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Purpose We create a viable, mechanically expanded autograft long head biceps tendon (LHBT) scaffold for biologically augmenting the repair of torn rotator cuffs. Methods The proximal aspect of the tenotomized LHBTs was harvested from patients during rotator cuff repair surgery and was mechanically formed into porous scaffolds using a surgical graft expander. LHBT scaffolds were evaluated for change in area, tensile properties, and tenocyte viability before and after expansion. The ability of endogenous tenocytes derived from the LHBT scaffold to promote tenogenic differentiation of human adipose‐derived mesenchymal stromal cells (ADMSCs) was also determined. Results Autograft LHBTs were successfully expanded using a modified surgical graft expander to create a porous scaffold containing viable resident tenoctyes from patients undergoing rotator cuff repair. LHBT scaffolds had significantly increased area (length: 24.91 mm [13.91, 35.90] × width: 22.69 mm [1.87, 34.50]; P = .011) compared with the native LHBT tendon (length: 27.16 mm [2.70, 33.62] × width: 6.68 mm [5.62, 7.74]). The structural properties of the autograft were altered, including the ultimate tensile strength (LHBT scaffold: .56 MPa [.06, 1.06] vs. native LHBT: 2.35 MPa [1.36, 3.33]; P = .002) and tensile modulus (LHBT scaffold: 4.72 MPa [−.80, 1.24] versus native LHBT: 37.17 MPa [24.56, 49.78]; P = .001). There was also a reduction in resident tenocyte percent viability (LHBT scaffold: 38.52% [17.94, 59.09] vs. native LHBT: 68.87% [63.67, 74.37]; P =.004). Tenocytes derived from the LHBT scaffold produced soluble signals that initiated ADMSC differentiation into an immature tenocyte‐like phenotype, as indicated by an 8.7× increase in scleraxis ( P = .040) and a 3.6× increase in collagen type III mRNA expression ( P = .050) compared with undifferentiated ADMSC controls. Conclusions The ability to produce a viable autologous scaffold from the proximal biceps tendon having dimensions, porosity, mechanical characteristics, native ECM components, and viable tenocytes that produce bioactive signals conducive to supporting the biologic augmentation of rotator cuff repair surgery has been demonstrated. Clinical Relevance This biologically active construct may help to improve the quality of healing and regeneration at the repair site of rotator cuff tears, especially those at high risk for retear.

Abstract Eating disorders and substance use disorders frequently co‐occur. Twin studies reveal shared genetic variance between liabilities to eating disorders and substance use, with the strongest associations between symptoms of bulimia nervosa and problem alcohol use (genetic correlation [ r g ], twin‐based = 0.23‐0.53). We estimated the genetic correlation between eating disorder and substance use and disorder phenotypes using data from genome‐wide association studies (GWAS). Four eating disorder phenotypes (anorexia nervosa [AN], AN with binge eating, AN without binge eating, and a bulimia nervosa factor score), and eight substance‐use‐related phenotypes (drinks per week, alcohol use disorder [AUD], smoking initiation, current smoking, cigarettes per day, nicotine dependence, cannabis initiation, and cannabis use disorder) from eight studies were included. Significant genetic correlations were adjusted for variants associated with major depressive disorder and schizophrenia. Total study sample sizes per phenotype ranged from ~2400 to ~537 000 individuals. We used linkage disequilibrium score regression to calculate single nucleotide polymorphism‐based genetic correlations between eating disorder‐ and substance‐use‐related phenotypes. Significant positive genetic associations emerged between AUD and AN ( r g = 0.18; false discovery rate q = 0.0006), cannabis initiation and AN ( r g = 0.23; q < 0.0001), and cannabis initiation and AN with binge eating ( r g = 0.27; q = 0.0016). Conversely, significant negative genetic correlations were observed between three nondiagnostic smoking phenotypes (smoking initiation, current smoking, and cigarettes per day) and AN without binge eating ( r gs = −0.19 to −0.23; qs < 0.04). The genetic correlation between AUD and AN was no longer significant after co‐varying for major depressive disorder loci. The patterns of association between eating disorder‐ and substance‐use‐related phenotypes highlights the potentially complex and substance‐specific relationships among these behaviors.