Benchmarking the Self-Assembly of Surfactin Biosurfactant at the Liquid–Air Interface to those of Synthetic Surfactants

The adsorption of surfactin, a lipopeptide biosurfactant, at the liquid–air interface has been investigated in this work. The maximum adsorption density and the nature and the extent of lateral interaction between the adsorbed surfactin molecules at the interface were estimated from surface tension data using the Frumkin model. The quantitative information obtained using the Frumkin model was also compared to those obtained using the Gibbs equation and the Langmuir–Szyszkowski model. Error analysis showed a better agreement between the experimental and the calculated values using the Frumkin model relative to the other two models. The adsorption of surfactin at the liquid–air interface was also compared to those of synthetic anionic, sodium dodecylbenzenesulphonate (SDBS), and nonionic, octaethylene glycol monotetradecyl ether (C14E8), surfactants. It has been estimated that the area occupied by a surfactin molecule at the interface is about 3- and 2.5-fold higher than those occupied by SDBS and C14E8 molecules, respectively. The interaction between the adsorbed molecules of the anionic biosurfactant (surfactin) was estimated to be attractive, unlike the mild repulsive interaction between the adsorbed SDBS molecules

Forebrain Deletion of the Vesicular Acetylcholine Transporter Results in Deficits in Executive Function, Metabolic, and RNA Splicing Abnormalities in the Prefrontal Cortex

One of the key brain regions in cognitive processing and executive function is the prefrontal cortex (PFC), which receives cholinergic input from basal forebrain cholinergic neurons. We evaluated the contribution of synaptically released acetylcholine (ACh) to executive function by genetically targeting the vesicular acetylcholine transporter (VAChT) in the mouse forebrain. Executive function was assessed using a pairwise visual discrimination paradigm and the 5-choice serial reaction time task (5-CSRT). In the pairwise test, VAChT-deficient mice were able to learn, but were impaired in reversal learning, suggesting that these mice present cognitive inflexibility. Interestingly, VAChT-targeted mice took longer to reach criteria in the 5-CSRT. Although their performance was indistinguishable from that of control mice during low attentional demand, increased attentional demand revealed striking deficits in VAChT-deleted mice. Galantamine, a cholinesterase inhibitor used in Alzheimer\u27s disease, significantly improved the performance of control mice, but not of VAChT-deficient mice on the 5-CSRT. In vivo magnetic resonance spectroscopy showed altered levels of two neurochemical markers of neuronal function, taurine and lactate, suggesting altered PFC metabolism in VAChT-deficient mice. The PFC of these mice displayed a drastic reduction in the splicing factor heterogeneous nuclear ribonucleoprotein A2/B1 (hnRNPA2/B1), whose cholinergic-mediated reduction was previously demonstrated in Alzheimer\u27s disease. Consequently, several key hnRNPA2/B1 target transcripts involved in neuronal function present changes in alternative splicing in VAChT-deficient mice, including pyruvate kinase M, a key enzyme involved in lactate metabolism. We propose that VAChT-targeted mice can be used to model and to dissect the neurochemical basis of executive abnormalities

Forebrain Cholinergic Signaling Regulates Innate Immune Responses and Inflammation

The brain regulates physiological functions integral to survival. However, the insight into brain neuronal regulation of peripheral immune function and the neuromediator systems and pathways involved remains limited. Here, utilizing selective genetic and pharmacological approaches, we studied the role of forebrain cholinergic signaling in the regulation of peripheral immune function and inflammation. Forebrain-selective genetic ablation of acetylcholine release and vagotomy abolished the suppression of serum TNF by the centrally-acting cholinergic drug galantamine in murine endotoxemia. Selective stimulation of acetylcholine action on the M1 muscarinic acetylcholine receptor (M1 mAChR) by central administration of the positive allosteric modulator benzyl quinolone carboxylic acid (BQCA) suppressed serum TNF (TNF alpha) levels in murine endotoxemia. This effect was recapitulated by peripheral administration of the compound. BQCA also improved survival in murine endotoxemia and these effects were abolished in M1 mAChR knockout (KO) mice. Selective optogenetic stimulation of basal forebrain cholinergic neurons innervating brain regions with abundant M1 mAChR localization reduced serum TNF in endotoxemic mice. These findings reveal that forebrain cholinergic neurons regulate innate immune responses and inflammation, suggesting the possibility that in diseases associated with cholinergic dysfunction, including Alzheimer\u27s disease this anti-inflammatory regulation can be impaired. These results also suggest novel anti-inflammatory approaches based on targeting forebrain cholinergic signaling in sepsis and other disorders characterized by immune dysregulation

Forebrain Cholinergic Signaling Regulates Innate Immune Responses and Inflammation

The brain regulates physiological functions integral to survival. However, the insight into brain neuronal regulation of peripheral immune function and the neuromediator systems and pathways involved remains limited. Here, utilizing selective genetic and pharmacological approaches, we studied the role of forebrain cholinergic signaling in the regulation of peripheral immune function and inflammation. Forebrain-selective genetic ablation of acetylcholine release and vagotomy abolished the suppression of serum TNF by the centrally-acting cholinergic drug galantamine in murine endotoxemia. Selective stimulation of acetylcholine action on the M1 muscarinic acetylcholine receptor (M1 mAChR) by central administration of the positive allosteric modulator benzyl quinolone carboxylic acid (BQCA) suppressed serum TNF (TNFα) levels in murine endotoxemia. This effect was recapitulated by peripheral administration of the compound. BQCA also improved survival in murine endotoxemia and these effects were abolished in M1 mAChR knockout (KO) mice. Selective optogenetic stimulation of basal forebrain cholinergic neurons innervating brain regions with abundant M1 mAChR localization reduced serum TNF in endotoxemic mice. These findings reveal that forebrain cholinergic neurons regulate innate immune responses and inflammation, suggesting the possibility that in diseases associated with cholinergic dysfunction, including Alzheimer's disease this anti-inflammatory regulation can be impaired. These results also suggest novel anti-inflammatory approaches based on targeting forebrain cholinergic signaling in sepsis and other disorders characterized by immune dysregulation

Remodeling of cholinergic input to the hippocampus after noise exposure and tinnitus induction in Guinea pigs

Here, we investigate remodeling of hippocampal cholinergic inputs after noise exposure and determine the relevance of these changes to tinnitus. To assess the effects of noise exposure on the hippocampus, guinea pigs were exposed to unilateral noise for 2 hr and 2 weeks later, immunohistochemistry was performed on hippocampal sections to examine vesicular acetylcholine transporter (VAChT) expression. To evaluate whether the changes in VAChT were relevant to tinnitus, another group of animals was exposed to the same noise band twice to induce tinnitus, which was assessed using gap‐prepulse Inhibition of the acoustic startle (GPIAS) 12 weeks after the first noise exposure, followed by immunohistochemistry. Acoustic Brainstem Response (ABR) thresholds were elevated immediately after noise exposure for all experimental animals but returned to baseline levels several days after noise exposure. ABR wave I amplitude‐intensity functions did not show any changes after 2 or 12 weeks of recovery compared to baseline levels. In animals assessed 2‐weeks following noise‐exposure, hippocampal VAChT puncta density decreased on both sides of the brain by 20–60% in exposed animals. By 12 weeks following the initial noise exposure, changes in VAChT puncta density largely recovered to baseline levels in exposed animals that did not develop tinnitus, but remained diminished in animals that developed tinnitus. These tinnitus‐specific changes were particularly prominent in hippocampal synapse‐rich layers of the dentate gyrus and areas CA3 and CA1, and VAChT density in these regions negatively correlated with tinnitus severity. The robust changes in VAChT labeling in the hippocampus 2 weeks after noise exposure suggest involvement of this circuitry in auditory processing. After chronic tinnitus induction, tinnitus‐specific changes occurred in synapse‐rich layers of the hippocampus, suggesting that synaptic processing in the hippocampus may play an important role in the pathophysiology of tinnitus.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/150542/1/hipo23058.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/150542/2/hipo23058_am.pd

Lysozyme binding to tethered bilayer lipid membranes prepared by rapid solvent exchange and vesicle fusion methods

Tethered bilayer lipid membranes (tBLMs) are important tools for studying protein-lipid interactions. The widely used methodology for the perparation of these membranes is the fusion of phospholipid vesicles from an aqueous medium onto an anchored phospholipid layer. The preparation of phospholipid vesicles is a long and tedious procedure. There is another simple method, rapid solvent exchange, for preparing lipid membranes. However, there is a lack of information on the effects of the preparation method of tBLMs on their interactions with proteins. Therefore, we present in this paper a comparative study on the binding of lysozyme onto tBLMs prepared by the above mentioned methods. The prepared tBLMs have either zwitterionic or anionic characteristics. The results show that lysozyme binding onto the prepared tBLMS is unaffected by the preparation method of the tBLMs, suggesting that the tedious fusion method might be replaced by the simple rapid solvent exchange method without altering the level of protein-lipid interactions

Langmuir-Hinshelwood kinetic study for palm oil catalytic cracking over Al-MCM-41

Palm oil catalytic cracking over a mesoporous aluminosilicate material (Al-MCM-41) containing 5 % alumina was studied in order to evaluate the Langmuir-Hinshelwood (LH) kinetic parameters. The Al-MCM-41 catalyst was prepared by the sol-gel technique and was characterized by X-ray diffraction and nitrogen adsorption techniques. The Brunauer-Emmett-Teller surface area of the catalyst was found to be 1,278 m2g-1. A 400 mL stirred batch autoclave reactor was used for catalytic cracking of 100 g refined palm oil and 1 g catalyst at a reaction temperature ranging from 573 to 673 K. The pressure-time data at different reaction temperatures were analyzed statistically in order to minimize experimental errors in the recorded pressures, whereas the statistically predicted pressure data were used to calculate the kinetic parameters. It was found that the fitting quality of the statistical model data using the LH model is similar to that of the raw experimental data. However, the values of the predicted parameters are significantly different. The estimated activation energy from LH kinetics was found to be 87 and 112 kJ mol-1 calculated from statistical model data and raw experimental data, respectively. The predicted parameters obtained from statistical model data are found to be more accurate as the influence of experimental error is minimized prior to data analysis

Directed disassembly of an interfacial rubisco protein network

We present the first study of the directed disassembly of a protein network at the air-water interface by the synergistic action of a surfactant and an enzyme. We seek to understand the fundamentals of protein network disassembly by using rubisco adsorbed at the air-water interface as a model. We propose that rubisco adsorption at the air-water interface results in the formation of a fishnet-like network of interconnected protein molecules, capable of transmitting lateral force. The mechanical properties of the rubisco network during assembly and disassembly at the air-water interface were characterized by direct measurement of laterally transmitted force through the protein network using the Cambridge interfacial tensiometer. We have shown that, when used individually, either 2 ppm of the surfactant, sodium dodecyl benzyl sulfonate (SDOBS), or 2 ppm of the enzyme, subtilisin A (SA), were insufficient to completely disassemble the rubisco network within 1 h of treatment. However, a combination of 2 ppm SDOBS and 2 ppm SA led to almost complete disassembly within 1 h. Increasing the concentration of SA in the mixture from 2 to 10 ppm, while keeping the SDOBS concentration constant, significantly decreased the time required to completely disassemble the rubisco network. Furthermore, the initial rate of network disassembly using formulations containing SDOBS was surprisingly insensitive to this increase in SA concentration. This study gives insight into the role of lateral interactions between protein molecules at interfaces in stabilizing interfacial protein networks and shows that surfactant and enzyme working in combination proves more effective at disrupting and mobilizing the interfacial protein network than the action of either agent alone

Aqueous Pb(II) Removal Using ZIF-60: Adsorption Studies, Response Surface Methodology and Machine Learning Predictions

Zeolitic imidazolate frameworks (ZIFs) are increasingly gaining attention in many application fields due to their outstanding porosity and thermal stability, among other exceptional characteristics. However, in the domain of water purification via adsorption, scientists have mainly focused on ZIF-8 and, to a lesser extent, ZIF-67. The performance of other ZIFs as water decontaminants is yet to be explored. Hence, this study applied ZIF-60 for the removal of lead from aqueous solutions; this is the first time ZIF-60 has been used in any water treatment adsorption study. The synthesized ZIF-60 was subjected to characterization using FTIR, XRD and TGA. A multivariate approach was used to investigate the effect of adsorption parameters on lead removal and the findings revealed that ZIF-60 dose and lead concentration are the most significant factors affecting the response (i.e., lead removal efficiency). Further, response surface methodology-based regression models were generated. To further explore the adsorption performance of ZIF-60 in removing lead from contaminated water samples, adsorption kinetics, isotherm and thermodynamic investigations were conducted. The findings revealed that the obtained data were well-fitted by the Avrami and pseudo-first-order kinetic models, suggesting that the process is complex. The maximum adsorption capacity (qmax) was predicted to be 1905 mg/g. Thermodynamic studies revealed an endothermic and spontaneous adsorption process. Finally, the experimental data were aggregated and used for machine learning predictions using several algorithms. The model generated by the random forest algorithm proved to be the most effective on the basis of its significant correlation coefficient and minimal root mean square error (RMSE)