No abstract

Mesenchymal stem/stromal cells or medicinal signaling cells (MSC)-based therapy holds promise as a beneficial strategy for treating knee OA (osteoarthritis), but there is no standardized protocols nor mechanistic understanding. In order to gain a better insight into the human MSC from adipose tissue applied for autologous OA treatment, we performed extensive comparative immunophenotyping of the stromal vascular fraction from lipoaspirate or microfragmented lipoaspirates by polychromatic flow cytometry and investigated the cellular components considered responsible for cartilage regeneration. We found an enrichment of the regenerative cellular niche of the clinically applied microfragmented stromal vascular fraction. Sex-related differences were observed in the MSC marker expression and the ratio of the progenitor cells from fresh lipoaspirate, which, in female patients, contained a higher expression of CD90 on the three progenitor cell types including pericytes, a higher expression of CD105 and CD146 on CD31highCD34high endothelial progenitors as well as of CD73 on supra-adventitialadipose stromal cells. Some of these MSC-expression differences were present after microfragmentation and indicated a differential phenotype pattern of the applied MSC mixture in female and male patients. Our results provide a better insight into the heterogeneity of the adipose MSC subpopulations serving as OA therapeutics, with an emphasis on interesting differences between women and men.

Aim To expand our previous findings by increasing the number of patients in a study characterizing medicinal signaling cells (MSC) of stromal vascular fraction from lipoaspirate (SVF-LA) and from microfragmented lipoaspirate (SVF-MLA) applied for the treatment of osteoarthritis (OA).Methods Twenty OA patients, including 8 new patients, acquiring autologous microfragmented adipose tissue were enrolled. In-parallel immunophenotyping of SVF-LA and SVF-MLA was performed. The samples were incubated in a DuraClone SC prototype tube targeting the CD31, CD34, CD45, CD73, CD90, CD105, and CD146 surface markers, stained with the DRAQ7 cell nuclear dye and Live/Dead Yellow Fixable Stain, and analyzed by flow cytometry.

SUMMARY The aim of this study was to compare the incidence of mild psychomotor delay in infants whose mothers were treated for thyroid dysfunction regardless of the cause during first trimester of pregnancy with those whose mothers did not use medications prenatally. The sample included 200 infants up to 4 months of age. Half of the infants were examined by a pediatric physiatrist, while the other half were chosen randomly from the primary pediatric clinic. Binary logistic regression was performed to assess the impact of factors on psychomotor delay. The model contained seven independent variables derived from bivariate analyses and clinical relevance. Results showed that the infant’s chance of having psychomotor delay was 5.53 times higher if the mother had drug-compensated thyroid dysfunction. Younger gestational age increased the likelihood of delay 2.12 times per each gestational week. The likelihood of psychomotor delay also rose by 1% per 1 g of birth weight reduction. We found strong positive linear correlation between maternal drug-compensated thyroid dysfunction during pregnancy and psychomotor delay in infants, which has not been reported elsewhere. This differentiates an important and common prenatal risk factor and lays the foundation for faster initiation of habilitation of infants at risk. These insights provide a basis for planning the National Screening Program for Neurorisk Infants.