Poly(L-lactic acid) (PLLA) microfibrous scaffolds with three-dimensional (3D) structures were fabricated using an electrospinning technique with a subsequent mechanical expansion process. To achieve a 3D fibrous structure, the fusion at the contact points of the as-spun PLLA microfibers was avoided using an appropriate binary solvent system of methylene chloride and acetone. The solvent composition was optimized based on the solvent power, volatility, and viscosity (methylene chloride:acetone = 9:1 volume ratio). The final 3D structure of the electrospun scaffolds was obtained after mechanical expansion of the electrospun microfibrous mats. The pore sizes of the scaffolds were controlled by varying the degree of expansion of the nonbonded microfibrous mats, and they were in the range of several microns up to 400 μm. The 3D scaffolds were examined for their morphological properties and their potential use for the proliferation of osteoblasts. Generally recognized electrospun 2D nanofibrous membranes were also tested in order to compare the cell behaviors using different scaffold geometries. The 3D scaffolds demonstrated a high level of osteoblast proliferation (1.8-fold higher than nanofibrous membranes in a week). The osteoblasts actively penetrated the inside of the 3D scaffold and showed a spatial cell distribution, as confirmed by SEM and H&E staining, while a monolayer formed in the case of the 2D nanofibrous membranes with limited cell infiltration. In vivo results further showed that 3D electrospun microfibrous matrices were a favorable substrate for cell infiltration and bone formation after 2 and 4 weeks, using a rabbit calvarial defect model. In this study, the 3D microfibrous PLLA scaffolds fabricated using electrospinning techniques might be an innovative addition to tissue engineering applications.
Background/Aims:A cross-sectional study was undertaken to investigate the association between severity of periodontitis and clinical manifestation of rheumatoid arthritis (RA).Methods:Two hundred sixty-four RA patients and 88 age- and sex-matched controls underwent dental exam. Additionally, clinical manifestations including disease activity and anti-citrullinated protein antibodies were evaluated in RA patients.Results:The prevalence of moderate or severe periodontitis was higher in RA patients compared to controls (63.6% vs 34.1%, p < 0.001). In markers of periodontal inflammation, bleeding on probing was correlated with disease activity score 28 (r = 0.128, p = 0.041), RA disease duration (r = 0.211, p = 0.001), erythrocyte sedimentation rate (ESR; r = 0.141, p = 0.023), anti-cyclic citrullinated peptide antibody (r = 0.183, p = 0.009), and anti-citrullinated α-enolase peptide-1 antibody (r = 0.143, p = 0.025). Gingival index was correlated with RA duration (r = 0.262, p < 0.001), ESR (r = 0.162, p = 0.009), anti-cyclic citrullinated peptide antibody (r = 0.203, p = 0.004) and anti-citrullinated α-enolase peptide-1 antibody (r = 0.225, p < 0.001). Periodontal structural damage represented by probing pocket depth and clinical attachment level were less in RA patients with human leukocyte antigen (HLA)-DRB1 shared epitope compared than those without shared epitope (p = 0.005 and p =0.006, respectively).Conclusions:The prevalence of moderate or severe periodontitis was increased in RA patients compared to controls. Periodontal inflammation was correlated with RA disease duration, ESR, and anti-citrullinated protein antibodies. Periodontal structural damage was less in RA patients with HLA-DRB1 shared epitope.
The pathogenesis of Alzheimer's disease (AD), especially the early events of AD pathology, remains unknown because of the complexity of AD and limitation of analysis methods. Transcriptome analysis has provided comprehensive insights to investigate the complex cellular activity in brain, but the transcriptome profiles from AD patients with microarray have generated discordant results. Here, for the first time, we performed transcriptome analysis of frontal cortex and cerebellum in 7-week-old 5XFAD transgenic mice (before extracellular amyloid plaque deposits) using high-throughput RNA-Seq analysis. Specific functional annotations were identified with differentially expressed genes (DEGs) of frontal cortex (a typically vulnerable region of AD pathology) and cerebellum (a typically non-vulnerable region of AD pathology). Cardiovascular disease-related genes were significantly found in down-regulated DEGs of frontal cortex, and mitochondrial dysfunction-related genes were evident in down-regulated DEGs of cerebellum. Additionally, we found RNA variants at the nucleotide level in transgenic mice compared with non-transgenic mice. Our results indicate that both frontal cortex and cerebellum in 5XFAD transgenic mice show specific pathological processes in the early pathophysiology of AD.
Hindlimb muscle atrophy occurs in both ipsilateral and contralateral sides following induction of neuropathic pain by unilateral peripheral nerve damage. Muscle changes of the ipsilateral side are more pronounced than those of the contralateral side.
Collectively, these results indicate that F20 induces osteoblast differentiation with a pattern similar to that mediated by BMP2 signaling pathway. The authors' previous data also showed that FN-derived oligopeptide improved wound healing, and it is suggested that F20 might serve as a therapeutic biomolecule to facilitate periodontal tissue regeneration.
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