Neoliberalism can (and should) be saved by macroprudential financial regulation

Terrence Casey argues that macroprudential regulation, by smoothening the credit cycle, can temper the major problems with the neoliberal growth model. It is the tendency toward excessive credit growth, producing booms and subsequent damaging busts, and not productive exhaustions that weakens neoliberalism. If financial volatility can be removed, it is indeed a model worth saving as it has undoubtedly produced real growth, albeit in a two steps forward, one step back process

The teachable moment: engaging students in social justice movements

Social justice has long been at the forefront of the core values of the social work profession. Social workers are charged to confront social injustices and advocate for social change. In 2014, there was a societal response across the United States to the deaths of two African-American men, Mike Brown and Eric Garner, and the decision to not indict the police officers who killed them. The collective reaction was reflective of a country unsettled by the criminal justice system’s ongoing acceptance of structural discrimination. This article will focus on one university’s social work faculty’s collective response to the brutal killings of African-American men by police officers. With a main campus located in the suburbs and a satellite campus situated in a major city, the faculty felt compelled to guide students from both campuses through an understanding of what was happening locally and nationally by facilitating forums and programs to engage in dialog, not only in the classroom, but throughout the campus community. The concept of the living classroom is introduced and applied as a way to combat discrimination and advocate for social justice and human rights

Alcohol and HIV Decrease Proteasome and Immunoproteasome Function in Macrophages: Implications for Impaired Immune Function During Disease

Proteasomes (proteinase complexes, PR) and immunoproteasomes (IPR) degrade damaged proteins and affect protein processing required for antigen presentation by mononuclear phagocytes. These critical immune processes are attenuated during progressive HIV-1 infection and are affected by alcohol abuse. To investigate the mechanisms underlying these functional changes, we measured PR and CYP2E1 activities [an ethanol (EtOH) metabolizing enzyme] and reactive oxygen species (ROS) in human monocyte-derived macrophages (MDM) following HIV-1 infection and EtOH treatment. We observed progressive declines of PR activity and PR/IPR contents in HIV-1-infected MDM. PR activity and IPR expression increased after IFN-γ stimulation but reduced after HIV-1 infection. EtOH inhibited both IFN-γ -induced PR and IPR. Paradoxically, EtOH attenuated PR catalytic activity in infected MDM and suppressed viral replication. Elevated ROS followed EtOH exposure and paralleled decreased PR activity. The latter was restored by anti-oxidant. The data support the notion that HIV-1 infection and EtOH may work in concert to affect immune function including antigen presentation and thereby affect disease progression

Fluid Flow Thermometry Using Thermographic Phosphors

Phosphor thermometry is a non-intrusive thermometry technique that allows for spatially and temporally resolved surface temperature measurements. The thermographic method has been employed in a number of applications that include combustion, sprays, and gas flows. In the current work, we investigate the implementation of thermographic phosphors in liquid flows, which is of interest in a wide range of applications in heat transfer, fluid mechanics, and thermal systems. Zinc oxide doped with Zinc (ZnO:Zn) was the phosphor employed for experimentation due to its high emission intensity and insolubility. In order to explore this application, the phosphor powder was uniformly dispersed in water using a magnetic stirring rod. The phosphor was excited by the third harmonic 355 nm output of a Nd:YAG laser, and the luminescence was examined using a fiber-coupled spectrometer. Analysis of the spectral data showed a significant redshift as the temperature approached boiling point. Further characterization of effects of temperature and experimental parameters such as ZnO:Zn concentration on the luminescence signal was performed

Lipophagy and Alcohol-Induced Fatty Liver

This review describes the influence of ethanol consumption on hepatic lipophagy, a selective form of autophagy during which fat-storing organelles known as lipid droplets (LDs) are degraded in lysosomes. During classical autophagy, also known as macroautophagy, all forms of macromolecules and organelles are sequestered in autophagosomes, which, with their cargo, fuse with lysosomes, forming autolysosomes in which the cargo is degraded. It is well established that excessive drinking accelerates intrahepatic lipid biosynthesis, enhances uptake of fatty acids by the liver from the plasma and impairs hepatic secretion of lipoproteins. All the latter contribute to alcohol-induced fatty liver (steatosis). Here, our principal focus is on lipid catabolism, specifically the impact of excessive ethanol consumption on lipophagy, which significantly influences the pathogenesis alcohol-induced steatosis. We review findings, which demonstrate that chronic ethanol consumption retards lipophagy, thereby exacerbating steatosis. This is important for two reasons: (1) Unlike adipose tissue, the liver is considered a fat-burning, not a fat-storing organ. Thus, under normal conditions, lipophagy in hepatocytes actively prevents lipid droplet accumulation, thereby maintaining lipostasis; (2) Chronic alcohol consumption subverts this fat-burning function by slowing lipophagy while accelerating lipogenesis, both contributing to fatty liver. Steatosis was formerly regarded as a benign consequence of heavy drinking. It is now recognized as the first hit in the spectrum of alcohol-induced pathologies that, with continued drinking, progresses to more advanced liver disease, liver failure, and/or liver cancer. Complete lipid droplet breakdown requires that LDs be digested to release their high-energy cargo, consisting principally of cholesteryl esters and triacylglycerols (triglycerides). These subsequently undergo lipolysis, yielding free fatty acids that are oxidized in mitochondria to generate energy. Our review will describe recent findings on the role of lipophagy in LD catabolism, how continuous heavy alcohol consumption affects this process, and the putative mechanism(s) by which this occurs

Lipophagy and Alcohol-Induced Fatty Liver

This review describes the influence of ethanol consumption on hepatic lipophagy, a selective form of autophagy during which fat-storing organelles known as lipid droplets (LDs) are degraded in lysosomes. During classical autophagy, also known as macroautophagy, all forms of macromolecules and organelles are sequestered in autophagosomes, which, with their cargo, fuse with lysosomes, forming autolysosomes in which the cargo is degraded. It is well established that excessive drinking accelerates intrahepatic lipid biosynthesis, enhances uptake of fatty acids by the liver from the plasma and impairs hepatic secretion of lipoproteins. All the latter contribute to alcohol-induced fatty liver (steatosis). Here, our principal focus is on lipid catabolism, specifically the impact of excessive ethanol consumption on lipophagy, which significantly influences the pathogenesis alcohol-induced steatosis. We review findings, which demonstrate that chronic ethanol consumption retards lipophagy, thereby exacerbating steatosis. This is important for two reasons: (1) Unlike adipose tissue, the liver is considered a fat-burning, not a fat-storing organ. Thus, under normal conditions, lipophagy in hepatocytes actively prevents lipid droplet accumulation, thereby maintaining lipostasis; (2) Chronic alcohol consumption subverts this fat-burning function by slowing lipophagy while accelerating lipogenesis, both contributing to fatty liver. Steatosis was formerly regarded as a benign consequence of heavy drinking. It is now recognized as the “first hit” in the spectrum of alcohol-induced pathologies that, with continued drinking, progresses to more advanced liver disease, liver failure, and/or liver cancer. Complete lipid droplet breakdown requires that LDs be digested to release their high-energy cargo, consisting principally of cholesteryl esters and triacylglycerols (triglycerides). These subsequently undergo lipolysis, yielding free fatty acids that are oxidized in mitochondria to generate energy. Our review will describe recent findings on the role of lipophagy in LD catabolism, how continuous heavy alcohol consumption affects this process, and the putative mechanism(s) by which this occurs

Lipid Droplet Membrane Proteome Remodeling Parallels Ethanol-Induced Hepatic Steatosis and its Resolution

Lipid droplets (LDs) are composed of neutral lipids enclosed in a phospholipid monolayer, which harbors membrane-associated proteins that regulate LD functions. Despite the crucial role of LDs in lipid metabolism, remodeling of LD protein composition in disease contexts, such as steatosis, remains poorly understood. We hypothesized that chronic ethanol consumption, subsequent abstinence from ethanol, or fasting differentially affects the LD membrane proteome content and that these changes influence how LDs interact with other intracellular organelles. Here, male Wistar rats were pair-fed liquid control or ethanol diets for 6 weeks, and then, randomly chosen animals from both groups were either refed a control diet for 7 days or fasted for 48 h before euthanizing. From all groups, LD membrane proteins from purified liver LDs were analyzed immunochemically and by MS proteomics. Liver LD numbers and sizes were greater in ethanol-fed rats than in pair-fed control, 7-day refed, or fasted rats. Compared with control rats, ethanol feeding markedly altered the LD membrane proteome, enriching LD structural perilipins and proteins involved in lipid biosynthesis, while lowering LD lipase levels. Ethanol feeding also lowered LD-associated mitochondrial and lysosomal proteins. In 7-day refed (i.e., ethanol-abstained) or fasted-ethanol-fed rats, we detected distinct remodeling of the LD proteome, as judged by lower levels of lipid biosynthetic proteins, and enhanced LD interaction with mitochondria and lysosomes. Our study reveals evidence of significant remodeling of the LD membrane proteome that regulates ethanol-induced steatosis, its resolution after withdrawal and abstinence, and changes in LD interactions with other intracellular organelles

Lipid droplet membrane proteome remodeling parallels ethanol-induced hepatic steatosis and its resolution

Abstract Lipid droplets (LDs) are composed of neutral lipids enclosed in a phospholipid monolayer, which harbors membrane-associated proteins that regulate LD functions. Despite the crucial role of LDs in lipid metabolism, remodeling of LD protein composition in disease contexts, such as steatosis, remains poorly understood. We hypothesized that chronic ethanol consumption, subsequent abstinence from ethanol, or fasting differentially affects the LD membrane proteome content and that these changes influence how LDs interact with other intracellular organelles. Here, male Wistar rats were pair-fed liquid control or ethanol diets for 6 weeks, and then, randomly chosen animals from both groups were either refed a control diet for 7 days or fasted for 48 h before euthanizing. From all groups, LD membrane proteins from purified liver LDs were analyzed immunochemically and by MS proteomics. Liver LD numbers and sizes were greater in ethanolfed rats than in pair-fed control, 7-day refed, or fasted rats. Compared with control rats, ethanol feeding markedly altered the LD membrane proteome, enriching LD structural perilipins and proteins involved in lipid biosynthesis, while lowering LD lipase levels. Ethanol feeding also lowered LDassociated mitochondrial and lysosomal proteins. In 7-day refed (i.e., ethanol-abstained) or fasted-ethanolfed rats, we detected distinct remodeling of the LD proteome, as judged by lower levels of lipid biosynthetic proteins, and enhanced LD interaction with mitochondria and lysosomes. Our study reveals evidence of significant remodeling of the LD membrane proteome that regulates ethanol-induced steatosis, its resolution after withdrawal and abstinence, and changes in LD interactions with other intracellular organelles

Natural Recovery by the Liver and Other Organs after Chronic Alcohol Use

Chronic, heavy alcohol consumption disrupts normal organ function and causes structural damage in virtually every tissue of the body. Current diagnostic terminology states that a person who drinks alcohol excessively has alcohol use disorder. The liver is especially susceptible to alcohol-induced damage. This review summarizes and describes the effects of chronic alcohol use not only on the liver, but also on other selected organs and systems affected by continual heavy drinking-including the gastrointestinal tract, pancreas, heart, and bone. Most significantly, the recovery process after cessation of alcohol consumption (abstinence) is explored. Depending on the organ and whether there is relapse, functional recovery is possible. Even after years of heavy alcohol use, the liver has a remarkable regenerative capacity and, following alcohol removal, can recover a significant portion of its original mass and function. Other organs show recovery after abstinence as well. Data on studies of both heavy alcohol use among humans and animal models of chronic ethanol feeding are discussed. This review describes how (or whether) each organ/tissue metabolizes ethanol, as metabolism influences the organ\u27s degree of injury. Damage sustained by the organ/tissue is reviewed, and evidence for recovery during abstinence is presented

The Origin of the Virgo Stellar Substructure

We present three-dimensional space velocities of stars selected to be consistent with membership in the Virgo stellar substructure. Candidates were selected from SA 103, a single 40x40 arcmin field from our proper motion (PM) survey in Kapteyn's Selected Areas (SAs), based on the PMs, SDSS photometry, and follow-up spectroscopy of 215 stars. The signature of the Virgo substructure is clear in the SDSS color-magnitude diagram (CMD) centered on SA 103, and 16 stars are identified that have high Galactocentric-frame radial velocities (V_GSR > 50 km/s) and lie near the CMD locus of Virgo. The implied distance to the Virgo substructure from the candidates is 14+/-3 kpc. We derive mean kinematics from these 16 stars, finding a radial velocity V_GSR = 153+/-22 km/s and proper motions (mu_alpha*cos(delta), mu_delta) = (-5.24, -0.91)+/-(0.43, 0.46) mas/yr. From the mean kinematics of these members, we determine that the Virgo progenitor was on an eccentric (e ~ 0.8) orbit that recently passed near the Galactic center (pericentric distance R_p ~ 6 kpc). This destructive orbit is consistent with the idea that the substructure(s) in Virgo originated in the tidal disruption of a Milky Way satellite. N-body simulations suggest that the entire cloud-like Virgo substructure (encompassing the "Virgo Overdensity" and the "Virgo Stellar Stream") is likely the tidal debris remnant from a recently-disrupted massive (~10^9 M_sun) dwarf galaxy. The model also suggests that some other known stellar overdensities in the Milky Way halo (e.g., the Pisces Overdensity and debris near NGC 2419 and SEGUE 1) are explained by the disruption of the Virgo progenitor.Comment: Accepted to ApJ; preprint format, 41 pages, 17 figures (some with degraded resolution). Full-resolution version (in emulateapj format) available at http://homepages.rpi.edu/~carlij/virgo_paper/carlin_etal2012_virgo.pd