Both adipose-derived stem cells (ADSCs) and fat grafting promote burn wound healing, but whether adipogen-derived cells using various inducers such as 3-isobutyl-1-methylxanthine (IBMX) and insulin affect wound healing is unknown. Herein, ADSC-differentiated adipogenic lineages were used in rat burn wounds to evaluate wound healing potential. ADSCs were cultivated using six different adipogenic differentiation conditions (IBMX ± insulin, IBMX for 5 days, high and low Dulbecco's modified Eagle's medium) and in vitro morphological changes and cell proliferations during adipogenic differentiation were recorded. Intermediate burn wounds were inflicted in 15 Wistar male rats. Afterwards, the rats were divided into five groups for subcutaneous injections under the wounds: control; ADSCs; differentiated adipocytes (-IBMX+INSULIN and +IBMX[D1-5]+INSULIN) and fat prepared by Coleman technique. Macroscopic changes and histology were documented for 3 weeks. Repeated measures analysis of variance was performed to analyze cell growth and wound healing with a statistical level set of P < .05. Induction cocktails significantly reduced proliferation and induced lipid droplet accumulation. Conditioning without insulin induced the least lipid accumulation, while discontinuing IBMX generated larger adipocytes (P < .001). Adipogenic differentiated ADSCs had similar wound healing abilities with ADSC and fat injections, but differentiated adipocytes (+IBMX[D1-5]+INSULIN) and fat grafting accelerated the early healing process relative to ADSC (P < .001). Reduced fibrosis and mild inflammatory infiltration limited to superficial dermis were observed in +IBMX(D1-5)+INSULIN and fat injection groups, while those reactions were mild to moderate in ADSC group. Differentiated adipocytes achieve similar wound healing results compared with ADSC and fat injections, but differentiated adipocytes (+IBMX[D1-5]+INSULIN) and fat grafting accelerate early healing relative to ADSC.

Burns have become an important public health problem in the last two decades, with just over a quarter of a million deaths annually. Major burns are accompanied by a strong inflammatory response, which will most often lead to systemic response inflammatory syndrome, followed by sepsis and finally induce multiple organ failure. The main mechanism involved in wound healing after burns is the inflammatory process, characterized by the recruitment of myeloid and T cells and by the involvement of numerous cytokines, chemokines, complement fractions, as well as various growth factors. Inflammasomes, protein-based cytosolic complexes, activated during metabolic stress or infection, play a role in modulating and improving the defense capacity of the innate immune system. Nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) inflammasome has been studied predominantly and several hypotheses have been issued. Restoring the balance between the pro-inflammatory response and the anti-inflammatory activity is the key element to effective therapy in burns. Severe burns require nutritional support and pharmacotherapy not only for burn area but for different pathological complications of burn injury. In-depth research is required to find new ways to modulate the defense capacity, to prevent the complications of abnormal immune response and to treat burn injuries efficiently. Contents 1. Introduction 2. Burns and host immune response 3. The involvement of inflammasomes in burn and host immune response 4. Burns and the therapy 5. Conclusions

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Dissection of aorta is a serious condition; the main factors are hypertension and diseases of the connective tissue or of collagen. Aortitis syndrome in combination with hypertension and atherosclerosis in association with ascending aortic dissection is rarely seen. We present the case of a 53-year-old hypertensive patient whose ascending aortic dissection was associated with pericardial effusion without rupture of the aorta and with pleural effusion. Several unusual aspects of transesophageal echocardiography are described. The intraoperative biopsy revealed inflammatory aortitis with mural hematoma, without giant cells. The literature concerning aortic dissection and aortitis is reviewed.