PubMed · 7393569
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G J Beekhuis. 1980. Blepharoplasty.. https://pubmed.ncbi.nlm.nih.gov/7393569/
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Decellularized tissues provide biological cues owing to the wealth of structural and regulatory factors that promote angiogenesis, adipogenesis, and myogenesis and facilitate neurite outgrowth. Here, we demonstrated the advantages of decellularized adipose tissue (adipoECM) over defined collagen-based biomaterials for host tissue integration. Three batches of human adipose tissue were decellularized using a rapid decellularization protocol and analyzed using mass spectrometry. To assess the biological activity of the decellularized materials, adipoECM and a reference standard of care biomaterial (Integra®DRT, also containing collagen I and glycosaminoglycans) were implanted subcutaneously, but far from the wound bed (in anatomical potential spaces) of immunocompetent BALB/c mice. The mice were euthanized in the acute (1 day) and chronic (day 60) inflammatory reaction phases, followed by biomaterial excision and Masson’s trichrome immunohistofluorescence imaging of the paraffin-embedded specimens. Each batch of processed tissue passed a quality control check, showing a low level of donor genomic DNA, lack of nuclei, lipids, endotoxins, and bacterial contamination. Mass spectrometry revealed that all batches of decellularized tissue mainly contained collagen I and, to a lesser degree, collagen III, collagen IV, collagen V, laminin, fibrillin, fibronectin, tenascin, and elastin. No acute inflammatory reaction was observed in either material one day post-transplantation. At 60 days post-implantation, different cell types were detected in adipoECM specimens, whereas Integra®DRT remained acellular. Additional immunohistochemical staining of adipoECM revealed CD31-positive cells in the blood vessels. Mesenchymal (CD90 positive) and myeloid (CD14 positive) cells were also detected. Primary cell types involved in soft tissue healing and remodeling were found in the adipoECM-treated group. The ingrowth of blood vessels and mesenchymal cells confirmed the effective integration of adipoECM with host tissues. Our results demonstrate that decellularized adipose tissue implanted away from the wound bed possesses contextual biological activities that promote efficient integration with host tissues.
The purpose of this study was to determine whether alterations in body composition, resting energy expenditure (REE), and dietary energy intake are associated with growth retardation in HIV-positive children. Body composition (deuterium oxide dilution, skinfold measurements), REE (indirect calorimetry), and energy intake (24-hour weighed food intake) were evaluated in three groups: HIV-positive with growth retardation (HIV+Gr), HIV-positive with normal growth (HIV+); and HIV-uninfected with normal growth (HIV-). Children were between 2 and 11 years of age, afebrile, and free from acute infection. Forty-two children (13 HIV+Gr, 19 HIV+, 10 HIV-) were studied. Lean body mass was significantly reduced in HIV+Gr compared with HIV- (p < .05), and fat mass was significantly reduced in HIV+Gr and HIV+ compared with HIV- (p < .05). The percentages of lean and fat mass were not significantly different between groups, suggesting that differences in lean and fat mass were proportional to differences in body size. Consistent with reduced lean body mass, mean REE was significantly lower in HIV+Gr compared with HIV- (p < .05). Differences in mean REE/kg of body weight or lean body mass between groups were not statistically significant. A significant negative correlation was found between REE (kcal/kg/day) and weight-for-age (p = .04), and a trend with height-for-age Z-score (p = .07). Mean energy intake was not significantly different between groups. This study suggests that lean and fat mass are proportionately reduced in HIV-positive children with growth retardation. Further studies are necessary to delineate the relationship between energy balance and growth in children with HIV infection.
Melatonin, the principal pineal gland hormone, exerts a direct antiproliferative effect on estrogen-responsive MCF-7 cells in culture. The purpose of the current study was to investigate the effects of melatonin on the invasion capacity of MCF-7 cells. In vitro, melatonin at physiological doses (1 nM) reduced (P < 0.001) the invasiveness of tumoral cells measured in Falcon invasion chambers. Subphysiological (0.1 pM) and pharmacological concentrations (10 microM) of melatonin failed to inhibit cell invasion. Melatonin was also able to block 17beta-estradiol-induced invasion (P < 0.001). Pretreatment of MCF-7 cells with 1 nM melatonin increased the response of tumoral cells to the anti-invasive effects of this indolamine. To explore possible mechanisms by which melatonin reduces invasiveness, we measured the attachment of MCF-7 cells to a basement membrane, the chemotactic response of the cells, and their type IV collagenolytic activity. The presence of melatonin (1 nM) in the culture medium significantly reduced the ability of MCF-7 cells to attach to the basement membrane; this effect was enhanced by pretreating the cells with the same indolamine (P < 0.001). Melatonin also counteracts the stimulatory effects of 17beta-estradiol on cell adhesion (P < 0.001). The chemotactic response of MCF-7 cells also decreased in the presence of 1 nM melatonin, and this melatonin-induced reduction of cell migration was more effective on cells that were previously incubated for 5 days with melatonin than it was on nonpretreated cells (P < 0.001). The simultaneous addition of 17beta-estradiol and melatonin resulted in a significantly lower chemotactic response than that of 17beta-estradiol-treated cells (P < 0.001). However, type IV collagenolytic activity was not influenced by melatonin. Our results demonstrate that melatonin reduces the invasiveness of MCF-7 cells, causing a decrease in cell attachment and cell motility, probably by interacting with the estrogen-mediated mechanisms of MCF-7 cell invasiveness. In addition, we also studied the influence of melatonin on the expression of two cell surface adhesion molecules (E-cadherin and beta1 integrin) and an intermediate filament protein (vimentin), the expression of which has been correlated with the relative invasive capacity of human breast cancer cells. The culture of tumor cells in the presence of melatonin (1 nM) increased the membrane staining for E-cadherin and beta1 integrin as well as the number of E-cadherin and beta1 integrin immunoreactive cells (P < 0.01). Neither control MCF-7 cells nor those treated with melatonin stained for vimentin. Preliminary in vivo experiments carried out on ovariectomized athymic nude mice implanted with 17beta-estradiol pellets and inoculated with 5 x 10(6) MCF-7 cells in the inguinal mammary fat pad suggest that melatonin could decrease the tumorigenicity of these tumor cells. However, these results need further confirmation. Taken together, our results suggest that melatonin shifts MCF-7 human breast cancer cells to a lower invasive status by increasing the beta1 integrin subunit and E-cadherin expression and promoting the differentiation of tumor cells. Finally, our study points out the existence of the anti-invasive actions of melatonin as a part of the oncostatic action of melatonin.