Romanian River Basins Lag Time Analysis. The SCS-CN Versus RNS Comparative Approach Developed for Small Watersheds

Romanian policy makers have to perceive that human intervention on river basins land cover is influencing rainfall-runoff relation and the used methodology cannot accurately estimate watershed surface flow transformations. Global water cycles and energy fluxes understanding is leading to better predictions of land atmosphere interaction and local hydro-climates evolution. The water transfer time determination from rainfall to runoff needs accurate measurements of river basins hydrological parameters. Here, we analyzed and compared the lag time value results of two different methodologies (curve number and rational methodology) used for 54 Romanian small catchment areas study. The focus of this paper is the lag time evaluation and interpretation for an effective implementation of the best methodology approach in the Romanian geographical space. Our research in small river basins was developed using remote sensing technology maps, GIS and environmental datasets in combination with field work on every drainage basin in order to assess the specific morphological features and validate the land cover typology. We found that Soil Conservation Service - Curve Number (SCS-CN) method is widely used according to USA landscape features classification, but not necessarily applicable to Romanian river basins characteristics. Our results show how the official Romanian rational methodology national standard (RNS) can be improved and the limits of SCS-CN method.

     

Group sequential crossover trial designs with strong control of the familywise error rate

Crossover designs are an extremely useful tool to investigators, and group sequential methods have proven highly proficient at improving the efficiency of parallel group trials. Yet, group sequential methods and crossover designs have rarely been paired together. One possible explanation for this could be the absence of a formal proof of how to strongly control the familywise error rate in the case when multiple comparisons will be made. Here, we provide this proof, valid for any number of initial experimental treatments and any number of stages, when results are analyzed using a linear mixed model. We then establish formulae for the expected sample size and expected number of observations of such a trial, given any choice of stopping boundaries. Finally, utilizing the four-treatment, four-period TOMADO trial as an example, we demonstrate that group sequential methods in this setting could have reduced the trials expected number of observations under the global null hypothesis by over 33%.     

Oxidative degradation of polyamide reverse osmosis membranes: Studies of molecular model compounds and selected membranes

Selected aromatic amides were used to model the chemical reactivity of aromatic polyamides found in thin‐film composite reverse osmosis (RO) membranes. Chlorination and possible amide bond cleavage of aromatic amides upon exposure to aqueous chlorine, which can lead to membrane failure, were investigated. Correlations are made of the available chlorine concentration, pH, and exposure time with chemical changes in the model compounds. From the observed reactivity trends, insights are obtained into the mechanism of RO membrane performance loss upon chlorine exposure. Two chemical pathways for degradation are shown, one at constant pH and another that is pH‐history dependent. An alternative strategy is presented for the design of chlorine‐resistant RO membranes, and an initial performance study of RO membranes incorporating this strategy is reported. © 2003 Wiley Periodicals, Inc. J Appl Polym Sci 90: 1173–1184, 2003     

A demonstration of melt rate control during VAR of “Cracked” electrodes

A particularly challenging problem associated with vacuum arc remelting occurs when trying to maintain accurate control of electrode melt rate as the melt zone passes through a transverse crack in the electrode. As the melt zone approaches the crack, poor heat conduction across the crack drives the local temperature in the electrode tip above its steady-state value, causing the controller to cut back on melting current in response to an increase in melting efficiency. The difficulty arises when the melt zone passes through the crack and encounters the relatively cold metal on the other side, giving rise to an abrupt drop in melt rate. This extremely dynamic melting situation is very difficult to handle using standard load-cell based melt rate control, resulting in large melt rate excursions. We have designed and tested a new generation melt rate controller that is capable of controlling melt rate through crack events. The controller is designed around an accurate dynamic melting model that uses four process variables: electrode tip thermal boundary layer, electrode gap, electrode mass and melting efficiency. Tests, jointly sponsored by the Specialty Metals Processing Consortium and Sandia National Laboratories, were performed at Carpenter Technology Corporation wherein two 0.43 m diameter Pyromet® 718 electrodes were melted into 0.51 m diameter ingots. Each electrode was cut approximately halfway through its diameter with an abrasive saw to simulate an electrode crack. Relatively accurate melt rate control through the cuts was demonstrated despite the observation of severe arc disturbances and loss of electrode gap control. Subsequent to remelting, one ingot was sectioned in the “as cast” condition, whereas the other was forged to 0.20 m diameter billet. Macrostructural characterization showed solidification white spots in regions affected by the cut in the electrode.     

Metastatic parathyroid carcinoma in the MEN2A syndrome

We report a patient with a metastatic parathyroid carcinoma and medullary carcinoma of the thyroid. This patient represents a variation of the multiple endocrine neoplasia syndrome (MEN) type 2A. There was no evidence of a phaeochromocytoma. The case illustrates the difficulties that may be encountered in localising the source of PTH secretion; the patient underwent four unsuccessful exploratory operations of the neck and mediastinum before further investigations revealed a single metastatic deposit of parathyroid carcinoma involving the first thoracic vertebra. PCR amplification and sequencing of the RET oncogene from the metastatic parathyroid carcinoma and genomic DNA revealed a heterozygous mutation (Cys634Tyr) in exon 11, as has previously been described to occur in MEN 2A. In addition, loss of tumour heterozygosity was demonstrated at loci from chromosomes 1, 2, 3p, 13q and 16p. This represents the first report of a parathyroid carcinoma in a MEN2A patient, in which the multiple allelic deletions are consistent with the generalised losses observed in aggressive tumours.     

Genetic mapping of a major susceptibility locus for juvenile myoclonic epilepsy on chromosome 15q

The epilepsies are a group of disorders characterised by recurrent seizures caused by episodes of abnormal neuronal hyperexcitability involving the brain. Up to 60 million people are affected worldwide and genetic factors may contribute to the aetiology in up to 40% of patients. The most common human genetic epilepsies display a complex pattern of inheritance. These are categorised as idiopathic in the absence of detectable structural or metabolic abnormalities. Juvenile myoclonic epilepsy (JME) is a distinctive and common variety of familial idiopathic generalised epilepsy (IGE) with a prevalence of 0.5-1.0 per 1000 and a ratio of sibling risk to population prevalence (lambda(s)) of 42. The molecular genetic basis of these familial idiopathic epilepsies is entirely unknown, but a mutation in the gene CHRNA4, encoding the alpha4 subunit of the neuronal nicotinic acetylcholine receptor (nAChR), was recently identified in a rare Mendelian variety of idiopathic epilepsy. Chromosomal regions harbouring genes for nAChR subunits were therefore tested for linkage to the JME trait in 34 pedigrees. Significant evidence for linkage with heterogeneity was found to polymorphic loci encompassing the region in which the gene encoding the alpha7 subunit of nAChR (CHRNA7) maps on chromosome 15q14 (HLOD = 4.4 at alpha = 0.65; Z(all) = 2.94, P = 0.0005). This major locus contributes to genetic susceptibility to JME in a majority of the families studied.