ZIF-8 Vibrational Spectra: Peak Assignments and Defect Signals.

Zeolitic imidazolate framework (ZIF-8) is a promising material for gas separation applications. It also serves as a prototype for numerous ZIFs, including amorphous ones, with a broader range of possible applications, including sensors, catalysis, and lithography. It consists of zinc coordinated with 2-methylimidazolate (2mIm) and has been synthesized with methods ranging from liquid-phase to solvent-free synthesis, which aim to control its crystal size and shape, film thickness and microstructure, and incorporation into nanocomposites. Depending on the synthesis method and postsynthesis treatments, ZIF-8 materials may deviate from the nominal defect-free ZIF-8 crystal structure due to defects like missing 2mIm, missing zinc, and physically adsorbed 2mIm trapped in the ZIF-8 pores, which may alter its performance and stability. Infrared (IR) spectroscopy has been used to assess the presence of defects in ZIF-8 and related materials. However, conflicting interpretations by various authors persist in the literature. Here, we systematically investigate ZIF-8 vibrational spectra by combining experimental IR spectroscopy and first-principles molecular dynamics simulations, focusing on assigning peaks and elucidating the spectroscopic signals of putative defects present in the ZIF-8 material. We attempt to resolve conflicting assignments from the literature and to provide a comprehensive understanding of the vibrational spectra of ZIF-8 and its defect-induced variations, aiming toward more precise quality control and design of ZIF-8-based materials for emerging applications.

In Situ Tracking of Nonthermal Plasma Etching of ZIF-8 Films.

Surface characterization is critical for understanding the processes used for preparing catalysts, sorbents, and membranes. Nonthermal plasma (NTP) is a process that achieves high reactivity at low temperatures and is used to tailor the surface properties of materials. In this work, we combine the capabilities of infrared reflection absorption spectroscopy (IRRAS) with NTP for the in situ interrogation of zeolitic imidazolate framework-8 (ZIF-8) thin films to probe modifications in the material induced by oxygen and nitrogen plasmas. The IRRAS measurements in oxygen plasma reveal etching of organic ligands with sequential removal of the methyl group and imidazole ring and with the formation of carbonyl moieties (C═O). In contrast, nitrogen plasma induces mild etching and grafting of nitrile groups (-C≡N). Scanning electron microscopy imaging shows that oxygen plasma, at prolonged times, significantly degrades the ZIF-8 film at the grain boundaries. Treatment of ZIF-8 membranes using mild plasma conditions yields a fivefold enhancement for H2/N2 and CO2/CH4 ideal selectivities and an eightfold enhancement for CO2/N2 ideal selectivity. Additionally, the new tools described here can be used for spectroscopic in situ tracking of plasma-induced chemistry on thin films in general.

Solvent-free bottom-up patterning of zeolitic imidazolate frameworks.

Patterning metal-organic frameworks (MOFs) at submicrometer scale is a crucial yet challenging task for their integration in miniaturized devices. Here we report an electron beam (e-beam) assisted, bottom-up approach for patterning of two MOFs, zeolitic imidazolate frameworks (ZIF), ZIF-8 and ZIF-67. A mild pretreatment of metal oxide precursors with linker vapor leads to the sensitization of the oxide surface to e-beam irradiation, effectively inhibiting subsequent conversion of the oxide to ZIFs in irradiated areas, while ZIF growth in non-irradiated areas is not affected. Well-resolved patterns with features down to the scale of 100 nm can be achieved. This developer-free, all-vapor phase technique will facilitate the incorporation of MOFs in micro- and nanofabrication processes.

An in vivo tracer study of noise-induced damage to the reticular lamina.

An in vivo tracer was used to determine if the reticular lamina and/or the cell membranes abutting the endolymphatic space are temporarily disrupted after intense noise exposure (4-kHz OBN, 108-dB SPL, 1.75 h). Using a double-barreled micropipette, the endolymphatic potential (EP) was recorded and artificial endolymph containing 10% carbon particles was injected into the endolymphatic space either 0 days or 28 days post-exposure. The cochleae were fixed 30-45 min post-injection, then dehydrated, embedded in plastic and dissected as flat preparations. Damage in the organ of Corti (OC) was quantified, the location of carbon was determined, and some OC segments were then sectioned radially. EP averaged 72+/-5 mV in five controls. These cochleae had carbon tracer in the endolymphatic space only. Four of five noise-exposed chinchillas examined 3-4 h post-exposure had a low EP (30+/-6 mV). The cochleae from these 0-day animals had several focal lesions in which nearly all outer hair cells had just degenerated. At these lesions, carbon was attached to cell membranes and debris between the reticular lamina and basilar membrane. By transmission electron microscopy, discontinuities were found in the apical membranes of sensory and supporting cells. Carbon particles were found in the cytoplasm of these cells. Four of five animals examined at 28 days had an average EP of 70+/-11 mV. The cochleae from these animals had multiple lesions in the basal turn, all of which were healed by phalangeal scars or squamous epithelial cells. In these cochleae, no carbon was found within the OC. Acute disruption of the reticular lamina and the apical membranes of sensory and supporting cells from noise appears to be a major mechanism to account for degeneration in the cochlea that spreads or continues for days to weeks post-exposure.

DPOAE level shifts and ABR threshold shifts compared to detailed analysis of histopathological damage from noise.

A detailed comparison of 2f(1)-f(2) distortion product otoacoustic emission (DPOAE) level shifts (LS) and auditory brainstem response (ABR) threshold shifts with noise-induced histopathology was conducted in chinchillas. DPOAE levels (i.e., L(1) and L(2)) at f(1) and f(2), respectively, ranged from 55-75 dB sound pressure level (SPL), with f(2)/f(1)=1.23, 6 points/octave, f(2)=0.41-20 kHz, and ABR thresholds at 0.5-20 kHz, 2 points/octave, were determined pre-exposure. The exposure was a 108 dB SPL octave band of noise centered at 4 kHz (1-1.75 h, n=6) or 80-86 dB SPL (24 h, n=5). DPOAE LSs (magnitude pre- minus post-exposure) and ABR threshold shifts (TS) were determined at 0 days and up to 28 days post-exposure. The cochleae were fixed, embedded in plastic and dissected into flat preparations. The length of the organ of Corti (OC) was measured; missing inner (IHC) and outer (OHC) hair cells counted; stereocilia damage rated; and regions of OC and nerve-fiber loss determined. Cytocochleograms were made showing functional loss and structural damage with the LS and TS overlaid. Some unexpected results were obtained. First, the best correlation of LS with histopathology required plotting the DPOAE data at f(1) with respect to the chinchilla-place map. The best correlation of TS was with IHC and nerve-fiber loss. Second, wide regions of up to 10% scattered OHC loss in the apical half of the OC showed little or no LS. Third, with the 108 dB SPL noise, there was 20-40 dB of recovery for DPOAEs at mid-high frequencies (3-10 kHz) in eight of 12 cochleae where there was 70-100% OHC loss in the basal half of the OC. The largest recovery at mid-high frequencies occurred in regions where the OC was entirely missing. Fourth, with the 80-86 dB SPL noise, there was no LS at small focal lesions (100% loss of OHCs over 0.4 mm) when the frequency place of either f(1) or f(2) was within the lesion but not both. There was no correlation of LS with OHC stereocilia loss, fusion or disarray. These results suggest that, after noise exposure, DPOAEs at mid-high frequencies can originate from or be augmented by generators located at someplace other than the frequency place of f(2), possibly the basal 20% of the OC when this region is intact. Also, noise-induced DPOAE LSs seemed to reflect differing mechanisms for temporary and permanent hearing loss.