BACKGROUND: Along with the emergence of porcelain-fused-to-metal (PFM) technique, Ni-Cr alloy has been shown to be the most available non-novel metal alloy used for preparation of PFM materials. The metal margin of Ni-Cr based PFM crown possibly produces some effects on periodontal tissue for it is primarily contacted with gingiva. OBJECTIVE: To investigate the influences of Ni-Cr alloy PFM crown on periodontal tissue. DESIGN, TIME AND SETTING: A retrospective case analysis was performed. All cases were from Department of Stomatology, the 476 Hospital of Fuzhou General Hospital of Nanjing Military Area Command of Chinese PLA between January 2006 and January 2007.PARTICIPANTS: Totally 23 maxillary incisors were included from 19 patients who averaged (32.5±10.8)years old and received tooth restoration using Ni-Cr based PFM crowns. Healthy contralateral corresponding teeth were used as controls. METHODS: All clinical operations were conducted by one dentist. Dental restoration principles should be strictly followed during preparation of dental prosthesis. A routine tooth preparation was performed. Specifically, gingival retraction cords were used for gingival recession, with a shoulder prepared 0.5 mm below the labial gingiva and concave shoulder thickness 0.5 mm. A temporary crown was made using silicon rubber. The normal physiological anatomical profile of complete crown should be recovered as possible while preparation. Dental axial crown overcontour should be increased within 0.2 mm. Finally, a permanent sticking was followed.MAIN OUTCOME MEASURES: At 6-9 months after wearing Ni-Cr alloy PFM crown, the gingival crevicular fluid was collected from affected and control teeth for quantitation and laboratory examinations (C reactive protein and tumor necrosis factor- a included),PARTICIPANTS: Alter placement of Ni-Cr alloy PFM crown which was clinically accepted, plaque index of affected tooth did not alter significantly, but gingival crevicular fluid volume, probing depth, sulcus bleeding index, and levels of C reactive protein and tumor necrosis factor-α were significantly greater in affected teeth than in control teeth (P < 0.05).CONCLUSION: Ni-Cr alloy PFM crown produces some harmful effects on periodontal tissue.

Objective To evaluate the impact of HIV co-infection with HCV or HBV on the efficacy of highly active anti-retroviral therapy (HARRT). Methods The patients were divided into three groups: HIV + HBV + HCV co-infection group ( 23 patients), HIV + HCV co-infection group ( 166 patients), and HIV-only group (178 patients). HIV RNA, HCV RNA or HBV DNA were detected by real time PCR before treatment and 1,3,6,9 and 12 monthes after treatment, meanwhile the counts of CD4+ T lymphocyte and liver function including ALT, AST and TBil were tested. Results During one-year HAART, HIV RNA of HIV-only group, HIV + HBV + HCV co-infection group and HIV + HCV co-infection group decreased significantly from (6.78 ± 1.08), (6.23 ± 1.34), (6.54 ± 1.23) lg copies/ml to (0.53 ±0.15), (0.67 ±0.16),(0.43 ±0.11 ) lg copies/ml respectively (P＜.001 ). And CD4+ T lymphocyte counts of the three groups elevated significantly from ( 197 ± 127), (184 ± 113), (213 ± 143) cells/μl to (382 ±74), (383 ±70),(378 ±76) cells/μl respectively (P ＜0.001 ). However there were no differences among the three groups in HIV RNA and CD4+ T lymphocyte counts. There were no differences in liver functions including ALT,AST and TBil among the three groups. Conclusiom HIV co-infected with HBV and/or HCV does not impact on the efficacy of HAART. What more, HAART does not impact HCV replication.

Spiramycin and midecamycin are 16-membered macrolide antibiotics with very similar chemical structures. Spiramycin has three components, namely spiramycin I, II and III. Spiramycin II and III are, respectively, the O-acetyl and propionyl derivatives at C3-hydroxyl group of spiramycin I. Midecamycin has four components, and the C3-hydroxyl group of midecamycin is all O-propionylated. The enzyme adding acyl group(s) at the C3-hydroxyl group during the biosynthesis of spiramycin and midecamycin is 3-O-acyltransferase. The 3-O-acyltransferases for spiramycin and midecamycin are also very similar, and presume to function when exchanged. To explore whether the 3-O-acyltransferase for midecamycin biosynthesis hold still the character of selective and efficient propionylation for spiramycin I at its C3-hydroxyl group, we inserted mdmB, the 3-O-acyltransferase gene from Streptomyces mycarofaciens ATCC 21454 for midecamycin biosynthesis, into a mutant strain of S. spiramyceticus F21, in which the 3-O-acyltransferase gene for spiramycin biosynthesis, sspA, was deleted; and the mdmB was integrated exactly into the chromosomal site where the sspA was deleted. We name this "hybrid" strain as SP-mdmB. HPLC analysis of the spiramycin produced by SP-mdmB showed that spiramycin I was still the major component, although the relative proportions of both spiramycin II and III increased significantly. We thus conclude that MdmB from Streptomyces mycarofaciens ATCC 21454 for midecamyicn biosynthesis do not hold the character of selective and efficient propionylation for spiramycin I within S. spiramyceticus F21, and this character is possibly limited in Streptomyces mycarofaciens ATCC 21454 for midecamycin biosynthesis.
Acylation ; Acyltransferases ; genetics ; metabolism ; Culture Media ; Genes, Bacterial ; Genetic Engineering ; methods ; Leucomycins ; biosynthesis ; Spiramycin ; biosynthesis ; Streptomyces ; enzymology ; genetics ; Substrate Specificity