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PubMed1996

Cholesterol oxidation in butter and dairy spread during storage.

In a dairy spread (800 g lipid/kg, 10 g salt/kg) based on 750 g milk fat/kg and 250 g rapeseed oil/kg fat in 15 g extruded catering packaging, there was a more significant accumulation of cholesterol oxidation products than in butter (minimum 800 g lipid/kg, 12 g salt/kg) in 10 g extruded catering packaging when stored at 4 or at 20 degrees C. There was a lag phase of 7 weeks in cholesterol oxidation in dairy spread stored at 4 degrees C, while no lag phase was observed for storage at 20 degrees C. Total concentrations of oxysterols were, however, very similar for dairy spread stored at 4 and 20 degrees C after 13 weeks storage (approximately 12 micrograms/g milk lipid); storage at -18 degrees C almost prevented cholesterol oxidation (approximately 4 micrograms/g milk lipid). For butter, cholesterol oxidation was less pronounced at 4 degrees C (<3 micrograms/g milk lipid) than at -18 degrees C (approximately 4 micrograms/g milk lipid) and 20 degrees C (approximately 7 micrograms/g milk lipid). 7-Ketocholesterol was the dominant oxidation product, with 1.3 and 5.7 micrograms/g milk lipid in butter and dairy spread respectively after 13 weeks storage at 4 degrees C.

Butter↗
PubMed1980

Weather, host and vector--their interplay in the spread of insect-borne animal virus diseases.

The spread of insect-borne animal virus diseases is influenced by a number of factors. Hosts migrate, move or are conveyed over long distances: vectors are carried on the wind for varying distances in search of hosts and breeding sites; weather and climate affect hosts and vectors through temperature, moisture and wind. As parasites of host and vector, viruses are carried by animals, birds and insects, and their spread can be correlated with the migration of hosts and the carriage of vectors on winds associated with the movements of the Intertropical Convergence Zone (ITCZ) and warm winds to the north and south of the limits of the ITCZ. The virus is often transmitted from a local cycle to a migratory cycle and back again.Examples of insect-borne virus diseases and their spread are analysed. Japanese, Murray Valley, Western equine, Eastern equine and St Louis encephalitis represent viruses transmitted by mosquito-bird or pig cycles.THE AREAS EXPERIENCING INFECTION WITH THESE VIRUSES CAN BE DIVIDED INTO A NUMBER OF ZONES: A, B, C, D, E and F. In zone A there is a continuous cycle of virus in host and vector throughout the year; in zone B, there is an upsurge in the cycle during the wet season, but the cycle continues during the dry season; there is movement of infected vectors between and within zones A and B on the ITCZ and the virus is introduced to zone C by infected vectors on warm winds; persistence may occur in zone C if conditions are right. In zone D, virus is introduced each year by infected vectors on warm winds and the arrival of the virus coincides with the presence of susceptible nestling birds and susceptible piglets. The disappearance of virus occurs at the time when migrating mosquitoes and birds are returning to warmer climates. The virus is introduced to zone E only on occasions every 5-10 years when conditions are suitable. Infected hosts introduced to zone F do not lead to circulation of virus, since the climate is unsuitable for vectors. Zones A, B and C correspond to endemic and zones D and E to epidemic conditions.Similar zones can be recognized for African horse sickness, bluetongue, Ibaraki disease and bovine ephemeral fever - examples of diseases transmitted in a midge-mammal cycle. In zones A and B viruses are transported by infected midges carried on the wind in association with the movement of ITCZ and undergo cycles in young animals. In these zones and in zone C there is a continual movement of midges on the warm wind between one area and another, colonizing new sites or reinforcing populations of midges already present. Virus is introduced at times into fringe areas (zones D and E) and, as there is little resistance in the host, gives rise to clinical signs of disease. In some areas there is persistence during adverse conditions; in others, the virus is carried back to the endemic zones by infected midges or vectors.Examples of viruses maintained in a mosquito/biting fly-mammal cycle are Venezuelan equine encephalitis and vesicular stomatitis. These viruses enter a migratory cycle from a local cycle and the vectors in the migratory cycle are carried over long distances on the wind. Further examples of virus spread by movement of vectors include West Nile, Rift Valley fever, yellow fever, epizootic haemorrhagic disease of deer and Akabane viruses.In devising means of control it is essential to decide the relationship of host, vector and virus and the nature of the zone in which the area to be controlled lies. Because of the continual risk of reintroduction of infected vectors, it is preferable to protect the host by dipping, spraying or by vaccination rather than attempting to eliminate the local population of insects.

African Horse Sickness↗
PubMed2000

Band spreading in two-dimensional microchannel turns for electrokinetic species transport

Analytical and numerical methods are employed to investigate species transport by electrophoretic or electroosmotic motion in the curved geometry of a two-dimensional turn. Closed-form analytical solutions describing the turn-induced diffusive and dispersive spreading of a species band are presented for both the low and high Peclet number limits. We find that the spreading due to dispersion is proportional to the product of the turn included angle and the Peclet number at low Peclet numbers. It is proportional to the square of the included angle and independent of the Peclet number when the Peclet number is large. A composite solution applicable to all Peclet numbers is constructed from these limiting behaviors. Numerical solutions for species transport in a turn are also presented over a wide range of the included angle and the mean turn radius. On the basis of comparisons between the analytical and numerical results, we find that the analytical solutions provide very good estimates of both dispersive and diffusive spreading provided that the mean turn radius exceeds the channel width. These new solutions also agree well with data from a previous study. Optimum conditions minimizing total spreading in a turn are presented and discussed.

Journal Article↗
PubMed1997

An all-D amino acid peptide model of alpha1(IV)531-543 from type IV collagen binds the alpha3beta1 integrin and mediates tumor cell adhesion, spreading, and motility.

Type IV collagen promotes integrin-mediated cell adhesion, spreading, and motility. Several regions within the triple-helical domain of type IV collagen have been identified as tumor cellular recognition sites. Among these regions, the alpha1(IV)531-543 sequence, designated L-Hep-III, promotes integrin-mediated tumor cell adhesion and directly binds to the alpha3beta1 integrin [Miles, A. J., et al. (1994) J. Biol. Chem. 269, 30939-30945; Miles, A. J., et al. (1995) J. Biol. Chem. 270, 29047-29050]. We have presently compared the activities of the all-d enantiomeric peptide model of alpha1(IV)531-543, designated D-Hep-III, with L-Hep-III, for promoting the adhesion, spreading, and motility of metastatic melanoma and breast carcinoma cells. D-Hep-III was found to support melanoma and breast carcinoma cell adhesion, spreading, and motility in a dose-dependent fashion similar to that of L-Hep-III. The adhesions of melanoma and breast carcinoma cells to both type IV collagen and fibronectin were effectively inhibited by L-Hep-III and D-Hep-III. Melanoma cell invasion of the basement membrane was also inhibited by D-Hep-III. Characterization of the cell surface receptor for D-Hep-III was acheived via cell adhesion assays and affinity chromatography using monoclonal antibodies against integrin subunits. Immunoprecipitation analysis following EDTA elution from a D-Hep-III affinity column indicated that D-Hep-III binds to the alpha3beta1 integrin but not to the alpha2 or alpha6 integrin subunits. In summary, these studies demonstrate that an all-D model of the alpha1(IV)531-543 sequence mimics the biological activities of the all-L peptide. D-Hep-III is the first all-D peptide that has been shown to promote tumor cell adhesion, spreading, and migration, inhibit tumor cell adhesion and migration on type IV collagen and invasion of the basement membrane, and bind directly to an integrin. Due to the resistance to proteolysis, all-D receptor-binding peptides such as D-Hep-III have great potential for in vivo studies and as therapeutic agents.

Antibodies, Monoclonal↗
PubMedDate not supplied

Measurement of adhesion and spreading kinetics of baby hamster kidney and hybridoma cells using an integrated optical method.

A novel optical method was used for quantitative characterization and continuous measurement of both the adhesion and spreading of mammalian cells on inorganic surfaces. It is based upon the effective refractive index change caused by cells when they adhere to a planar optical waveguide. We have applied this technique to measure the kinetics of the adhesion and spreading processes of baby hamster kidney (BHK) cells adhering to surfaces coated with fibronectin and under different culture conditions (PBS, medium, serum, EDTA). In comparison, hybridoma cells are only adsorbed to the surface and do not spread at all. Moreover, this technique also allows the mass of an adsorbed protein adlayer to be determined very precisely and thus provides a valuable tool for screening suitable substrata as well as determining the influence of different culture conditions on cell adhesion and spreading. This sensitive test for substrate influence could be important in toxicity tests using adherent animal cells.

Animals↗
PubMedDate not supplied

Quartz crystal microbalance study of endothelial cell number dependent differences in initial adhesion and steady-state behavior: evidence for cell-cell cooperativity in initial adhesion and spreading.

The quartz crystal microbalance (QCM) technique has been applied to the real time monitoring of endothelial cell (EC) adhesion and spreading on the QCM gold surface. We previously showed that the measured QCM Deltaf and DeltaR shifts were due to cells adhering to the gold crystal surface, requiring proteolytic enzyme treatment to be removed from the surface, in order for the Deltaf and DeltaR shifts to return to zero. In the present report, we demonstrate the quantitative dependence and saturation of the measured Deltaf and DeltaR shifts on the number of firmly attached ECs as measured by electronic counting of the cells. We demonstrate through a light microscope simulation experiment that the different Deltaf and DeltaR regions of the QCM temporal response curve correspond to the incident ECs contacting the surface, followed by their adhesion and spreading, which reflect cellular mass distribution and cytoskeletal viscoelasticity changes. Also, we demonstrate that the dose response curve of Deltaf and DeltaR values versus attached EC number is more sensitive and possesses less scatter for the hydrophilically treated surface compared to the native gold surface of the QCM. For both surfaces, a Deltaf and DeltaR versus trypsinized, attached EC number plot 1 h post-seeding exhibits a sigmoid curve shape whereas a similar plot 24 h post-seeding exhibits a hyperbolic curve shape. This number dependence suggests cell-cell cooperativity in the initial cell adhesion and spreading processes. These QCM data and our interpretation are corroborated by differences in cell appearance and spreading behavior we observed for ECs in a light microscope fluorescence simulation experiment of the cell density effect. For a stably attached EC monolayer at 24 h post-addition, steady-state Deltaf and DeltaR values are higher and exhibit saturation behavior for both the hydrophilically treated gold surface as compared to the untreated surface. The steady-state 24 h Deltaf and DeltaR values of stably attached ECs are shifted from the 1 h attached ECs. The 24 h values are characteristic of a more energy-dissipative structure. This is consistent with the time-dependent elaboration of surface contacts in anchorage-dependent ECs via the attachment of intregrins to underlying extracellular matrix. It is also in agreement with the known energy dissipation function of the ECs that cover the interior of blood vessels and are exposed to continuous pulsatile blood flow.

Animals↗
PubMed2005

Controlling molecular diffusion in self-spreading lipid bilayer using periodic array of ultra-small metallic architecture on solid surface.

Diffusion of target molecules incorporated in the self-spreading lipid bilayer was controlled by the introduction of periodic array of metallic architecture on solid surface. Retardation of the progress of target molecules became significant when the size of gap between small metal architectures was less than a few hundred nanometers. The self-spreading dynamics of the lipid bilayer depending on the size of the small gap were analyzed semiquantitatively. Estimated change in the driving force of the spreading layer suggests that highly localized compression of the spreading layer causes selective segregation of molecules.

Chemical Phenomena↗
PubMed2005

Chemical and physical properties of butterfat-vegetable oil blend spread prepared with enzymatically transesterified canola oil and caprylic acid.

Structured Lipid was synthesized from canola oil and caprylic acid with sn-1,3 specific lipase from Rhizomucor miehei. Cold spreadable butter was made by blending butterfat with the SL at a weight ratio of 80:20. Its chemical and physical properties were compared with pure butter and butterfat-canola oil 80:20 blend spread. The butterfat-SL blend had lower contents of hypercholesterolemic fatty acids (FAs) and the lowest atherogenic index (AI) as compared to the others. Melting and crystallization behaviors of butterfat-SL blend were similar to those of butterfat-canola oil blend above 0 degrees C. It showed solid fat contents (SFCs) similar to butterfat-canola oil blend but lower than pure butterfat. The butterfat-SL blend was shown to crystallize in the beta' form. There were no differences between the hardness of butterfat-SL blend spread and butterfat-canola oil blend spread. Rheological analysis showed that butterfat-SL blend spread lost its elastic behavior at 5 degrees C, a lower temperature than pure butter.

Butter↗
PubMed2005

Levels of phytosterol oxides in enriched and nonenriched spreads: application of a thin-layer chromatography-gas chromatography methodology.

The content of phytosterol oxidation products (POPs) in enriched and nonenriched commercial spreads was evaluated by thin-layer chromatography-gas chromatography (TLC-GC). Oxides of beta-sitosterol, campesterol, and stigmasterol were produced by thermo-oxidation (7-hydroxy, 7-keto, and epoxy derivatives) and chemical synthesis (triol derivatives), which were then separated and identified by TLC-GC. Their identification was further confirmed by GC-mass spectrometry (GC-MS). The total amounts of phytosterols found were 6.07 and 0.33 g/100 g of sample in phytosterol-enriched and nonenriched spread, respectively, whereas the total POPs contents were 45.60 and 13.31 mg/kg of sample in the enriched and nonenriched products. The main POPs found were the 7-keto derivatives of all phytosterols analyzed; 7-ketositosterol was the most abundant one (14.96 and 5.93 mg/kg of sample in phytosterol-enriched and nonenriched spread). No beta-epoxy and triol derivatives were detected in both types of samples. The enriched spread presented a lower phytosterol oxidation rate (0.07%) than the nonenriched one (0.41%).

Cholesterol↗
PubMed2004

Spreading of 16-mercaptohexadecanoic acid in microcontact printing.

Spreading in microcontact printing refers to the process or processes by which the ink molecules end up in the parts of the substrate that are adjacent to the contacted areas but which are not contacted themselves. This has been investigated for different inking concentrations of 16-mercaptohexadecanoic acid (MHDA). Spreading of MHDA takes place with retention of a well-defined demarcation. Feature sizes can be controlled by varying the contact times. Spreading, however, only takes place beyond a certain threshold concentration. For low ink concentrations the edges of stamp features dominate the ink transfer. For these low concentrations the extent of this edge dominance depends strongly on ink concentration rather than on contact time. These observations indicate a dominant role of the stamp surface in the processes of pattern formation and spreading.

Journal Article↗
PubMed2006

Spreading of silicone oils on glass in two geometries.

A basic problem in liquid spreading is the hydrodynamic description of the viscous breaking force near the moving contact line. A solution to the problem of divergence at the triple line has been illustrated with two experimental configurations. It consists of observing that the rheological behavior of a Newtonian liquid is modified near the triple line due to high shear rates. Above a critical value of the shear rate, near the triple line and near the solid surface, the liquid becomes shear-thinning, meaning that the apparent viscosity of the liquid decreases as the shear rate increases. As a result, there is no divergence of the viscous energy dissipation and of the braking force as observed for a purely Newtonian behavior. This description of the viscous braking phenomenon in liquid spreading is well supported by spreading experiments of silicone oils on glass substrates in two different wetting configurations. The liquids used are two silicone oils (10,000 and 100,000 cSt). These liquids are Newtonian below a critical value of the shear rate. Above this critical value, the liquid viscosity decreases according to a power law of the shear rate. One series of experiments consider the spreading of silicone oil droplets on treated and untreated glass substrates. The other configuration consists of using the glass substrates as Wilhelmy plates and to determine the advancing dynamic contact angle as a function of the imposed speed of sinking of the plate into oil reservoirs. The two series of experiments satisfy the same dynamic wetting laws. The overall experimental results are compatible with the hypothesis of a Newtonian/non Newtonian transition of the rheological properties of liquids near the wetting front although the main origin of dissipation appears to result from Newtonian viscous braking. The same dynamic law applies for the drop and Wilhelmy plate geometries.

Journal Article↗
PubMed2006

Wetting and spreading of a surfactant film on solid particles: influence of sharp edges and surface irregularities.

In addition to particle size and surface chemistry, the shape of particles plays an important role in their wetting and displacement by the surfactant film in the lung. The role of particle shape was the subject of our investigations using a model system consisting of a modified Langmuir-Wilhelmy surface balance. We measured the influence of sharp edges (lines) and other highly curved surfaces, including sharp corners or spikes, of different particles on the spreading of a dipalmitoylphosphatidyl (DPPC) film. The edges of cylindrical sapphire plates (circular curved edges, 1.65 mm radius) were wetted at a surface tension of 10.7 mJ/m2 (standard error (SE) = 0.45, n = 20) compared with that of 13.8 mJ/m2 (SE = 0.20, n = 20) for cubic sapphire plates (straight linear edges, edge length 3 mm) (p < 0.05). The top surfaces of the sapphire plates (cubic and cylindrical) were wetted at 8.4 mJ/m2 (SE = 0.54, n = 20) and 9.1 mJ/m2 (SE = 0.50, n = 20), respectively, but the difference was not significant (p > 0.05). The surfaces of the plates showed significantly higher resistance to spreading compared to that of the edges, as substantially lower surface tensions were required to initiate wetting (p < 0.05). Similar results were found for talc particles, were the edges of macro- and microcrystalline particles were wetted at 7.2 mJ/m2 (SE = 0.52, n = 20) and 8.2 mJ/m2 (SE = 0.30, n = 20) (p > 0.05), respectively, whereas the surfaces were wetted at 3.8 mJ/m2 (SE = 0.89, n = 20) and 5.8 mJ/m2 (SE = 0.52, n = 20) (p < 0.05), respectively. Further experiments with pollen of malvaceae and maize (spiky and fine knobbly surfaces) were wetted at 10.0 mJ/m2 (SE = 0.52, n = 10) and 22.75 mJ/m2 (SE = 0.81, n = 10), respectively (p < 0.05). These results show that resistance to spreading of a DPPC film on various surfaces is dependent on the extent these surfaces are curved. This is seen with cubic sapphire plates which have at their corners a radius of curvature of about 0.75 microm, spiky malvaceae pollen with an even smaller radius on top of their spikes, or talc with various highly curved surfaces. These highly curved surfaces resisted wetting by the DPPC film to a higher degree than more moderately curved surfaces such as those of cylindrical sapphire plates, maize pollens, or polystyrene spheres, which have a surface free energy similar to that of talc but a smooth surface. The macroscopic plane surfaces of the particles demonstrated the greatest resistance to spreading. This was explained by the extremely fine grooves in the nanometer range, as revealed by electron microscopy. In summary, to understand the effects of airborne particles retained on the surfaces of the respiratory tract, and ultimately their pathological potential, not only the particle size and surface chemistry but also the particle shape should be taken in consideration.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed2003

Which administration route of fentanyl better enhances the spread of spinal anaesthesia: intravenous, intrathecal or both?

BACKGROUND: To enhance the spread of spinal anaesthesia, fentanyl may be administered intrathecally (i.t.) or intravenously (i.v.). The purpose of this prospective study was to investigate the effects of fentanyl administered i.v., i.t. or concurrently by both i.v. and spinal routes on the spread of spinal anaesthesia. METHODS: Sixty patients were randomly assigned to one of three groups. In Groups I and II, spinal anaesthesia was performed with plain bupivacaine 10 mg plus 20 micro g fentanyl and in Group III with 10 mg of plain bupivacaine. The level of first peak sensory block was marked. In addition, fentanyl 50 micro g was administered i.v. in Groups II and III or by saline in Group I after the sensory blockade reached the highest dermatomal level. Ten minutes after i.v. administration, the level of the second peak sensory block was marked. The distance between the first- and second-highest levels of sensory block was measured. RESULTS: The distance between the first- and second-highest level of sensory block was significantly different for the three groups: Group II (5.8 +/- 2.6 cm) > Group III (2.9 +/- 2.1 cm) > Group I (-0.15 +/- 1.7 cm). The peak dermatomal level of spinal block was significantly higher in Group II [T4 (T3-T7)] than in Group I [T6 (T4-T9)] and Group III [T6 (T4-T8)]. In Groups I and II the sensory block regressed to S2 for a longer period of time than it did in Group III. CONCLUSION: Both the spinal and systemic administration of fentanyl enhanced the spread of spinal anaesthesia. The co-administration of spinal and i.v. fentanyl produced a greater increase in the cephalad spread of spinal block.

Adult↗
PubMedDate not supplied

Monensin inhibits initial spreading of cultured human fibroblasts.

The monovalent ionophore, monensin, inhibits the secretion of both pro-collagen and fibronectin in cultured human fibroblasts and other cell types. The block to secretion is due to the ability of monensin to suppress the export of these secretory proteins from the Golgi apparatus. As such proteins are known to be implicated in the adhesion, spreading and movement of cultured fibroblasts, it might be expected that monensin treatment would interfere with these processes. However, it has recently been reported that monensin-treated human embryonal fibroblasts attached and spread onto glass substrata to the same extent as untreated cells, although at later stages they fail to develop focal adhesion sites. However, these experiments were performed using medium supplemented with fetal calf serum (FCS). We now demonstrate that in the absence of FCS, while monensin has little or no effect on the initial adhesion of fibroblasts to the substratum, subsequent spreading is much reduced. The inhibition of spreading is noticeable within 30 min of plating and is maintained for at least 100 min in monensin-free medium following prolonged pre-incubation of the cells with monensin.

Cell Adhesion↗
PubMed1991

Genetic evidence for the spread of agriculture in Europe by demic diffusion.

European agriculture originated in the Near East about 9,000 years ago. The Neolithic reached almost all areas suitable for agriculture by 5,000 yr BP (before present). The routes and times of the spread of agriculture through Europe are relatively well established, but not its manner of spreading. This could have been by cultural diffusion with few genetic consequences. By contrast, Ammerman and Cavalli-Sforza proposed that the spread of farming increased local population densities, causing demic expansion into new territory and diffusive gene flow between the neolithic farmers and mesolithic groups. We have now tested observed genetic patterns against expectations derived from the demic expansion hypothesis. We found significant partial correlations of genetic distances with a distance matrix especially designed to represent the spread of agriculture on that continent, when geographic distances are held constant. These findings support the hypothesis of Ammerman and Cavalli-Sforza and invite further investigation into Renfrew's hypothesis on the origin of the Indo-European languages.

Agriculture↗
PubMed2006

Activation of c-jun N-terminal kinase is associated with cell proliferation and shorter relapse-free period in superficial spreading malignant melanoma.

Signaling pathways regulating cell proliferation and survival have become attractive targets for anticancer strategies. In the present study, we analyzed by immunohistochemistry, a panel of benign nevi, superficial spreading and nodular primary melanomas and metastases for expression of activated p38/mitogen-activated protein kinase (p-p38) and c-jun N-terminal kinase (JNK) (p-JNK) and correlated the findings with known prognostic variables. Twenty-five and 35% of the primaries and 9 and 25% of the metastases expressed variable levels of p-p38 and p-JNK, respectively. In benign nevi, 73.5% expressed p-JNK and 7% expressed p-p38. For patients with superficial spreading melanomas, high level of cytoplasmic p-JNK was associated with thicker tumors (P=0.017) and shorter disease-free survival (P=0.003) as well as with markers of cell proliferation (cyclin A (P=0.017) and p21 (P=0.021)). In nodular melanomas, nuclear p-p38 was associated with Ki-67 (P=0.012), but neither cytoplasmic nor nuclear localized p-p38 was associated with disease outcome. Of note, in superficial spreading melanomas, a positive correlation between cytoplasmic p-JNK and cytoplasmic p-extracellular signal-regulated kinase ERK(1/2) (P=0.005) and p-p38 (P=0.003) was observed. Likewise, p-p38 in cytoplasm was positively associated with cytoplasmic p-ERK1/2 (P<0.0005) and p-Akt (P=0.047). In contrast, except for a positive correlation between nuclear p-p38 and membranous p-TrkA (P=0.02), no correlation between the activation status of the different signaling pathways was observed in nodular melanomas. In conclusion, our results suggest that in benign nevi activated JNK may have a role in restricting uncontrolled cell proliferation or survival. However, during tumor progression, activation of JNK is associated with cell proliferation and shorter relapse-free period for patients with superficial spreading melanomas, suggesting that the JNK activation status could be a marker for clinical outcome in at least a subgroup of malignant melanoma. In contrast, activation of p38 seems to play a less important role in development and progression of malignant melanomas.

Biomarkers, Tumor↗
PubMed2002

Host-induced epidemic spread of the cholera bacterium.

The factors that enhance the transmission of pathogens during epidemic spread are ill defined. Water-borne spread of the diarrhoeal disease cholera occurs rapidly in nature, whereas infection of human volunteers with bacteria grown in vitro is difficult in the absence of stomach acid buffering. It is unclear, however, whether stomach acidity is a principal factor contributing to epidemic spread. Here we report that characterization of Vibrio cholerae from human stools supports a model whereby human colonization creates a hyperinfectious bacterial state that is maintained after dissemination and that may contribute to epidemic spread of cholera. Transcriptional profiling of V. cholerae from stool samples revealed a unique physiological and behavioural state characterized by high expression levels of genes required for nutrient acquisition and motility, and low expression levels of genes required for bacterial chemotaxis.

Animals↗
PubMed2003

Discovery of abundant hydrothermal venting on the ultraslow-spreading Gakkel ridge in the Arctic Ocean.

Submarine hydrothermal venting along mid-ocean ridges is an important contributor to ridge thermal structure, and the global distribution of such vents has implications for heat and mass fluxes from the Earth's crust and mantle and for the biogeography of vent-endemic organisms. Previous studies have predicted that the incidence of hydrothermal venting would be extremely low on ultraslow-spreading ridges (ridges with full spreading rates <2 cm x yr(-1)-which make up 25 per cent of the global ridge length), and that such vent systems would be hosted in ultramafic in addition to volcanic rocks. Here we present evidence for active hydrothermal venting on the Gakkel ridge, which is the slowest spreading (0.6-1.3 cm x yr(-1)) and least explored mid-ocean ridge. On the basis of water column profiles of light scattering, temperature and manganese concentration along 1,100 km of the rift valley, we identify hydrothermal plumes dispersing from at least nine to twelve discrete vent sites. Our discovery of such abundant venting, and its apparent localization near volcanic centres, requires a reassessment of the geologic conditions that control hydrothermal circulation on ultraslow-spreading ridges.

Journal Article↗