On generalized surjective codes

We consider generalized surjective codes, together with their connection to covering codes and covering arrays. We prove new bounds on sigma(q) (n, s; r), the minimal cardinality of a q-ary code of length n, which is s-surjective with radius r. For covering codes we deduce the new records K-6 (10, 7) <= 18 and K-6 (9, 6) <= 24

Muscle mitochondrial function in patients with type 2 diabetes mellitus and peripheral arterial disease: implications in vascular surgery

AbstractObjectives(1) To review the available information on mitochondrial function in type 2 diabetes mellitus (T2DM) and peripheral arterial disease (PAD) obtained by non-invasive phosphor magnetic resonance spectroscopy (31PMRS), near-infrared spectroscopy (NIRS) in vivo and respirometry on mitochondria isolated from muscle biopsies in vitro (2) to evaluate the usefulness of such data in the diagnosis, treatment and prognosis of these patients.DesignReview.MethodsSearch strategy: PubMed (http://www.ncbi.nlm.nih.gov/PubMed) and manual literature search.Main resultsFifty-three articles were retrieved, which included 31PMRS, 15, NIRS, 11, Combined, 1 and Respirometry, 2 and background literature, 24.ConclusionMuscle mitochondrial function is impaired in both T2DM and PAD patients, but differently. Patients suffering from both pathological conditions will display more serious impairment of the mitochondrial function. Mitochondrial function and the degree of ischaemic disease as evaluated by 31PMRS and NIRS are well correlated. The NIRS technique appears to determine the degree of PAD better than 31PMRS. It is argued that systematic testing of mitochondrial function may be a useful prognostic tool with PAD and T2DM, but clinical studies are needed

Economic Development of Urban Areas

In this dissertation I study the development of urban areas. At the aggregate level I investigate how they may be affected by climate change policies and by being designated the seat of governmental power. At the household level I study with coauthors how microfinance could improve the health of urban residents. In Chapter 1, I investigate how local employment may be affected by electricity price increases, which is a likely consequence of climate change policies. I outline how previous studies that find large, negative effects may be biased. To overcome these biases I develop a novel estimation strategy that blends border-pair regressions with the synthetic control methodology. I show the conditions for consistent estimation. Using this estimator, I find no effect of contemporaneous price changes on employment. Consistent with the longer time-frame for manufacturing decisions, I do find evidence for negative effects from perceived permanent price shocks. These estimates are much smaller than previous research has found. National capital cities are often substantially larger than other cities in their countries. In Chapter 2, I investigate whether there is a causal effect from being a capital by studying the 1960 relocation of the Brazilian capital from Rio de Janeiro to Brasília. Using a synthetic controls strategy I find that losing the capital had no significant effects on Rio de Janeiro in terms of population, employment, or gross domestic product (GDP). I find that Brasília experienced large and significant increases in population, employment, and GDP. I find evidence of large spillovers from the public to the private sector. Chapter 3 investigates how microfinance could increase the uptake of costly health goods. We study the effect of time payments (micro-loans or micro-savings) on willingness-to-pay (WTP) for a water filter among households in the slums of Dhaka, Bangladesh. We find that time payments significantly increase WTP: compared to a lump-sum up-front purchase, median WTP increases 83% with a six-month loan and 115% with a 12-month loan. We find that households are quite patient with respect to consumption of health inputs. We find evidence for the presence of credit and savings constraints

Three-dimensional reconstructions of intrahepatic bile duct tubulogenesis in human liver

<p>Abstract</p> <p>Background</p> <p>During liver development, intrahepatic bile ducts are thought to arise by a unique asymmetric mode of cholangiocyte tubulogenesis characterized by a series of remodeling stages. Moreover, in liver diseases, cells lining the Canals of Hering can proliferate and generate new hepatic tissue. The aim of this study was to develop protocols for three-dimensional visualization of protein expression, hepatic portal structures and human hepatic cholangiocyte tubulogenesis.</p> <p>Results</p> <p>Protocols were developed to digitally visualize portal vessel branching and protein expression of hepatic cell lineage and extracellular matrix deposition markers in three dimensions. Samples from human prenatal livers ranging from 7 weeks + 2 days to 15½ weeks post conception as well as adult normal and acetaminophen intoxicated liver were used. The markers included cytokeratins (CK) 7 and 19, the epithelial cell adhesion molecule (EpCAM), hepatocyte paraffin 1 (HepPar1), sex determining region Y (SRY)-box 9 (SOX9), laminin, nestin, and aquaporin 1 (AQP1).</p> <p>Digital three-dimensional reconstructions using CK19 as a single marker protein disclosed a fine network of CK19 positive cells in the biliary tree in normal liver and in the extensive ductular reactions originating from intrahepatic bile ducts and branching into the parenchyma of the acetaminophen intoxicated liver. In the developing human liver, three-dimensional reconstructions using multiple marker proteins confirmed that the human intrahepatic biliary tree forms through several developmental stages involving an initial transition of primitive hepatocytes into cholangiocytes shaping the ductal plate followed by a process of maturation and remodeling where the intrahepatic biliary tree develops through an asymmetrical form of cholangiocyte tubulogenesis.</p> <p>Conclusions</p> <p>The developed protocols provide a novel and sophisticated three-dimensional visualization of vessels and protein expression in human liver during development and disease.</p