Why Does Activation of the Weaker CS Bond in CS₂ by P/N-Based Frustrated Lewis Pairs Require More Energy Than That of the CO Bond in CO₂? A DFT Study

The sequestration of carbon disulfide (CS₂), a common pollutant in environmental systems, is of great importance due to its physical harm to human beings. Compared with CO₂ capture, that of CS₂ is much less developed. The use of P/N-based frustrated Lewis pairs (FLPs) has been proven, both experimentally and theoretically, to be an alternative strategy to efficiently sequestrate CO₂. Therefore, we pose the question of whether the analogue CS₂ could also be sequestrated by the same FLPs, given that the CS bond in CS₂ is weaker than the CO bond in CO₂. Herein, we carry out a thorough DFT study to theoretically examine this hypothesis for a series of P/N-based FLPs. Our results reveal unexpectedly higher reaction barriers in CS₂ capture by most of the P/N-based FLPs, although the bond dissociation energy of the CS bond in CS₂ (105.3 kcal mol^–1) is smaller than that of the CO bond in CO₂ (127.2 kcal mol^–1). The unexpected higher energy required for CS₂ activation can be rationalized by its larger bond distortion and its reverse bond polarization, as revealed by energy decomposition analysis and natural bond orbital analysis, respectively. Our findings could be helpful for experimentalists investigating the sequestration of CS₂ with P/N-based FLPs

Stress-induced charge-ordering process in LiMn₂O₄

In this letter we report the stress-induced Mn charge-ordering process in the LiMn2O4 spinel, evidenced by the lattice strain evolutions due to the Jahn–Teller effects. In situ neutron diffraction reveals the initial stage of this process at low stress, indicating the eg electron localization at the preferential Mn sites during the early phase transition as an underlying charge-ordering mechanism in the charge-frustrated LiMn2O4. The initial stage of this transition exhibits as a progressive lattice and charge evolution, without showing a first-order behavior. IMPACT STATEMENT The newly reported continuous charge-ordering process will refresh the fundamental understanding of the structural evolution along with the anomalous physical properties in the frustrated LiMn2O4 spinel.</p

Dexamethasone as Adjuvant to Bupivacaine Prolongs the Duration of Thermal Antinociception and Prevents Bupivacaine-Induced Rebound Hyperalgesia via Regional Mechanism in a Mouse Sciatic Nerve Block Model

<div><p>Background</p><p>Dexamethasone has been studied as an effective adjuvant to prolong the analgesia duration of local anesthetics in peripheral nerve block. However, the route of action for dexamethasone and its potential neurotoxicity are still unclear.</p><p>Methods</p><p>A mouse sciatic nerve block model was used. The sciatic nerve was injected with 60ul of combinations of various medications, including dexamethasone and/or bupivacaine. Neurobehavioral changes were observed for 2 days prior to injection, and then continuously for up to 7 days after injection. In addition, the sciatic nerves were harvested at either 2 days or 7 days after injection. Toluidine blue dyeing and immunohistochemistry test were performed to study the short-term and long-term histopathological changes of the sciatic nerves. There were six study groups: normal saline control, bupivacaine (10mg/kg) only, dexamethasone (0.5mg/kg) only, bupivacaine (10mg/kg) combined with low-dose (0.14mg/kg) dexamethasone, bupivacaine (10mg/kg) combined with high-dose (0.5mg/kg) dexamethasone, and bupivacaine (10mg/kg) combined with intramuscular dexamethasone (0.5mg/kg).</p><p>Results</p><p>High-dose perineural dexamethasone, but not systemic dexamethasone, combined with bupivacaine prolonged the duration of both sensory and motor block of mouse sciatic nerve. There was no significant difference on the onset time of the sciatic nerve block. There was “rebound hyperalgesia” to thermal stimulus after the resolution of plain bupivacaine sciatic nerve block. Interestingly, both low and high dose perineural dexamethasone prevented bupivacaine-induced hyperalgesia. There was an early phase of axon degeneration and Schwann cell response as represented by S-100 expression as well as the percentage of demyelinated axon and nucleus in the plain bupivacaine group compared with the bupivacaine plus dexamethasone groups on post-injection day 2, which resolved on post-injection day 7. Furthermore, we demonstrated that perineural dexamethasone, but not systemic dexamethasone, could prevent axon degeneration and demyelination. There was no significant caspase-dependent apoptosis process in the mouse sciatic nerve among all study groups during our study period.</p><p>Conclusions</p><p>Perineural, not systemic, dexamethasone added to a clinical concentration of bupivacaine may not only prolong the duration of sensory and motor blockade of sciatic nerve, but also prevent the bupivacaine-induced reversible neurotoxicity and short-term “rebound hyperalgesia” after the resolution of nerve block.</p></div

Motor recovery of mouse sciatic nerve block with various medication.

<p>* indicates P<0.05 when compared with other groups. # indicates P<0.05 when compared with baseline control. The data were reported as mean ± SEM. NS, normal saline; Bup, bupivacaine; Dexa, dexamethasone; i.m., intramuscularly.</p

Paw withdrawal latency behavioral changes in response to thermal stimulation after sciatic nerve block with various medications.

<p>* indicates P<0.05 when compared with other groups. # indicates P<0.05 when compared with baseline control. The data were reported as mean ± SEM. NS, normal saline; Bup, bupivacaine; Dexa, dexamethasone; i.m., intramuscularly.</p

S-100 expression in sciatic nerves.

<p>5A. S-100 protein immunostaining in sciatic nerves (200×); 5B. Immunoreactivity of S-100 expression in different treatment groups on day 2 and day 7. Bupivacaine with or without intramuscular dexamethasone treatment group showed significantly lower S-100 expression on day 2 (red box) than that on day 7 (*<i>P</i><0.05), while S-100 was expressed significantly higher when treated with perineural bupivacaine and high-dose dexamethasone than treated with perineural bupivacaine and low-dose of dexamethasone (^#<i>P</i><0.05); 5C. Immunohistochemical assay for S-100 protein staining (deep brown, black arrows) in each group was primarily localized in the myelin sheath (400×, counterstained with hematoxylin). NS, normal saline; Bup, bupivacaine; Dexa, dexamethasone. Scale bar: 45 μm (black color),10 μm (red color).</p

Additional file 3 of Bioinformatics analysis of diagnostic biomarkers for Alzheimer's disease in peripheral blood based on sex differences and support vector machine algorithm

Additional file 3: Supplementary Data 3. Intersected DEGs lists of males and females

Microscopic changes of sciatic nerves after sciatic nerve block.

<p>3A. istomorphological changes of paraffin-embedded sciatic nerves on day 2 and day 7 after injection (400×, toluidine blue staining). Nerves appeared normal on day 2 and day 7 after injection in most groups, while nerves in the bupivacaine treated group (red box) showed fiber degeneration with vague myelin sheath appearance (arrows) at 2 days after injection; 3B. Percentage of demyelinated axons in sections (n = 5 per group). The percentage of unmyelinated axons in bupivacaine group was significant higher on post-injection day 2 than on day 7 (*<i>P</i><0.05), while no significant difference was observed in other groups. NS, normal saline; Bup, bupivacaine; Dexa, dexamethasone. Sale bar is at 10μm.</p

Additional file 4 of Bioinformatics analysis of diagnostic biomarkers for Alzheimer's disease in peripheral blood based on sex differences and support vector machine algorithm

Additional file 4: Supplementary Data 4. Significantly enriched GO entries and KEGG pathways in females

Caspase-3 expression in sciatic nerves.

<p>4A. Immunohistochemical assays for cleaved caspase-3 staining (200×, nucleus counterstained with hematoxylin). There was no significant caspase expression in sciatic nerve axoplasm in all groups; 4B. Caspase-3 expression in positive control tissue (red arrows) (hippocampal neurons, 200×); 4C. Percentage of nucleus in sciatic nerves. The percentage of nucleus staining (blue arrows) in sciatic nerve was significant higher in bupivacaine treated mice on day 2 than day 7 (red box, *<i>P</i><0.05), while no significant difference was found in other groups. 4D. Caspase-3 expression in mouse sciatic nerve after bupivacaine and high-dose dexamethasone block (400×). NS, normal saline; Bup, bupivacaine; Dexa, dexamethasone. Scale bar: 45 μm (black color),10 μm (red color).</p