Influence of Ti-incorporated Zeolite Topology and Pore Condensation on Vapor Phase Propylene Epoxidation Kinetics with Gaseous H2O2.

Vapor-phase propylene (C3H6) epoxidation kinetics with hydrogen peroxide (H2O2) strongly reflects the physical properties of Ti-incorporated zeolite catalysts and the presence of spectating molecules ("solvent") near active sites even without a bulk liquid phase. Steady-state turnover rates of C3H6 epoxidation and product selectivities vary by orders of magnitudes, depending on the zeolite silanol ((SiOH)x) density, pore topology (MFI, *BEA, FAU), and the quantity of condensed acetonitrile (CH3CN) molecules nearby active sites, under identical reaction mechanisms sharing activated H2O2 intermediates on Ti surfaces. Individual kinetic analyses for propylene oxide (PO) ring-opening, homogeneous diol oxidative cleavage, and homogeneous aldehyde oxidation reveal that secondary reaction kinetics following C3H6 epoxidation responds more sensitively to the changes in zeolite physical properties and pore condensation with CH3CN. Thus, higher PO selectivities achieved in hydrophilic Ti-MFI at steady-state reflect the preferential stabilization of transition states for C3H6 epoxidation (a primary reaction) relative to PO ring-opening and oxidative cleavage (secondary reactions) that solvation effects that reflect interactions among condensed CH3CN within pores and the extended pore structure.

Distinct Site Motifs Activate O2 and H2 on Supported Au Nanoparticles in Liquid Water.

Au nanoparticles catalyze the activation and conversion of small molecules with rates and kinetic barriers that depend on the dimensions of the nanoparticle, composition of the support, and presence of catalytically culpable water molecules that solvate these interfaces. Here, molecular interpretations of steady-state rate measurements, kinetic isotope effects, and structural characterizations reveal how the interface of Au nanoparticles, liquid water, and metal oxide supports mediate the kinetically relevant activation of H2 and sequential reduction of O2-derived intermediates during the formation of H2O2 and H2O. Rates of H2 consumption are 10-100 fold greater on Au nanoparticles supported on metal oxides (e.g., titania) compared to more inert and hydrophobic materials (carbon, boron nitride). Similarly, Au nanoparticles on reducible and Lewis acidic supports (e.g., lanthana) bind dioxygen intermediates more strongly and present lower barriers (<22 kJ mol-1) for O-O bond dissociation than inert interfaces formed with silica (>70 kJ mol-1). Selectivities for H2O2 formation increase significantly as the diameters of the Au nanoparticles increase because differences in nanoparticle size change the relative fractions of exposed sites that exist at Au-support interfaces. In contrast, site-normalized rates and barriers for H2 activation depend weakly on the size of Au nanoparticles and the associated differences in active site motifs. These findings suggest that H2O aids the activation of H2 at sites present across all surface Au atoms when nanoparticles are solvated by water. However, molecular O2 preferentially binds and dissociates at Au-support interfaces, leading to greater structure sensitivity for barriers of O-O dissociation across different support identities and sizes of Au nanoparticles. These insights differ from prior knowledge from studies of gas-phase reactions of H2 and O2 upon Au nanoparticle catalysts within dilute vapor pressures of water (10-4 to 0.1 kPa H2O), in which catalysis occurs at the perimeter of the Au-support interface. In contrast, contacting Au catalysts with liquid water (55.5 M H2O) expands catalysis to all surface Au atoms and enables appreciable H2O2 formation.

Cell-type-specific and disease-associated expression quantitative trait loci in the human lung.

Common genetic variants confer substantial risk for chronic lung diseases, including pulmonary fibrosis. Defining the genetic control of gene expression in a cell-type-specific and context-dependent manner is critical for understanding the mechanisms through which genetic variation influences complex traits and disease pathobiology. To this end, we performed single-cell RNA sequencing of lung tissue from 66 individuals with pulmonary fibrosis and 48 unaffected donors. Using a pseudobulk approach, we mapped expression quantitative trait loci (eQTLs) across 38 cell types, observing both shared and cell-type-specific regulatory effects. Furthermore, we identified disease interaction eQTLs and demonstrated that this class of associations is more likely to be cell-type-specific and linked to cellular dysregulation in pulmonary fibrosis. Finally, we connected lung disease risk variants to their regulatory targets in disease-relevant cell types. These results indicate that cellular context determines the impact of genetic variation on gene expression and implicates context-specific eQTLs as key regulators of lung homeostasis and disease.

Incidental Cardiovascular Abnormalities in the Abdominal Aortic Aneurysm (AAA) Surveillance Population During the AAA Get Fit Trial: A Case Series and Review of the Literature.

Background The prevalence of cardiovascular disease and incidence of major adverse cardiovascular events (MACEs) is very high among the abdominal aortic aneurysm (AAA) surveillance population. Formal assessments of and interventions to reduce cardiovascular risk are not a routine part of the surveillance programme at present. However, its potential importance is highlighted by incidental findings during the AAA Get Fit Trial, a randomised controlled trial which included baseline cardiopulmonary exercise testing (CPET). We speculate that CPET can act as an opportunistic screening programme to identify cardiovascular disease in AAA surveillance patients. Methods The AAA Get Fit Trial was a prospective, randomised controlled trial at a tertiary vascular centre, Manchester University NHS Foundation Trust, conducted between November 2017 and August 2019. Patients underwent CPET at baseline, 8, 16, 24 and 36 weeks as well as clinical history and examination and blood tests. We report on incidental cardiovascular abnormalities diagnosed during the trial. Results Of the 59 participants in the trial, four (6.8%) were identified to have abnormal findings suggestive of unstable cardiovascular disease. On subsequent further investigation, two patients were diagnosed and treated for severe coronary artery disease after abnormal ECG findings were noted during CPET. One patient was diagnosed with unstable angina after obtaining a detailed history on baseline assessment which was treated medically before going on to have a successful elective AAA repair. Conclusions There is a high incidence of MACEs among this high-risk population both pre and perioperatively. Identifying and treating cardiovascular disease among the AAA surveillance population must be a focus of the future AAA screening programme.

Brace for Impact: A Retrospective Analysis of the Modified Broström-Gould Procedure With and Without Internal Brace Augmentation.

Background Chronic lateral ankle instability (CLAI) is caused by lateral ankle ligament weakness or rupture secondary to recurrent sprains. The surgical management has traditionally involved a modified Broström-Gould (MBG) procedure with or without internal brace (IB) augmentation. This study aims to demonstrate the improved outcomes for patients undergoing an MBG procedure with IB augmentation for CLAI. Methodology A retrospective analysis was performed among 40 patients undergoing an MBG procedure with or without IB for CLAI at a large teaching hospital between January 2012 and June 2019. Functional outcomes were measured using the Manchester-Oxford Foot Questionnaire (MOxFQ). Clinic letters were reviewed to assess additional outcomes including postoperative complications, revision surgery rate, time in a plaster cast, and time to full weight-bearing. Results A total of 23 patients were included in the study, with seven undergoing both MBG and IB procedures and 16 undergoing MBG intervention alone. The average age was 37.1 years in the IB group and 35.7 years in the MBG group. The mean MOxFQ overall raw scores (10.9 vs. 33.6, p < 0.016), standing and walking MOxFQ subscale (4 vs. 15.2, p < 0.012), pain MOxFQ subscale (4.86 vs. 10.9, p < 0.042), and social interaction subscale (2 vs. 7.5 p < 0.023) all showed significantly better results for the IB group versus the MBG group. Patients in the IB group had significantly less number of weeks in plaster than the MBG group and were able to fully weight bear sooner (4.14 vs. 6, p < 0.01). The MBG group suffered a postoperative complication in seven patients compared to zero in the IB group (p < 0.057). There were three re-ruptures in the MBG group requiring further revision surgery compared to zero in the IB group (3 vs. 0, p < 0.53). Conclusions MBG surgery with IB augmentation for CLAI appears to have better outcomes in terms of overall function and may have fewer overall complications. The IB group displayed a lower recurrence of pain, less time in a plaster cast, and a quicker return to walking.

Cell type-specific and disease-associated eQTL in the human lung.

Common genetic variants confer substantial risk for chronic lung diseases, including pulmonary fibrosis (PF). Defining the genetic control of gene expression in a cell-type-specific and context-dependent manner is critical for understanding the mechanisms through which genetic variation influences complex traits and disease pathobiology. To this end, we performed single-cell RNA-sequencing of lung tissue from 67 PF and 49 unaffected donors. Employing a pseudo-bulk approach, we mapped expression quantitative trait loci (eQTL) across 38 cell types, observing both shared and cell type-specific regulatory effects. Further, we identified disease-interaction eQTL and demonstrated that this class of associations is more likely to be cell-type specific and linked to cellular dysregulation in PF. Finally, we connected PF risk variants to their regulatory targets in disease-relevant cell types. These results indicate that cellular context determines the impact of genetic variation on gene expression, and implicates context-specific eQTL as key regulators of lung homeostasis and disease.

Engineering intraporous solvent environments: effects of aqueous-organic solvent mixtures on competition between zeolite-catalyzed epoxidation and H2O2 decomposition pathways.

Solvent molecules alter the free energies of liquid phase species and adsorbed intermediates during catalytic reactions, thereby impacting rates and selectivities. Here, we examine these effects through the epoxidation of 1-hexene (C6H12) with hydrogen peroxide (H2O2) over hydrophilic and hydrophobic Ti-BEA zeolites immersed in aqueous solvent mixtures (acetonitrile, methanol, and γ-butyrolactone). Greater H2O mole fractions provide greater epoxidation rates, lower H2O2 decomposition rates, and hence improved H2O2 selectivities to the desired epoxide product in each combination of solvent and zeolite. The mechanisms for epoxidation and H2O2 decomposition remain constant across solvent compositions; however, H2O2 activates reversibly in protic solutions. Differences in rates and selectivities reflect the disproportionate stabilization of transition states within zeolite pores with respect to surface intermediates and fluid phase reactants, as evinced by turnover rates normalized by the activity coefficients of C6H12 and H2O2. Opposing trends in activation barriers suggest that the hydrophobic epoxidation transition state disrupts hydrogen bonds with solvent molecules, while the hydrophilic decomposition transition state forms hydrogen bonds with surrounding solvent molecules. Solvent compositions and adsorption volumes within pores, from 1H NMR spectroscopy and vapor adsorption, depend on the composition of the bulk solution and the density of silanol defects within pores. Strong correlations between epoxidation activation enthalpies and epoxide adsorption enthalpies from isothermal titration calorimetry indicate that the reorganization of solvent molecules (and associated entropy gains) required to accommodate transition states provides the most significant contribution to the stability of transition states that determine rates and selectivities. These results demonstrate that replacing a portion of organic solvents with H2O offers opportunities to increase rates and selectivities for zeolite-catalyzed reactions while reducing usage of organic solvents for chemical manufacturing.

Ester Reduction with H2 on Bifunctional Metal-Acid Catalysts: Implications of Metal Identity on Rates and Selectivities.

Esters reduce to form ethers and alcohols on contact with metal nanoparticles supported on Brønsted acidic faujasite (M-FAU) that cleave C-O bonds by hydrogenation and hydrogenolysis pathways. Rates and selectivities for each pathway depend on the metal identity (M=Co, Ni, Cu, Ru, Rh, Pd, and Pt). Pt-FAU gives propyl acetate consumption rates up to 100 times greater than other M-FAU catalysts and provides an ethyl propyl ether selectivity of 34 %. Measured formation rates, kinetic isotope effects, and site titrations suggest that ester reduction involves a bifunctional mechanism that implicates the stepwise addition of H* atoms to the carbonyl to form hemiacetals on the metal sites, followed by hemiacetal diffusion to a nearby Brønsted acid site to dehydrate to ethers or decompose to alcohol and aldehyde. The rates of reduction of propyl acetate appear to be determined by the H* addition to the carbonyl and by the C-O cleavage of hemiacetal.

Neutrophil trafficking to the site of infection requires Cpt1a-dependent fatty acid ß-oxidation.

Cellular metabolism influences immune cell function, with mitochondrial fatty acid ß-oxidation and oxidative phosphorylation required for multiple immune cell phenotypes. Carnitine palmitoyltransferase 1a (Cpt1a) is considered the rate-limiting enzyme for mitochondrial metabolism of long-chain fatty acids, and Cpt1a deficiency is associated with infant mortality and infection risk. This study was undertaken to test the hypothesis that impairment in Cpt1a-dependent fatty acid oxidation results in increased susceptibility to infection. Screening the Cpt1a gene for common variants predicted to affect protein function revealed allele rs2229738_T, which was associated with pneumonia risk in a targeted human phenome association study. Pharmacologic inhibition of Cpt1a increases mortality and impairs control of the infection in a murine model of bacterial pneumonia. Susceptibility to pneumonia is associated with blunted neutrophilic responses in mice and humans that result from impaired neutrophil trafficking to the site of infection. Chemotaxis responsible for neutrophil trafficking requires Cpt1a-dependent mitochondrial fatty acid oxidation for amplification of chemoattractant signals. These findings identify Cpt1a as a potential host determinant of infection susceptibility and demonstrate a requirement for mitochondrial fatty acid oxidation in neutrophil biology.

Extending the Bioavailability of Hydrophilic Antioxidants for Metal Ion Detoxification via Crystallization with Polysaccharide Dopamine.

Although metal ions, such as silver and gold, have been shown to have strong antimicrobial properties, their potential to have toxic effects on human and environmental health has gained interest with an improved understanding of their mechanisms to promote oxidative stress. Redox control is a major focus of many drug delivery systems and often incorporates an antioxidant as the active pharmaceutical ingredient (API) to neutralize overproduced reactive oxygen species (ROS). Nevertheless, there are still limitations with bioavailability and extended redox control with regard to antioxidant drug delivery. Herein, this study develops a colloidal antioxidant crystal system that dissolves sustainably through polymer stabilization using sodium hyaluronate conjugated with dopamine (HA-dopa). We explore the role of dopamine incorporation into crystal-stabilizing polymers and quantify the balance between drug-polymer interactions and competing polymer-polymer interactions. We propose that this type of analysis is useful in the engineering of and provides insight into the release behavior of polymer-crystal complexes. In developing our crystal complex, N-acetylcysteine (NAC) was used as the model antioxidant to protect against silver ion toxicity. We found that our optimized HA-dopa-stabilized NAC crystals prolong the release time of NAC 5-fold compared to a polymer-free NAC crystal. Therefore, following sublethal exposure to AgNO3, the extended lifetime of NAC was able to maintain normal intracellular ROS levels, modulate metabolic function, mitigate fluctuations in ATP levels and ATP synthase activity, and preserve contraction frequency in engineered cardiac muscle tissue. Furthermore, the protective effects of the HA-dopa-stabilized NAC crystals were extended to a Daphnia magna model where silver-ion-induced change to both cell-level biochemistry and organ function was alleviated. As such, we propose that the packaging of hydrophilic antioxidants as colloidal crystals drastically extends the lifetime of the API, better maintains ROS homeostasis post metal ion exposure, and therefore preserves both intracellular biochemistry and tissue functionality.

Increased Development of Th1, Th17, and Th1.17 Cells Under T1 Polarizing Conditions in Juvenile Idiopathic Arthritis.

In juvenile idiopathic arthritis (JIA) inflammatory T cells and their produced cytokines are drug targets and play a role in disease pathogenesis. Despite their clinical importance, the sources and types of inflammatory T cells involved remain unclear. T cells respond to polarizing factors to initiate types of immunity to fight infections, which include immunity types 1 (T1), 2 (T2), and 3 (T17). Polarizing factors drive CD4+ T cells towards T helper (Th) cell subtypes and CD8+ T cells towards cytotoxic T cell (Tc) subtypes. T1 and T17 polarization are associated with autoimmunity and production of the cytokines IFNγ and IL-17 respectively. We show that JIA and child healthy control (HC) peripheral blood mononuclear cells are remarkably similar, with the same frequencies of CD4+ and CD8+ naïve and memory T cell subsets, T cell proliferation, and CD4+ and CD8+ T cell subsets upon T1, T2, and T17 polarization. Yet, under T1 polarizing conditions JIA cells produced increased IFNγ and inappropriately produced IL-17. Under T17 polarizing conditions JIA T cells produced increased IL-17. Gene expression of IFNγ, IL-17, Tbet, and RORγT by quantitative PCR and RNA sequencing revealed activation of immune responses and inappropriate activation of IL-17 signaling pathways in JIA polarized T1 cells. The polarized JIA T1 cells were comprised of Th and Tc cells, with Th cells producing IFNγ (Th1), IL-17 (Th17), and both IFNγ-IL-17 (Th1.17) and Tc cells producing IFNγ (Tc1). The JIA polarized CD4+ T1 cells expressed both Tbet and RORγT, with higher expression of the transcription factors associated with higher frequency of IL-17 producing cells. T1 polarized naïve CD4+ cells from JIA also produced more IFNγ and more IL-17 than HC. We show that in JIA T1 polarization inappropriately generates Th1, Th17, and Th1.17 cells. Our data provides a tool for studying the development of heterogeneous inflammatory T cells in JIA under T1 polarizing conditions and for identifying pathogenic immune cells that are important as drug targets and diagnostic markers.

Self-locomotive, antimicrobial microrobot (SLAM) swarm for enhanced biofilm elimination.

Biofilm is a major cause of infections and infrastructure deterioration, largely due to molecular diffusion restrictions that hamper the antimicrobial activity of traditional antibiotics and disinfectants. Here, we present a self-locomotive, antimicrobial microrobot (SLAM) swarm that can penetrate, fracture, and detach biofilm and, in turn, nullify bacterial resistance to antibiotics. The SLAM is assembled by loading a controlled mass of manganese oxide nanosheets on diatoms with the polydopamine binder. In hydrogen peroxide solution, SLAMs produce oxygen bubbles that generate thrust to penetrate the rigid and dense Pseudomonas aeruginosa biofilm and self-assemble into a swarm that repeatedly surrounds, expands, and bursts oxygen bubbles. The resulting cavities continue to deform and fracture extracellular polymeric substances from microgrooved silicone substrates and wounded skin explants while decreasing the number of viable bacterial cells. Additionally, SLAM allows irrigating water or antibiotics to access the residual biofilm better, thus enhancing the synergistic efficacy in killing up to 99.9% of bacterial cells.

Foot and ankle injuries related to the use of E-scooters - A case series and a review of literature.

INTRODUCTION: As E-scooter use is increasing with the introduction of urban rental schemes in the United Kingdom, associated foot and ankle injuries will become more prevalent. The aim of this study is to assess the injury pattern and injury severity of foot and ankle trauma associated with E-scooter use. METHODS: A retrospective case analysis of all E-scooter foot and ankle injuries presenting to three London hospitals between 1st January and 31st December 2020 was conducted. Data including demographics, mechanism and location of injury sustained, management, duration of hospital stay and mortality were collected. RESULTS: 20 patients were identified with a total of 27 foot and ankle fractures. Eight patients had fracture dislocations, four sustained open injuries and 45% (9/20) of patients required surgical treatment. Those travelling over 15.5 mph were significantly more likely to require operative intervention (70%) than those travelling below 15.5 mph (20%) (P < 0.033) and were more likely to have an open fracture (40% compared to 0%) (P < 0.0886), however the latter was not of statistical significance. 85% (17/20) of rider's injuries involved the foot and/or ankle only. There were no mortalities at 30 days. CONCLUSIONS: E-scooter use can cause serious foot and ankle injuries. Robust guidelines and legislation restricting top speeds and enforcing the wearing of protective clothing could be implemented. This may protect the E-scooter user from significant foot and ankle injury.

Synergistic action of WDR5 and HDM2 inhibitors in SMARCB1-deficient cancer cells.

Rhabdoid tumors (RT) are rare and deadly pediatric cancers driven by loss of SMARCB1, which encodes the SNF5 component of the SWI/SNF chromatin remodeler. Loss of SMARCB1 is associated with a complex set of phenotypic changes including vulnerability to inhibitors of protein synthesis and of the p53 ubiquitin-ligase HDM2. Recently, we discovered small molecule inhibitors of the 'WIN' site of WDR5, which in MLL-rearranged leukemia cells decrease the expression of a set of genes linked to protein synthesis, inducing a translational choke and causing p53-dependent inhibition of proliferation. Here, we characterize how WIN site inhibitors act in RT cells. As in leukemia cells, WIN site inhibition in RT cells causes the comprehensive displacement of WDR5 from chromatin, resulting in a decrease in protein synthesis gene expression. Unlike leukemia cells, however, the growth response of RT cells to WIN site blockade is independent of p53. Exploiting this observation, we demonstrate that WIN site inhibitor synergizes with an HDM2 antagonist to induce p53 and block RT cell proliferation in vitro. These data reveal a p53-independent action of WIN site inhibitors and forecast that future strategies to treat RT could be based on dual WDR5/HDM2 inhibition.

WIN site inhibition disrupts a subset of WDR5 function.

WDR5 nucleates the assembly of histone-modifying complexes and acts outside this context in a range of chromatin-centric processes. WDR5 is also a prominent target for pharmacological inhibition in cancer. Small-molecule degraders of WDR5 have been described, but most drug discovery efforts center on blocking the WIN site of WDR5, an arginine binding cavity that engages MLL/SET enzymes that deposit histone H3 lysine 4 methylation (H3K4me). Therapeutic application of WIN site inhibitors is complicated by the disparate functions of WDR5, but is generally guided by two assumptions-that WIN site inhibitors disable all functions of WDR5, and that changes in H3K4me drive the transcriptional response of cancer cells to WIN site blockade. Here, we test these assumptions by comparing the impact of WIN site inhibition versus WDR5 degradation on H3K4me and transcriptional processes. We show that WIN site inhibition disables only a specific subset of WDR5 activity, and that H3K4me changes induced by WDR5 depletion do not explain accompanying transcriptional responses. These data recast WIN site inhibitors as selective loss-of-function agents, contradict H3K4me as a relevant mechanism of action for WDR5 inhibitors, and indicate distinct clinical applications of WIN site inhibitors and WDR5 degraders.

The association of bone bruising and grade of MCL injury in patients sustaining isolated MCL injuries.

OBJECTIVES: To investigate the incidence of bone bruising with isolated medial collateral ligament injury and to assess whether the presence of bone bruising is related to the injury grade. MATERIALS AND METHODS: Patients who sustained an acute isolated medial collateral ligament injury demonstrated on knee MRI between 2016 and 2020 were included in this study. Patient's characteristics and injury classification (clinical and radiological) were reviewed from clinical notes and imaging. The patients were divided into two groups, based on the presence of bone bruising. Fisher's exact test was used for dichotomous variables and odds ratios were computed in areas of clinical significance. RESULTS: Sixty patients with a median age of 37.6 ± 13.8 were included. Twenty-eight (46.7%) had bone bruising demonstrated on MRI scan. The bone bruising group were 7 times (95% CI [1.4;36.5]) more likely to have a complete disruption of the superficial medial collateral ligament and MRI grade III injury. Injury to the deep medial collateral ligament was more often observed in this group (p < 0.05). The most common location of bone bruising was the lateral femoral condyle (57.1%, 16/28) and/or the medial femoral condyle (57.1%, 16/28). CONCLUSIONS: The incidence of bone bruising with isolated medial collateral ligament injury is significant and is more common with radiologically higher grade injuries. There was no statistically significant difference between the anatomical location of bone bruise and the grade of MCL injury. Bone bruising patterns can help determine the mechanism of injury, with a valgus impact or avulsion type injury most commonly seen.

Medial collateral ligament injury of the knee: correlations between MRI features and clinical gradings.

OBJECTIVE: To evaluate the degree of correlation between MRI and clinical gradings of medial collateral ligament (MCL) injuries and assess for associated structures on MRI which may influence the clinical perception of MCL laxity. MATERIALS AND METHODS: All knee MRIs with acute MCL injuries between 2016 and 2020 at our centre were retrospectively reviewed by two blinded musculoskeletal radiologists. The clinic notes were reviewed for clinical gradings. RESULTS: One hundred and nineteen MRIs included. Forty-eight percent (57/119) agreement between MRI and clinical gradings (κ = 0.21, standard error (SE) 0.07). MRI grades: I 29% (34/119), II 50% (60/119), III 21% (25/119). Clinical grades: I 67% (80/119), II 26% (31/119), III 7% (8/119). In patients with clinical grade III MCL injury, there was waviness of the superficial MCL on MRI in 100% (8/8), deep meniscofemoral ligament tear in 75% (6/8), anterior cruciate ligament (ACL) partial or complete tear in 75% (6/8) and posteromedial corner (PMC) injury in 100% (8/8); compared with 0% (0/111), 34% (38/111), 44% (49/111) and 41% (46/111) respectively in clinical grade I or II injuries (p < 0.05). CONCLUSION: Agreement between MRI and clinical gradings of MCL injuries was only 'fair', with MRI almost always overestimating the grade of the injury when there was a mismatch. Waviness of the superficial MCL and injuries to the deep MCL, ACL and PMC correlate with clinical instability.

Influence of solvent structure and hydrogen bonding on catalysis at solid-liquid interfaces.

Solvent molecules interact with reactive species and alter the rates and selectivities of catalytic reactions by orders of magnitude. Specifically, solvent molecules can modify the free energies of liquid phase and surface species via solvation, participating directly as a reactant or co-catalyst, or competitively binding to active sites. These effects carry consequences for reactions relevant for the conversion of renewable or recyclable feedstocks, the development of distributed chemical manufacturing, and the utilization of renewable energy to drive chemical reactions. First, we describe the quantitative impact of these effects on steady-state catalytic turnover rates through a rate expression derived for a generic catalytic reaction (A → B), which illustrates the functional dependence of rates on each category of solvent interaction. Second, we connect these concepts to recent investigations of the effects of solvents on catalysis to show how interactions between solvent and reactant molecules at solid-liquid interfaces influence catalytic reactions. This discussion demonstrates that the design of effective liquid phase catalytic processes benefits from a clear understanding of these intermolecular interactions and their implications for rates and selectivities.

Unifying Concepts in Electro- and Thermocatalysis toward Hydrogen Peroxide Production.

We examine relationships between H2O2 and H2O formation on metal nanoparticles by the electrochemical oxygen reduction reaction (ORR) and the thermochemical direct synthesis of H2O2. The similar mechanisms of such reactions suggest that these catalysts should exhibit similar reaction rates and selectivities at equivalent electrochemical potentials (µÌ…i), determined by reactant activities, electrode potential, and temperature. We quantitatively compare the kinetic parameters for 12 nanoparticle catalysts obtained in a thermocatalytic fixed-bed reactor and a ring-disk electrode cell. Koutecky-Levich and Butler-Volmer analyses yield electrochemical rate constants and transfer coefficients, which informed mixed-potential models that treat each nanoparticle as a short-circuited electrochemical cell. These models require that the hydrogen oxidation reaction (HOR) and ORR occur at equal rates to conserve the charge on nanoparticles. These kinetic relationships predict that nanoparticle catalysts operate at potentials that depend on reactant activities (H2, O2), H2O2 selectivity, and rate constants for the HOR and ORR, as confirmed by measurements of the operating potential during the direct synthesis of H2O2. The selectivities and rates of H2O2 formation during thermocatalysis and electrocatalysis correlate across all catalysts when operating at equivalent µÌ…i values. This analysis provides quantitative relationships that guide the optimization of H2O2 formation rates and selectivities. Catalysts achieve the greatest H2O2 selectivities when they operate at high H atom coverages, low temperatures, and potentials that maximize electron transfer toward stable OOH* and H2O2* while preventing excessive occupation of O-O antibonding states that lead to H2O formation. These findings guide the design and operation of catalysts that maximize H2O2 formation, and these concepts may inform other liquid-phase chemistries.