A BIOCHEMICAL MULTI-SPECIES QUALITY MODEL OF A DRINKING WATER DISTRIBUTION SYSTEM FOR SIMULATION AND DESIGN

Drinking Water Distribution Systems (DWDSs) play a key role in sustainable development of modern society. They are classified as critical infrastructure systems. This imposes a large set of highly demanding requirements on the DWDS operation and requires dedicated algorithms for on-line monitoring and control to tackle related problems. Requirements on DWDS availability restrict the usability of the real plant in the design phase. Thus, a proper model is crucial. Within this paper a DWDS multi-species quality model for simulation and design is derived. The model is composed of multiple highly inter-connected modules which are introduced to represent chemical and biological species and (above all) their interactions. The chemical part includes the processes of chloramine decay with additional bromine catalysis and reaction with nitrogen compounds. The biological part consists of both heterotrophic and chemo-autotrophic bacteria species. The heterotrophic bacteria are assumed to consume assimilable organic carbon. Autotrophs are ammonia oxidizing bacteria and nitrite oxidizing bacteria species which are responsible for nitrification processes. Moreover, Disinfection By-Products (DBPs) are also considered. Two numerical examples illustrate the derived model’s behaviour in normal and disturbance operational states

Polarimetry and the Long Awaited Superoutburst of BZ UMa

BZ UMa is a cataclysmic variable star whose specific classification has eluded researchers since its discovery in 1968. It has outburst and spectral properties consistent with both U Gem class dwarf novae and intermediate polars. We present new photometric and polarimetric measurements of recent outbursts, including the first detected superoutburst of the system. Statistical analysis of these and archival data from outbursts over the past 40 years present a case for BZ UMa as a non-magnetic, U Gem class, SU-UMa subclass dwarf novae.Comment: Accepted by PASP for the November, 2009 issu

As tests evolve and costs of cancer care rise: reappraising stool-based screening for colorectal neoplasia

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73533/1/j.1365-2036.2008.03632.x.pd

Cost-effectiveness and budget impact analyses of a colorectal cancer screening programme in a high adenoma prevalence scenario using MISCAN-Colon microsimulation model

This economic evaluation showed a screening intervention with a major health gain that also produced net savings when a long follow-up was used to capture the late economic benefit. The number of colonoscopies required was high but remain within the capacity of the Basque Health Service. So far in Europe, no other population Colorectal Cancer screening programme has been evaluated by budget impact analysis

The role of inherited genetic variants in colorectal polyposis syndromes

Colorectal carcinoma (CRC) is the third most common cancer in men and the second most common cancer in women across the world. Most CRCs occur sporadically, but in 15–35% of cases, hereditary factors are important. Some patients with an inherited predisposition to CRC will be diagnosed with a “genetic polyposis syndrome” such as familial adenomatous polyposis (FAP), MUTYH-associated polyposis (MAP), polymerase proofreading associated polyposis (PPAP), NTHL1-associated polyposis, MSH3-associated polyposis or a hamartomatous polyposis syndrome. Individuals with ≥ 10 colorectal polyps have traditionally been referred for genetic diagnostic testing to identify APC and MUTYH mutations which cause FAP and MAP respectively. Mutations are found in most patients with > 100 adenomas but in only a minority of those with 10–100 adenomas. The reasons that diagnostic laboratories are not identifying pathogenic variants include mutations occurring outside of the open reading frames of genes, individuals exhibiting generalized mosaicism and the involvement of additional genes. It is important to identify patients with an inherited polyposis syndrome, and to define the mutations causing their polyposis, so that the individuals and their relatives can be managed appropriately