A Clinical Overview of Anorexia Nervosa and Overcoming Treatment Resistance.

Anorexia nervosa (AN) is a type of eating disorder that has been increasing in incidence and has been encountered more commonly by physicians in their daily practice. Both environmental and genetic risk factors paired along with a more susceptible neurobiology are at play in the emerging resistance to treatment in AN. Preoccupations with intense fear of weight gain, dietary restrictions, excessive exercise, and how the individual is perceived by society mixed with underlying psychopathology all further add to the issue. Many patients who fall into this cycle of obsessive and restrictive patterns refuse to get treatment. As clinicians, it is essential we recognize the early signs of both eating disorders during the initial primary care appointments. To review the literature on the etiology of AN, possible misdiagnosis leading to inappropriate management of this condition, and understand the treatment-resistant AN and its management. Additionally, it will explore possible reasons that contribute to the resistance to treatment, the underlying psychopathology of anorexics, its genetic predisposition, psychiatric comorbidities, identification of the early signs and symptoms, and timely prevention. Early recognition by a physician includes a thorough history and physical examination, pertinent laboratory, and electrolyte studies, and identifying comorbid psychiatric conditions. The treatment of AN is intricate and requires a holistic approach. Treatment includes multiple modalities such as nutritional rehabilitation and psychosocial and pharmacological therapies. An interdisciplinary team of medical professionals for managing chronic AN is recommended.

Three dimensional porous scaffolds derived from collagen, elastin and fibrin proteins orchestrate adipose tissue regeneration.

Current gold standard to treat soft tissue injuries caused by trauma and pathological condition are autografts and off the shelf fillers, but they have inherent weaknesses like donor site morbidity, immuno-compatibility and graft failure. To overcome these limitations, tissue-engineered polymers are seeded with stem cells to improve the potential to restore tissue function. However, their interaction with native tissue is poorly understood so far. To study these interactions and improve outcomes, we have fabricated scaffolds from natural polymers (collagen, fibrin and elastin) by custom-designed processes and their material properties such as surface morphology, swelling, wettability and chemical cross-linking ability were characterised. By using 3D scaffolds, we comprehensive assessed survival, proliferation and phenotype of adipose-derived stem cells in vitro. In vivo, scaffolds were seeded with adipose-derived stem cells and implanted in a rodent model, with X-ray microtomography, histology and immunohistochemistry as read-outs. Collagen-based materials showed higher cell adhesion and proliferation in vitro as well as higher adipogenic properties in vivo. In contrast, fibrin demonstrated poor cellular and adipogenesis properties but higher angiogenesis. Elastin formed the most porous scaffold, with cells displaying a non-aggregated morphology in vitro while in vivo elastin was the most degraded scaffold. These findings of how polymers present in the natural polymers mimicking ECM and seeded with stem cells affect adipogenesis in vitro and in vivo can open avenues to design 3D grafts for soft tissue repair.