Insight into the direct conversion of methane to methanol on modified ZIF-204 from the perspective of DFT-based calculations.

Direct oxidation of methane over oxo-doped ZIF-204, a bio-mimetic metal-organic framework, is investigated under first-principles calculations based on density functional theory. In the pristine ZIF-204, the tetrahedral methane molecule anchors to an open monocopper site via the so-called η2 configuration with a physisorption energy of 0.24 eV. This weak binding arises from an electrostatic interaction between the negative charge of carbon in the methane molecule and the positive Cu2+ cation in the framework. In the modified ZIF-204, the doped oxo species is stabilized at the axial position of a CuN4-base square pyramid at a distance of 2.06 Å. The dative covalent bond between Cu and oxo is responsible for the formation energy of 1.06 eV. With the presence of the oxo group, the presenting of electrons in the O_pz orbital accounts for the adsorption of methane via hydrogen bonding with an adsorption energy of 0.30 eV. The methane oxidation can occur via either a concerted direct oxo insertion mechanism or a hydrogen-atom abstraction radical rebound mechanism. Calculations on transition-state barriers show that reactions via the concerted direct oxo insertion mechanism can happen without energy barriers. Concerning the hydrogen-atom abstraction radical rebound mechanism, the C-H bond dissociation of the CH4 molecule is barrierless, but the C-O bond recombination to form the CH3OH molecule occurs through a low barrier of 0.16 eV. These predictions suggest the modified ZIF-204 is a promising catalyst for methane oxidization.

The human cathelicidin LL-37 host defense peptide upregulates tight junction-related proteins and increases human epidermal keratinocyte barrier function.

Both psoriasis and atopic dermatitis (AD) are not only associated with an impaired stratum corneum barrier, but also with abnormal expression of the tight junction (TJ) proteins. Because host defense peptides, including LL-37, are overexpressed in lesional psoriatic skin but are downregulated in lesional AD skin, we hypothesized that LL-37 might regulate the TJ function in keratinocytes. We demonstrated that LL-37 selectively increased the expression of several claudins and occludin, and enhanced their membrane distribution. Furthermore, LL-37 elevated the transepithelial electrical resistance while reducing the paracellular permeability of keratinocyte layers, and this activity was weakened by the claudin inhibitor ochratoxin A. A characterization of the molecular mechanism underlying the regulation of the TJ barrier by LL-37 revealed that LL-37 induced the activation of the Rac1, atypical PKC, glycogen synthase kinase-3 and PI3K pathways, and the specific inhibition of these pathways reversed the LL-37-mediated regulation of TJ function. In addition, LL-37 enhanced the expression of differentiation markers under the control of ochratoxin A, suggesting an association between LL-37-induced TJ function and keratinocyte differentiation. These data provide novel evidence that, in addition to its antimicrobial and other immunoregulatory functions, LL-37 contributes to cutaneous immunity by strengthening the skin's barrier function.