Among US veterans, ST131, primarily its H30 subclone, accounts for most antimicrobial-resistant E. coli and is the dominant E. coli strain overall. Possible contributors include multidrug resistance, extensive virulence gene content, and ongoing transmission. Focused attention to ST131, especially its H30 subclone, could reduce infection-related morbidity, mortality, and costs among veterans.
Tissue engineering has emerged as a promising alternative approach to current clinical treatments for restoration of soft tissue defects. The purpose of this study was to investigate adipose tissue formation in vitro and in vivo by using human adipose-derived stromal cells (ADSCs) utilizing a gelatin sponge (Gelform®) as a scaffold. Adipogenic potentials of human ADSCs were demonstrated by Oil-O-red staining and cellular morphology. After seeding human ADSCs in a density of 3 × 106 cells/ml on three-dimensional gelatin sponges, tissue-engineered constructs were exposed to adipogenic differentiation medium for in vitro studies and implanted in the backs of severe combined immunodeficient (SCID) mice for in vivo adipose regeneration. Adipogenesis of ADSC-seeded gelatin sponges was confirmed by Oil-O-red staining after 4 weeks of in vitro incubation. The optical density of the elution from Oil-O-red staining of adipogenic constructs is significantly higher than that of the control group (p < 0.05, n = 4). With short-term in vitro differentiation, adipogenic constructs turned into fat tissue 4 weeks after in vivo implantation, confirmed by biochemical and immunohistochemical examination. No adipogenic-morphological change or fat formation was observed in in vitro or in vivo studies when ADSCs were exposed to a control medium without adipogenic stimulation. These results indicate that engineered adipose tissue can be achieved using human ADSCs and biocompatible and degradable gelatin sponges.
41 Brucella strains isolated from blood and cerebrospinal fluid cultures were identified to species level and biotypes detected. All of the isolates were Brucella melitensis: 2 strains of B. melitensis biotype-1 and 39 strains of B. melitensis biotype-3. In vitro activities of these strains were detected by the E test method. According to the 90% minimal inhibitory concentration (MIC90) values, the most active agent was doxycycline (MIC90 0.064 microg/ml), followed by ciprofloxacin (MIC90 0.25 microg/ml), trimethoprim-sulfamethoxazole and ceftriaxone (MIC90 0.38 microg/ml). Rifampin exhibited the highest MIC90 value (0.75 microg/ml).
Adipose-derived stromal cells (ASCs) possess multiple differentiation potentials and may serve as a cell source, if effectively modulated, for regenerative medicine and tissue engineering. Due to estrogen's function in tissue and organ development through regulating cell proliferation and differentiation, we hypothesized that an estrogen supplement may effectively enhance the multiple differentiation potentials of human ASCs. 17-Beta estradiol (E2) was investigated for modulating in vitro osteogenic and adipogenic differentiation in human ASCs isolated from a healthy female donor. After ASCs' exposure to osteogenic and adipogenic differentiation medium supplemented with different concentrations of E2, osteogenic markers (alkaline phosphatase activity, extracellular matrix, calcium deposition, and osteocalcin expression) and adipogenic parameters (lipid accumulation and differentiated cell population) significantly improved. Estrogen's enhancement is dose dependent and linked to differing alpha and beta estrogen receptors. Our data preliminarily demonstrate that estrogen can modulate the differentiation, and potentially improve the efficiency of ASCs in stem cell-based tissue engineering and regeneration. However, further study is needed to verify the regulatory functions of estrogen on ASC differentiations of donors with different ages and genders.
Central nervous system involvement occurs less than 5% of patients with brucellosis. A prospective analysis of 73 patients with brucellosis identified 13 (17.8%) neurobrucellosis cases from February 2001 to May 2002. 10 patients had chronic meningitis and 3 acute meningitis. Two patients had only psychiatric disorders. Cranial nerve involvement was observed in 3 patients (6th, 7th and 8th nerves). Three patients had positive blood cultures and 3 others had positive cerebrospinal fluid (CSF) cultures. 12 patients had positive agglutination titres in CSF. All patients received antibiotic therapy with ceftriaxone, rifampicin and doxycycline initially, and after 1 month they were continued with rifampicin and doxycycline up to 4 months. All patients were completely cured. Hearing loss developed in 1 patient as a sequela.
Bone marrow mesenchymal stem cells (MSCs) are a promising cell source for tissue engineering and regenerative medicine applications. However, effective regulation to improve differentiation potentials of MSCs plays a critical role in promoting successful tissue formation. Because estrogen has been demonstrated to modulate tissue and organ development and differentiation, we hypothesized that adding estrogen could effectively improve the multiple differentiation potentials of human bone marrow MSCs in vitro. In the present study, 17-beta estradiol (E2) was investigated for in vitro osteogenic and adipogenic differentiations of MSCs isolated from a healthy male human donor. After MSCs were exposed to osteogenic differentiation medium supplemented with E2 at different concentrations, osteocalcin expression is upregulated and calcium deposition (21.0%) is significantly improved ( p < 0.01; n = 4). Under adipogenic stimulation, E2 increased 35.4% lipid accumulations more than that of the group without the E2 supplement ( p < 0.01; n = 4). Estrogen's effect on osteogenesis occurs via estrogen receptors (ER)-alpha and -beta, whereas the effect on adipogenesis is through ER-alpha. Estrogen's regulation of differentiations of MSCs is dose dependent. The present study indicated that estrogen could potentially improve the role of MSCs in tissue engineering and regeneration by serving as a modulator of differentiation.
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