Gomezbraswell9570

Importance Body fat contouring procedures have increasingly grown in popularity over the years. As such, there is a need for inexpensive, minimally invasive, and simple fat reduction/contouring technique. Objective To examine the acid-base and histological changes in ex vivo human adipose tissue after electrochemolipolysis (ECL). Design, Setting, and Participants Panniculus tissue specimens obtained after abdominoplasty procedures were tumesced with normal saline. Two platinum needle electrodes were inserted into each sample and connected to a DC power supply. Voltage (3-6 V) was varied and applied for 5 min. Specimens were sectioned through a sagittal midline across both electrode insertion sites and immediately stained with pH-sensitive dye. A numerical algorithm was used to calculate the area of the dye color change for each dosimetry pair. Samples were also evaluated utilizing light microscopy (hematoxylin and eosin). An ex vivo human adipose tissue model was used for evaluating the effects of ECL. Resultnonsurgical fat reduction as an ultralow cost alternative to current lipolytic devices and pharmaceuticals. Level of Evidence NA.Background The adult mammalian heart has limited regenerative capacity, mostly due to postnatal cardiomyocyte (CM) cell cycle arrest. In the last two decades, numerous studies have explored CM cell cycle regulatory mechanisms to enhance myocardial regeneration post myocardial infarction (MI). Pyruvate kinase muscle isozyme 2 (Pkm2) is an isoenzyme of the glycolytic enzyme pyruvate kinase. The role of Pkm2 in CM proliferation, heart development and cardiac regeneration is unknown. Methods We investigated the effect of Pkm2 in CM through models of loss (CM-specific Pkm2 deletion during cardiac development) or gain using CM-specific Pkm2 modified mRNA (CMSPkm2 modRNA) to evaluate Pkm2 function and regenerative affects post-acute or -chronic MI in mice. Results Here, we identify Pkm2 as an important regulator of the CM cell cycle. We show that Pkm2 is expressed in CMs during development and immediately after birth but not during adulthood. Loss of function studies show that CM-specific Pkm2 deletion during cardiac development resulted in significantly reduced CM cell cycle, CM numbers and myocardial size. In addition, using CMSPkm2 modRNA, our novel CM-targeted strategy, following acute or chronic MI resulted in increased CM cell division, enhanced cardiac function and improved long-term survival. We mechanistically show that Pkm2 regulates the CM cell cycle and reduces oxidative stress damage through anabolic pathways and β-catenin. Conclusions We demonstrate that Pkm2 is an important intrinsic regulator of the CM cell cycle and oxidative stress and highlight its therapeutic potential using CMSPkm2 modRNA as a gene delivery platform.Hyperglycemia mediates oxidative stress, thus inducing transcription factor nuclear factor kappa B (NF-κB) activation, increasing endothelial adhesion molecule expression and monocyte/endothelial interaction, and resulting in endothelial injury. Ketamine was reported to attenuate oxidative stress in many cases. In this research, we determined whether and how ketamine protects against high-glucose-mediated augmentation of monocyte/endothelial interaction and endothelial adhesion molecule expression in human umbilical vein endothelial cells. High glucose augmented monocyte/endothelial adhesion and endothelial adhesion molecule expression. High glucose induced reactive oxygen species (ROS) production and augmented phospho-protein kinase C (p-PKC) βII expression and PKC activity. Moreover, high glucose inhibited the inhibitory subunit of nuclear factor-κBα (IκBα) expression in the cytoplasm and induced NF-κB nuclear translocation. Importantly, the effects induced by high glucose were counteracted by ketamine treatment. find more Further, CGP53353, a PKC βII inhibitor, inhibited high-glucose-mediated NF-κB nuclear translocation, attenuated adhesion molecule expression, and reduced monocyte/endothelial interaction. Further, these effects of ketamine against high-glucose-induced endothelial injury were inhibited by phorbol 12-myristate 13-acetate, a PKC βII activator. In conclusion, ketamine, via reducing ROS accumulation, inhibited PKC βII Ser660 phosphorylation and PKC and NF-κB activation and reduced high-glucose-induced expression of endothelial adhesion molecules and monocyte/endothelial interaction.Objective The present study used a longitudinal design to examine associations between paternal depressive symptoms in toddlerhood and children's psychosocial adjustment during the preschool and school-age periods. Maternal depressive symptoms and intervention status were tested as moderators of associations between paternal depressive symptoms and child maladjustment.Method The sample (n = 264, 48% female, 62% White, 14% Black, 14% bi-racial, 11% another racial group, and 86% non-Hispanic/Latinx) represented a subsample of families from the Early Steps Multisite Study, a clinical randomized trial testing the effectiveness of the Family Check-Up among low-income families using Women, Infants, and Children Nutritional Supplement Services in three communities varied in urbanicity. Fathers and mothers reported their levels of depressive symptoms at child age 2, primary caregivers (mostly mothers) contributed measures of child adjustment at ages 5, 8.5, and 9.5, and teachers completed questionnaires about child adjustment at ages 8.5 and 9.5.Results Direct relations were found between paternal depressive symptoms and primary caregivers' reports of children's preschool and school-age internalizing problems. Furthermore, higher levels of paternal depression were associated with higher levels of children's later adjustment problems at preschool-age when maternal depressive symptoms were mild or higher. The Family Check-Up attenuated relations between paternal depressive symptoms and children's internalizing problems at school-age.Conclusions These findings have important implications for future research on preventing children's early-emerging problem behaviors at home, suggesting that addressing paternal depressive symptoms in early childhood may be an important intervention target, especially in the context of maternal depression.