Financial Development and Economic Growth: The Case of Chinese Banking Sector

China’s economy has developed rapidly since the introduction of market reforms in 1978. In parallel came the reforms within the financial sector and the most of financial intermediation between savings and investment has been channelled through the banking sector. Thus far studies on the finance-growth nexus in China have focused on the financial sector as a whole. This thesis aims to determine the impact of different banking institutions on economic growth and assess the compatibility of state financial policies with country’s economic performance. The empirical analysis is performed using annual data for the period 1978 to 2005. Using the Granger-causality test procedure under vector autoregressive model I examine the relationship between economic growth and, respectively, different types of banks and different types of loans. The procedure provides evidence that presence and direction of causality is affected by the type of bank as well as type of loan. There is two-way causality between economic growth and policy banks as well as rural credit cooperatives. The development of state-owned commercial banks and other commercial banks merely follows economic growth. Furthermore, loans to construction sector Granger cause growth and there is a one-way causality between growth and loans to commercial sector. The fact that policy banks manage to positively influence China’s development might indicate that state policies concerning financial sector and economic growth are successful. However to sustain the growth it is important to further develop financial services, ensure better credit allocation and improve access to financing for private as well as small and medium-sized enterprises

UAL Research Online Ten Years

The Internet has fundamentally changed the practical and economic realities of distributing academic research. Scholarly knowledge can be digitally archived, and disseminated worldwide, at virtually no cost beyond that of providing it to the first reader. It’s easy to create many copies, easy to share instantly, easy to find publications and practice research, and easy to make many copies available. The historic barriers restricting access to research, scholarship and knowledge are falling. We now have much greater opportunities for reach and impact. UAL is part of the global Open Access movement, committed to removing access barriers to published scholarly research, making knowledge widely and readily available to anybody with an internet connection. UAL provides Open Access to the research produced by staff and PhD students through UAL Research Online. UAL Research Online is an open library of research. Its purpose is to showcase our work to the world, and to open global access to what we do here. Content in UAL Research Online is downloaded by interested users and scholars all over the world; by people who would not otherwise have known of or have access to our research. UAL Research Online was the first scholarly research repository designed specifically for research in arts, design and media. It was built in 2008 and 2009, and was opened to the world ten years ago. We built a light, open source repository designed to hold, share, and care for research with a strong visual component. We provide free, long term, managed storage for research, with clear terms for IP protection and reuse, according to internationally accepted standards. We’re globally accessible regardless of level of technology or connectivity, we are interoperable with other academic systems, and we conform to accepted academic citation style. In its tenth year, UALRO continues to be globally recognised as the most prominent open access collection of original research outputs in arts, design and media. No other online library of this type offers free open access to as large a collection of research within the creative arts. UAL Research Online now contains records of more than ten thousand research outputs. And we make available nearly a hundred thousand individual files, which document, support, and describe these outputs. We’re celebrating our ten year anniversary in 2020, and looking forward to continuing our role in providing free open access to the research we do at UAL

Childhood and the pandemic: Chronicle of an absence foretold

La infancia es el sur del virus, como ha visibilizado la pandemia de COVID-19: un mundo donde el cuidado no es un valor escogido desde el deseo, y donde la voz infantil es silenciada en virtud de una injusticia epistémica ancestral. Así, la transformación que las sociedades humanas están experimentando debido a la COVID-19 ha impactado significativamente en los derechos de la infancia, a niveles micro y macro. En España, como país especialmente golpeado por la pandemia, encontramos que tanto la primera infancia (a través especialmente de la violencia obstétrica) como ella misma en todas sus fases, están siendo víctimas de un paradigma adultocéntrico de control e injusticia epistémica basales. En este ensayo se analiza y discute algunas de las consecuencias negativas observadas en este país con relación al cuidado y el confinamiento de menores y sus familias, acaecidas a raíz de la pandemia, considerando que la crisis desencadenada por la COVID-19 puede ser una oportunidad para visibilizar situaciones de injusticia ancestral para con la niñez.As the COVID-19 pandemic has made visible, childhood is the virus’s proverbial south: a world where care is not a value chosen from a place of desire, and where children’s voices are silenced at the hands of an ancestral epistemic injustice. Thus, the transformation that human societies are undergoing due to COVID-19 has significantly impacted the rights of children, both at the micro and the macro levels. In Spain – a country that has been particularly hard-hit by the pandemic – we find that both infancy (especially through obstetric violence) and childhood at all its stages fall victim to an adultcentric paradigm based on control and epistemic injustice. This essay analyzes and discusses some of the negative consequences observed in this country related to the care for and the confinement of minors and their families – which has occurred as a result of the pandemic – and considers that the crisis triggered by COVID-19 may be an opportunity to shed light on situations of ancestral injustice towards children

Changes in MicroRNA Expression during Rabbit Hemorrhagic Disease Virus (RHDV) Infection.

Current knowledge on the role of microRNAs (miRNAs) in rabbit hemorrhagic disease virus (RHDV) infection and the pathogenesis of rabbit hemorrhagic disease (RHD) is still limited. RHDV replicates in the liver, causing hepatic necrosis and liver failure. MiRNAs are a class of short RNA molecules, and their expression profiles vary over the course of diseases, both in the tissue environment and in the bloodstream. This paper evaluates the expression of miRNAs in the liver tissue (ocu-miR-122-5p, ocu-miR-155-5p, and ocu-miR-16b-5p) and serum (ocu-miR-122-5p) of rabbits experimentally infected with RHDV. The expression levels of ocu-miR-122-5p, ocu-miR-155-5p, and ocu-miR-16b-5p in liver tissue were determined using reverse transcription quantitative real-time PCR (RT-qPCR), and the expression level of circulating ocu-miR-122-5p was established using droplet digital PCR (ddPCR). The expression levels of ocu-miR-155-5p and ocu-miR-16b-5p were significantly higher in the infected rabbits compared to the healthy rabbits (a fold-change of 5.8 and 2.5, respectively). The expression of ocu-miR-122-5p was not significantly di�erent in the liver tissue from the infected rabbits compared to the healthy rabbits (p = 0.990), while the absolute expression level of the circulating ocu-miR-122-5p was significantly higher in the infected rabbits than in the healthy rabbits (p < 0.0001). Furthermore, a functional analysis showed that ocu-miR-155-5p, ocu-miR-16b-5p, and ocu-miR-122-5p can regulate the expression of genes involved in processes correlated with acute liver failure (ALF) in rabbits. Search tool for the retrieval of interacting genes/proteins (STRING) analysis showed that the potential target genes of the three selected miRNAs may interact with each other in di�erent pathways. The results indicate the roles of these miRNAs in RHDV infection and over the course of RHD and may reflect hepatic inflammation and impairment/dysfunction in RHD

Hereditary xerocytosis - spectrum and clinical manifestations of variants in the PIEZO1 gene, including co-occurrence with a novel β-globin mutation

Hereditary xerocytosis (HX) is a rare, autosomal dominant congenital hemolytic anemia (CHA) characterized by erythrocyte dehydration with presentation of various degrees of hemolytic anemia. HX is often misdiagnosed as hereditary spherocytosis or other CHA. Here we report three cases of suspected HX and one case of HX associated with β-thalassemia. Sanger method was used for sequencing cDNA of the PIEZO1 gene. Variants were evaluated for potential pathogenicity by MutationTaster, PROVEAN, PolyPhen-2 and M-CAP software, and by molecular modeling. Four different variants in the PIEZO1 gene were found, including three substitutions (p.D669H, p.D1566G, p.T1732 M) and one deletion (p.745delQ). In addition, in the patient with the p.T1732 M variant we detected a 12-nucleotide deletion in the β-globin gene leading to a deletion of amino acids 62AHGK65. The joint presence of mutations in two different genes connected with erythrocytes markedly aggravated the presentation of the disease. Bioinformatic analysis and molecular modeling strongly indicated likely deleterious effects of all four PIEZO1 variants, but co-segregation analysis showed that the p.D1566G substitution is in fact non-pathogenic. Identification of causative mutations should improve the diagnosis and management of HX and provide a new insight into the molecular basis of this complex red blood cell abnormality

Serum microRNA in patients undergoing atrial fibrillation ablation.

MicroRNAs mediate posttranscriptional gene regulation. The aim of the study was to find a microRNA predictor of successful atrial fibrillation (AF) ablation. A total of 109 patients undergoing first-time AF ablation were included. Nineteen patients were selected to undergo serum microRNA sequencing (study group). The sequencing data were used to select several microRNAs that correlated with 12-month recurrences after AF ablation. Those microRNAs were validated by digital droplet PCR in samples from remaining 90 patients. All patients underwent pulmonary vein isolation (RF ablation, contact force catheter, electroanatomical system). The endpoint of the study was the 12-month AF recurrence rate; the overall recurrence rate was 42.5%. In total, levels of 34 miRNAs were significantly different in sera from patients with AF recurrence compared to patients without AF recurrence. Six microRNAs (miR-183-5p, miR-182-5p, miR-32-5p, miR-107, miR-574-3p, and miR-144-3p) were validated in the whole group. Data from the validation group did not confirm the observations from the study group, as no significant differences were found between miRNAs serum levels in patients with and without recurrences 12 months after AF ablation

Interindividual variability of atorvastatin treatment influence on the MPO gene expression in patients after acute myocardial infarction

Myeloperoxidase (MPO) and C-reactive protein (CRP) may play critical roles in generation of oxidative stress and the development of the systemic inflammatory response. The aim of the study was to determine the effect of atorvastatin therapy on the MPO gene expression and its plasma level in relation to lipids level lowering and an anti-inflammatory response in patients after acute myocardial infarction. The research material was represented by 112 samples. Thirty-eight patients with first AMI receiving atorvastatin therapy (40 mg/day) and followed up for one month were involved in the study. The relative MPO gene expression in peripheral blood mononuclear cells (PBMCs) was examined using RT-qPCR in 38 patients before-, 38 patients after-therapy and in 36 patients as the control group. The plasma concentrations of MPO and serum concentrations of biochemical parameters were determined using commercially available diagnostic tests. After one month of atorvastatin therapy, in 60.5% patients a decrease of MPO gene expression, whereas in 39.5% patients an increase, was observed. The plasma MPO levels behaved in the same way as the MPO gene expression. However, the serum lipids and CRP concentrations were significantly lower after one month of atorvastatin therapy in both groups of patients - with decreased and increased MPO gene expression. Atorvastatin exhibited a different effect on MPO gene expression and its plasma level. Short-term atorvastatin therapy resulted in lipid lowering and anti-inflammatory activity in patients after AMI, independently of its effect on MPO gene expression. The molecular mechanisms of this phenomenon are not yet defined and require further research

Molecular analysis of three novel G6PD variants : G6PD Pedoplis-Ckaro, G6PD Piotrkow and G6PD Krakow

We present three novel mutations in the G6PD gene and discuss the changes they cause in the 3-dimensional structure of the enzyme: 573C→G substitution that predicts Phe to Leu at position 191 in the C-terminus of helix αe, 851T→C mutation which results in the substitution 284Val→→Ala in the β+α domain close to the C-terminal part of helix αj, and 1175T→C substitution that predicts Ile to Thr change at position 392

Symmetric data-driven fusion of diffusion tensor MRI: Age differences in white matter

In the past 20 years, white matter (WM) microstructure has been studied predominantly using diffusion tensor imaging (DTI). Decreases in fractional anisotropy (FA) and increases in mean (MD) and radial diffusivity (RD) have been consistently reported in healthy aging and neurodegenerative diseases. To date, DTI parameters have been studied individually (e.g., only FA) and separately (i.e., without using the joint information across them). This approach gives limited insights into WM pathology, increases the number of multiple comparisons, and yields inconsistent correlations with cognition. To take full advantage of the information in a DTI dataset, we present the first application of symmetric fusion to study healthy aging WM. This data-driven approach allows simultaneous examination of age differences in all four DTI parameters. We used multiset canonical correlation analysis with joint independent component analysis (mCCA + jICA) in cognitively healthy adults (age 20–33, n = 51 and age 60–79, n = 170). Four-way mCCA + jICA yielded one high-stability modality-shared component with co-variant patterns of age differences in RD and AD in the corpus callosum, internal capsule, and prefrontal WM. The mixing coefficients (or loading parameters) showed correlations with processing speed and fluid abilities that were not detected by unimodal analyses. In sum, mCCA + jICA allows data-driven identification of cognitively relevant multimodal components within the WM. The presented method should be further extended to clinical samples and other MR techniques (e.g., myelin water imaging) to test the potential of mCCA+jICA to discriminate between different WM disease etiologies and improve the diagnostic classification of WM diseases

White matter plasticity in healthy older adults: The effects of aerobic exercise

White matter deterioration is associated with cognitive impairment in healthy aging and Alzheimer\u27s disease. It is critical to identify interventions that can slow down white matter deterioration. So far, clinical trials have failed to demonstrate the benefits of aerobic exercise on the adult white matter using diffusion Magnetic Resonance Imaging. Here, we report the effects of a 6-month aerobic walking and dance interventions (clinical trial NCT01472744) on white matter integrity in healthy older adults (n = 180, 60-79 years) measured by changes in the ratio of calibrated T1- to T2-weighted images (T1w/T2w). Specifically, the aerobic walking and social dance interventions resulted in positive changes in the T1w/T2w signal in late-myelinating regions, as compared to widespread decreases in the T1w/T2w signal in the active control. Notably, in the aerobic walking group, positive change in the T1w/T2w signal correlated with improved episodic memory performance. Lastly, intervention-induced increases in cardiorespiratory fitness did not correlate with change in the T1w/T2w signal. Together, our findings suggest that white matter regions that are vulnerable to aging retain some degree of plasticity that can be induced by aerobic exercise training. In addition, we provided evidence that the T1w/T2w signal may be a useful and broadly accessible measure for studying short-term within-person plasticity and deterioration in the adult human white matter