Publications by authors named "T B Krasieva"

Body contouring achieved via subcutaneous adipose tissue reduction has notably advanced over the past century, from suction assisted lipectomy to techniques with reduced degrees of invasiveness including laser, radiofrequency, high frequency focused ultrasound, cryolipolysis, and drug-based injection approaches. These costly techniques have focused on damaging adipocyte cell membranes, hydrolyzing triglycerides (TGs), or inducing apoptosis. Here, we present a simple, low-cost technique, termed electrochemical lipolysis (ECLL).

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  • - Mutations in the proto-oncogene in melanocytes lead to benign moles (nevi), but the same mutations can cause melanoma, with nevi commonly not progressing due to a process called 'oncogene-induced senescence.'
  • - Recent research using a mouse model reveals that nevus cells do not show signs of senescence when compared to other skin cells, suggesting they are still actively proliferating.
  • - The study proposes that the growth arrest of nevi is likely due to collective cell interactions and dynamics rather than an individual cell's programmed senescence mechanism.
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  • Scientists found a way to change skin scars using a method called electrochemical therapy (ECT), which uses electricity to alter the skin's collagen.
  • They tested this method on pig skin and found that ECT created acid and base in different spots, causing changes in the skin structure.
  • The results showed that ECT could be a cheap and easy way to improve scars because it safely changes the collagen in the skin.
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Objectives: Injury to healthy dermis and the dermoepidermal junction initiates a robust healing process consisting of fibrous tissue overgrowth, collagen deposition, and scar formation. The conventional management of scars and other skin injuries has largely relied upon surgical soft tissue transfer to resurface and/or replace damaged and dysmorphic tissue with new skin. However, these strategies are invasive, expensive, and may further exacerbate integumentary injury.

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Peripheral endothelial cells are capable of erythrophagocytosis, but data on brain endothelial erythrophagocytosis are limited. We studied the relationship between brain endothelial erythrophagocytosis and cerebral microhemorrhage, the pathological substrate of MRI-demonstrable cerebral microbleeds. To demonstrate the erythrophagocytic capability of the brain endothelium, we studied the interactions between brain endothelial cells and red blood cells exposed to oxidative stress , and developed a new cerebral microbleeds model to study the subsequent passage of hemoglobin across the brain endothelial monolayer.

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