Non-Places in Postwar Italian Film: Roma Città Aperta, Ladri di Biciclette, and Le Mani sulla Città

This work analyzes three postwar Italian films in the context of how spaces and places are portrayed through humanistic geographical conceptions of space and place such as Marc Augé’s ‘non-places’. Augé describes non-places as places which cannot be defined as relational, historical, or concerned with identity. Augé uses a poem of Baudelaire to say, if the spire of a church is a place, the chimney of a factory is a non-place. The most archetypal examples of non-places, he says, would be train stations and airports. From this, I will analyze Italy’s relationship with places and non-places through its films. As a modernized country with an extremely rich history, ever present on the landscape, Italy has a unique relationship with its places. Films such as Roma Città Aperta (Rossellini 1945), Ladri di Biciclette (De Sica 1948), and Le Mani Sulla Città (Rosi 1963) reveal the wariness or even disdain many Italians have had for non-places, lacking the cultural significance and alike in which their places are steeped. Through such film analysis I will examine Italy under the guiding question of those like Augé, Tuan, and Relph: how do people relate to the places they inhabit as the world moves forward, and as non-places like train stations and airports appear and places like cathedrals and ruins become spectacles and tourist attractions?Bachelor of Art

Diacylglycerol Kinase β Knockout Mice Exhibit Attention-Deficit Behavior and an Abnormal Response on Methylphenidate-Induced Hyperactivity

BACKGROUND: Diacylglycerol kinase (DGK) is an enzyme that phosphorylates diacylglycerol to produce phosphatidic acid. DGKβ is one of the subtypes of the DGK family and regulates many intracellular signaling pathways in the central nervous system. Previously, we demonstrated that DGKβ knockout (KO) mice showed various dysfunctions of higher brain function, such as cognitive impairment (with lower spine density), hyperactivity, reduced anxiety, and careless behavior. In the present study, we conducted further tests on DGKβ KO mice in order to investigate the function of DGKβ in the central nervous system, especially in the pathophysiology of attention deficit hyperactivity disorder (ADHD). METHODOLOGY/PRINCIPAL FINDINGS: DGKβ KO mice showed attention-deficit behavior in the object-based attention test and it was ameliorated by methylphenidate (MPH, 30 mg/kg, i.p.). In the open field test, DGKβ KO mice displayed a decreased response to the locomotor stimulating effects of MPH (30 mg/kg, i.p.), but showed a similar response to an N-methyl-d-aspartate (NMDA) receptor antagonist, MK-801 (0.3 mg/kg, i.p.), when compared to WT mice. Examination of the phosphorylation of extracellular signal-regulated kinase (ERK), which is involved in regulation of locomotor activity, indicated that ERK1/2 activation induced by MPH treatment was defective in the striatum of DGKβ KO mice. CONCLUSIONS/SIGNIFICANCE: These findings suggest that DGKβ KO mice showed attention-deficit and hyperactive phenotype, similar to ADHD. Furthermore, the hyporesponsiveness of DGKβ KO mice to MPH was due to dysregulation of ERK phosphorylation, and that DGKβ has a pivotal involvement in ERK regulation in the striatum

2,2′-(Biphenyl-2,2′-diyldi­oxy)diaceto­hydrazide

In the mol­ecule of the title compound, C16H18N4O4, the dihedral angle between the mean planes of the two benzene rings is 56.76 (5)°. The crystal structure reveals extensive inter­molecular hydrogen bonds between carbonyl O atoms and primary amines, as well as between primary and secondary amines of hydrazide, forming rings of R 2 2(10) and R 2 2(6) motifs, respectively. The structure is further stabilized by intra­molecular and non-classical hydrogen bonds of the types N—H⋯O and C—H⋯O, respectively. The structure does not show any π–π inter­actions

SGLT5 Reabsorbs Fructose in the Kidney but Its Deficiency Paradoxically Exacerbates Hepatic Steatosis Induced by Fructose

Although excessive fructose intake is epidemiologically linked with dyslipidemia, obesity, and diabetes, the mechanisms regulating plasma fructose are not well known. Cells transfected with sodium/glucose cotransporter 5 (SGLT5), which is expressed exclusively in the kidney, transport fructose in vitro; however, the physiological role of this transporter in fructose metabolism remains unclear. To determine whether SGLT5 functions as a fructose transporter in vivo, we established a line of mice lacking the gene encoding SGLT5. Sodium-dependent fructose uptake disappeared in renal brush border membrane vesicles from SGLT5-deficient mice, and the increased urinary fructose in SGLT5-deficient mice indicated that SGLT5 was the major fructose reabsorption transporter in the kidney. From this, we hypothesized that urinary fructose excretion induced by SGLT5 deficiency would ameliorate fructose-induced hepatic steatosis. To test this hypothesis we compared SGLT5-deficient mice with wild-type mice under conditions of long-term fructose consumption. Paradoxically, however, fructose-induced hepatic steatosis was exacerbated in the SGLT5-deficient mice, and the massive urinary fructose excretion was accompanied by reduced levels of plasma triglycerides and epididymal fat but fasting hyperinsulinemia compared with fructose-fed wild-type mice. There was no difference in food consumption, water intake, or plasma fructose between the two types of mice. No compensatory effect by other transporters reportedly involved in fructose uptake in the liver and kidney were indicated at the mRNA level. These surprising findings indicated a previously unrecognized link through SGLT5 between renal fructose reabsorption and hepatic lipid metabolism

Preventive effect of statin pretreatment on contrast-induced acute kidney injury in patients undergoing coronary angioplasty: Propensity score analysis from a multicenter registry

BackgroundThe prophylactic benefit of statins in reducing the incidence of contrast-induced acute kidney injury (CI-AKI) has been investigated in several studies with conflicting results. We sought to investigate whether statin pretreatment prevents CI-AKI in coronary artery disease (CAD) patients undergoing percutaneous coronary intervention (PCI).MethodsA total of 2198 CAD patients who underwent PCI, except for those undergoing dialysis or who died within 7 days after angioplasty, were analyzed from the ICAS (Ibaraki Cardiovascular Assessment Study) multicenter registry. Analyzed subjects were divided into 2 groups according to statin pretreatment: statin pretreatment (n = 839) and non-statin pretreatment (n = 1359). Selection bias of statin pretreatment was adjusted by propensity score-matching method: pretreatment statin (n = 565) and non-statin pretreatment (n = 565). CI-AKI was defined as an increase in serum creatinine of ≥ 25% or 0.5 mg/dl from baseline within 1 week of contrast medium exposure.ResultsA total of 192 (8.7%) patients developed CI-AKI. No significant differences were observed in baseline patient characteristics between the statin and non-statin pretreatment groups after propensity score matching. In the propensity score-matched groups, the incidence of CI-AKI was significantly lower in patients with statin pretreatment than in those without statin pretreatment (3.5% vs.10.6%, odds ratio [OR]: 0.31, 95% confidence interval [CI]: 0.18–0.52, P < 0.001). Multivariate logistic regression analysis showed that statin pretreatment remained an independent negative predictor of CI-AKI (OR: 0.31, 95% CI: 0.18–0.53, P < 0.001) among propensity score-matched subjects.ConclusionsStatin pretreatment was associated with a significant decrease in the risk of CI-AKI in CAD patients undergoing PCI in the ICAS Registry

Restraint-Induced Expression of Endoplasmic Reticulum Stress-Related Genes in the Mouse Brain

ABSTRACT Depression is a significant public health concern but its pathology remains unclear. Previously, increases in an end

SIRT1 silencing confers neuroprotection through IGF-1 pathway activation

The following study demonstrated that, in in vitro differentiated neurons, SIRT1 silencing induced an increase of IGF-1 protein expression and secretion and of IGF-1R protein levels which, in turn, prolonged neuronal cell survival in presence of an apoptotic insult. On the contrary, SIRT1 overexpression increased cell death. In particular, IGF-1 and IGF-1R expression levels were negatively regulated by SIRT1. In SIRT1 silenced cells, the increase in IGF-1 and IGF-1R expression was associated to an increase in AKT and ERK1/2 phosphorylation. Moreover, neuronal differentiation was reduced in SIRT1 overexpressing cells and increased in SIRT1 silenced cells. We conclude that SIRT1 silenced neurons appear more committed to differentiation and more resistant to cell death through the activation of IGF-1 survival pathway. J. Cell. Physiol. 228: 17541761, 2013. (c) 2013 Wiley Periodicals, Inc