Objective: Using computer-assisted navigation technology to guide the resection and reconstruction of mandibular ameloblastoma, evaluating its treatment effect. Methods : Twelve patients were selected from the Affiliated Stomatological Hospital of Nanjing University from January 2017 to May 2022. All 12 patients accepted same surgery which included resection of mandibular ameloblastoma and reconstruction by fibula musculocutaneous flap. Among them, 6 cases were included in the navigation group; 6 cases were in the non-navigation group. Advantages and disadvantages of computer-assisted navigation technology in this operation were evaluated with these cases. Results: The 12 operations were performed by the same operator. The average time for fixing the navigation bracket and performing navigation in the navigation group was about 15 minutes. Compared with the non-navigation group, the average operation time in the navigation group was shortened by about 10 minutes. In the navigation group, the mandible resection range matched the fibula musculocutaneous flap well, and the occlusal relationship recovered well. Conclusion Using the mandibular reference frame, under the guidance of computer-assisted navigation technology, the resection and reconstruction of mandibular ameloblastoma can be performed quickly and accurately.

Object To evaluate the efficacy and toxicity of L-asparaginase based regimen for extranodal nasal type NK/T cell lymphoma (ENKTL).Methods 36 patients were treated with L-asparaginase based regimen from February 2008 to November 2011. 20 stage Ⅰ /Ⅱ patients were administered with VLD regimen based chemo-radiotherapy. 4 of 16 stage Ⅲ/Ⅳ patients received modified SMILE regimen chemotherapy, followed by involved field radiation therapy (IFRT), while others received modified SMILE regimen chemotherapy alone.Results Among 36 patients,35 were eligible for treatment response evaluation.The overall response rate (RR) was 68.6％ (24/35) with complete response (CR) rate of 54.3％ (19/35).After the median follow-up of 13.5 (range 3-31) months,for all patients,the 1-year overall survival (OS) rate was 82 ％,and the rate of progression-free survival (PFS) at 1 year was 65 ％.The patients who attained response with treatment showed better 1-year OS (93 ％) and PFS (80 ％) as compared with patients without response (35 ％; 33 ％),and the differences were statistically significant (x2=13.909,P =0.000; x2=8.216,P =0.004).The major adverse event was myelosuppression. No chemotherapy-related mortality occurred. Conclusion L-asparaginase based regimen is obviously effective and well tolerant for ENKTL. The large prospective clinical trials of L-asparaginase based regimen in the first-line treatment for ENKTL are worth for further investigation.

OBJECTIVETo observe the ability of triple helix-forming oligonucleotides (TFOs) modified with manganese porphyrin to combine with and cleave HBV DNA fractions.

METHODSTFO were modified with manganese porphyrin and acridines, and then reacted with the (32)P labeled HBV DNA fragments at 37 degrees C in vitro (pH 7.4). Electrophoretic mobility shift assays and DNase I footprinting tests were used to show the affinity and specificity of TFO to bind to target sequences. The ability of TFO to cleave HBV DNA fragments was tested by cleavage experiments.

RESULTSTFO modified with manganese porphyrin and acridine could bind to the target sequence in a sequence-dependent manner, with a Kd value of 3.5 x 10(-7) mol/L and a relative affinity of 0.008. In the presence of potassium monopersulfate (KHSO(5)), TFO modified with manganese porphyrin and acridine could cleave the target sequence where the triplex DNA was formed.

CONCLUSIONIn the presence of KHSO(5), TFO modified with manganese porphyrin and acridine could bind and cleave the target HBV-DNA in a sequence-dependent manner.

DNA ; drug effects ; pharmacology ; DNA, Viral ; chemistry ; drug effects ; Hepatitis B virus ; genetics ; Manganese ; pharmacology ; Metalloporphyrins ; pharmacology ; Potassium Compounds ; pharmacology ; Sulfates ; pharmacology

To study the molecular mechanism for DNA hypomethylation of STAT3 promoter in CD4+ T cells from acute graft-versus-host disease (aGVHD) patients.
 Methods: We collected CD4+ T cells from peripheral blood of 42 patients who underwent allogeneic hematopoietic stem cell transplantation (allo-HSCT) from HLA-identical sibling donors. GADD45A expression level in CD4+ T cells was measured by real-time PCR and Western blot. The binding level between HMGB1 and GADD45A in CD4+ T cells was analyzed by co-immunoprecipitation, while the binding levels of HMGB1/GADD45A with STAT3 promoter were detected by chromatin immunoprecipitation-quantitative real-time PCR (ChIP-qPCR). After overexpression of HMGB1 and knockdown of GADD45A in normal CD4+ T cells, STAT3 expression and DNA methylation were measured by Western blot and bisulfite sequencing PCR, respectively.
 Results: GADD45A expression was significantly up-regulated in patients with aGVHD compared with that in the patients without aGVHD. More HMGB1-GADD45A complexes were found in CD4+ T cells from patients with aGVHD compared with that in patients without aGVHD. The bindings of HMGB1/GADD45A with STAT3 promoter were significantly increased, and the binding levels of HMGB1/GADD45A were negatively correlated with STAT3 promoter DNA methylation. The expression of STAT3 was significantly reduced and the DNA methylation of STAT3 promoter was significantly increased in CD4+ T cells with overexpression of HMGB1 and knockdown of GADD45A compared with CD4+ T cells only with overexpression of HMGB1.
 Conclusion: The increased expression of HMGB1/GADD45A plays an importent role in STAT3 promoter DNA hypomethylation, thereby promoting STAT3 expression in CD4+ T cells from aGVHD patients.
CD4-Positive T-Lymphocytes ; Cell Cycle Proteins ; metabolism ; DNA Demethylation ; Gene Expression Regulation ; genetics ; Graft vs Host Disease ; genetics ; HMGB1 Protein ; metabolism ; Hematopoietic Stem Cell Transplantation ; Humans ; Nuclear Proteins ; metabolism ; Promoter Regions, Genetic ; genetics ; STAT3 Transcription Factor ; genetics ; metabolism