Effects of applying procyanidins on the bond strength of bleached dentin to composite resin / 口腔疾病防治

Objective@#To study the influence of procyanidins on the bonding strength of dentin bleached by carbamide peroxide to composite resin.@*Methods @#By applying different treatments to dentin bonding interfaces, 120 human third molars were randomly divided into 12 groups (n = 10): W group (no bleaching+deionized water), Wa group (no bleaching+deionized water+aging), WT1 group (no bleaching+5% procyanidins for 1 min), WT1a group (no bleaching+5% procyanidins for 1 min+aging), WT2 group (no bleaching+5% procyanidins for 5 min), WT2a group (no bleaching+5% procyanidins for 5 min+aging), C group (carbamide peroxide+deionized water), Ca group (carbamide peroxide+deionized water+aging), CT1 group (carbamide peroxide+5% procyanidins for 1 min), CT1a group (carbamide peroxide+5% procyanidins for 1 min+aging), CT2 group (carbamide peroxide+5% procyanidins for 5 min), and CT2a group (carbamide peroxide+5% procyanidins for 5 min+aging). The bond strength to composite resin was measured by universal mechanical testing machine, microstructure and the nanoleakages were measured by scanning electron microscope immediately or after the thermal cycling aging test.@*Results@#The immediate bond strength of the bleached groups pretreated with procyanidins for 1 min (P<0.001) and 5 min (P<0.001) was higher than that of Group C, and the difference was statistically significant. Meanwhile, there was no statistically significant difference between Group CT1 and Group CT2 (P = 1.000). After the thermal cycles, the bond strength of each group declined. The differences between Group W and Group Wa (P<0.001) and Group C and Group Ca (P<0.001) were statistically significant, but no significant differences between Group CT1 and Group CT1a (P = 0.052) or Group CT2 and Group CT2a (P = 0.053) were found. The main effects of “aging” (P<0.001), “bleaching” (P<0.001) and “procyanidins” (P<0.001) and the second-order interaction effects of “bleaching * procyanidins” (P = 0.008), “bleaching * aging” (P = 0.024), and “aging * procyanidins” (P<0.001) were statistically significant. SEM observations showed that the hybrid layers in Groups C, CT1 and CT2 were not clear, and the hybrid layers in Groups Ca, CT1a and CT2a were partially destroyed and disintegrated. Under backscattering mode, it was observed that there were a large number of silver nitrate particles in the hybrid layer of Group Ca, and the residual silver ions in the hybrid layer of Groups CT1a and CT2a were decreased. @*Conclusion@# Pretreatment with 5% procyanidins for 1 min can improve the immediate bond strength of dentin bleached by carbamide peroxide to composite resin and maintain bonding durability.

Characterization of gyrA and gyrB mutations and fluoroquinolone resistance in Mycobacterium tuberculosis clinical isolates from Hubei Province, China

OBJECTIVE: The study aimed to investigate gyrA and gyrB mutations in Mycobacterium tuberculosis (MTB) clinical strains from 93 patients with pulmonary tuberculosis in Hubei Province, China, and analyze the association between mutation patterns of the genes and ofloxacin resistance level. RESULTS: Among 93 MTB clinical isolates, 61 were ofloxacin-resistant by the proportion method, and 32 were ofloxacin-susceptible MDR-TB. No mutation in the gyrB gene was found in any MTB strains. In the 61 ofloxacin-resistant isolates, 54 mutations were observed in the gyrA gene. Only one mutation in the gyrA gene was found in ofloxacin-susceptible MDR-TB isolates. In this study, the mutation patterns of gyrA involved seven patterns of single codon mutation (A90V, S91P, S91T, D94N, D94Y, D94G or D94A) and two patterns of double codons mutation (S91P & D94H, S91P & D94A). The ofloxacin minimal inhibitory concentrations (MICs) of three patterns of single codon mutations in the gyrA gene (codons 94, 90 and 91) showed a statistically significant difference (p < 0.0001). CONCLUSIONS: The gyrA mutations at codons 90, 91 and 94 constitute the primary mechanism of fluoroquinolone resistance in MTB, and mutations at codon 91 in the gyrA gene may be associated with low-level resistance to ofloxacin.

CD44 is involved in CXCL-12 induced acute myeloid leukemia HL-60 cell polarity

CXCL-12 and its receptor CXCR4 participate in breast cancer and melanoma cell metastasis to bone and lymphoid nodes. CD44, as a receptor for hyaluronic acid, is involved in lymphocyte recirculation, homing, adhesion and migration. But the role of CD44 in CXCL-12 induced leukemia cell migration still remains unclear. The present study showed that CXCL-12 stimulation induced the rapid internalization of CXCR4 and facilitated the formation of lamellipodia and uropod in acute leukemia cell line HL-60. CXCL-12 also induced CD44 translocation into the uropod, while CD44 remained evenly distributed on the untreated cell membranes. Results suggest that CD44 participates in CXCL-12 induced cell polarization and subsequent cell migration.