Triple negative breast cancer (TNBC) is one of the most aggressive cancers diagnosed amongst women with a high rate of treatment failure and a poor prognosis. Mitochondria have been found to be key players in oncogenesis and tumor progression by mechanisms such as altered metabolism, reactive oxygen species (ROS) production and evasion of apoptosis. Therefore, mitochondrial infusion is an area of interest for cancer treatment. Studies in vitro and in vivo demonstrate mitochondrial-mediated reduction in glycolysis, enhancement of oxidative phosphorylation (OXPHOS), reduction in proliferation, and an enhancement of apoptosis as effective anti-tumor therapies. This review focuses on mitochondrial dysregulation and infusion in malignancies, such as TNBC.

Treatment of advanced liver disease using surgical modalities is possible due to the liver's innate ability to regenerate following resection. Several key cellular events in the regenerative process converge at the mitochondria, implicating its crucial roles in liver regeneration. Mitochondria enable the regenerating liver to meet immense metabolic demands by coordinating energy production to drive cellular proliferative processes and vital homeostatic functions. Mitochondria are also involved in terminating the regenerative process by mediating apoptosis. Studies have shown that attenuation of mitochondrial activity results in delayed liver regeneration, and liver failure following resection is associated with mitochondrial dysfunction. Emerging mitotherapy strategies involve isolating healthy donor mitochondria for transplantation into diseased organs to promote regeneration. This review highlights mitochondria's inherent roles in liver regeneration. New & Noteworthy Mitochondrial therapy (Mitotherapy) could potentially be the next big wave in therapeutics to preserve, supplement or replace damaged mitochondria after injury. In liver, mitotherapy should be considered to not only improve organ function but as therapeutic modality that could accelerate liver regeneration after partial hepatectomy.

tions with a visible light spectrophotometer (Parrish amd Grammer, 2012). However, the shift in the absorption spectrum of the dye upon acidification, the pK of the shift, had to exactly match the pH range of the acidification, necessitating changes in dyes employed depending upon which pH decreases were observed. Moreover, the absorption properties of any colored additives to be investigated and the light scattering properties of any potential food sources, such as bacterial suspensions, made it difficult to interpret the spectral properties of the observed mixture due to the use of spectrophotometry. Thus, the use of pH probes was alternatively investigated.Due to the intracellular oxidation of glucose, phenol red and spectrophotometry can detect color change. It was assumed that exogenous glucose would produce significant acidification of the medium by the worms. As the sugar is oxidized through respiration, carbon dioxide is produced, which causes the medium to acidify. Previous studies have investigated the respiratory processes and demonstrated the dependence of absorption of pH indicators on time and weak dependence of respiration rate on glucose concentration (Parrish & Grammer, 2012).This study developed procedures to further detect respiration in C. elegans by using Vernier pH probes (Vernier Software and Technology, Beaverton, OR) and tested the effects of E. coli and different carbohydrates (glucose, fructose, and maltose) on respiration rates. It was hypothesized that Vernier pH probes could be utilized to detect respiration and that E. coli and glucose would show the highest respiration rates, even if all carbohydrates were metabolized to some degree. The addition of E. coli should reveal increased respiration rates because it serves as the main food source for C. elegans. Glucose was also expected to reveal high