Systemic risk determinants in the European banking industry during financial crises, 2006-2012

The recent financial turmoil has stimulated a rich debate in banking and financial literature on the identification of systemic risk determinants and devices to forecast and prevent crises. This paper explores the contribution of corporate variables to systemic risk using the CoVaR approach (Adrian and Brunnermeier, 2016). Using balanced panel data on 141 European banks from 24 countries, which were listed from 2006Q1 to 2012Q4, we investigated the impact of corporate variables during the three regimes that characterised the European banking sector-the subprime crisis (2007Q3-2008Q3), the European Great Financial Depression (2008Q4-2010Q2), and the sovereign debt crisis (2010Q3-2012Q4). Our results show that size did not play a significant role in spreading systemic risk, while maturity mismatch did. However, the nature and intensity of these two determinants varied across the three regimes

Fatal infection with Taenia martis metacestodes in a ring-tailed lemur (Lemur catta) living in an Italian zoological garden

A case of fatal infection caused by larval forms of Taenia martis in a ring-tailed lemur (Lemur catta) living in the Rome zoological garden is described. The animal, living in a semi-natural pen with other 15 conspecific individuals and being fed with fresh fruit and vegetables, yoghurt and eggs, was transported to the Istituto Zooprofilattico of Rome for post-mortem examination. The anamnesis included, ten days before the death, apathy, lack of appetite, abdominal distension and diarrhoea. A severe exudative fibrinous-purulent peritonitis with numerous adhesions between the abdominal wall and the bowel loops was detected. After intestine removal, two free and viable, 4cm long, whitish, leaf-like parasitic forms were pinpointed. Macroscopic examination of the two parasites allowed their identification as larval stages of cestodes, identified via molecular analysis as T. martis metacestodes. This report represents the first record of T. martis infection in the host species and in a zoological garden and for the pathological relevance of the infection

B-cell chronic lymphocytic leukaemia in an African lion (Panthera leo)

A 15-year-old female African lion (Panthera leo) maintained at the Zoological Garden of Pistoia, Tuscany (Italy), showed signs of malaise, dyspnoea, tremors, pale mucous membranes and ataxia for two days prior to death. Complete blood count showed anaemia, thrombocytopaenia and severe lymphocytosis. At autopsy, the most relevant finding was severe, generalised splenomegaly. Histologically, high numbers of neoplastic lymphocytes diffusely infiltrated the spleen, liver, heart, pancreas, kidney and lungs. The lymphoid cells were positive for CD79a and negative for CD3 on immunohistochemistry. The histologic features of the neoplastic cells and their immunophenotype are consistent with B-cell lymphocytes. Based on surface membrane co-expression of immunoglobulin M and immunoglobulin D in most neoplastic cells, which indicated that they were naïve, antigen-inexperienced and mature circulating resting B-cells, and consistent with their appearance as small lymphocytes with high nuclear-to-cytoplasmic ratios, a diagnosis of B-cell chronic lymphocytic leukaemia was made

State of the art on approved cystic fibrosis transmembrane conductance regulator (Cftr) modulators and triple-combination therapy

Cystic fibrosis (CF) is the most common life-limiting inherited disease in Caucasian populations, affecting approximately 80,000 people worldwide. CF is a complex multi-organ monogenic autosomal recessive disorder caused by a mutation in cystic fibrosis transmembrane conductance regulator (CFTR) gene. Since the discovery of the CFTR gene in 1989, more than 2000 mutations have been identified so far and about 240 can cause CF. Until recently, the treatment for CF was aimed to prevent and manage the manifestations of CFTR dysfunction, primarily recurrent pulmonary infections and pancreatic exocrine failure. Over the past few decades, the therapeutic approach to CF has been revolutionized by the development of a new class of small molecules called CFTR modulators that target specific defects caused by mutations in the CFTR gene. CFTR modulators have been shown to change profoundly the clinical course of the CF, leading to meaningful improvements in the lives of a large proportion of people of CF heterozygous for F508del, especially if started in young children. Further studies are needed to extend the use of triple CFTR modulation therapy also for young children in order to prevent the irreversible effects of the disease and for patients with very rare mutations with a personalized approach to treatment

How i do it: laparoscopic implantation of lower esophageal sphincter stimulator for the treatment of gastro-esophageal reflux disease

The principal medical treatment of gastro-esophageal reflux disease (GERD) is proton pump inhibitor (PPI) therapy. PPI lowers gastric acid secretion, but its long-term use is not free from adverse effects. However, PPI therapy has no effects on the dysfunctional lower esophageal sphincter (LES) and on reflux of stomach contents. Prior to the introduction of medical therapy, surgical gastric fundoplication was originally proposed in order to create a mechanical valve to prevent reflux. The postoperative results obtained after fundoplication depend on the surgical volume of the centers in which surgery is performed, and important functional sequelae, including dysphagia and gas bloat syndrome, have been reported. LES electrical stimulation therapy (EST) has been recently introduced as an alternative treatment option in the management of GERD. The rationale of this strategy is to electrically stimulate the LES in order to increase its tone and to reduce reflux. LES stimulator implantation is a feasible and safe minimally invasive technique. Data reported in the literature regarding the postoperative functional outcomes related to GERD, evaluated by 24 h-pH-manometry, and GERD specific questionnaire after the implantation of LES-EST, show significant improvement at both short and long-term follow up, up to three years after surgery. Although these data are encouraging, further prospective and randomized studies are required to draw definitive conclusions. We report the technique of laparoscopic LES stimulator surgical implantation, together with an explanatory video

Proteomic Analysis of GLUT4 Storage Vesicles Reveals Tumor Suppressor Candidate 5 (TUSC5) as a Novel Regulator of Insulin Action in Adipocytes.

Insulin signaling augments glucose transport by regulating glucose transporter 4 (GLUT4) trafficking from specialized intracellular compartments, termed GLUT4 storage vesicles (GSVs), to the plasma membrane. Proteomic analysis of GSVs by mass spectrometry revealed enrichment of 59 proteins in these vesicles. We measured reduced abundance of 23 of these proteins following insulin stimulation and assigned these as high confidence GSV proteins. These included established GSV proteins such as GLUT4 and insulin-responsive aminopeptidase, as well as six proteins not previously reported to be localized to GSVs. Tumor suppressor candidate 5 (TUSC5) was shown to be a novel GSV protein that underwent a 3.7-fold increase in abundance at the plasma membrane in response to insulin. siRNA-mediated knockdown of TUSC5 decreased insulin-stimulated glucose uptake, although overexpression of TUSC5 had the opposite effect, implicating TUSC5 as a positive regulator of insulin-stimulated glucose transport in adipocytes. Incubation of adipocytes with TNFα caused insulin resistance and a concomitant reduction in TUSC5. Consistent with previous studies, peroxisome proliferator-activated receptor (PPAR) γ agonism reversed TNFα-induced insulin resistance. TUSC5 expression was necessary but insufficient for PPARγ-mediated reversal of insulin resistance. These findings functionally link TUSC5 to GLUT4 trafficking, insulin action, insulin resistance, and PPARγ action in the adipocyte. Further studies are required to establish the exact role of TUSC5 in adipocytes

Three Month Follow-Up of Patients With COVID-19 Pneumonia Complicated by Pulmonary Embolism

Background: Previous studies have demonstrated persistent dyspnoea and impairment of respiratory function in the follow-up of patients who have recovered from COVID-19 pneumonia. However, no studies have evaluated the clinical and functional consequences of COVID-19 pneumonia complicated by pulmonary embolism. Objective: The aim of our study was to assess the pulmonary function and exercise capacity in COVID-19 patients 3 months after recovery from pneumonia, either complicated or not by pulmonary embolism. Methods: This was a retrospective, single-centre, observational study involving 68 adult COVID-19 patients with a positive/negative clinical history of pulmonary embolism (PE) as a complication of COVID-19 pneumonia. Three months after recovery all patients underwent spirometry, diffusion capacity of the lungs for carbon monoxide (DLCO), and 6 minute walk test (6MWT). In addition, high-resolution computed tomography (HRCT) of the lung was carried out and CT-pulmonary angiography was conducted only in the PE+ subgroup. Patients with a previous diagnosis of PE or chronic lung diseases were excluded from the study. Results: Of the 68 patients included in the study, 24 had previous PE (PE+) and 44 did not (PE-). In comparison with the PE- subgroup, PE+ patients displayed a FVC% predicted significantly lower (87.71 ± 15.40 vs 98.7 ± 16.7, p = 0.009) and a significantly lower DLCO% predicted (p = 0.023). In addition, a higher percentage of patients were dyspnoeic on exercise, as documented by a mMRC score ≥1 (75% vs 54.3%, p < 0.001) and displayed a SpO2 <90% during 6MWT (37.5% vs 0%, p < 0.001). HRCT features suggestive of COVID-19 pneumonia resolution phase were present in both PE+ and PE- subjects without any significant difference (p = 0.24) and abnormalities at CT pulmonary angiography were detected in 57% of the PE+ subgroup. Conclusion: At the 3 month follow-up, the patients who recovered from COVID-19 pneumonia complicated by PE showed more dyspnoea and higher impairment of pulmonary function tests compared with those without PE

Metabolomic analysis of insulin resistance across different mouse strains and diets

Insulin resistance is a major risk factor for many diseases. However, its underlying mechanism remains unclear in part because it is triggered by a complex relationship between multiple factors, including genes and the environment. Here, we used metabolomics combined with computational methods to identify factors that classified insulin resistance across individual mice derived from three different mouse strains fed two different diets. Three inbred ILSXISS strains were fed high-fat or chow diets and subjected to metabolic phenotyping and metabolomics analysis of skeletal muscle. There was significant metabolic heterogeneity between strains, diets, and individual animals. Distinct metabolites were changed with insulin resistance, diet, and between strains. Computational analysis revealed 113 metabolites that were correlated with metabolic phenotypes. Using these 113 metabolites, combined with machine learning to segregate mice based on insulin sensitivity, we identified C22:1-CoA, C2-carnitine, and C16-ceramide as the best classifiers. Strikingly, when these three metabolites were combined into one signature, they classified mice based on insulin sensitivity more accurately than each metabolite on its own or other published metabolic signatures. Furthermore, C22:1-CoA was 2.3-fold higher in insulin-resistant mice and correlated significantly with insulin resistance. We have identified a metabolomic signature composed of three functionally unrelated metabolites that accurately predicts whole-body insulin sensitivity across three mouse strains. These data indicate the power of simultaneous analysis of individual, genetic, and environmental variance in mice for identifying novel factors that accurately predict metabolic phenotypes like whole-body insulin sensitivity

Understanding how parents deal with the health advice they receive: A qualitative study and implications for the design of message-based health dissemination systems for child health

Message-based health information dissemination systems can potentially improve maternal and child health (MCH). By conveying health information to parents, SMS- and chatbot-based systems can support parents’ learning and empower them to make better health decisions for their children. However, there is limited design advice for creating message-based dissemination systems for MCH. To help address this gap, we conducted 14 participatory workshops with 42 parents from Portugal and South Africa, exploring how parents learned to care for their children’s health. Our findings showed how parents reflected on the health advice they received, by assessing the fit of the advice to their child’s characteristics, their values and beliefs, the advice’s feasibility, or the intention and competence of the advice giver. Based on these insights, we propose four design implications for creating message-based health information dissemination systems tailored to parents and their children

Mitochondrial CoQ deficiency is a common driver of mitochondrial oxidants and insulin resistance.

Insulin resistance in muscle, adipocytes and liver is a gateway to a number of metabolic diseases. Here, we show a selective deficiency in mitochondrial coenzyme Q (CoQ) in insulin-resistant adipose and muscle tissue. This defect was observed in a range of in vitro insulin resistance models and adipose tissue from insulin-resistant humans and was concomitant with lower expression of mevalonate/CoQ biosynthesis pathway proteins in most models. Pharmacologic or genetic manipulations that decreased mitochondrial CoQ triggered mitochondrial oxidants and insulin resistance while CoQ supplementation in either insulin-resistant cell models or mice restored normal insulin sensitivity. Specifically, lowering of mitochondrial CoQ caused insulin resistance in adipocytes as a result of increased superoxide/hydrogen peroxide production via complex II. These data suggest that mitochondrial CoQ is a proximal driver of mitochondrial oxidants and insulin resistance, and that mechanisms that restore mitochondrial CoQ may be effective therapeutic targets for treating insulin resistance