P<0.05). The expression of the SODD and phospho-NF-kappaB-p65 proteins in the high-risk (HR) group was significantly higher than that in the standard-risk (SR) group (P<0.05). The Pearson rank correlation analysis revealed that there was a positive correlation between SODD and phospho-NF-kappaB-p65 expression (P<0.01, r=0.69). VCR could effectively induce the apoptosis of Jurkat cells, and down-regulate the expression of SODD and phospho-NF-kappaB-p65 proteins in a time-dependent manner, but DNR could not down-regulate the expression of SODD effectively. It was concluded that SODD may be closely related to the clinical classification and prognosis of ALL in children. The expression of SODD and phospho-NF-kappaB-p65 had a definite synergistic relationship with the onset and development of ALL. VCR could down-regulate the expression of SODD and inhibit the NF-kappaB activation, which could recover the sensibility of apoptosis in leukemic cells.

[The regulating effect of antisense-S-Oligo on TYR gene expression and melanin production of melanocytes].

OBJECTIVE: Despite the causes for melanin increase, the increased gene expression of TYR is a common pathological process. Based on this viewpoint, antisense-S-Oligo of TYR was designed and synthesized to regulate synthesis of melanin in order to explore the treatment for skin pigmentation. METHODS: The cultured melanocytes were divided into 3 groups. The group 1 was treated with endothelin, group 2 treated with ultraviolet ray and group 3 was used as the control. In each group, the 5' antisense-S-Oligo, the 3' antisense-S-Oligo, the mixed antisense-S-Oligo of TYR or Dotap only was added. The melanin content and TYR gene expressions were examined. RESULTS: The 5' antisense-S-Oligo, the 3' antisense-S-Oligo and the mixed antisense-S-Oligo significantly inhibited the increase of melanin content and TYR gene expression, which were caused by endothelin or ultraviolet ray treatment. Of the three treatments, the 3' antisense-S-Oligo showed the strongest effect. CONCLUSION: Antisense-S-Oligo has significant regulating effects on TYR gene expression and melanin content. The 3' antisense-S-Oligo is more effective than the 5' antisense-S-Oligo.

[Repair of whole auricular defects with implant-plasty and prosthesis].

OBJECTIVE: To repair the whole auricular defects with implant-plasty and prosthesis technique. The indications, complications and implant sites of this method were discussed. METHODS: In reconstruction of the whole auricular defect, the self-developed pure titanium implants, specialized for plastic surgery, were used for intra-osseous fixation for retaining the artificial ear. 10 cases were treated with this method. RESULTS: Follow-up of three years demonstrated that this implant system, with stable function, could generate osseointegration and be used as an abutment of intra-osseous fixation to retain the auricular prosthesis for a long time. CONCLUSION: The operation is simple and convenient with little trauma and short-term of treatment. The artificial ear has lifelike appearance, proper color and satisfactory effects. This technique has wide indications and is worth popularization.