scholarly journals Aggregate-based sub-CMC solubilization of n-alkanes by monorhamnolipid biosurfactant

2016 ◽  
Vol 40 (3) ◽  
pp. 2028-2035 ◽  
Author(s):  
Hua Zhong ◽  
Xin Yang ◽  
Fei Tan ◽  
Mark L. Brusseau ◽  
Lei Yang ◽  
...  
Keyword(s):  
Formation Mechanism ◽  
Aggregate Size ◽  
Aggregate Formation ◽  
Surface Excess

Monorhamnolipid biosurfactant at concentrations lower than the CMC enhances solubilization ofn-alkanes due to an aggregate formation mechanism. The sub-CMC aggregate size decreases with increasing surface excess of monorhamnolipid.

scholarly journals Aggregate-based sub-CMC solubilization of hexadecane by surfactants

RSC Advances ◽  
2015 ◽  
Vol 5 (95) ◽  
pp. 78142-78149 ◽  
Author(s):  
Hua Zhong ◽  
Lei Yang ◽  
Guangming Zeng ◽  
Mark L. Brusseau ◽  
Yake Wang ◽  
...  
Keyword(s):  
Formation Mechanism ◽  
Aggregate Size ◽  
Aggregate Formation ◽  
Surface Excess ◽  
Triton X

SDBS or Triton X-100 at sub-CMC concentrations enhances hexadecane solubilization due to the aggregate formation mechanism. The sub-CMC aggregate size decreases with increasing surface excess of the surfactant.

scholarly journals Quorum sensing controls Vibrio cholerae multicellular aggregate formation

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Matthew Jemielita ◽  
Ned S Wingreen ◽  
Bonnie L Bassler
Keyword(s):  
Quorum Sensing ◽  
Vibrio Cholerae ◽  
Biofilm Formation ◽  
Aggregate Size ◽  
Extracellular Dna ◽  
Signal Molecules ◽  
Aggregate Formation ◽  
Multicellular Aggregate ◽  
Canonical Surface ◽  
Pandemic Strains

Bacteria communicate and collectively regulate gene expression using a process called quorum sensing (QS). QS relies on group-wide responses to signal molecules called autoinducers. Here, we show that QS activates a new program of multicellularity in Vibrio cholerae. This program, which we term aggregation, is distinct from the canonical surface-biofilm formation program, which QS represses. Aggregation is induced by autoinducers, occurs rapidly in cell suspensions, and does not require cell division, features strikingly dissimilar from those characteristic of V. cholerae biofilm formation. Extracellular DNA limits aggregate size, but is not sufficient to drive aggregation. A mutagenesis screen identifies genes required for aggregate formation, revealing proteins involved in V. cholerae intestinal colonization, stress response, and a protein that distinguishes the current V. cholerae pandemic strain from earlier pandemic strains. We suggest that QS-controlled aggregate formation is important for V. cholerae to successfully transit between the marine niche and the human host.

Effect of ADP and ATP Receptor Antagonism on Erythrocytosis-Induced Platelet Aggregate Formation under Dynamic Flow Conditions.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3903-3903
Author(s):  
Ellinor I.B. Peerschke ◽  
Richard T. Silver ◽  
Babette Weksler ◽  
Naphtali Savion ◽  
David Varon
Keyword(s):  
Adenine Nucleotides ◽  
Aggregate Size ◽  
Creatine Phosphate ◽  
Serotonin Release ◽  
Aggregate Formation ◽  
Flow Conditions ◽  
Platelet Factor ◽  
Thrombotic Risk ◽  
Platelet Aggregate ◽  
Granule Secretion

Abstract Red blood cells (RBC) contribute significantly to hemostasis and thrombosis under oscillatory flow conditions, and erythrocytosis has been associated with increased thrombotic risk. To capture dynamic effects of RBC on platelets, we used a recently described Cone and Plate (let) Analyzer (CPA), to evaluate the effect of hematocrit (Hct) on platelet function in whole blood under arterial flow conditions (1800 sec-1, 2 min, 25°C). Anticoagulated blood, reconstituted to varying hematocrits with autologous RBC, demonstrated a significant increase (30–50%, n= 12, p < 0.05) in adherent platelet aggregate size at Hct levels >45%. No significant effect on platelet adhesion was noted. Increases in aggregate size were not accompanied by significant platelet dense or alpha granule secretion, measured using 14C-serotonin release and Platelet Factor 4 ELISA assays, respectively. However, when cell-free supernatants (SNT) were prepared post shearing to investigate the presence of proaggregatory activity by adding SNT to fresh PRP (1:10 SNT: PRP ratio), and quantifying the formation of small platelet aggregates with a laser light scatter aggregometer, SNT derived from sheared high Hct samples contained nearly twice (1.75 + 0.16, n=5, p < 0.05) the activity of sheared normal Hct samples. The erythrocytosis-induced increase in platelet aggregate size was not affected by pretreatment of blood with 0.05 mM aspirin, but could be prevented completely by antagonism of P2Y1 (MRS2179, 200 μM), P2Y12 (2-methylthioadenosine 5′-monophosphate, 10–100 μM), or P2X1 (MRS2159, 200 μM), ADP and ATP receptors, respectively, as well as by converting exogenous ADP to ATP with a combination of creatine phosphate (2 mM) and creatine phosphokinase (20 U/ml). Whereas negligible platelet granule secretion was measured post shear, metabolic inhibition of RBC with 1% sodium azide or 0.25% glutaraldehyde fixation (2 h, 37°C) fully inhibited erythrocytosis-enhanced increases in platelet aggregate size. Thus, the adenine nucleotides contributing to erythrocytosis-enhanced platelet aggregate formation under physiologic shear appear to be derived predominantly from RBC. Taken together, the data suggest that ADP and ATP are both required for erythrocytosis-induced large platelet aggregate formation, but that the presence of ATP alone is not sufficient. The results may further suggest a role for direct ADP or ATP receptor blockade for the prevention of erythrocytosis-associated thrombotic complications.

scholarly journals The role of SOM and CaCO3 on soil aggregate development in reclaimed soils

2020 ◽  
Author(s):  
Evelin Pihlap ◽  
Markus Steffens ◽  
Ingrid Kögel-Knabner
Keyword(s):  
Organic Matter ◽  
Soil Organic Matter ◽  
Extracellular Polymeric Substances ◽  
Aggregate Size ◽  
Soil Aggregate ◽  
Parent Material ◽  
Size Class ◽  
Aggregate Formation ◽  
Structural Formation ◽  
Size Classes

&lt;p&gt;Soil organic matter (SOM) and extracellular polymeric substances (EPS) from biological processes are considered to be major contributors in aggregate formation. But there is limited knowledge on soil structural formation after reclamation &amp;#8211; the step when SOM content is low and soil properties are mostly controlled by the parent material. In our study we used a chronosequence approach in the reclaimed open-cast mining area near Cologne, Germany to elucidate the development of soil structure and soil organic matter during initial soil formation in a loess material. We selected six plots with different ages of agricultural management after reclamation (0, 1, 3, 6, 12, and 24 years after first seeding). In each reclaimed field 12 spatially independent locations were sampled with stainless steel cylinders (100 cm&lt;sup&gt;3&lt;/sup&gt;) at two depths in the topsoil (1-5 cm and 16-20 cm). Samples were wet sieved into four aggregate size classes of &lt;63 &amp;#181;m, 63-200 &amp;#181;m, 200-630 &amp;#181;m and 630-2000 &amp;#181;m. Each aggregate size class was characterized by organic carbon (OC), total nitrogen (TN) and CaCO&lt;sub&gt;3&lt;/sub&gt; concentration. The chemical composition of the SOM of selected samples was characterized using solid-state 13C NMR spectroscopy.&lt;/p&gt;&lt;p&gt;Wet sieving into aggregate size classes showed different trends along the chronosequence. Contradicting relation between CaCO&lt;sub&gt;3&lt;/sub&gt; and OC contribution to aggregate size classes display two different mechanisms on soil aggregate formation in young loess derived soils. CaCO&lt;sub&gt;3&lt;/sub&gt; influenced aggregation predominantly in finer aggregate size classes, where the highest concentration and contribution was measured. SOM, on the other hand, played an important role on formation of large macro-aggregates after organic manure application in year 4. Furthermore, the loss of total OC after year 12 was connected with the loss of OC contributing to the largest aggregate size class. Our findings reveal that SOM and CaCO&lt;sub&gt;3&lt;/sub&gt; role on stabilizing aggregates is not equally distributed and is aggregate size class dependent.&lt;/p&gt;

scholarly journals N-terminal ubiquitination of amyloidogenic proteins triggers removal of their oligomers by the proteasome holoenzyme

2019 ◽  
Author(s):  
Yu Ye ◽  
David Klenerman ◽  
Daniel Finley
Keyword(s):  
Single Molecule ◽  
Biological Process ◽  
Aggregate Size ◽  
Peptidase Activity ◽  
Aggregation Process ◽  
Aggregate Formation ◽  
Ubiquitinated Proteins ◽  
Amyloidogenic Proteins ◽  
Ubiquitin Moiety

Aggregation of amyloidogenic proteins is an abnormal biological process implicated in neurodegenerative disorders. While the aggregation process of amyloid-forming proteins has been studied extensively, the mechanism of aggregate removal is poorly understood. We recently demonstrated that proteasomes could fragment filamentous aggregates into smaller entities, restricting aggregate size[1]. Here, we show in vitro that UBE2W can modify the N-terminus of both αS and tauK18 with a single ubiquitin moiety. We demonstrate that an engineered N-terminal Ub modification changes the aggregation process of both proteins, resulting in the formation of structurally distinct aggregates. Single-molecule approaches further reveal that the proteasome can target soluble oligomers assembled from Ub-modified proteins independent of its peptidase activity, consistent with our recently reported fibril-fragmenting activity. Based on these results, we propose that proteasomes are able to target oligomers assembled from N-terminally ubiquitinated proteins. Our data suggest a possible disassembly mechanism by which N-terminal ubiquitination and the proteasome may together impede aggregate formation.

scholarly journals Turbulence mediates marine aggregate formation and destruction in the upper ocean

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Marika Takeuchi ◽  
Mark J. Doubell ◽  
George A. Jackson ◽  
Misuzu Yukawa ◽  
Yosuke Sagara ◽  
...  
Keyword(s):  
Surface Layer ◽  
Size Distribution ◽  
Aggregate Size ◽  
Euphotic Zone ◽  
Ocean Surface ◽  
Benthic Boundary Layer ◽  
Pump Efficiency ◽  
Field Observations ◽  
Aggregate Formation ◽  
Ocean Surface Layer

Abstract Marine aggregates formed through particle coagulation, large ones (>0.05 cm) also called marine snow, make a significant contribution to the global carbon flux by sinking from the euphotic zone, impacting the Earth’s climate. Since aggregate sinking velocity and carbon content are size-dependent, understanding the physical mechanisms controlling aggregate size distribution is fundamental to determining the biological carbon pump efficiency. Theoretical, laboratory and in-situ studies of flocculation have suggested that turbulence in the benthic boundary layer is important for aggregate formation and destruction, but the small number of field observations has limited our understanding of the role of turbulence on aggregation processes in the ocean surface layer away from energetic boundaries. Using simultaneous field observations of turbulence and aggregates, we show how aggregate formation, destruction, morphology and size distribution in the ocean surface layer (10–100 m) are mediated by interactions between turbulence and aggregate concentration. Our findings suggest that turbulence enhances aggregate formation up to a critical turbulent kinetic energy dissipation rate of 10−6 (W kg−1), above which the smallest turbulent eddies limit aggregate size.

The Effect of Red Blood Cells on the ADP-induced Aggregation of Human Platelets in Flow Through Tubes

1990 ◽  
Vol 63 (01) ◽  
pp. 112-121 ◽  
Author(s):  
David N Bell ◽  
Samira Spain ◽  
Harry L Goldsmith
Keyword(s):  
Platelet Aggregation ◽  
Shear Rate ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Platelet Rich Plasma ◽  
Mean Transit Time ◽  
White Blood Cells ◽  
Aggregate Size ◽  
Human Platelets ◽  
Induced Aggregation

SummaryThe effect of red blood cells, rbc, and shear rate on the ADPinduced aggregation of platelets in whole blood, WB, flowing through polyethylene tubing was studied using a previously described technique (1). Effluent WB was collected into 0.5% glutaraldehyde and the red blood cells removed by centrifugation through Percoll. At 23°C the rate of single platelet aggregtion was upt to 9× greater in WB than previously found in platelet-rich plasma (2) at mean tube shear rates Ḡ = 41.9,335, and 1,920 s−1, and at both 0.2 and 1.0 µM ADP. At 0.2 pM ADP, the rate of aggregation was greatest at Ḡ = 41.9 s−1 over the first 1.7 s mean transit time through the flow tube, t, but decreased steadily with time. At Ḡ ≥335 s−1 the rate of aggregation increased between t = 1.7 and 8.6 s; however, aggregate size decreased with increasing shear rate. At 1.0 µM ADP, the initial rate of single platelet aggregation was still highest at Ḡ = 41.9 s1 where large aggregates up to several millimeters in diameter containing rbc formed by t = 43 s. At this ADP concentration, aggregate size was still limited at Ḡ ≥335 s−1 but the rate of single platelet aggregation was markedly greater than at 0.2 pM ADP. By t = 43 s, no single platelets remained and rbc were not incorporated into aggregates. Although aggregate size increased slowly, large aggregates eventually formed. White blood cells were not significantly incorporated into aggregates at any shear rate or ADP concentration. Since the present technique did not induce platelet thromboxane A2 formation or cause cell lysis, these experiments provide evidence for a purely mechanical effect of rbc in augmenting platelet aggregation in WB.

A Simple and Rapid Method to Determine GPIIb/IIIa-Receptor Inhibitor Activity in Whole Blood

1999 ◽  
Vol 19 (03) ◽  
pp. 134-138
Author(s):  
Gitta Kühnel ◽  
A. C. Matzdorff
Keyword(s):  
Flow Cytometry ◽  
Platelet Count ◽  
Blood Sample ◽  
Platelet Activation ◽  
Whole Blood ◽  
Receptor Occupancy ◽  
Aggregate Formation ◽  
Inhibitor Activity ◽  
Receptor Inhibitor

SummaryWe studied the effect of GPIIb/IIIa-inhibitors on platelet activation with flow cytometry in vitro. Citrated whole blood was incubated with increasing concentrations of three different GPIIb/IIIa-inhibitors (c7E3, DMP728, XJ757), then thrombin or ADP were added and after 1 min the sample was fixed. Samples without c7E3 but with 0.1 U/ml thrombin had a decrease in platelet count. Samples with increasing concentrations of c7E3 had a lesser or no decrease in platelet count. The two other inhibitors (DMP 725, XJ757) gave similar results. GPIIb/IIIa-inhibitors prevent aggregate formation and more single platelets remain in the blood sample. The agonist-induced decrease in platelet count correlates closely with the concentration of the GPIIb/IIIa inhibitor and receptor occupancy. This correlation may be used as a simple measure for inhibitor activity in whole blood.

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