[Treatment of severe medial tibial bone defect in primary total knee arthroplasty with autogenous bone graft and plate fixation].

OBJECTIVE: To explore the technique of autogenous bone graft combined with plate fixation in total knee arthroplasty(TKA) with severe proximal medial tibial bone defect. METHODS: From March 2012 to October 2018, 21 patients (9 males and 12 females) with severe bone defects in the proximal medial tibia during primary total knee arthroplasty were treated with autogenous structural bone grafting and steel plate fixation, with an age of 61 to 77 years old with an average of (69.6±9.1) years and a course of 64 to 257 months with an average of (73.6±170.7) months. According to Rand classification, there were 13 cases of type Ⅲb and 8 cases of type Ⅳb. Postoperative complications were observed, and knee joint function was evaluated by the Hospital for Special Surgery (HSS) score and SF-36 quality of life score. RESULTS: All 21 patients were followed up for 37 to 64 months with an average of (49.5±13.7) months. The incisions of all patients healed smoothly, and 2 patients developed lower limb intermuscular venous plexus thrombosis after operation. There were no periprosthetic infection, loosening of prosthesis and other complications. The autogenous bone grafts of all patients achieved bony healing during postoperative X-ray follow-up, and the healing time was 8 to 13 months with an average of (10.1±2.3) months. The HSS score of patients increased significantly from 30 to 48 with an average of (53.4±4.2) before operation to 75 to 92 with an average of (81.2±8.4) at the final follow-up (P<0.05). The SF-36 quality of life score of patients after operation was significantly different from that before operation (P<0.05). CONCLUSION: The technique of autogenous bone graft combined with steel plate fixation can achieve satisfactory osseointegration effect in the treatment of severe proximal tibial bone defects in primary knee arthroplasty, with less complications and obvious improvement in knee function.

A Novel ATM Antisense Transcript ATM-AS Positively Regulates ATM Expression in Normal and Breast Cancer Cells.

OBJECTIVE: The ataxia telangiectasia mutated (ATM) gene is a master regulator in cellular DNA damage response. The dysregulation of ATM expression is frequent in breast cancer, and is known to be involved in the carcinogenesis and prognosis of cancer. However, the underlying mechanism remains unclear. The bioinformatic analysis predicted a potential antisense transcript ATM-antisense (AS) from the opposite strand of the ATM gene. The purpose of this study was to identify ATM-AS and investigate the possible effect of ATM-AS on the ATM gene regulation. METHODS: Single strand-specific RT-PCR was performed to verify the predicted antisense transcript ATM-AS within the ATM gene locus. qRT-PCR and Western blotting were used to detect the expression levels of ATM-AS and ATM in normal and breast cancer cell lines as well as in tissue samples. Luciferase reporter gene assays, biological mass spectrometry, ChIP-qPCR and RIP were used to explore the function of ATM-AS in regulating the ATM expression. Immunofluorescence and host-cell reactivation (HCR) assay were performed to evaluate the biological significance of ATM-AS in ATM-mediated DNA damage repair. Breast cancer tissue samples were used for evaluating the correlation of the ATM-AS level with the ATM expression as well as prognosis of the patients. RESULTS: The ATM-AS significantly upregulated the ATM gene activity by recruiting KAT5 histone acetyltransferase to the gene promoter. The reduced ATM-AS level led to the abnormal downregulation of ATM expression, and impaired the ATM-mediated DNA damage repair in normal breast cells in vitro. The ATM-AS level was positively correlated with the ATM expression in the examined breast cancer tissue samples, and the patient prognosis. CONCLUSION: The present study demonstrated that ATM-AS, an antisense transcript located within the ATM gene body, is an essential positive regulator of ATM expression, and functions by mediating the binding of KAT5 to the ATM promoter. These findings uncover the novel mechanism underlying the dysregulation of the ATM gene in breast cancer, and enrich our understanding of how an antisense transcript regulates its host gene.

Functionalized ferrocenes and ferroceniums: synthesis, crystal structures and electrochemical properties based on carbazole/phenothiazine-ferrocene conjugated molecules.

Four new D-pi-D (or D-pi-D-pi-D) complexes 9-ethyl-3-E-((1-ferrocenyl)vinyl)-carbazole (1), 9-ethyl-3,6-E,E-((1,1-diferrocenyl)vinyl)- carbazole(2), 10-ethyl-3-E-((1-ferrocenyl)vinyl)-phenothiazine (3), 10-ethyl- 3,7-E,E- ((1,1-diferrocenyl)vinyl)-phenothiazine (4), have been obtained by solid-phase Wittig reactions and fully characterized. The four complexes were treated with iodine leading to four corresponding [D-pi-A](+) I(3)(-) ferrocenium triiodides (+)I(3)(-) (5), (+)I(3)(-) (6), (+)I(3)(-) (7) and 4(+)I(3)(-) (8), respectively. The results of single crystal X-ray diffraction analysis show that and display better coplanarity between the Fc and carbazole subunits than that between the phenothiazine and ferrocene moieties, which leads to a better pi-electron delocalization. Both the poor pi-electron in [D-pi-A](+) ferroceniums and the heavy iodine atom have a negative effect on the electrochemical properties. The complexes 1-8 undergo multi-step redox processes and show lower oxidation potentials compared with those of ferrocene. Density functional theory (DFT) calculations are performed and the experimental redox properties of the complexes are studied. The eight complexes show MLCT and pi-pi transitions in the UV-visible range in solution, which have been verified by TD-DFT theoretical calculations. In all cases the highest-lying occupied molecular orbitals of the eight complexes are mainly localized on the Fe d orbitals and show a greater Fe proportion than that of alkyl in the complexes, whereas the LUMOs and LUMO+1 are mainly from the pi orbitals of the conjugated vinyl carbazole or phenothiazine unit.