PubMed · 15673815
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R John Davenport. 2005-01-26. Coming back for seconds.. https://doi.org/10.1126/sageke.2005.4.nf7
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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.
INTRODUCTION: The incidence of breast cancer varies among women living in the Southwestern part of the US. We evaluate how body size influences breast cancer risk among these women. METHODS: Cases (n = 2,325) diagnosed with breast cancer between October 1, 1999 and May 2004 residing in Arizona, Colorado, New Mexico, or Utah were matched to controls (n = 2,525). Participants were interviewed; height, weight, waist, and hip circumference were measured at the time of interview; blood was drawn. RESULTS: A large body mass index (BMI) at age 15 was inversely associated with pre-menopausal breast cancer risk in both non-Hispanic white (NHW) and Hispanic women (Odds ratio, ORs 0.68 95% CI 0.44, 1.04, and 0.65 95% CI 0.39, 1.08, respectively); BMI at age 15 also had an impact on subsequent breast cancer associated with obesity after menopause. Among post-menopausal women, recent exposure to hormones was an important modifier of risk associated with body size. Among women not recently exposed to hormones risk associated with obesity was 1.61 (95% CI 1.05, 2.45) for NHW women; gaining > or = 25 kg between 15 and age 50 was inversely associated with breast cancer among Hispanic women (OR 0.51, 95% CI 0.23, 1.14). A large weight gain and a large waist-to-hip ratio (WHR) was associated with an increased odds of having an estrogen receptor negative tumor among NHW only (OR 1.81, 95% CI 1.07, 3.08, and 2.04 95% CI 1.20,3.50). CONCLUSIONS: These findings suggest that the metabolic consequences of obesity on breast cancer risk differ between NHW and Hispanic women living in the Southwest.
Overproduction of VLDL (very-low-density lipoprotein) particles is an important cause of FCHL (familial combined hyperlipidaemia). It has been shown recently that VLDL production is driven by the amount of hepatic fat. The present study was conducted to determine the prevalence of fatty liver in relation to the different fat compartments and lipid parameters in FCHL. A total of 68 FCHL patients, 110 normolipidaemic relatives and 66 spouses underwent ultrasound of the abdominal region to estimate the amount of subcutaneous, visceral and hepatic fat. Skinfold callipers were used to measure subcutaneous fat of the biceps, triceps, subscapular and supra-iliacal regions. Fatty liver was observed in 18% of the spouses, 25% of the normolipidaemic relatives and 49% of the FCHL patients. After adjustment for age, gender and body mass index, the prevalence of fatty liver was significantly higher in FCHL patients compared with spouses [OR (odds ratio), 3.1; P=0.03], and also in the normolipidaemic relatives compared with spouses (OR, 4.0; P=0.02), whereas no differences were observed between FCHL patients and normolipidaemic relatives (OR, 0.8; P=0.58). In the normolipidaemic relatives and FCHL patients combined, both visceral fat mass and subcutaneous abdominal fat were independent predictors of fatty liver (P<0.001 for both fat compartments; FCHL status corrected). Of interest, fatty liver stages were correlated with both VLDL-apoB (apolipoprotein B) and VLDL-triacylglycerols (triglycerides) in a representative subset (n=69) of patients and relatives (r(2)=0.12, P=0.006; and r(2)=0.18, P=0.001 respectively). These results show that fatty liver is a central aspect of FCHL, i.e. patients and normolipidaemic relatives. Both visceral and subcutaneous adiposity contribute to its 3-4-fold higher risk in FCHL.