Cadmium is an environmental toxin strongly associated with the development of cancer, kidney and liver disease, and bone demineralization. Whether cadmium causes obesity in humans remains a subject of controversy in the literature. An NHANES study that examined the effect of various toxic metals on central obesity demonstrated a decrease in the BMI of subjects exposed to cadmium. The purpose of this study is to examine the effect of cadmium on visceral adipose tissue (VAT), the potential for chelation to reverse cadmium‐induced changes, and to investigate the mechanism by which these changes occur. VAT is the subset of adipose tissue most heavily implicated in the pathogenesis of obesity, insulin resistance, and metabolic syndrome. ICR mice were placed into one of three groups: control, cadmium followed by washout, and cadmium followed by chelation. Mice in the two experimental groups were treated with 100ppm CdCl2 drinking water for 8 weeks followed by either 8 weeks of washout or 8 weeks of chelation with DMSA. Digital analysis of H&E images was performed using ImageJ and morphometric parameters of approximately 400 adipocytes per group were obtained. A 14.6% reduction in adipocyte size was observed in the group treated with cadmium followed by washout relative to the control group (p < 0.0001). In the group that underwent chelation after cadmium exposure, there was an increase in adipocyte size relative to the cadmium‐washout group (p<0.002). Additionally, animals in the cadmium‐washout group had a 5% reduction in body weight relative to control (p<0.0001). There was no significant difference in weight between the control group and the cadmium‐chelation group. In conclusion, the mouse model we have developed demonstrates that chronic low dose cadmium exposure causes weight loss and that chelation has the potential to reverse this change. Although the effect of cadmium on body weight remains controversial, this mouse model may serve to clarify this relationship and address the mechanism of cadmium’s action. Support or Funding Information NIEHS Grant # P30 ES027792‐02

O presente trabalho traz uma abordagem de como a figura feminina é representada nas histórias em quadrinhos. O objetivo do trabalho é identificar o discurso criado em torno da imagem feminina, que intercala da heroína destemida a mocinha em perigo que necessita da proteção masculina. Vamos realizar uma análise a partir das histórias em quadrinhos da MulherMaravilha. Fica evidente que são necessários abordagens mais acurada a respeito das HQs, ainda mais quando tratamos de gênero, pode parecer exagerado mas essa visão redutora da mulher que é passada nos quadrinhos é parte de um problema maior, é algo que é reflexo da nossa sociedade, que necessita ser desconstruído.PalavrasChave: Representação; HQs; Gênero; MulherMaravilha.This article presents an approach of how the female figure is represented in comics. The objective is to identify the discourse created about the female image in this genre, that merges the fearless heroine with the damsel in distress, who needs male protection. We will perform an analysis of the Wonder Woman comics. It is evident that a more accurate approach about those comics is needed, especially when dealing with gender. However exaggerated it may seem, the reductive view of women that is passed on by the comics is part of a larger problem, it is something that reflects our society, and needs to be deconstructed.

Environmental cadmium exposure has been established as a promotor of vascular inflammation and risk factor for atherosclerosis. Inflammation causes histone release, which was shown to increase macrophage low‐density lipoprotein (LDL) phagocytosis, which initiates foam cell formation, a crucial step in atherosclerosis. The link between histones and macrophages suggests cadmium may increase atherogenesis by upregulating scavenger receptors, which function to bind LDL and Oxidized LDL (OxLDL).RAW 264.7 (murine) macrophages were incubated in a solution of DMEM (Dulbecco's Modified Eagle Medium) and treated with 2 μg LDL, 2 μg histones, and 10 nM, 50 nM, and 200 nM CdCl2 concentrations with varying incubation times (24 hr, 48 hr, and 72 hr). Cells were stained using Oil Red O (lipid sensitive dye) and imaged using a microplate reader at 500 nm. LDL was oxidized by incubation in 10 μM CuSO4 and centrifugal filtration in a PD‐10 spin column. OxLDL was diluted to 2 μg/ml and applied to macrophage cells with the aforementioned conditions, excluding histones. Oil Red O staining and absorbance measurement were performed with similar time constraintsIn vivo studies for measurement of serum LOX‐1, CD‐36 and SR‐A I/II were also performed. LOX‐1, CD‐36, and SR‐A I/II are the main macrophage and endothelial receptors for oxidized LDL. ICR male Mice were exposed to cadmium through drinking water for 8 weeks. Mice were sacrificed, and serum was extracted for assessment of scavenger receptor expression by ELISA assay.Oil Red O staining of RAW 264.7 cells incubated with 2 μg LDL, 2 μg histones and 10 nM, 50 nM, and 200 nM CdCl2 concentrations showed significant dose‐dependent and time‐dependent (24, 48, and 72 hr.) increases in lipid absorbance. Those at the highest CdCl2 concentrations showed the largest increase in LDL uptake, further augmented by histones. Similar results were found in macrophage cells incubated with 2 μg OxLDL. The serum ELISA provided inconclusive results to LOX‐1 serum concentrations.Our data indicates cadmium modulates macrophage function to promote the uptake of LDL, histone‐LDL and OxLDL. We are currently studying the in vitro expression of major scavenger receptors, including LOX‐1, CD‐36 and SR‐A I/II that may provide insight into the mechanism of action for cadmium adverse effects on macrophages.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Nanomolar cadmium concentrations have been shown to increase the risk for atherosclerosis and promote endothelial damage. Atherosclerotic plaque formation is regulated by scavenger receptors, which are cell surface receptors crucial to macrophage apoptosis and foam cell formation. LOX‐1, CD‐36, and SR‐A I/II are the main macrophage and endothelial receptors responsible for internalization of oxidized LDL. Incubation with CdCl2 caused a four‐fold increase in LDL absorption by RAW 264.7 (murine) macrophages. To study mechanisms of this increase, macrophages were treated with 2 mg/ml of LDL only, 5nM to 200 nM CdCl2 and then both treatments combined, all for a 48 hour period. Cell lysates were then subjected to a phospho‐kinase array, which simultaneously analyzes the rate of phosphorylation for 43 kinases. When exposed to 10 nM CdCl2, Signal Transducer and Activator of Transcription 5 (STAT5) had a 5 fold increase in phosphorylation compared to control (macrophage cells only), which was the highest in the array. 30 kinases had a significant increase in phosphorylation, while 13 kinases showed a significant decrease in phosphorylation, the greatest decrease being p53 which was knocked down to half. Interestingly, the cadmium induced changes in phosphorylation were attenuated by LDL co‐incubation. In vitro studies were performed to assess levels of LOX‐1, CD‐36 and SR‐A I/II. Macrophage cells were exposed to 200 nM CdCl2, STAT5 inhibitor AC‐4‐130, and 2 mg/ml of LDL for 48 hrs. Lysates were assessed for scavenger receptor expression by ELISA assay. Both the 200 nM CdCl2 and STAT5 inhibitor groups showed significantly increased expression of all 3 scavenger receptors, and the 200 nM CdCl2 STAT5 inhibitor combination resulted in an even higher fold expression. Overall, cadmium plays a role in the progression of atherosclerosis which could in part be via the phosphorylation cascade. STAT5 inhibits the transcription of CD36, hence the increased expression of CD36 and other scavenger receptors noted in the presence of a STAT5 inhibitor. However, cadmium increases the phosphorylation and subsequent function of STAT5 while also increasing the expression of CD36, LOX‐1 and SR‐A I/II. This implies a non‐STAT5 mediated mechanism. It would be interesting to examine the function of the other cadmium‐modulated highly phosphorylated or dephosphorylated kinases in scavenger receptor expression.

Introdução: O processo de envelhecimento é responsável pelo declínio progressivo da saúde geral do idoso que, poderá culminar na dependência e consequente institucionalização. A PTH e a vitamina D são as principais hormonas responsáveis pela regulação da fisiologia óssea. Objetivos: O presente estudo objetiva avaliar as hormonas envolvidas na regulação do cálcio em idosos institucionalizados e, nos que habitam em zona rural, com estilo de vida independente e ativo. Conclusion:The adoption of an active lifestyle and the contact with nature, carry profit to a better aging process.