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1.
J Orthop Trauma ; 37(3): e118-e121, 2023 03 01.
Article in English | MEDLINE | ID: mdl-36162060

ABSTRACT

OBJECTIVE: Cefazolin is a heat-labile antibiotic that is not usually added to polymethylmethacrylate (PMMA) cement spacers because it is believed to be inactivated by the high polymerization temperatures. The purpose of this study was to compare cefazolin versus vancomycin high-dose antibiotic cement spacers. METHODS: High-dose antibiotic PMMA spacers with either cefazolin or vancomycin were fabricated. Setting time, compressive strength, and compression modulus of spacers were measured. Spacers were emerged in saline, and the eluent was tested on days 1, 2, 3, 7, 14, and 30 to determine the zone of inhibition of methicillin-sensitive Staphylococcus aureus and estimate the cumulative antibiotic released. RESULTS: Cefazolin, compared with vancomycin-loaded spacers, had significantly shorter setting time [mean difference (MD) -1.8 minutes, 95% confidence interval (CI), -0.6 to -3.0], greater compressive strength (MD 20.1 megapascal, CI, 15.8 to 24.5), and compression modulus (MD 0.15 megapascal, CI, 0.06 to 0.23). The zone of inhibition of eluent from PMMA-C spacers was significantly greater than PMMA-V spacers at all time points, an average of 11.7 ± 0.8 mm greater across time points. The estimated cumulative antibiotic released from cefazolin spacers was significantly greater at all time points ( P < 0.0001). CONCLUSIONS: Cefazolin was not inactivated by PMMA polymerization and resulted in spacers with superior antimicrobial and biomechanical properties than those made with vancomycin, suggesting that cefazolin could play a role in the treatment of infected bone defects with high-dose antibiotic PMMA spacers.


Subject(s)
Anti-Bacterial Agents , Vancomycin , Humans , Vancomycin/pharmacology , Cefazolin , Polymethyl Methacrylate/pharmacology , Bone Cements/pharmacology
2.
Biomedicines ; 10(10)2022 Sep 29.
Article in English | MEDLINE | ID: mdl-36289702

ABSTRACT

Since ancient times aging has also been regarded as a disease, and humankind has always strived to extend the natural lifespan. Analyzing the genes involved in aging and disease allows for finding important indicators and biological markers for pathologies and possible therapeutic targets. An example of the use of omics technologies is the research regarding aging and the rare and fatal premature aging syndrome progeria (Hutchinson-Gilford progeria syndrome, HGPS). In our study, we focused on the in silico analysis of differentially expressed genes (DEGs) in progeria and aging, using a publicly available RNA-Seq dataset (GEO dataset GSE113957) and a variety of bioinformatics tools. Despite the GSE113957 RNA-Seq dataset being well-known and frequently analyzed, the RNA-Seq data shared by Fleischer et al. is far from exhausted and reusing and repurposing the data still reveals new insights. By analyzing the literature citing the use of the dataset and subsequently conducting a comparative analysis comparing the RNA-Seq data analyses of different subsets of the dataset (healthy children, nonagenarians and progeria patients), we identified several genes involved in both natural aging and progeria (KRT8, KRT18, ACKR4, CCL2, UCP2, ADAMTS15, ACTN4P1, WNT16, IGFBP2). Further analyzing these genes and the pathways involved indicated their possible roles in aging, suggesting the need for further in vitro and in vivo research. In this paper, we (1) compare "normal aging" (nonagenarians vs. healthy children) and progeria (HGPS patients vs. healthy children), (2) enlist genes possibly involved in both the natural aging process and progeria, including the first mention of IGFBP2 in progeria, (3) predict miRNAs and interactomes for WNT16 (hsa-mir-181a-5p), UCP2 (hsa-mir-26a-5p and hsa-mir-124-3p), and IGFBP2 (hsa-mir-124-3p, hsa-mir-126-3p, and hsa-mir-27b-3p), (4) demonstrate the compatibility of well-established R packages for RNA-Seq analysis for researchers interested but not yet familiar with this kind of analysis, and (5) present comparative proteomics analyses to show an association between our RNA-Seq data analyses and corresponding changes in protein expression.

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