The relationship between the pitting potential of an oxide‐covered metal, and the pH of zero charge of its oxide, pHnormalpzc , was studied by ion implanting aluminum (99.999% purity) with elements whose oxides were of known pHnormalpzc (Mg, Al, Si, Cr, Zr, Nb, Mo, and Zn). The results showed that all the implants chosen because of the low pHnormalpzc of their oxides (Si, Cr, Zr, Nb, and Mo) produced binary surface alloys that had higher (more positive) pitting potentials than aluminum. The implants chosen because of the high pHnormalpzc of their oxides (Zn and Mg) produced binary surface alloys that had pitting potentials that were either lower than (Zn) or the same as (Mg) that of aluminum. The Mg‐Al surface alloy results are explained by selective leaching of the Mg from the oxide. The implantation of aluminum into aluminum had no effect on the pitting potential, indicating that the increased and decreased pitting potentials observed for the other implants was a chemical effect.

Explosive blast-induced mild traumatic brain injury (mTBI), a "signature wound" of recent military conflicts, commonly affects service members. While past blast injury studies have provided insights into TBI with moderate- to high-intensity explosions, the impact of primary low-intensity blast (LIB)-mediated pathobiology on neurological deficits requires further investigation. Our prior considerations of blast physics predicted ultrastructural injuries at nanoscale levels. Here, we provide quantitative data using a primary LIB injury murine model exposed to open field detonation of 350 g of high-energy explosive C4. We quantified ultrastructural and behavioral changes up to 30 days post blast injury (DPI). The use of an open-field experimental blast generated a primary blast wave with a peak overpressure of 6.76 PSI (46.6 kPa) at a 3-m distance from the center of the explosion, a positive phase duration of approximate 3.0 milliseconds (ms), a maximal impulse of 8.7 PSI × ms and a sharp rising time of 9 × 10 ms, with no apparent impact/acceleration in exposed animals. Neuropathologically, myelinated axonal damage was observed in blast-exposed groups at 7 DPI. Using transmission electron microscopy, we observed and quantified myelin sheath defects and mitochondrial abnormalities at 7 and 30 DPI. Inverse correlations between blast intensities and neurobehavioral outcomes including motor activities, anxiety levels, nesting behavior, spatial learning and memory occurred. These observations uncover unique ultrastructural brain abnormalities and associated behavioral changes due to primary blast injury and provide key insights into its pathogenesis and potential treatment.

We describe a technique for rapid stand-off detection of trace explosives and other analytes of interest. An infrared ͑IR͒ laser is directed to a surface of interest, which is viewed using a thermal imager. Resonant absorption by the analyte at specific IR wavelengths selectively heats the analyte, providing a thermal contrast with the substrate. The concept is demonstrated using trinitrotoluene and cyclotrimethylenetrinitramine on transparent, absorbing, and reflecting substrates. Trace explosives have been detected from particles as small as 10 m.

Alzheimer’s disease (AD), the most prevalent form of dementia, is characterized by two pathological hallmarks: Tau-containing neurofibrillary tangles and amyloid-β protein (Aβ)-containing neuritic plaques. The goal of this study is to understand mild traumatic brain injury (mTBI)-related brain proteomic changes and tau-related biochemical adaptations that may contribute to AD-like neurodegeneration. We found that both phosphorylated tau (p-tau) and the ratio of p-tau/tau were significantly increased in brains of mice collected at 3 and 24 h after exposure to 82-kPa low-intensity open-field blast. Neurological deficits were observed in animals at 24 h and 7 days after the blast using Simple Neuroassessment of Asymmetric imPairment (SNAP) test, and axon/dendrite degeneration was revealed at 7 days by silver staining. Liquid chromatography-mass spectrometry (LC-MS/MS) was used to analyze brain tissue labeled with isobaric mass tags for relative protein quantification. The results from the proteomics and bioinformatic analysis illustrated the alterations of axonal and synaptic proteins in related pathways, including but not being limited to substantia nigra development, cortical cytoskeleton organization, and synaptic vesicle exocytosis, suggesting a potential axonal damage caused by blast-induced mTBI. Among altered proteins found in brains suffering blast, microtubule-associated protein 1B, stathmin, neurofilaments, actin binding proteins, myelin basic protein, calcium/calmodulin-dependent protein kinase, and synaptotagmin I were representative ones involved in altered pathways elicited by mTBI. Therefore, TBI induces elevated phospho-tau, a pathological feature found in brains of AD, and altered a number of neurophysiological processes, supporting the notion that blast-induced mTBI as a risk factor contributes to AD pathogenesis. LC/MS-based profiling has presented candidate target/pathways that could be explored for future therapeutic development.

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