Better banks for Eastern Europe

Grossly inefficient banking systems are one of the major impediments to a rapid and sustained upswing in Europe's emerging market economies (EMEs for short). Although the transition from plan to market necessitates a large-scale re-allocation of domestic capital and easy access to foreign capital, the EMEs have adopted slow and inefficient approaches to the transformation of their banking systems. The EMEs can create optimal conditions for financial intermediation and a substantial import of capital and skills if they immediately import an efficient banking system and enter into an East-West Banking Union with the EC. A Banking Union goes far beyond the adoption of some relevant EC regulations for local banks; it gives all financial intermediaries licensed in one EC country free access to the EMEs subject to the same rules that apply in the EC internal market. At present, non-performing loans still tie state banks to insolvent state enterprises; the precarious portfolio positions of domestic banks serve as a convenient excuse for not allowing efficient and experienced Western banks to enter the market in the EMEs. To resolve the portfolio problem at one stroke, all loans that state banks had granted to state firms prior to a certain date should be written off; tight ceilings on the amount of new credits each state firm can receive from state banks would prevent a recurrence of the problem. The ceilings should not apply to private banks, which are controlled by self-interested owners. State banks should be recapitalized using government bonds that are indexed to inflation. Since a programme of debt write-off and recapitalization raises the value of state firms and state banks and thus the potential proceeds of privatization, it need not constitute a drain on the state budget. A clean sweep, which eases the privatization of firms and banks, is preferable to a time-consuming and arbitrary case-by-case approach. Even if it is no longer politically possible to fully discard the present gradualist policies, the EMEs should at least upgrade their piecemeal debt-reduction and recapitalization programmes. Thereafter, the residual portfolio problems should no longer pose an obstacle to immediate and free market access for foreign banks within an East-West Banking Union. --

Evaluation of genome-wide loci of iron metabolism in hereditary hemochromatosis identifies PCSK7 as a host risk factor of liver cirrhosis

Genome-wide association studies (GWAS) have revealed genetic determinants of iron metabolism, but correlation of these with clinical phenotypes is pending. Homozygosity for HFE C282Y is the predominant genetic risk factor for hereditary hemochromatosis (HH) and may cause liver cirrhosis. However, this genotype has a low penetrance. Thus, detection of yet unknown genetic markers that identify patients at risk of developing severe liver disease is necessary for better prevention. Genetic loci associated with iron metabolism (TF, TMPRSS6, PCSK7, TFR2 and Chr2p14) in recent GWAS and liver fibrosis (PNPLA3) in recent meta-analysis were analyzed for association with either liver cirrhosis or advanced fibrosis in 148 German HFE C282Y homozygotes. Replication of associations was sought in additional 499 Austrian/Swiss and 112 HFE C282Y homozygotes from Sweden. Only variant rs236918 in the PCSK7 gene (proprotein convertase subtilisin/kexin type 7) was associated with cirrhosis or advanced fibrosis (P = 1.02 × 10−5) in the German cohort with genotypic odds ratios of 3.56 (95% CI 1.29-9.77) for CG heterozygotes and 5.38 (95% CI 2.39-12.10) for C allele carriers. Association between rs236918 and cirrhosis was confirmed in Austrian/Swiss HFE C282Y homozygotes (P = 0.014; ORallelic = 1.82 (95% CI 1.12-2.95) but not in Swedish patients. Post hoc combined analyses of German/Swiss/Austrian patients with available liver histology (N = 244, P = 0.00014, ORallelic = 2.84) and of males only (N = 431, P = 2.17 × 10−5, ORallelic = 2.54) were consistent with the premier finding. Association between rs236918 and cirrhosis was not confirmed in alcoholic cirrhotics, suggesting specificity of this genetic risk factor for HH. PCSK7 variant rs236918 is a risk factor for cirrhosis in HH patients homozygous for the HFE C282Y mutatio

Federated Learning for Breast Density Classification: A Real-World Implementation

Building robust deep learning-based models requires large quantities of diverse training data. In this study, we investigate the use of federated learning (FL) to build medical imaging classification models in a real-world collaborative setting. Seven clinical institutions from across the world joined this FL effort to train a model for breast density classification based on Breast Imaging, Reporting & Data System (BI-RADS). We show that despite substantial differences among the datasets from all sites (mammography system, class distribution, and data set size) and without centralizing data, we can successfully train AI models in federation. The results show that models trained using FL perform 6.3% on average better than their counterparts trained on an institute's local data alone. Furthermore, we show a 45.8% relative improvement in the models' generalizability when evaluated on the other participating sites' testing data.Comment: Accepted at the 1st MICCAI Workshop on "Distributed And Collaborative Learning"; add citation to Fig. 1 & 2 and update Fig.

Evaluation of genome-wide loci of iron metabolism in hereditary hemochromatosis identifies PCSK7 as a host risk factor of liver cirrhosis

Genome-wide association studies (GWAS) have revealed genetic determinants of iron metabolism, but correlation of these with clinical phenotypes is pending. Homozygosity for HFE C282Y is the predominant genetic risk factor for hereditary hemochromatosis (HH) and may cause liver cirrhosis. However, this genotype has a low penetrance. Thus, detection of yet unknown genetic markers that identify patients at risk of developing severe liver disease is necessary for better prevention. Genetic loci associated with iron metabolism (TF, TMPRSS6, PCSK7, TFR2 and Chr2p14) in recent GWAS and liver fibrosis (PNPLA3) in recent meta-analysis were analyzed for association with either liver cirrhosis or advanced fibrosis in 148 German HFE C282Y homozygotes. Replication of associations was sought in additional 499 Austrian/Swiss and 112 HFE C282Y homozygotes from Sweden. Only variant rs236918 in the PCSK7 gene (proprotein convertase subtilisin/kexin type 7) was associated with cirrhosis or advanced fibrosis (P = 1.02 × 10(-5)) in the German cohort with genotypic odds ratios of 3.56 (95% CI 1.29-9.77) for CG heterozygotes and 5.38 (95% CI 2.39-12.10) for C allele carriers. Association between rs236918 and cirrhosis was confirmed in Austrian/Swiss HFE C282Y homozygotes (P = 0.014; ORallelic = 1.82 (95% CI 1.12-2.95) but not in Swedish patients. Post hoc combined analyses of German/Swiss/Austrian patients with available liver histology (N = 244, P = 0.00014, ORallelic = 2.84) and of males only (N = 431, P = 2.17 × 10(-5), ORallelic = 2.54) were consistent with the premier finding. Association between rs236918 and cirrhosis was not confirmed in alcoholic cirrhotics, suggesting specificity of this genetic risk factor for HH. PCSK7 variant rs236918 is a risk factor for cirrhosis in HH patients homozygous for the HFE C282Y mutation