Signature polymorphisms in the internal transcribed spacer region relevant for the differentiation of zoophilic and anthropophilic strains of Trichophyton interdigitale and other species of T. mentagrophytes sensu lato.

Summary Background Dermatophytes are the main cause of superficial mycoses in humans and animals. Molecular research has given useful insights into the phylogeny and taxonomy of the dermatophytes to overcome the difficulties with conventional diagnostics. Objectives The Trichophyton mentagrophytes complex consists of anthropophilic as well as zoophilic species. Although several molecular markers have been developed for the differentiation of strains belonging to T. mentagrophytes sensu lato, correct identification still remains problematic, especially concerning the delineation of anthropophilic and zoophilic strains of T. interdigitale. This differentiation is not academic but is essential for selection of the correct antimycotic therapy to treat infected patients. Methods One hundred and thirty isolates identified by morphological characteristics as T. mentagrophytes sensu lato were investigated using restriction fragment length polymorphism (RFLP) and sequence analysis of the polymerase chain reaction-amplified internal transcribed spacer (ITS) region of the rDNA. Results Species of this complex produced individual RFLP patterns obtained by the restriction enzyme MvaI. Subsequent sequence analysis of the ITS1, 5.8S and ITS2 region of all strains, but of T. interdigitale in particular, revealed single unique polymorphisms in anthropophilic and zoophilic strains. Conclusions Signature polymorphisms were observed to be useful for the differentiation of these strains and epidemiological data showed a host specificity among zoophilic strains of T. interdigitale/Arthroderma vanbreuseghemii compared with A. benhamiae as well as characteristic clinical pictures in humans when caused by zoophilic or anthropophilic strains. The delineation is relevant because it helps in determining the correct treatment and provides clues regarding the source of the infection.

Evolution and sedimentology of a channel fill in the sandy braided South Saskatchewan River and its comparison to the deposits of an adjacent compound bar

The depositional stratigraphy of within-channel deposits in sandy braided rivers is dominated by a variety of barforms (both singular `unit' bars and complex `compound' bars), as well as the infill of individual channels (herein termed `channel fills'). The deposits of bars and channel fills define the key components of facies models for braided rivers and their within-channel heterogeneity, knowledge of which is important for reservoir characterization. However, few studies have sought to address the question of whether the deposits of bars and channel fills can be readily differentiated from each other. This paper presents the first quantitative study to achieve this aim, using aerial images of an evolving modern sandy braided river and geophysical imaging of its subsurface deposits. Aerial photographs taken between 2000 and 2004 document the abandonment and fill of a 1 3 km long, 80 m wide anabranch channel in the sandy braided South Saskatchewan River, Canada. Upstream river regulation traps the majority of very fine sediment and there is little clay (<1%) in the bed sediments. Channel abandonment was initiated by a series of unit bars that stalled and progressively blocked the anabranch entrance, together with dune deposition and stacking at the anabranch entrance and exit. Complete channel abandonment and subsequent fill of up to 3 m of sediment took approximately two years. Thirteen kilometres of ground-penetrating radar surveys, coupled with 18 cores, were obtained over the channel fill and an adjacent 750 m long, 400 m wide, compound bar, enabling a quantitative analysis of the channel and bar deposits. Results show that, in terms of grain-size trends, facies proportions and scale of deposits, there are only subtle differences between the channel fill and bar deposits which, therefore, renders them indistinguishable. Thus, it may be inappropriate to assign different geometric and sedimentological attributes to channel fill and bar facies in object-based models of sandy braided river alluvial architecture.

β1- and β3- voltage-gated sodium channel subunits modulate cell surface expression and glycosylation of Nav1.7 in HEK293 cells.

Voltage-gated sodium channels (Navs) are glycoproteins composed of a pore-forming α-subunit and associated β-subunits that regulate Nav α-subunit plasma membrane density and biophysical properties. Glycosylation of the Nav α-subunit also directly affects Navs gating. β-subunits and glycosylation thus comodulate Nav α-subunit gating. We hypothesized that β-subunits could directly influence α-subunit glycosylation. Whole-cell patch clamp of HEK293 cells revealed that both β1- and β3-subunits coexpression shifted V ½ of steady-state activation and inactivation and increased Nav1.7-mediated I Na density. Biotinylation of cell surface proteins, combined with the use of deglycosydases, confirmed that Nav1.7 α-subunits exist in multiple glycosylated states. The α-subunit intracellular fraction was found in a core-glycosylated state, migrating at ~250 kDa. At the plasma membrane, in addition to the core-glycosylated form, a fully glycosylated form of Nav1.7 (~280 kDa) was observed. This higher band shifted to an intermediate band (~260 kDa) when β1-subunits were coexpressed, suggesting that the β1-subunit promotes an alternative glycosylated form of Nav1.7. Furthermore, the β1-subunit increased the expression of this alternative glycosylated form and the β3-subunit increased the expression of the core-glycosylated form of Nav1.7. This study describes a novel role for β1- and β3-subunits in the modulation of Nav1.7 α-subunit glycosylation and cell surface expression.

Regulation of the expression of Nav1.5, the cardiac voltage-gated sodium channel

Abstract The cardiac sodium channel Nav1.5 plays a key role in cardiac excitability and conduction. Its importance for normal cardiac function has been highlighted by descriptions of numerous mutations of SCN5A (the gene encoding Nav1.5), causing cardiac arrhythmias which can lead to sudden cardiac death. The general aim of my PhD research project has been to investigate the regulation of Nav1.5 along two main axes: (1) We obtained experimental evidence revealing an interaction between Nav1.5 and a multiprotein complex comprising dystrophin. The first part of this study reports the characterization of this interaction. (2) The second part of the study is dedicated to the regulation of the cardiac sodium channel by the mineralocorticoid hormone named aldosterone. (1) Early in this study, we showed that Nav1.5 C-terminus was associated with dystrophin and that this interaction was mediated by syntrophin proteins. We used dystrophin-deficient mdx5cv mice to study the role of this interaction. We reported that dystrophin deficiency led to a reduction of both Nav1.5 protein level and the sodium current (INa). We also found that mdx5cv mice displayed atrial and ventricular conduction defects. Our results also indicated that proteasome inhibitor MG132 treatment of mdx5cv mice rescued Nav1.5 protein level and INa in cardiac tissue. (2) We showed that aldosterone treatment of mice cardiomyocytes led to an increase of the sodium current with no modification of Nav1.5 transcript and protein level. Altogether, these results suggest that the sodium current can be increased by distribution of intracellular pools of protein to the plasma membrane (e.g. upon aldosterone stimulation) and that interaction with dystrophin multiprotein complex is required for the stabilization of the channel at the plasma membrane. Finally, we obtained preliminary results suggesting that the proteasome could regulate Nav1.5 in mdx5cv mice. This study defines regulatory mechanisms of Nav1.5 which could play an important role in cardiac arrhythmia and bring new insight in cardiac conduction alterations observed in patients with dystrophinopathies. Moreover, this work suggests that Brugada syndrome, and some of the cardiac alterations seen in Duchenne patients may be caused by overlapping molecular mechanisms leading to a reduction of the cardiac sodium current.

Modulation of the epithelial sodium channel by serine proteases

Abstract The epithelial sodium channel (ENaC) is composed of three homologous subunits α, ß, and γ. This channel is involved in the regulation of sodium balance, which influences the periciliary liquid level in the lung, and blood pressure via the kidney. ENaC expressed in Xenopus laevis oocytes is preferentially and rapidly assembled into heteromeric αßγ complexes. Expression of homomeric α or heteromeric αß and αγ complexes lead to channel expression at the cell surface wíth low activities. Recent studies have demonstrated that α and γ (but not ß) ENaC subunits undergo proteolytic cleavage by endogenous proteases (i.e. furin) correlating with increased channel activity. We therefore assayed the full-length subunits and their cleavage products at the cell surface, as well as in the intracellular pool for all homo- and heteromeric combínations (α, ß, γ, ßγ, αß, αγ, ßγ and αßγ) and measured the corresponding channel activities as amiloride-sensitive sodíum transport (INa). We showed that upon assembly, cleavage of the y ENaC subunit ís responsible for increasing INa. We further demonstrated that in disease states such as cystic fibrosis (CF) where there is disequilibrium in the proteaseprotease inhibitor balance, ENaC is over-activated by the serine protease elastase (NE). We demonstrated that elevated NE concentrations can cleave cell surface expressed γ ENaC (but not α, or ß ENaC), suggesting a causal relationship between γ ENaC cleavage and ENaC activation, taking place at the plasma membrane. In addition, we demonstrated that the serine protease inhibitor (serpin) serpinH1, which is co-expressed with ENaC in the distal nephron is capable of inhibiting the channel by preventing cleavage of the γ ENaC subunit. Aldosterone mediated increases in INa aze known to be inhibted by TGFß. TGFß is also known to increase serpinHl expression. The demonstrated inhibition of γ ENaC cleavage and channel activation by serpinH1 may be responsible for the effect of TGFß on aldosterone stimulation in the distal nephron. In summary, we show that cleavage of the γ subunit, but not the α or ß subunit is linked to channel activation in three seperate contexts. Résumé Le canal épithélial à sodium (ENaC) est constitué de trois sous-unités homologues α, ß, and γ. Ce canal est impliqué dans le maintien de la balance sodique qui influence le niveau du liquide périciliaire du poumon et la pression sanguine via le rein. Dans les ovocytes de Xenopus laevis ENaC est préférentiellement et rapidement exprimé en formant un complexe hétéromérique αßγ. En revanche, l'expression homomérique de α ou hétéromérique des complexes αß et αγ conduit à une expression à la surface cellulaire d'un canal ENaC ne possédant qu'une faible activité. Des études récentes ont mis en évidence que les sous-unités α et γ d'ENaC (mais pas ß) sont coupées par des protéases endogènes (les farines) et que ces clivages augmentent l'activité du canal. Nous avons donc analysé, aussi bien à la surface cellulaire que dans le cytoplasme, les produits des clivages de combinaison homo- et hétéromérique des sous-unités d'ENaC (α, ß, γ, ßγ, αß, αγ, ßγ et αßγ). En parallèle, nous avons étudié l'activité correspondante à ces canaux par la mesure du transport de sodium sensible à l'amiloride (INa). Nous avons montré que lors de l'assemblage des sous-unités d'ENaC, le clivage de γ correspond à l'augmentation de INa. Nous avons également mis en évidence que dans une maladie telle que la fibrose cystique (CF) caractérisée par un déséquilibre de la balance protéase-inhibiteur de protéase, ENaC est suractivé par une sérine protéase nommée élastase (NE). L'augmentation de la concentration de NE clive γ ENaC exprimé à la surface cellulaire (mais pas α, ni ß ENaC) suggérant une causalité entre le clivage d'ENaC et son activation à la membrane plasmique. De plus, nous avons démontré que l'inhibiteur de sérine protéase (serpin) serpinH1, qui est co-exprimé avec ENaC dans le néphron distal, inhibe l'activité du canal en empêchant le clivage de la sous-unité γ ENaC. Il est connu que le INa induit par l'aldostérone peut être inhibé par TGFß. Or TGFß augmente l'expression de serpinH1. L'inhibition du clivage de γ ENaC et de l'activation du canal par la serpinH1 que nous avons mis en évidence pourrait ainsi être responsable de l'effet de TGFß sur la stimulation du courant par l'aldostérone dans le néphron distal. En résumé, nous avons montré que le clivage de la sous-unité γ, mais pas des sous-unités α et ß, est lié à l'activation du canal dans trois contextes distincts. Résumé tout public Le corps humain est composé d'environ 10 000 milliards de cellules et d'approximativement 60% d'eau. Les cellules du corps sont les unités fondamentales de la vie et elles sont dépendantes de certains nutriments et molécules. Ces nutriments et molécules sont dissous dans l'eau qui est présente dans et hors des cellules. Le maintien d'une concentration adéquate - de ces nutriments et de ces molécules dans l'eau à l'intérieur et à l'extérieur des cellules est -..essentiel pour leur survie. L'eau hors des cellules est nommée le fluide extracellulaire et peut être subdivisée en fluide interstitiel, qui se trouve autour des cellules, et en plasma, qui est le fluide des vaisseaux sanguins. Les fluides, les nutriments et les molécules sont constamment échangés entre les cellules, le fluide interstitiel, et le plasma. Le plasma circule dans le système circulatoire afin de distribuer les nutriments et molécules dans tout le corps et afin d'enlever les déchets cellulaires. Le rein joue un rôle essentiel dans la régulation du volume et de la concentration du plasma en éliminant sélectivement les nutriments et les molécules via la formation de l'urine. L'être humain possède deux reins, constitués chacun d'environ 1 million de néphrons. Ces derniers sont responsables de réabsorber et de sécréter sélectivement les nutriments et les molécules. Le canal épithélial à sodium (ENaC) est localisé à la surface cellulaire des néphrons et est responsable de la réabsorption du sodium (Na+). Le Na+ est présent dans quasiment toute la nourriture que nous mangeons et représente, en terme de molécule, 50% du sel de cuisine. Si trop de sodium est consommé, ENaC est inactif, si bien que le Na+ n'est pas réabsorbé et quitte le corps par l'urine. Ce mécanisme permet d'éviter que la concentration plasmatique de Na+ ne devienne trop grande, ce qui résulterait en une augmentation de la pression sanguine. Si trop peu de Na+ est consommé, ENaC réabsorbe le Na+ de l'urine primaire ce qui permet de conserver la concentration de Na+ et de prévenir une diminution de la pression sanguine par une perte de Na+. ENaC est aussi présent dans les cellules des poumons qui sont les organes permettant la respiration. La respiration est aussi essentielle pour la survie des cellules. Les poumons ne doivent pas contenir trop de liquide afin de permettre la respiration, mais en même temps ils ne doivent pas non plus être trop secs. En effet, ceci tuerait les cellules et empêcherait aussi la respiration. ENaC permet de maintenir un niveau d'humidité approprié dans les poumons en absorbant du Na+ ce qui entraîne un mouvement osmotique d'eau. L'absorption de sodium par ENaC ~ est augmentée par les protéases (in vitro et ex vivo). Les protéases sont des molécules qui peuvent couper d'autres molécules à des endroits précis. Nous avons démonté que certaines protéases augmentent l'absorption de Na+ en coupant ENaC à des endroits spécifiques. L'inhibition de ces protéases diminue le transport de Na+ et empêche le clivage d'ENaC. Dans certaines maladies telle que la mucoviscidose, des protéases sont suractivées et augmentent l'activité d'ENaC de manière inappropriée conduisant à une trop forte absorption de Na+ et à un déséquilibre de la muqueuse des poumons. Cette étude est donc particulièrement importante dans le cadre de la recherche thérapeutique de ce genre de maladie.

Scales and causes of heterogeneity in bars in a large multi-channel river: Rio Parana, Argentina

To date, published studies of alluvial bar architecture in large rivers have been restricted mostly to case studies of individual bars and single locations. Relatively little is known about how the depositional processes and sedimentary architecture of kilometre-scale bars vary within a multi-kilometre reach or over several hundreds of kilometres downstream. This study presents Ground Penetrating Radar and core data from 11, kilometre-scale bars from the Rio Parana, Argentina. The investigated bars are located between 30km upstream and 540km downstream of the Rio Parana - Rio Paraguay confluence, where a significant volume of fine-grained suspended sediment is introduced into the network. Bar-scale cross-stratified sets, with lengths and widths up to 600m and thicknesses up to 12m, enable the distinction of large river deposits from stacked deposits of smaller rivers, but are only present in half the surface area of the bars. Up to 90% of bar-scale sets are found on top of finer-grained ripple-laminated bar-trough deposits. Bar-scale sets make up as much as 58% of the volume of the deposits in small, incipient mid-channel bars, but this proportion decreases significantly with increasing age and size of the bars. Contrary to what might be expected, a significant proportion of the sedimentary structures found in the Rio Parana is similar in scale to those found in much smaller rivers. In other words, large river deposits are not always characterized by big structures that allow a simple interpretation of river scale. However, the large scale of the depositional units in big rivers causes small-scale structures, such as ripple sets, to be grouped into thicker cosets, which indicate river scale even when no obvious large-scale sets are present. The results also show that the composition of bars differs between the studied reaches upstream and downstream of the confluence with the Rio Paraguay. Relative to other controls on downstream fining, the tributary input of fine-grained suspended material from the Rio Paraguay causes a marked change in the composition of the bar deposits. Compared to the upstream reaches, the sedimentary architecture of the downstream reaches in the top ca 5m of mid-channel bars shows: (i) an increase in the abundance and thickness (up to metre-scale) of laterally extensive (hundreds of metres) fine-grained layers; (ii) an increase in the percentage of deposits comprised of ripple sets (to >40% in the upper bar deposits); and (iii) an increase in bar-trough deposits and a corresponding decrease in bar-scale cross-strata (<10%). The thalweg deposits of the Rio Parana are composed of dune sets, even directly downstream from the Rio Paraguay where the upper channel deposits are dominantly fine-grained. Thus, the change in sedimentary facies due to a tributary point-source of fine-grained sediment is primarily expressed in the composition of the upper bar deposits.

Deposits of the sandy braided South Saskatchewan River: Implications for the use of modern analogs in reconstructing channel dimensions in reservoir characterization

Estimation of the dimensions of fluvial geobodies from core data is a notoriously difficult problem in reservoir modeling. To try and improve such estimates and, hence, reduce uncertainty in geomodels, data on dunes, unit bars, cross-bar channels, and compound bars and their associated deposits are presented herein from the sand-bed braided South Saskatchewan River, Canada. These data are used to test models that relate the scale of the formative bed forms to the dimensions of the preserved deposits and, therefore, provide an insight as to how such deposits may be preserved over geologic time. The preservation of bed-form geometry is quantified by comparing the Alluvial architecture above and below the maximum erosion depth of the modem channel deposits. This comparison shows that there is no significant difference in the mean set thickness of dune cross-strata above and below the basal erosion surface of the contemporary channel, thus suggesting that dimensional relationships between dune deposits and the formative bed-form dimensions are likely to be valid from both recent and older deposits. The data show that estimates of mean bankfull flow depth derived from dune, unit bar, and cross-bar channel deposits are all very similar. Thus, the use of all these metrics together can provide a useful check that all components and scales of the alluvial architecture have been identified correctly when building reservoir models. The data also highlight several practical issues with identifying and applying data relating to cross-strata. For example, the deposits of unit bars were found to be severely truncated in length and width, with only approximately 10% of the mean bar-form length remaining, and thus making identification in section difficult. For similar reasons, the deposits of compound bars were found to be especially difficult to recognize, and hence, estimates of channel depth based on this method may be problematic. Where only core data are available (i.e., no outcrop data exist), formative flow depths are suggested to be best reconstructed using cross-strata formed by dunes. However, theoretical relationships between the distribution of set thicknesses and formative dune height are found to result in slight overestimates of the latter and, hence, mean bankfull flow depths derived from these measurements. This article illustrates that the preservation of fluvial cross-strata and, thus, the paleohydraulic inferences that can be drawn from them, are a function of the ratio of the size and migration rate of bed forms and the time scale of aggradation and channel migration. These factors must thus be considered when deciding on appropriate length:thickness ratios for the purposes of object-based modeling in reservoir characterization.

An infrared spectral signature of human lymphocyte subpopulations from peripheral blood.

Metastatic melanomas are frequently refractory to most adjuvant therapies such as chemotherapies and radiotherapies. Recently, immunotherapies have shown good results in the treatment of some metastatic melanomas. Immune cell infiltration in the tumor has been associated with successful immunotherapy. More generally, tumor infiltrating lymphocytes (TILs) in the primary tumor and in metastases of melanoma patients have been demonstrated to correlate positively with favorable clinical outcomes. Altogether, these findings suggest the importance of being able to identify, quantify and characterize immune infiltration at the tumor site for a better diagnostic and treatment choice. In this paper, we used Fourier Transform Infrared (FTIR) imaging to identify and quantify different subpopulations of T cells: the cytotoxic T cells (CD8+), the helper T cells (CD4+) and the regulatory T cells (T reg). As a proof of concept, we investigated pure populations isolated from human peripheral blood from 6 healthy donors. These subpopulations were isolated from blood samples by magnetic labeling and purities were assessed by Fluorescence Activated Cell Sorting (FACS). The results presented here show that Fourier Transform Infrared (FTIR) imaging followed by supervised Partial Least Square Discriminant Analysis (PLS-DA) allows an accurate identification of CD4+ T cells and CD8+ T cells (>86%). We then developed a PLS regression allowing the quantification of T reg in a different mix of immune cells (e.g. Peripheral Blood Mononuclear Cells (PBMCs)). Altogether, these results demonstrate the sensitivity of infrared imaging to detect the low biological variability observed in T cell subpopulations.

Chromosome 7 gain and DNA hypermethylation at the HOXA10 locus are associated with expression of a stem cell related HOX-signature in glioblastoma.

BACKGROUND: HOX genes are a family of developmental genes that are expressed neither in the developing forebrain nor in the normal brain. Aberrant expression of a HOX-gene dominated stem-cell signature in glioblastoma has been linked with increased resistance to chemo-radiotherapy and sustained proliferation of glioma initiating cells. Here we describe the epigenetic and genetic alterations and their interactions associated with the expression of this signature in glioblastoma. RESULTS: We observe prominent hypermethylation of the HOXA locus 7p15.2 in glioblastoma in contrast to non-tumoral brain. Hypermethylation is associated with a gain of chromosome 7, a hallmark of glioblastoma, and may compensate for tumor-driven enhanced gene dosage as a rescue mechanism by preventing undue gene expression. We identify the CpG island of the HOXA10 alternative promoter that appears to escape hypermethylation in the HOX-high glioblastoma. An additive effect of gene copy gain at 7p15.2 and DNA methylation at key regulatory CpGs in HOXA10 is significantly associated with HOX-signature expression. Additionally, we show concordance between methylation status and presence of active or inactive chromatin marks in glioblastoma-derived spheres that are HOX-high or HOX-low, respectively. CONCLUSIONS: Based on these findings, we propose co-evolution and interaction between gene copy gain, associated with a gain of chromosome 7, and additional epigenetic alterations as key mechanisms triggering a coordinated, but inappropriate, HOX transcriptional program in glioblastoma.

Establishment and characterization of models of chemotherapy resistance in colorectal cancer: Towards a predictive signature of chemoresistance.

Current standard treatments for metastatic colorectal cancer (CRC) are based on combination regimens with one of the two chemotherapeutic drugs, irinotecan or oxaliplatin. However, drug resistance frequently limits the clinical efficacy of these therapies. In order to gain new insights into mechanisms associated with chemoresistance, and departing from three distinct CRC cell models, we generated a panel of human colorectal cancer cell lines with acquired resistance to either oxaliplatin or irinotecan. We characterized the resistant cell line variants with regards to their drug resistance profile and transcriptome, and matched our results with datasets generated from relevant clinical material to derive putative resistance biomarkers. We found that the chemoresistant cell line variants had distinctive irinotecan- or oxaliplatin-specific resistance profiles, with non-reciprocal cross-resistance. Furthermore, we could identify several new, as well as some previously described, drug resistance-associated genes for each resistant cell line variant. Each chemoresistant cell line variant acquired a unique set of changes that may represent distinct functional subtypes of chemotherapy resistance. In addition, and given the potential implications for selection of subsequent treatment, we also performed an exploratory analysis, in relevant patient cohorts, of the predictive value of each of the specific genes identified in our cellular models.

Electrical signature of modern and ancient tectonic processes in the crust of the Atlas mountains of Morocco.

The Atlas Mountains in Morocco are considered as type examples of intracontinental chains, with high topography that contrasts with moderate crustal shortening and thickening. Whereas recent geological studies and geodynamic modeling have suggested the existence of dynamic topography to explain this apparent contradiction, there is a lack of modern geophysical data at the crustal scale to corroborate this hypothesis. Newly-acquired magnetotelluric data image the electrical resistivity distribution of the crust from the Middle Atlas to the Anti-Atlas, crossing the tabular Moulouya Plain and the High Atlas. All the units show different and unique electrical signatures throughout the crust reflecting the tectonic history of development of each one. In the upper crust electrical resistivity values may be associated to sediment sequences in the Moulouya and Anti-Atlas and to crustal scale fault systems in the High Atlas developed during the Cenozoic times. In the lower crust the low resistivity anomaly found below the Mouluya plain, together with other geophysical (low velocity anomaly, lack of earthquakes and minimum Bouguer anomaly) and geochemical (Neogene-Quaternary intraplate alkaline volcanic fields) evidence, infer the existence of a small degree of partial melt at the base of the lower crust. The low resistivity anomaly found below the Anti-Atlas may be associated with a relict subduction of Precambrian oceanic sediments, or to precipitated minerals during the release of fluids from the mantle during the accretion of the Anti-Atlas to the West African Supercontinent during the Panafrican orogeny ca. 685 Ma).

Measurement of a Structured Backflow in an Open Small Channel Induced by Surface-Tension Gradients

We present experiments in which the laterally confined flow of a surfactant film driven by controlled surface tension gradients causes the subtended liquid layer to self-organize into an inner upstream microduct surrounded by the downstream flow. The anomalous interfacial flow profiles and the concomitant backflow are a result of the feedback between two-dimensional and three-dimensional microfluidics realized during flow in open microchannels. Bulk and surface particle image velocimetry data combined with an interfacial hydrodynamics model explain the dependence of the observed phenomena on channel geometry.

Implementation of Customer Relationship Management system to support channel partners

Työn tavoitteena oli selvittää, kokevatko matkapuhelinalalla toimivat kanavapartnerit heitä varten suunnitellun asiakassuhdehallintajärjestelmän lisäarvopalveluna vaiko eivät. Työ toteutettiin asiakastyytyväisyystutkimuksen avulla, jossa mitattiin erilaisten partnereiden asennetta palvelua kohtaan. Työn tuloksena ilmeni, että palvelussa olevan informaation määrällä ei ollut suurta vaikutusta asiakkaiden tyytyväisyyteen. Syyt ovat pikemminkin yleisissä asenteissa vastaavia palveluja kohtaan.

Nutrient signature of Quebec (Canada) cranberry (Vaccinium macrocarpon Ait.)

Fertilizer recommendations for cranberry crops are guided by plant and soil tests. However, critical tissue concentration ranges used for diagnostic purposes are inherently biased by nutrient interactions and physiological age. Compositional data analysis using isometric log ratios (ilr) of nutrients as well as time detrending can avoid numerical biases. The objective was to derive unbiased nutrient signature standards for cranberry in Quebec and compare those standards to literature data. Field trials were conducted during 3 consecutive years with varying P treatments at six commercial sites in Quebec. Leaf tissues were analyzed for N, P, K, Ca, Mg, B, Cu, Zn, Mn and Fe. The analytical results were transformed into ilr nutrient balances of parts and groups of parts. High-yield reference ilr values were computed for cranberry yielding greater than 35 Mg ha-1. Many cranberry fields appeared to be over-supplied with K and either under-supplied with Mn or over-supplied with Fe as shown by their imbalanced [K | Ca, Mg] and [Mn | Fe] ratios. Nutrient concentration ranges from Maine and Wisconsin, USA, were combined into ilr values to generate ranges of balances. It was found that these nutrient ranges were much too broad for application in Quebec or outside the Quebec ranges for the [Ca | Mg] and the [Mn | Fe] balances, that were lower compared to those of high yielding cranberry crops in Quebec.