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•Calcium-activated biochar was prepared from rice straw-derived black liquor.•The Ca(OH)2 creates the pores and provides active adsorption sites for phosphate.•The Ca-biochar showed ...excellent performance for phosphate adsorption.•A high maximum adsorption capacity of 197 mg/g was achieved by the Ca-biochar.•The P-adsorbed Ca-biochar samples can be used as fertilizer in soil.
Black liquor-derived calcium-activated biochars (Ca-biochar) were synthesized by treating rice straw with Ca(OH)2 to create an adsorbent that was effective for removing phosphate from aqueous waste streams. The Ca(OH)2 acts to separate lignin from the biomass, create pores in the biochar solids and form active adsorption sites. The Ca-biochar adsorbent was efficient for the removal of phosphate from aqueous solutions (pH 1.0 to pH 13.0) with a highest phosphate adsorption capacity of 197 mg/g. Phosphate adsorption was correlated with pseudo-second-order kinetics and the Langmuir model with primary mechanisms being attributed to chemical precipitation and ligand exchange. Application of the Ca-biochar (0.2 g/L) to actual wastewater from a cattle farm (phosphorus content 3.78 mg/L) reduced the phosphorus content to 0.021 mg/L. This work utilizes waste black liquor to prepare functionalized biochar materials, providing a promising approach for black liquor reuse and phosphate removal and recovery from phosphorus-rich waste streams.
SynGAP is a Ras-GTPase activating protein highly enriched at excitatory synapses in the brain. Previous studies have shown that CaMKII and the RAS-ERK pathway are critical for several forms of ...synaptic plasticity including LTP. NMDA receptor-dependent calcium influx has been shown to regulate the RAS-ERK pathway and downstream events that result in AMPA receptor synaptic accumulation, spine enlargement, and synaptic strengthening during LTP. However, the cellular mechanisms whereby calcium influx and CaMKII control Ras activity remain elusive. Using live-imaging techniques, we have found that SynGAP is rapidly dispersed from spines upon LTP induction in hippocampal neurons, and this dispersion depends on phosphorylation of SynGAP by CaMKII. Moreover, the degree of acute dispersion predicts the maintenance of spine enlargement. Thus, the synaptic dispersion of SynGAP by CaMKII phosphorylation during LTP represents a key signaling component that transduces CaMKII activity to small G protein-mediated spine enlargement, AMPA receptor synaptic incorporation, and synaptic potentiation.
The olfactory system's receptor cells are uniquely exposed to the outside environment, making them, along with other epithelial cells crucial for their function, susceptible to damage from airborne ...viruses, bacteria, and nanoparticles. ...damage is cumulative and can lead to greater pathogenic epithelial vulnerability later in life.6 Environmental factors, including viruses, seem to be more important than genetic ones in relation to age-related olfactory decrements.6 Rats reared in pathogen-free environments have less age-related decline in mature olfactory neurons than rats reared in standard laboratory conditions.7 Although the olfactory epithelium can regenerate, the process of regeneration is rarely complete after severe viral infections, resulting in a patchy and thin epithelium containing islands of interspersed metaplastic squamous epithelia and fewer cilia, olfactory receptor cells, and supporting cells.8 The proportion of the roughly 6 000 000 receptor cells in the human olfactory epithelium that needs to be damaged to produce noticeable olfactory deficits is unknown. Smell loss could also reflect underlying subtle inflammation or damage to the olfactory epithelium during infection. ...when objectively measured, some degree of smell dysfunction can remain for days after the resolution of common cold-related congestion.10 Since, unlike the common cold, COVID-19 is rarely accompanied by noticeable nasal congestion, the absence of an obvious explanation for the associated smell loss would magnify the apparent uniqueness of the loss.
Throughout the bacterial domain, the alarmone ppGpp dramatically reprograms transcription following nutrient limitation. This “stringent response” is critical for survival and antibiotic tolerance ...and is a model for transcriptional regulation by small ligands. We report that ppGpp binds to two distinct sites 60 Å apart on E. coli RNA polymerase (RNAP), one characterized previously (site 1) and a second identified here at an interface of RNAP and the transcription factor DksA (site 2). The location and unusual tripartite nature of site 2 account for the DksA-ppGpp synergism and suggest mechanisms for ppGpp enhancement of DksA’s effects on RNAP. Site 2 binding results in the majority of ppGpp’s effects on transcription initiation in vitro and in vivo, and strains lacking site 2 are severely impaired for growth following nutritional shifts. Filling of the two sites at different ppGpp concentrations would expand the dynamic range of cellular responses to changes in ppGpp levels.
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•ppGpp still regulates a DksA-RNAP complex lacking the known ppGpp binding site•A ppGpp binding site forms at the DksA-RNAP interface, ∼60 Å from the first site•ppGpp binding to this second site strongly affects transcription in vitro and in vivo•Cells lacking both sites have dramatic defects in recovery from nutritional shifts
To survive starvation, bacteria reprogram their transcriptomes by producing ppGpp, a signaling molecule that coordinates the stringent response by regulating hundreds of promoters. Unexpectedly, there are two widely separated ppGpp binding sites on RNA polymerase required for regulation. Cells lacking both sites are severely limited for adaptation to nutritional changes.
The field of molecular electronics has grown rapidly since its experimental realization in the late 1990s, with thousands of publications on how molecules can act as circuit components and the ...possibility of extending microelectronic miniaturization. Our research group developed molecular junctions (MJs) using conducting carbon electrodes and covalent bonding, which provide excellent temperature tolerance and operational lifetimes. A carbon-based MJ based on quantum mechanical tunneling for electronic music represents the world's first commercial application of molecular electronics, with >3000 units currently in consumer hands. The all-carbon MJ consisting of aromatic molecules and oligomers between vapor-deposited carbon electrodes exploits covalent, C-C bonding which avoids the electromigration problem of metal contacts. The high bias and temperature stability as well as partial transparency of the all-carbon MJ permit a wide range of experiments to determine charge transport mechanisms and observe photoeffects to both characterize and stimulate operating MJs. As shown in the Conspectus figure, our group has reported a variety of electronic functions, many of which do not have analogs in conventional semiconductors. Much of the described research is oriented toward the rational design of electronic functions, in which electronic characteristics are determined by molecular structure.In addition to the fabrication of molecular electronic devices with sufficient stability and operating life for practical applications, our approach was directed at two principal questions: how do electrons move through molecules that are components of an electronic circuit, and what can we do with molecules that we cannot do with existing semiconductor technology? The central component is the molecular junction consisting of a 1-20+ nm layer of covalently bonded oligomers between two electrodes of conducting, mainly sp
-hybridized carbon. In addition to describing the unique junction structure and fabrication methods, this Account summarizes the valuable insights available from photons used both as probes of device structure and dynamics and as prods to stimulate resonant transport through molecular orbitals.Short-range (<5 nm) transport by tunneling and its properties are discussed separately from the longer-range transport (5-60 nm) which bridges the gap between tunneling and transport in widely studied organic semiconductors. Most molecular electronic studies deal with the <5 nm thickness range, where coherent tunneling is generally accepted as the dominant transport mechanism. However, the rational design of devices in this range by changing molecular structure is frustrated by electronic interactions with the conducting contacts, resulting in weak structural effects on electronic behavior. When the molecular layer thickness exceeds 5 nm, transport characteristics change completely since molecular orbitals become the conduits for transport. Incident photons can stimulate transport, with the observed photocurrent tracking the absorption spectrum of the molecular layer. Low-temperature, activationless transport of photogenerated carriers is possible for up to at least 60 nm, with characteristics completely distinct from coherent tunneling and from the hopping mechanisms proposed for organic semiconductors. The Account closes with examples of phenomena and applications enabled by molecular electronics which may augment conventional microelectronics with chemical functions such as redox charge storage, orbital transport, and energy-selective photodetection.
Skeletal muscle design studies, based on anatomical structure, extend back several hundred years. Accurate anatomical drawings show that many muscle fibers are oriented at an angle relative to a ...muscle’s axis of force generation. This pennation angle has been reported in the skeletal muscle biomechanics literature, primarily in the context of trying to understand muscle force generation. In this perspective, I will describe several discoveries that changed my understanding of pennation and I will suggest that muscle pennation has little if any functional significance. I believe that the correct view of pennation is that it represents a packing strategy whereby short fibers can be packed into a limited volume. While surface pennation angle is easily measured, is very descriptive, and changes during force generation, I believe it has no functional significance.
Olfactory dysfunction is among the earliest nonmotor features of Parkinson disease (PD). Such dysfunction is present in approximately 90% of early-stage PD cases and can precede the onset of motor ...symptoms by years. The mechanisms responsible for olfactory dysfunction are currently unknown. As equivalent deficits are observed in Alzheimer disease, Down syndrome, and the Parkinson-dementia complex of Guam, a common pathological substrate may be involved. Given that olfactory loss occurs to a lesser extent or is absent in disorders such as multiple system atrophy, corticobasal degeneration, and progressive supranuclear palsy, olfactory testing can be useful in differential diagnosis. The olfactory dysfunction in PD and a number of related diseases with smell loss correlates with decreased numbers of neurons in structures such as the locus coeruleus, the raphe nuclei, and the nucleus basalis of Meynart. These neuroanatomical findings, together with evidence for involvement of the autonomic nervous system in numerous PD-related symptoms, suggest that deficits in cholinergic, noradrenergic and serotonergic function may contribute to the olfactory loss. This Review discusses the current understanding of olfactory dysfunction in PD, including factors that may be related to its cause.
Stroke, the third leading cause of death and disability worldwide, is undergoing a change in perspective with the emergence of new ideas on neurodegeneration. The concept that stroke is a disorder ...solely of blood vessels has been expanded to include the effects of a detrimental interaction between glia, neurons, vascular cells, and matrix components, which is collectively referred to as the neurovascular unit. Following the acute stroke, the majority of which are ischemic, there is secondary neuroinflammation that both promotes further injury, resulting in cell death, but conversely plays a beneficial role, by promoting recovery. The proinflammatory signals from immune mediators rapidly activate resident cells and influence infiltration of a wide range of inflammatory cells (neutrophils, monocytes/macrophages, different subtypes of T cells, and other inflammatory cells) into the ischemic region exacerbating brain damage. In this review, we discuss how neuroinflammation has both beneficial as well as detrimental roles and recent therapeutic strategies to combat pathological responses. Here, we also focus on time-dependent entry of immune cells to the ischemic area and the impact of other pathological mediators, including oxidative stress, excitotoxicity, matrix metalloproteinases (MMPs), high-mobility group box 1 (HMGB1), arachidonic acid metabolites, mitogen-activated protein kinase (MAPK), and post-translational modifications that could potentially perpetuate ischemic brain damage after the acute injury. Understanding the time-dependent role of inflammatory factors could help in developing new diagnostic, prognostic, and therapeutic neuroprotective strategies for post-stroke inflammation.
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