Titanium-based
substrates are widely used in orthopedic treatments
and hard tissue engineering. However, many of these titanium (Ti)
substrates fail to interact properly between the cell-to-implant interface,
which can lead to loosening and dislocation from the implant site.
As a result, scaffold implant-associated complications and the need
for multiple surgeries lead to an increased clinical burden. To address
these challenges, we engineered osteoconductive and osteoinductive
biosubstrates of chitosan (CS)-cross-linked polyaniline (PANI) nanonets
coated on titanium nanotubes (TiO2NTs) in an attempt to
mimic bone tissue’s major extracellular matrix. Inspired by
the architectural and tunable mechanical properties of such tissue,
the TiO2NTs-PANI@CS-based biofilm conferred strong anticorrosion,
the ability to nucleate hydroxyapatite nanoparticles, and excellent
biocompatibility with human bone marrow-derived mesenchymal stem cells
(hBM-MSCs). An in vitro study showed that the substrate-supported
cell activities induced greater cell proliferation and differentiation
compared to cell-TiO2NTs alone. Notably, the bone-related
genes (collagen-I, OPN, OCN, and RUNX 2) were highly expressed within
TiO2NTs-PANI@CS over a period of 14 days, indicating greater
bone cell differentiation. These findings demonstrate that the in
vitro functionality of the cells on the osteoinductive-like platform
of TiO2NTs-PANI@CS improves the efficiency for osteoblastic
cell regeneration and that the substrate potentially has utility in
bone tissue engineering applications.
(1) Background: Acinetobacter baumannii has emerged as a leading cause of nosocomial infections as they are capable of evolving resistance to various classes of antibiotics. The ability of A. baumannii to form biofilm might also be associated with increased antibiotic resistance and hence treatment failure. This study was carried to associate the biofilm formation with the drug resistance pattern of A. baumannii and to detect blaOXA-23, blaOXA-24, and blaOXA-51 from carbapenem resistance isolates. (2) Methods: Among different clinical samples, a total of 19 Acinetobacter spp. were identified with conventional microbiological procedures. The biofilm production was determined by a quantitative adherence assay. The antimicrobial susceptibility test was carried out by the Kirby-Bauer disc diffusion method, carbapenemase production detection was confirmed by Modified Hodge Test. And target resistant genes were detected by polymerase chain reaction. (3) Results: Out of 90 clinical specimens, 64.44% (58/90) showed bacterial growth. Whereas, 32.75% (19/58) isolates were identified as A. baumannii. Among all A. baumannii isolates, 84.21% (16/19) were multidrug-resistance and 63.16% (12/19) carbapenem resistance phenotypically. blaOXA-51 was detected in all the isolates and blaOXA-23 was detected only in 63.16% (12/19) isolates. However, blaOXA-24 was not detected in any of the isolates. Among A. baumannii, 89.47% (17/19) isolates produced biofilm with 47.37% (9/19) strong biofilm producers. (4) Conclusions: In the majority of MDR A. baumannii, blaOXA-51 and blaOXA-23 were detected as the determinant factor for carbapenem resistance having a direct relation with biofilm formation. This study provided a valuable clue for the management of A. baumannii infections in clinical settings.
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