PubMed · 15693532
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S Slavin. 2004. Liposuction in the consensus document.. https://pubmed.ncbi.nlm.nih.gov/15693532/
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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.
OBJECTIVES: To determine the effect of the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, pravastatin, on markers of cardiovascular risk and lipodystrophy in HIV-infected, protease inhibitor (PI)-treated men with hypercholesterolaemia. METHODS: A randomized, placebo-controlled, 16-week study was carried out on 33 HIV-infected, hypercholesterolaemic men (fasting total cholesterol > 6.5 mmol/L) on PI-containing therapy. Patients commenced dietary assessment and advice at week 0 and were randomized to 12 weeks pravastatin (40 mg each night) or placebo from week 4. The primary endpoint was the time-weighted change (TWAUC) in total cholesterol from week 0. Secondary endpoints included TWAUC cholesterol from week 4 (start of pravastatin), total and regional body fat, fasting lipids, glucose, insulin, and markers of cardiovascular risk. RESULTS: Of 33 men randomized (pravastatin n = 16, mean age 48 years), 31 completed the study. Groups were matched for baseline cholesterol and body composition. Although there was no significant between-group difference in TWAUC cholesterol from week 0 (pravastatin -0.6 +/- 1.0 versus placebo -0.4 +/- 1.0 mmol/L/week; P = 0.8), TWAUC cholesterol from week 4 decreased more in the pravastatin group (-0.8 +/- 1.0 versus -0.3 +/- 0.9 mmol/L/week; P = 0.04). Neither triglycerides nor dietary intake changed. Subcutaneous fat increased significantly with pravastatin (+0.72 +/- 1.55 versus +0.19 +/- 0.48 kg change in limb fat, P < 0.04; +5.2 +/- 8.7 versus -1.3 +/- 13.7 cm change in abdominal subcutaneous fat, P = 0.02). Apart from homocystine, which decreased in the pravastatin group, there were no significant differences in other cardiovascular, lipid or glucose parameters. CONCLUSIONS: Despite limited effects on cholesterol, 12 weeks use of pravastatin 40 mg each night in HIV-infected men with hypercholesterolaemia resulted in significant increases in subcutaneous fat.
The purpose of the present study was to study the aromatase mRNA expression as well as promoter usage (I.4, I.3, PII and I.7) in axillary adipose tissue (AA), mammary adipose tissue (MA), breast tumor tissue (BT) and adjacent normal breast tissue (NB), and to study the relationship between aromatase mRNA expression and tumor necrosis factor (TNF)-alpha, interleukin (IL)-6 and cyclooxygenase (COX)-2 mRNA expression. BT (n=108), NB (n=54), AA (n=41) and MA (n=34) from patients with breast cancer were subjected to real-time PCR assays for the mRNA levels of aromatase, TNF-alpha, IL-6 and COX-2. We also studied the usage of promoters I.4, I.3, PII and the recently reported endothelial promoter I.7. Total aromatase mRNA levels were significantly up-regulated in BT as compared with NB, AA and MA. Proportion of promoter l.4-specific transcripts against the total transcripts was significantly decreased and that of promoter l.3- and l.7-specific transcripts was significantly increased in BT than NB, AA and MA. However, the amount of transcripts from all the 4 promoters was significantly up-regulated in BT than NB, AA and MA. Estrogen receptor-alpha (ER-alpha) positive tumors showed a higher percentage of promoter I.7 usage than ER-alpha negative tumors with a marginal significance (p=0.05), and tumor with high microvessel counts tended (p=0.06) to show a higher percentage of promoter I.7 usage than those with low microvessel counts. There was a significant association between aromatase mRNA levels and TNF-alpha, IL-6 or COX-2 mRNA levels in BT, AA and MA but not in NB. These results suggest that enhanced transcription of promoters l.4, I.3, PII and I.7 explains the up-regulation of aromatase mRNA levels in BT. It has also been suggested that angiogenesis might stimulate the growth of ER-alpha positive tumors through the enhanced transcription of aromatase from promoter I.7 in endothelial cells in BT, and that TNF-alpha, IL-6 and COX-2 might be implicated in the up-regulation of aromatase mRNA in BT, AA and MA but not in NB.