Reactive oxygen species- (ROS-) induced lipid peroxidation plays a critical role in cell death including apoptosis, autophagy, and ferroptosis. This fundamental and conserved mechanism is based on an excess of ROS which attacks biomembranes, propagates lipid peroxidation chain reactions, and subsequently induces different types of cell death. A highly evolved sophisticated antioxidant system exists that acts to protect the cells from oxidative damage. In this review, we discussed how ROS propagate lipid peroxidation chain reactions and how the products of lipid peroxidation initiate apoptosis and autophagy in current models. We also discussed the mechanism of lipid peroxidation during ferroptosis, and we summarized lipid peroxidation in pathological conditions of critical illness. We aim to bring a more global and integrative sight to know how different ROS-induced lipid peroxidation occurs among apoptosis, autophagy, and ferroptosis.

To assess the mortality and resource utilization that results from acute renal failure associated with amphotericin B therapy, 707 adult admissions in which parenteral amphotericin B therapy was given were studied at a tertiary-care hospital. Main outcome measures were mortality, length of stay, and costs; we controlled for potential confounders, including age, sex, insurance status, baseline creatinine level, length of stay before beginning amphotericin B therapy, and severity of illness. Among 707 admissions, there were 212 episodes (30%) of acute renal failure. When renal failure developed, the mortality rate was much higher: 54% versus 16% (adjusted odds of death, 6.6). When acute renal failure occurred, the mean adjusted increase in length of stay was 8.2 days, and the adjusted total cost was $29,823. Although residual confounding exists despite adjustment, the increases in resource utilization that we found are large and the associated mortality is high when acute renal failure occurs following amphotericin B therapy.

Preliminary data support the feasibility of this comprehensive study to help determine the focus of public health efforts to reduce racial disparities in prostate cancer mortality.

BACKGROUND: Health literacy deficits affect half of the US overall patient population, especially the elderly, and are linked to poor health outcomes among noncancer patients. Yet little is known about how health literacy affects cancer populations. The authors examined the relation between health‐related quality of life (HRQOL) and health literacy among men with prostate cancer. METHODS: Data analysis included 1581 men with newly diagnosed clinically localized prostate cancer from a population‐based study, the North Carolina‐Louisiana Prostate Cancer Project (PCaP). Participants completed assessment of health literacy using Rapid Estimate of Adult Literacy in Medicine (REALM) and HRQOL using the Short Form‐12 General Health Survey (SF12). Bivariate and multivariate regression was used to determine the potential association between REALM and HRQOL, while controlling for sociodemographic and illness‐related variables. RESULTS: Higher health literacy level was significantly associated with better mental well‐being (SF12‐Mental Component Summary [MCS]; P < .001) and physical well‐being (SF12‐Physical Component Summary [PCS]; P < .001) in bivariate analyses. After controlling for sociodemographic (age, marital status, race, income, and education) and illness‐related factors (types of cancer treatment, tumor aggressiveness, and comorbidities), health literacy remained significantly associated with SF12‐MCS scores (P < .05) but not with SF12‐PCS scores. CONCLUSIONS: Among patients with newly diagnosed localized prostate cancer, those with low health literacy levels were more vulnerable to mental distress than those with higher health literacy levels, but physical well‐being was no different. These findings suggest that health literacy may be important in patients managing prostate cancer and the effects of treatment, and provide the hypothesis that supportive interventions targeting patients with lower health literacy may improve their HRQOL. Cancer 2012. © 2011 American Cancer Society.

Renal ischemia/reperfusion injury (IRI) is a significant challenge in perioperative medicine and is related to oxidative programmed cell death. However, the role of ferroptosis, a newly discovered form of oxidative cell death, has not been evaluated widely. Pannexin 1 (PANX1), an ATP-releasing pathway family protein, has pro-apoptotic effects during kidney injury. Here, we demonstrate that PANX1 deletion protects against renal IRI by regulating ferroptotic cell death. Panx1 knockout mice subjected to renal IRI had decreased plasma creatinine, malondialdehyde (MDA) levels in kidney tissues, and tubular cell death (visible as decreased TUNEL-positive renal tubular cells) compared with WT mice. In cultured human kidney 2 (HK-2) cells, silenced Panx1 expression significantly attenuated ferroptotic lipid peroxidation and iron accumulation induced by the ferroptosis inducer erastin. Moreover, the Panx1 silencing significantly modulated ferroptosis-related protein expression. Furthermore, Panx1 deletion induced the expression of a cytoprotective chaperone, heme oxygenase-1 (HO-1), and inhibited ferroptinophagy via the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathway. In summary, Panx1 deletion protects against renal IRI by attenuating MAPK/ERK activation in a ferroptotic pathway. Our findings provide critical insights into the role of PANX1 in ferroptotic cell death and highlight a potential therapeutic target for the management of acute kidney injury (AKI) during the perioperative period.Acute kidney injury (AKI) 2 is a frequent complication after cardiac surgery, which contributes to increased mortality, and

Social support has been shown to influence health outcomes in later life. In this study, we focus on social engagement as an umbrella construct that covers select social behaviors in a lifespan sample that included oldest-old adults, a segment of the adult population for whom very little data currently exist. We examined relationships among social engagement, positive health behaviors, and physical health to provide new evidence that addresses gaps in the extant literature concerning social engagement and healthy aging in very old adults. Participants were younger (21–59 years), older (60–89 years), and oldest-old (90–97 years) adults (N = 364) in the Louisiana Healthy Aging Study (LHAS). Linear regression analyses indicated that age, gender, and hours spent outside of the house were significantly associated with self-reported health. The number of clubs and hours outside of home were more important factors in the analyses of objective health status than positive health behaviors, after considering age group and education level. These data strongly suggest that social engagement remains an important determinant of physical health into very late adulthood. The discussion focuses on practical applications of these results including social support interventions to maintain or improve late life health.

In this article, we examined memory for pictures and words in middle-age (45-59 years), young-old (60-74 years), old-old (75-89 years) and the oldest-old adults (90-97 years) in the Louisiana Healthy Aging Study. Stimulus items were presented and retention was tested in a blocked order where half of the participants studied 16 simple line drawings and the other half studied matching words during acquisition. Free recall and recognition followed. In the next acquisition/test block, a new set of items was used where the stimulus format was changed relative to the first block. Results yielded pictorial superiority effects in both retention measures for all age groups. Follow-up analyses of clustering in free recall revealed a greater number of categories were accessed (which reflects participants' retrieval plan) and more items were recalled per category (which reflects participants' encoding strategy) when pictures served as stimuli compared to words. Cognitive status and working memory span were correlated with picture and word recall. Regression analyses confirmed that these individual difference variables accounted for significant age-related variance in recall. These data strongly suggest that the oldest-old can utilize nonverbal memory codes to support long-term retention as effectively as do younger adults. KeywordsEpisodic memory; healthy aging; oldest-old; picture superiority effect; verbal recall Age-related declines in episodic memory are well documented in the cognitive aging literature (for reviews, Craik, 2000;Zacks, Hasher, & Li, 2000). Much of the prior work on memory aging consists of studies where younger (20s to 30s) and older adults (60s to 70s) were Address correspondence to Katie E. Cherry, Department of Psychology, Louisiana State University, Baton Rouge, LA 70803-5501 (telephone: 225 578-8745, fax: 225 578-4125, email: pskatie@lsu.edu).. Correspondence concerning this article should be addressed to Katie E. Cherry, Department of Psychology, Louisiana State University, Baton Rouge, LA 70803-5501 (e-mail: pskatie@lsu.edu). . Other evidence has shown that demographic and life style variables influence the extent to which older adults benefit from cognitive support to enhance episodic memory (Hill, Wahlin, Winblad & Bäckman, 1995). These studies highlight the critical role of individual difference and task variables in episodic memory functioning in late life, consistent with a contextualist view of episodic memory (Bäckman, Mantyla, & Herlitz, 1990). NIH Public AccessOne issue that has received scant attention in studies of episodic memory in late adulthood is whether the oldest-old demonstrate pictorial superiority effects in retention. The pictorial superiority effect (PSE) refers to the finding that concrete items are better remembered when presented in a pictorial format than in a verbal format. Paivio (1971) advanced the dual-coding theory to explain the memorial advantage of pictures relative to their verbal referents. This theory holds that pictures can be dually represented i...

Mitophagy is an essential mitochondrial quality control mechanism that eliminates damaged mitochondria and the production of reactive oxygen species (ROS). The relationship between mitochondria oxidative stress, ROS production and mitophagy are intimately interwoven, and these processes are all involved in various pathological conditions of acute kidney injury (AKI). The elimination of damaged mitochondria through mitophagy in mammals is a complicated process which involves several pathways. Furthermore, the interplay between mitophagy and different types of cell death, such as apoptosis, pyroptosis and ferroptosis in kidney injury is unclear. Here we will review recent advances in our understanding of the relationship between ROS and mitophagy, the different mitophagy pathways, the relationship between mitophagy and cell death, and the relevance of these processes in the pathogenesis of AKI. Abbreviations: AKI: acute kidney injury; AMBRA1: autophagy and beclin 1 regulator 1; ATP: adenosine triphosphate; BAK1: BCL2 antagonist/killer 1; BAX: BCL2 associated X, apoptosis regulator; BCL2: BCL2 apoptosis regulator; BECN1: beclin 1; BH3: BCL2 homology domain 3; BNIP3: BCL2 interacting protein 3; BNIP3L/NIX: BCL2 interacting protein 3 like; CASP1: caspase 1; CAT: catalase; CCCP: carbonyl cyanide m-chlorophenylhydrazone; CI-AKI: contrast-induced acute kidney injury; CISD1: CDGSH iron sulfur domain 1; CL: cardiolipin; CNP: 2’,3’-cyclic nucleotide 3’-phosphodiesterase; DNM1L/DRP1: dynamin 1 like; E3: enzyme 3; ETC: electron transport chain; FA: folic acid; FUNDC1: FUN14 domain containing 1; G3P: glycerol-3-phosphate; G6PD: glucose-6-phosphate dehydrogenase; GPX: glutathione peroxidase; GSH: glutathione; GSK3B: glycogen synthase kinase 3 beta; GSR: glutathione-disulfide reductase; HIF1A: hypoxia inducible factor 1 subunit alpha; HUWE1: HECT, UBA and WWE domain containing 1; IL1B: interleukin 1 beta; IMM: inner mitochondrial membrane; IPC: ischemic preconditioning; IRI: ischemia-reperfusion injury; LIR: LC3-interacting region; LPS: lipopolysaccharide; MA: malate-aspartate; MPT: mitochondrial permeability transition; MUL1: mitochondrial E3 ubiquitin protein ligase 1; mtROS: mitochondrial ROS; NLR: NOD-like receptor; NLRP3: NLR family pyrin domain containing 3; NOX: NADPH oxidase; OGD-R: oxygen-glucose deprivation-reperfusion; OMM: outer mitochondrial membrane; OPA1: OPA1 mitochondrial dynamin like GTPase; OXPHOS: oxidative phosphorylation; PARL: presenilin associated rhomboid like; PINK1: PTEN induced kinase 1; PLSCR3: phospholipid scramblase 3; PMP: peptidase, mitochondrial processing; PRDX: peroxiredoxin; PRKN: parkin RBR E3 ubiquitin protein ligase; RPTC: rat proximal tubular cells; ROS: reactive oxygen species; SLC7A11/xCT: solute carrier family 7 member 11; SOD: superoxide dismutase; SOR: superoxide reductase; SQSTM1/p62: sequestosome 1; TCA: tricarboxylic acid; TIMM: translocase of inner mitochondrial membrane; TOMM: translocase of outer mitochondrial membrane; TXN: thi...