Financial phantasmagoria: corporate image-work in times of crisis

Our purpose in this article is to relate the real movements in the economy during 2008 to the ?image-work? of financial institutions. Over the period January?December 2008 we collected 241 separate advertisements from 61 financial institutions published in the Financial Times. Reading across the ensemble of advertisements for themes and evocative images provides an impression of the financial imaginaries created by these organizations as the global financial crisis unfolded. In using the term ?phantasmagoria? we move beyond its colloquial sense of a set of strange images designed to dazzle towards the more technical connotation used by Ranci�re (2004) who suggested that words and images can offer a trace of an overall determining set-up if they are torn from their obviousness so they become phantasmagoric figures. The key phantasmagoric figure we identify here is that of the financial institution as timeless, immortal and unchanging; a coherent and autonomous entity amongst other actors. This notion of uniqueness belies the commonality of thinking which precipitated the global financial crisis as well as the limited capacity for control of financial institutions in relation to market events. It also functions as a powerful naturalizing force, making it hard to question certain aspects of the recent period of ?capitalism in crisis?

Prospective validation of the bedside sonographic acute cholecystitis score in emergency department patients

Acute cholecystitis can be difficult to diagnose in the emergency department (ED); no single finding can rule in or rule out the disease. A prediction score for the diagnosis of acute cholecystitis for use at the bedside would be of great value to expedite the management of patients presenting with possible acute cholecystitis. The 2013 Tokyo Guidelines is a validated method for the diagnosis of acute cholecystitis but its prognostic capability is limited. The purpose of this study was to prospectively validate the Bedside Sonographic Acute Cholecystitis (SAC) Score utilizing a combination of only historical symptoms, physical exam signs, and point-of-care ultrasound (POCUS) findings for the prediction of the diagnosis of acute cholecystitis in ED patients. This was a prospective observational validation study of the Bedside SAC Score. The study was conducted at two tertiary referral academic centers in Boston, Massachusetts. From April 2016 to March 2019, adult patients (≥18 years old) with suspected acute cholecystitis were enrolled via convenience sampling and underwent a physical exam and a focused biliary POCUS in the ED. Three symptoms and signs (post-prandial symptoms, RUQ tenderness, and Murphy's sign) and two sonographic findings (gallbladder wall thickening and the presence of gallstones) were combined to calculate the Bedside Sonographic Acute Cholecystitis (SAC) Score. The final diagnosis of acute cholecystitis was determined from chart review or patient follow-up up to 30 days after the initial assessment. In patients who underwent operative intervention, surgical pathology was used to confirm the diagnosis of acute cholecystitis. Sensitivity, specificity, PPV and NPV of the Bedside SAC Score were calculated for various cut off points. 153 patients were included in the analysis. Using a previously defined cutoff of ≥ 4, the Bedside SAC Score had a sensitivity of 88.9% (95% CI 73.9%–96.9%), and a specificity of 67.5% (95% CI 58.2%–75.9%). A Bedside SAC Score of < 2 had a sensitivity of 100% (95% CI 90.3%–100%) and specificity of 35% (95% CI 26.5%–44.4%). A Bedside SAC Score of ≥ 7 had a sensitivity of 44.4% (95% CI 27.9%–61.9%) and specificity of 95.7% (95% CI 90.3%–98.6%). A bedside prediction score for the diagnosis of acute cholecystitis would have great utility in the ED. The Bedside SAC Score would be most helpful as a rule out for patients with a low Bedside SAC Score < 2 (sensitivity of 100%) or as a rule in for patients with a high Bedside SAC Score ≥ 7 (specificity of 95.7%). Prospective validation with a larger study is required

The POZ-ZF Transcription Factor Kaiso (ZBTB33) Induces Inflammation and Progenitor Cell Differentiation in the Murine Intestine

<div><p>Since its discovery, several studies have implicated the POZ-ZF protein Kaiso in both developmental and tumorigenic processes. However, most of the information regarding Kaiso’s function to date has been gleaned from studies in <i>Xenopus laevis</i> embryos and mammalian cultured cells. To examine Kaiso’s role in a relevant, mammalian organ-specific context, we generated and characterized a Kaiso transgenic mouse expressing a murine Kaiso transgene under the control of the intestine-specific <i>villin</i> promoter. Kaiso transgenic mice were viable and fertile but pathological examination of the small intestine revealed distinct morphological changes. Kaiso transgenics (<i>Kaiso^Tg/+</i>) exhibited a crypt expansion phenotype that was accompanied by increased differentiation of epithelial progenitor cells into secretory cell lineages; this was evidenced by increased cell populations expressing Goblet, Paneth and enteroendocrine markers. Paradoxically however, enhanced differentiation in <i>Kaiso^Tg/+</i> was accompanied by reduced proliferation, a phenotype reminiscent of Notch inhibition. Indeed, expression of the Notch signalling target HES-1 was decreased in <i>Kaiso^Tg/+</i> animals. Finally, our Kaiso transgenics exhibited several hallmarks of inflammation, including increased neutrophil infiltration and activation, villi fusion and crypt hyperplasia. Interestingly, the Kaiso binding partner and emerging anti-inflammatory mediator p120^ctn is recruited to the nucleus in <i>Kaiso^Tg/+</i> mice intestinal cells suggesting that Kaiso may elicit inflammation by antagonizing p120^ctn function.</p></div

Generation of transgenic mouse lines ectopically expressing <i>villin</i>-Kaiso.

<p>(<b>A</b>) Myc-tagged murine <i>Kaiso</i> cDNA was cloned downstream of the 9 kb v<i>illin</i> promoter sequence. (<b>B</b>) The transgene copy number in each transgenic line was evaluated via PCR. Line A transgenic animals have the greatest copy number. (<b>C</b>) RT-PCR confirmed expression of the Kaiso transgene in <i>villin</i>-expressing tissues of transgenic mice, <i>i.e.</i> the small intestine, large intestine, and kidneys. (<b>D</b>) Immunoblot analysis shows increased Kaiso expression in both small and large intestines in Kaiso transgenic (<i>Kaiso^Tg</i>^/+) Line A mice compared to non-transgenic (Non-Tg) siblings.</p

Secretory cell lineages are expanded in the intestines of <i>Kaiso^Tg</i>^/+ mice.

<p>(<b>A</b>) PAS stain for Goblet cells (black arrowheads) revealed increased numbers of Goblet cells in both the villi and crypts of <i>Kaiso^Tg</i>^/+ intestines, p = 0.011 & 0.002. (<b>B</b>) Lysozyme staining revealed increased Paneth cell numbers in <i>Kaiso^Tg</i>^/+ mice, p = 0.017. (<b>C</b>) Synaptophysin positive enteroendocrine cells (arrowheads) are increased in <i>Kaiso^Tg</i>^/+ mice, p = 0.031. n = 3 mice/genotype; measurements performed by two independent blind observers; T-test used for p-value. ** represents significance.</p

Kaiso transgenic mice exhibit inflammation of the intestinal mucosa.

<p>(<b>A</b>) <b><u>H</u></b>ematoxylin and <b><u>e</u></b>osin (H&E) stained sections were used to measure villi length (red bracket; ∼80 villi/mouse) and crypt depth (black bracket; ∼800 open crypts/mouse). <i>Kaiso^Tg</i>^/+ display increased crypt depth compared to their Non-Tg siblings, p = 0.001. (<b>B</b>) <i>Kaiso^Tg</i>^/+ mice exhibit increased immune cell infiltration of the lamina propria (yellow demarcated area) accompanied by increased MPO activity compared to their Non-Tg siblings, p = 0.014. (<b>C</b>) Line B mice do not exhibit immune cell infiltration or enhanced MPO activity compared to Non-Tg siblings. ** represents significance.</p

Subcellular localization and expression of ectopic Kaiso in Line A <i>Kaiso^Tg</i>^/+ small intestines.

<p><i>Kaiso^Tg</i>^/+ mice display strong nuclear Kaiso in the villi and crypt cells, compared to non-transgenic mice (Non-Tg), which mainly display weak Kaiso staining in the cytoplasm. Additionally, <i>Kaiso^Tg/+</i> mice display strong nuclear c-Myc staining corresponding to ectopic myc-tagged Kaiso expression, while Non-Tg mice display cytoplasmic c-Myc expression.</p

<i>Kaiso^Tg</i>^/+ mice display decreased HES-1 expression in the small intestine.

<p>Both Non-Tg and <i>Kaiso^Tg</i>^/+ tissues displayed nuclear HES-1 expression in the crypts of the small intestine, however <i>Kaiso^Tg</i>^/+ tissue displays significantly decreased HES-1 expression in the villi. Quantitative RT-PCR showed a significant decrease in HES-1 expression in <i>Kaiso^Tg</i>^/+ mice. Values were first normalized to the GAPDH housekeeping gene, followed by normalizing to non-Tg HES-1 expression (** represents p<0.05).</p