‘Everything … as a Gloss on Everything Else' : Life and Work in Paul Auster

The thesis examines a variety of philosophical implications in Paul Auster’s works, crossing American culture with Continental thought. Focusing on such subjects as solitude, community, the idea of America, the idea of the work (of art), the ontology of film, the disastrous and the ordinary, it aims to develop intersections of Auster’s works with the thoughts of Stanley Cavell and Maurice Blanchot. Blanchot has already been introduced into recent Auster criticism. But this is not the main reason why I use Cavell, instead of Blanchot, to set the tone for my study. Contrary to past research, which tends to divide into discrete areas, emphasising either Auster’s postmodern textuality or critical engagement, his American roots or European affiliations, my study is concerned with how these divisions can be reassessed and negotiated. A Cavellian reading of Auster is valuable not only because the themes Cavell discovers in Thoreau and Emerson (such as Moral Perfectionism) provide insight into Auster’s engagement with American Transcendentalism, but also because his way of reading is indissociable from his interests in Continental tradition, as well as in film and literature. I share these interests in my own reading of Auster; they help reconstruct the pictures of life and work, of self and other, of singularity and commonality, of ordinariness and extraordinariness. Additionally, I look at certain Blanchotian aspects of Auster’s writing, highlighting what has not been previously noted, such as the withdrawal and exigency of community in Moon Palace. Blanchot’s ideas of unworking (désoeuvrement) and disaster further define the ethico-ontological dimension of being. This does not essentially counter Cavell’s emphasis on the ordinary but rather reveals its difficulty. On the whole my reading suggests a logic of eternal return that underlies the entwinement of Cavellian and Blanchotian strands in Auster, which reflects both human vulnerability and responsibility

Regulation of RhoA/ROCK1 signaling pathway by miR 26b in sepsis induced acute lung injury

Purpose: To investigate the role of miR-26b in the regulation of RhoA/ ROCK1 signaling pathway in acute lung injury (ALI) caused by sepsis. Methods: Thirty male rats were randomized into sham group (SG), cecal ligation and puncture (CLP) group (CG) and miR-26b mimic group (MG). Hematoxylin and eosin (H & E) staining assay was performed to determine the pathological characteristics of rat lung tissues in each group, while enzyme-linked immunosorbent assay (ELISA) was conducted to determine TNF-α and IL-1β levels. The miR-26b expression was evaluated by quantitative reverse transcription polymerase chain reaction (qRT-PCR), while RhoA and Rock1 protein levels were assessed using western blotting. Results: The CG had significant lung injury in comparison with the SG. There were significant elevation in TNF-α and IL-1β levels (p < 0.05). RhoA and ROCK1 levels in lung tissue were noticeably elevated in CG (p < 0.05). After treatment, lung injury in MG was reduced in contrast to CG. The MG showed statistically significant decrease (p < 0.05) in the levels of TNF-α and IL-1β, while the lung tissue mRNA expression and the RhoA and ROCK1 expression levels were significantly reduced in MG (p < 0.05). Conclusion: The MiR-26b mimics plays an important role in the treatment of ALI induced by sepsis in rats by regulating RhoA/ROCK1 signaling pathway. Thus, the findings of this study provide a theoretical basis for clinical studies on the use of miR-26b in the therapy of sepsis

Non-equilibrium behaviour in coacervate-based protocells under electric-field-induced excitation

Although numerous strategies are now available to generate rudimentary forms of synthetic cell-like entities, minimal progress has been made in the sustained excitation of artificial protocells under non-equilibrium conditions. Here we demonstrate that the electric field energization of coacervate microdroplets comprising polylysine and short single strands of DNA generates membrane-free protocells with complex, dynamical behaviours. By confining the droplets within a microfluidic channel and applying a range of electric field strengths, we produce protocells that exhibit repetitive cycles of vacuolarization, dynamical fluctuations in size and shape, chaotic growth and fusion, spontaneous ejection and sequestration of matter, directional capture of solute molecules, and pulsed enhancement of enzyme cascade reactions. Our results highlight new opportunities for the study of non-equilibrium phenomena in synthetic protocells, provide a strategy for inducing complex behaviour in electrostatically assembled soft matter microsystems and illustrate how dynamical properties can be activated and sustained in microcompartmentalized media.</p

MiR-455 targeting SOCS3 improve liver lipid disorders in diabetic mice

MiR-455 has been verified a key regulator of brown adipose tissue and adipose tissue-specific overexpression of miR-455 (ap2-miR-455) mice could combat high-fat-diet-induced obesity. This study is to verify overexpression of miR-455 could ameliorate the lipid accumulation and metabolism in the liver of db/db diabetic mice and explore the potential mechanisms. Diabetic mice (db/db) and control mice (db/m) were randomly divided into four groups. After overexpression of miR-455 in the liver of db/db mice, the triglycerides level in both serum and liver decreased, the lipid deposit in liver was improved, the expression of fatty acid synthase, stearoyl-CoA desaturase 1, sterol regulatory element binding protein 1c (SREBP-1c) and acetyl-CoA carboxylase (ACCα) was also significantly down-regulated. TargetScan indicated that suppressor of cytokine signalling 3 (SOCS3) is predicated to target miR-455 and the protein of SOCS3 in the liver of db/db mice after intervention was significantly decreased. The dual luciferase reporter assay showed that SOCS3 was target gene of miR-455. In vitro, in Palmitate (PA)-stimulated human normal liver (LO2) cells, transfected miR-455 mimic could significantly inhibit the expression of SOCS3, while transfected miR-455 inhibitor could up-regulate the expression of SOCS3. Transfecting LO2 cells with siRNA of SOCS3 could significantly down-regulate the protein expression of SREBP-1c and ACCα. Our study showed that overexpression of miR-455 in the liver could improve lipid metabolism in diabetic mice by down-regulating its target gene SOCS3

Arecoline induces dual modulation of blood pressure in rat, including an initial downregulation and a subsequent upregulation

Purpose: To determine the role of arecoline in cardiovascular modulation in rats.Methods: After rats were anaesthetized with intraperitoneal urethane (1.4 g/kg body weight), saline or arecoline (at doses of 1.0, 3.0 and 10.0 mg/kg) was intraperitoneally administered, and blood pressure (BP) was continuously recorded using a physiological apparatus. Mean arterial pressure (MAP), maximum changes in MAP and reaction time due to arecoline stimulations were calculated and analyzed.Results: Arecoline induced biphasic modulation in BP, including an initial downregulation followed by a subsequent upregulation. The MAP and maximum change in MAP exhibited a concentration-dependent effect in the downregulation phase (p &lt; 0.001 within each group), but not in the upregulation phase (p &gt; 0.05 within each group), while BP reaction time showed a dose-dependent prolongation in both downregulation and upregulation phases (ps &lt; 0.01 within each group). Remarkably, arecoline-induced BP downregulation more rapidly and drastically than upregulation in each arecoline group.Conclusion: These results indicate that arecoline exerts a complex effect in cardiovascular modulation that should be considered as side effects in the clinical use of arecoline and/or with the habitual chewing of areca nuts. Keywords: Arecoline, Blood pressure, Downregulation, Upregulatio