Recent studies indicate that extracellular vesicles are an important source material for many clinical applications, including minimally-invasive disease diagnosis. However, challenges for rapid and simple extracellular vesicle collection have hindered their application. We have developed and validated a novel class of peptides (which we named venceremin, or Vn) that exhibit nucleotide-independent specific affinity for canonical heat shock proteins. The Vn peptides were validated to specifically and efficiently capture HSP-containing extracellular vesicles from cell culture growth media, plasma, and urine by electron microscopy, atomic force microscopy, sequencing of nucleic acid cargo, proteomic profiling, immunoblotting, and nanoparticle tracking analysis. All of these analyses confirmed the material captured by the Vn peptides was comparable to those purified by the standard ultracentrifugation method. We show that the Vn peptides are a useful tool for the rapid isolation of extracellular vesicles using standard laboratory equipment. Moreover, the Vn peptides are adaptable to diverse platforms and therefore represent an excellent solution to the challenge of extracellular vesicle isolation for research and clinical applications.
The Bay of Bengal receives large amounts of freshwater from the Ganga‐Brahmaputra (GB) river during the summer monsoon. The resulting upper‐ocean freshening influences seasonal rainfall, cyclones, and biological productivity. Sparse in situ observations and previous modeling studies suggest that the East India Coastal Current (EICC) transports these freshwaters southward after the monsoon as an approximately 200 km wide, 2,000 km long “river in the sea” along the East Indian coast. Sea surface salinity (SSS) from the Soil Moisture Active Passive (SMAP) satellite provides unprecedented views of this peculiar feature from intraseasonal to interannual timescales. SMAP SSS has a 0.83 correlation and 0.49 rms‐difference to 0–5 m in situ measurements. SMAP and in stu data both indicate a SSS standard deviation of ∼0.7 to 1 away from the coast, that rises to 2 pss within 100 km of the coast, providing a very favorable signal‐to‐noise ratio in coastal areas. SMAP also captures the strong northern BoB, postmonsoon cross‐shore SSS contrasts (∼10 pss) measured along ship transects. SMAP data are also consistent with previous modeling results that suggested a modulation of the EICC/GB plume southward extent by the Indian Ocean Dipole (IOD). Remote forcing associated with the negative Indian Ocean Dipole in the fall of 2016 indeed caused a stronger EICC and “river in the sea” that extended by approximately 800 km further south than that in 2015 (positive IOD year). The combination of SMAP and altimeter data shows eddies stirring the freshwater plume away from the coast.
This study investigates sea surface salinity (SSS) and sea surface temperature (SST) variations in the tropical Atlantic east of the Lesser Antilles, a region where freshwater advection from the Amazon and Orinoco Rivers, may potentially impact air‐sea interaction. Observations are used to document later‐summer variability and evaluate offshore riverine transport from 2010 to 2014. During this period, the largest difference in plume‐affected areas, defined as the extent covered by SSS lower than 35.5 pss, is found between 2011 and 2014. Plume waters covered 92% of the study region in 2011 and 60% in 2014, with the average SSS in the study region being 2 pss lower in 2011. Lagrangian particle tracking based on satellite‐derived ocean currents is used to diagnose the impact of the river plumes on SSS and SST from 2010 to 2014. Northward freshwater flux in summer 2014 was significantly weaker than fluxes in 2010–2013. This difference is not due to interannual discharge variability, but to significant changes in eddy‐driven transport and cross‐shore winds. In particular, the stronger cross‐shore wind in May 2014 restricted offshore freshwater flow and lead to a smaller plume‐affected area. Persistent SST gradients are often found near the plume edge, which may have implications for ocean‐atmosphere coupling associated with atmospheric convection. SST in the study region was 1°C higher in 2010 compared to other years, and is related to basin‐scale ocean‐atmosphere processes. Interannual variation in Amazon advective pathways and the associated SSS changes are also influenced by changes in the ITCZ position between 2011 and 2014.
Recurrent apneas are important causes of hospitalization and morbidity in newborns. Gestational stress (GS) compromises fetal brain development. Maternal stress and anxiety during gestation are linked to respiratory disorders in newborns; however, the mechanisms remain unknown. Here, we tested the hypothesis that repeated activation of the neuroendocrine response to stress during gestation is sufficient to disrupt the development of respiratory control and augment the occurrence of apneas in newborn rats. Pregnant dams were displaced and exposed to predator odor from days 9 to 19 of gestation. Control dams were undisturbed. Experiments were performed on male and female rats aged between 0 and 4 d old. Apnea frequency decreased with age but was consistently higher in stressed pups than controls. At day 4, GS augmented the proportion of apneas with O 2 desaturations by 12%. During acute hypoxia (12% O 2 ), the reflexive increase in breathing augmented with age; however, this response was lower in stressed pups. Instability of respiratory rhythm recorded from medullary preparations decreased with age but was higher in stressed pups than controls. GS reduced medullary serotonin (5-HT) levels in newborn pups by 32%. Bath application of 5-HT and injection of 8-OH-DPAT [(Ϯ)-8-hydroxy-2-di-(n-propylamino) tetralin hydrobromide; 5-HT 1A agonist; in vivo] reduced respiratory instability and apneas; these effects were greater in stressed pups than controls. Sex-specific effects were observed. We conclude that activation of the stress response during gestation is sufficient to disrupt respiratory control development and promote pathological apneas in newborn rats. A deficit in medullary 5-HT contributes to these effects.
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