Two-Year Monitoring of Water Samples from Dam of Iskar and the Black Sea, Bulgaria, by Molecular Analysis: Focus on Mycobacterium spp

<p>The coast of the Bulgarian Black Sea is a popular summer holiday destination. The Dam of Iskar is the largest artificial dam in Bulgaria, with a capacity of 675 million m3. It is the main source of tap water for the capital Sofia and for irrigating the surrounding valley. There is a close relationship between the quality of aquatic ecosystems and human health as many infections are waterborne. Rapid molecular methods for the analysis of highly pathogenic bacteria have been developed for monitoring quality. Mycobacterial species can be isolated from waste, surface, recreational, ground and tap waters and human pathogenicity of nontuberculose mycobacteria (NTM) is well recognized. The objective of our study was to perform molecular analysis for key-pathogens, with a focus on mycobacteria, in water samples collected from the Black Sea and the Dam of Iskar. In a two year period, 38 water samples were collected-24 from the Dam of Iskar and 14 from the Black Sea coastal zone. Fifty liter water samples were concentrated by ultrafiltration. Molecular analysis for 15 pathogens, including all species of genus Mycobacterium was performed. Our results showed presence of Vibrio spp. in the Black Sea. Rotavirus A was also identified in four samples from the Dam of Iskar. Toxigenic Escherichia coli was present in both locations, based on markers for stx1 and stx2 genes. No detectable amounts of Cryptosporidium were detected in either location using immunomagnetic separation and fluorescence microscopy. Furthermore, mass spectrometry analyses did not detect key cyanobacterial toxins. On the basis of the results obtained we can conclude that for the period 2012-2014 no Mycobacterium species were present in the water samples. During the study period no cases of waterborne infections were reported.p>

A note on the prediction of liquid hold-up with the stratified roll wave regime for gas/liquidco-current flow in horizontal pipes.

This note presents a simple model for prediction of liquid hold-up in two-phase horizontal pipe flow for the stratified roll wave (St+RW) flow regime. Liquid hold-up data for horizontal two-phase pipe flow [1, 2, 3, 4, 5 and 6] exhibit a steady increase with liquid velocity and a more dramatic fall with increasing gas rate as shown by Hand et al. [7 and 8] for example. In addition the liquid hold-up is reported to show an additional variation with pipe diameter. Generally, if the initial liquid rate for the no-gas flow condition gives a liquid height below the pipe centre line, the flow patterns pass successively through the stratified (St), stratified ripple (St+R), stratified roll wave, film plus droplet (F+D) and finally the annular (A+D, A+RW, A+BTS) regimes as the gas rate is increased. Hand et al. [7 and 8] have given a detailed description of this progression in flow regime development and definitions of the patterns involved. Despite the fact that there are over one hundred models which have been developed to predict liquid hold-up, none have been shown to be universally useful, while only a handful have proven to be applicable to specific flow regimes [9, 10, 11 and 12]. One of the most intractable regimes to predict has been the stratified roll wave pattern where the liquid hold-up shows the most dramatic change with gas flow rate. It has been suggested that the momentum balance-type models, which give both hold-up and pressure drop prediction, can predict universally for all flow regimes but particularly in the case of the difficult stratified roll wave pattern. Donnelly [1] recently demonstrated that the momentum balance models experienced some difficulties in the prediction of this regime. Without going into lengthy details, these models differ in the assumed friction factor or shear stress on the surfaces within the pipe particularly at the liquid–gas interface. The Baker–Jardine model [13] when tested against the 0.0454 m i.d. data of Nguyen [2] exhibited a wide scatter for both liquid hold-up and pressure drop as shown in Fig. 1. The Andritsos–Hanratty model [14] gave better prediction of pressure drop but a wide scatter for liquid hold-up estimation (cf. Fig. 2) when tested against the 0.0935 m i.d. data of Hand [5]. The Spedding–Hand model [15], shown in Fig. 3 against the data of Hand [5], gave improved performance but was still unsatisfactory with the prediction of hold-up for stratified-type flows. The MARS model of Grolman [6] gave better prediction of hold-up (cf. Fig. 4) but deterioration in the estimation of pressure drop when tested against the data of Nguyen [2]. Thus no method is available that will accurately predict liquid hold-up across the whole range of flow patterns but particularly for the stratified plus roll wavy regime. The position is particularly unfortunate since the stratified-type regimes are perhaps the most predominant pattern found in multiphase lines.

The Septin-Binding Protein Anillin is Over-Expressed in Diverse Human Tumours

<p>Anillin is an actin-binding protein that can bind septins and is a component of the cytokinetic ring. We assessed the anillin expression in 7,579 human tissue samples and cell lines by DNA micro-array analysis. Anillin is expressed ubiquitously but with variable levels of expression, being highest in the central nervous system. The median level of anillin mRNA expression was higher in tumors than normal tissues (median fold increase 2.58; 95% confidence intervals, 2.19-5.68, P < 0.0001) except in the central nervous system where anillin in RNA levels were lower in tumors. We developed a sensitive reverse transcription-PCR strategy to show that anillin mRNA is expressed in cell lines and in cDNA panels derived from fetal and adult tissues, thus validating the microarray data. We compared anillin with Ki67 in RNA expression and found a significant linear relationship between anillin and Ki67 mRNA expression (Spearmann r similar to 0.6, P < 0.0001). Anillin mRNA expression was analyzed during tumor progression in breast, ovarian, kidney, colorectal, hepatic, lung, endometrial, and pancreatic tumors and in all tissues there was progressive, increase in anillin mRNA expression from normal to benign to malignant to metastatic disease. Finally, we used anti-anillin sera and found nuclear anillin immuncireactivity to be widespread in normal tissues, often not correlating with proliferative compartments. These data provide insight into the existence of non proliferation-associated activities of anillin and roles in interphase nuclei. Thus, anillin is overexpressed in diverse common human tumors, but not simply as a consequence of being a proliferation marker. Anillin may have potential as a novel biomarker.p>

SEPT9_v4 expression induces morphological change, increased motility and disturbed polarity

<p>Several lines of evidence indicate that altered expression of SEPT9 is seen in human neoplasia. In particular there is evidence of altered expression of the SEPT9_v4 isoform. The functional consequences of this remain unclear. We have studied the expression of wild-type- and GTP-binding mutants (G144V and S148N) of the SEPT9_v4 isoform in the MCF7 cell line as a model for its deregulation in neoplasia. We find that SEPT9_v4 expression induces dramatic actin cytoskeletal reorganization with the formation of processes around the cell periphery. Expression of the SEPT9_v4 isoform and a G144V mutant cause delocalization of endogenous SEPT9 from filamentous structures but the S148N mutant does not have this effect. In addition SEPT9_v4 isoform expression enhances cell motility and is associated with perturbation of directional movement. Expression of SEPT9_v4 GTP binding mutants also has potent effects on morphology and motility and causes loss of normal polarity, as judged by Golgi reorientation assays. The phenotypes induced by expression of the SEPT9_v4 isoform and the GTP mutants provide an insight into possible mechanisms of SEPT9_v4 function and suggest that the GTPase functions have both ras- and rab-like features. We propose a model in which overexpression of the SEPT9_v4 isoform in neoplasia is associated with perturbation of SEPT9 complexes, leading to phenotypes associated with neoplasia. Copyright (c) 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley &amp; Sons, Ltd.p>