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Aluminum powder, ≥91% (complexometric); CAS Number: 7429-90-5; EC Number: 231-072-3; find Sigma-Aldrich-11009 MSDS, related peer-reviewed papers, technical documents, similar products & more at Sigma-Aldrich

Aluminum powder, ≥91% (complexometric) | Sigma-Aldrich

Aluminum powder, &#8805;91% (complexometric)

Aluminum

Structural features of oxide coatings on aluminum.

Aluminum ion diffusion in aluminum oxide.

Electrochemistry of Cd (II) in the basic 1-ethyl-3-methylimidazolium chloride/tetrafluoroborate room temperature molten salt.	

Using a combination of experimental techniques such as optical absorption, Raman scattering, continuous wave and pulse Electron Spin Resonance (ESR), we characterize a set of γ-irradiated Yb(3+) doped silica glass preforms with different contents of phosphorous and aluminum. We demonstrate that when P is introduced in excess compared to Al, nearly no radiodarkening is induced by γ-rays. On the other hand, when Al>P, a large absorption band is induced by radiation. Thermal annealing experiments reveal the correlation between the decrease of the optical absorption band and the decrease of the Al-Oxygen Hole Center (AlOHC) ESR signal, demonstrating the main role of AlOHC defects in the fiber darkening. HYSCORE (HYperfine Sublevel CORElation) pulse-ESR experiments show a high Al-P nuclear spin coupling when P>Al and no coupling when Al>P. This result suggests that both AlOHC and POHC creation is inhibited by Al-O-P linkages. Confronting our data with previous works, we show that the well-known photodarkening process, meaning losses induced by the IR pump, can also be explained in this framework.

Evidence of AlOHC responsible for the radiation-induced darkening in Yb doped fiber.

Laser treatment has emerged as a novel treatment modality for onychomycosis. We sought to determine thermal response and optical effects of a submillisecond neodymium:yttrium-aluminum-garnet (Nd:YAG) 1064-nm laser on common fungal nail pathogens, and the clinical efficacy and safety of the Nd:YAG 1064-nm laser on onychomycotic toenails. A 4-part in vitro and in vivo study was conducted using a Nd:YAG 1064-nm laser. The first portion evaluated 3 different nail pathogens in suspension at 7 heat and time exposures. The second and third parts of the study irradiated pure fungal colonies. The final portion involved an in vivo treatment of toenails over 5 treatment sessions. A fungicidal effect for Trichophyton rubrum was seen at 50°C after 15 minutes, and for Epidermophyton floccosum at 50°C after 10 minutes. Limited growth of Scytalidium was seen at 55°C after 5 minutes. No inhibition was observed after laser treatment of fungal colonies or suspensions. In vivo treatment of toenails showed no improvement in Onychomycosis Severity Index score. The Nd:YAG 1064-nm laser was the only laser tested. Laser treatment of onychomycosis was not related to thermal damage or direct laser effects. In vivo treatment did not result in onychomycosis cure.

Treatment of onychomycosis using a submillisecond 1064-nm neodymium:yttrium-aluminum-garnet laser.

Refractory inclusions [calcium-aluminum-rich inclusions, (CAIs)] represent the oldest Solar System solids and provide information regarding the formation of the Sun and its protoplanetary disk. CAIs contain evidence of now extinct short-lived radioisotopes (e.g., (26)Al, (41)Ca, and (182)Hf) synthesized in one or multiple stars and added to the protosolar molecular cloud before or during its collapse. Understanding how and when short-lived radioisotopes were added to the Solar System is necessary to assess their validity as chronometers and constrain the birthplace of the Sun. Whereas most CAIs formed with the canonical abundance of (26)Al corresponding to (26)Al/(27)Al of ∼5 × 10(-5), rare CAIs with fractionation and unidentified nuclear isotope effects (FUN CAIs) record nucleosynthetic isotopic heterogeneity and (26)Al/(27)Al of <5 × 10(-6), possibly reflecting their formation before canonical CAIs. Thus, FUN CAIs may provide a unique window into the earliest Solar System, including the origin of short-lived radioisotopes. However, their chronology is unknown. Using the (182)Hf-(182)W chronometer, we show that a FUN CAI recording a condensation origin from a solar gas formed coevally with canonical CAIs, but with (26)Al/(27)Al of ∼3 × 10(-6). The decoupling between (182)Hf and (26)Al requires distinct stellar origins: steady-state galactic stellar nucleosynthesis for (182)Hf and late-stage contamination of the protosolar molecular cloud by a massive star(s) for (26)Al. Admixing of stellar-derived (26)Al to the protoplanetary disk occurred during the epoch of CAI formation and, therefore, the (26)Al-(26)Mg systematics of CAIs cannot be used to define their formation interval. In contrast, our results support (182)Hf homogeneity and chronological significance of the (182)Hf-(182)W clock.

182Hf-182W age dating of a 26Al-poor inclusion and implications for the origin of short-lived radioisotopes in the early Solar System.

With the global population predicted to grow by at least 25 per cent by 2050, the need for sustainable production of nutritious foods is critical for human and environmental health. Recent advances show that specialized plant membrane transporters can be used to enhance yields of staple crops, increase nutrient content and increase resistance to key stresses, including salinity, pathogens and aluminium toxicity, which in turn could expand available arable land.

Using membrane transporters to improve crops for sustainable food production.

When a material is heated, generally, it dilates. Here, we find a general trend that the average distance between a center atom and atoms in the first nearest-neighbor shell contracts for several metallic melts upon heating. Using synchrotron X-ray diffraction technique and molecular dynamics simulations, we elucidate that this anomaly is caused by the redistribution of polyhedral clusters affected by temperature. In metallic melts, the high-coordinated polyhedra are inclined to evolve into low-coordinated ones with increasing temperature. As the coordination number decreases, the average atomic distance between a center atom and atoms in the first shell of polyhedral clusters is reduced. This phenomenon is a ubiquitous feature for metallic melts consisting of various-sized polyhedra. This finding sheds light on the understanding of atomic structures and thermal behavior of disordered materials and will trigger more experimental and theoretical studies of liquids, amorphous alloys, glasses, and casting temperature effect on solidification process of crystalline materials.

Negative expansions of interatomic distances in metallic melts.

To evaluate the effect of nozzle distance, nozzle angle, and deposition duration on the silica content attained on zirconia by air abrasion. Disk-shaped zirconia (LAVA, 3M ESPE) (diameter: 10 mm, thickness: 2 mm) specimens (N = 54) were obtained. They were wet-ground finished using 600-, 800-, and 1200-grit silicone carbide abrasive papers in sequence and ultrasonically cleaned. The specimens were mounted in a specially designed apparatus that allowed the chairside air-abrasion device to be operated under standard conditions. Alumina-coated silica particles (CoJet Sand, 3M ESPE) were deposited on the zirconia disk surfaces varying the following parameters: a) nozzle distance (2, 5, 10 mm), and b) deposition duration (5, 13, 20 s) at two nozzle angles (45 and 90 degrees) under 2.5 bar pressure at three locations on each ceramic disk. The specimen surfaces were then gently air dried for 20 s. Silica content in weight percentage (wt%) was measured from 3 surfaces on each disk using Energy Dispersive X-ray Spectroscopy (EDS) (150X) in an area of 0.8 mm x 0.6 mm (n = 3 per group). Surface topographies were evaluated using SEM. Data were analyzed using ANOVA and Tukey's tests (α = 0.05). Nozzle angle (p = 0.003) and deposition duration (p = 0.03) significantly affected the results, but nozzle distance (p = 0.569) did not. A significantly higher amount of silica (wt%) was achieved when the nozzle angle was 45 degrees to the surface in all distance-duration combinations (16.7 to 28.2 wt%) compared to the 90-degree nozzle angle (10.7 to 18.6 wt%) (p < 0.001). The silica amount was significantly higher after 20-s deposition duration than after 13 s (p < 0.05). EDS analysis demonstrated not only Si but also Al, Zr, and O traces on the substrate. SEM images indicated that deposition at a nozzle distance of 2 mm often created cavitations in zirconia. Effective silica deposition using a charside air-abrasion device can be achieved when the nozzle is held at 45 degrees to the surface with more than 2-mm nozzle distance for 20 s.

Effect of particle deposition parameters on silica coating of zirconia using a chairside air-abrasion device.

The neuroanatomic specificity with which Alzheimer's disease (AD) progresses could provide clues to AD etiopathology. Magnetic resonance imaging studies of AD clinical progression have confirmed general conclusions from earlier studies of AD neuropathological progression wherein neurofibrillary tangle pathology was observed to spread along a well-defined sequence of corticocortical and corticosubcortical connections, preferentially affecting certain cell types, while sparing others. Identical and non-identical twin studies have consistently shown AD has mixed (environmental and genetic) etiopathogenesis. The decades-long prodromal phase over which AD develops suggests slow but progressive accumulation of a toxic or infective agent over time. Major environmental candidates are reviewed to assess which best fits the profile of an agent that slowly accrues in susceptible cell types of AD-vulnerable brain regions to toxic levels by old age, giving rise to AD neuropathology without rapid neuronal lysis. Chronic aluminum neurotoxicity best matches this profile. Many humans routinely ingest aluminum salts as additives contained in processed foods and alum-treated drinking water. The physical properties of aluminum and ferric iron ions are similar, allowing aluminum to use mechanisms evolved for iron to enter vulnerable neurons involved in AD progression, accumulate in those neurons, and cause neurofibrillary damage. The genetic component of AD etiopathogenesis apparently involves a susceptibility gene, yet to be identified, that increases aluminum absorption because AD and Down syndrome patients have higher than normal plasma, and brain, aluminum levels. This review describes evidence for aluminum involvement in AD neuropathology and the clinical progression of sporadic AD.

Aluminum involvement in the progression of Alzheimer's disease.

In 1991, treatment with low dose intramuscular desferrioxamine (DFO), a trivalent chelator that can remove excessive iron and/or aluminum from the body, was reported to slow the progression of Alzheimer's disease (AD) by a factor of two. Twenty years later this promising trial has not been followed up and why this treatment worked still is not clear. In this critical interdisciplinary review, we provide an overview of the complexities of AD and involvement of metal ions, and revisit the neglected DFO trial. We discuss research done by us and others that is helping to explain involvement of metal ion catalyzed production of reactive oxygen species in the pathogenesis of AD, and emerging strategies for inhibition of metal-ion toxicity. Highlighted are insights to be considered in the quests to prevent potentially toxic effects of aluminum toxicity and prevention and intervention in AD.

Towards the prevention of potential aluminum toxic effects and an effective treatment for Alzheimer's disease.

We have examined the neurotoxicity of aluminum in humans and animals under various conditions, following different routes of administration, and provide an overview of the various associated disease states. The literature demonstrates clearly negative impacts of aluminum on the nervous system across the age span. In adults, aluminum exposure can lead to apparently age-related neurological deficits resembling Alzheimer's and has been linked to this disease and to the Guamanian variant, ALS-PDC. Similar outcomes have been found in animal models. In addition, injection of aluminum adjuvants in an attempt to model Gulf War syndrome and associated neurological deficits leads to an ALS phenotype in young male mice. In young children, a highly significant correlation exists between the number of pediatric aluminum-adjuvanted vaccines administered and the rate of autism spectrum disorders. Many of the features of aluminum-induced neurotoxicity may arise, in part, from autoimmune reactions, as part of the ASIA syndrome.

Aluminum in the central nervous system (CNS): toxicity in humans and animals, vaccine adjuvants, and autoimmunity.

Most humans living in industrialized societies are routinely exposed to bioavailable aluminum salts in the form of additives-in commercially-prepared foods, alum-clarified drinking water, certain pharmaceuticals, sunscreens, and other topical applications. Minute amounts of this aluminum are absorbed into the circulation. Trace aluminum levels cross the blood-brain barrier and progressively accumulate in large pyramidal neurons of the hippocampus, cortex, and other brain regions vulnerable in Alzheimer's disease. More aluminum enters the brain than leaves, resulting in a net increase in intraneuronal aluminum with advancing age. Aluminum is responsible for two main types of toxic damage in cells. As a pro-oxidant, aluminum causes oxidative damage both on its own and in synergy with iron. Aluminum also competes with, and substitutes for, essential metals-primarily Mg2+, iron and Ca2+ ions-in or on proteins and their co-factors. The author hypothesizes that intraneuronal aluminum interferes with Ca2+ metabolism in the aged brain and describes a way to test this hypothesis. This paper reviews: 1) major changes that occur in brain Ca2+ homeostasis and Ca2+ signaling, subtly with aging and more overtly in Alzheimer's disease; and 2) evidence from the scientific literature that aluminum causes these same changes in neurons.

Aluminum disruption of calcium homeostasis and signal transduction resembles change that occurs in aging and Alzheimer's disease.

Magnetic resonance imaging of multiple sclerosis (MS) patients often shows active inflammatory lesions despite clinical remission. No immunological marker of disease activity has been identified in these patients. Concentrations of neopterin, interleukin-2 (IL-2), soluble interleukin-2 receptor (sIL-2R) and tumour necrosis factor-alpha (TNF-alpha) were measured in the serum and cerebrospinal fluid of 19 clinically-inactive MS patients and compared with those of 19 non-inflammatory controls. Cerebrospinal fluid (CSF) neopterin concentrations were significantly higher in the MS group than in controls (mean 9.1 mM vs 3.4 nM, P < 0.01) and 10 of 19 MS patients had levels above the control range. This finding provides evidence of ongoing T-cell-directed and interferon-gamma-mediated macrophage activation in the central nervous system. Analysis of IL-2, sIL-2R and TNF-alpha concentrations revealed no significant differences between MS patients and controls. We conclude that CSF neopterin concentration may correlate with disease activity in asymptomatic patients.

Measurement of immune markers in the serum and cerebrospinal fluid of multiple sclerosis patients during clinical remission.

1-Benzyl-1,2,3,4-tetrahydroisoquinoline (1BnTIQ) was detected as a novel endogenous amine in mouse brain and parkinsonian CSF by using the gas chromatography-selected ion-monitoring method. The level of 1BnTIQ was very high in CSF of some parkinsonian patients compared with that of controls with other neurological diseases, the mean value being three times higher (parkinsonians: 1.17 +/- 0.35 ng/ml of CSF, n = 18; vs. controls: 0.40 +/- 0.10 ng/ml of CSF, n = 11; mean +/- SEM, not significantly different). The pole test, a toxicological examination to evaluate behavior abnormalities related to Parkinson's disease, was used to examine the pharmacological effect of 1BnTIQ in mice. Repeated administration of 1BnTIQ induced behavior abnormalities, which pretreatment with 1-methyl-1,2,3,4-tetrahydroisoquinoline could prevent. We suggest that 1BnTIQ may be related to the idiopathic Parkinson's disease.

1-Benzyl-1,2,3,4-tetrahydroisoquinoline as a parkinsonism-inducing agent: a novel endogenous amine in mouse brain and parkinsonian CSF.

In a recent publication [Diestel, A., O. Aktas, D. Hackel, I. Hake, S. Meier, C. S. Raine, R. Nitsch, F. Zipp, and O. Ullrich. 2003. Activation of microglial poly (ADP-ribose)-polymerase-1 by cholesterol breakdown products during neuroinflammation: a link between demyelination and neuronal damage. J. Exp. Med. 198: 1729-1740], extremely high levels of 7-oxocholesterol were reported in cerebrospinal fluid (CSF) of 11 patients with multiple sclerosis (MS) [7.4 +/- 0.3 mg/l (mean +/- SEM)]. The corresponding level of 12 subjects with other kinds of neurological diseases was reported to be 0.5 +/- 0.1 mg/l. Such high levels of 7-oxocholesterol were found to cause neuronal damage of living brain tissues. Using a highly accurate method for an assay of 7-oxocholesterol based on isotope dilution-mass spectrometry and anaerobic conditions during workup, we found that the level of 7-oxocholesterol in CSF from 29 Swedish patients with MS was only 1.2 microg/l (median, ranging from 0.4 to 4.6 microg/l), less than 1/1,000 th of the previously reported level. The level of 7-oxocholesterol in CSF from 24 Swedish control patients was 0.9 microg/l (0.3-2.3 microg/l), slightly but significantly lower than the CSF level in MS patients (P=0.002). In vitro-induced lipid peroxidation of the endogenous cholesterol in CSF increased the level of 7-oxygenated cholesterol metabolites, particularly 7-oxocholesterol, up to approximately 0.3 mg/l. These results are discussed in relation to the fact that 7-oxygenated steroids are easily artificially formed by autoxidation of cholesterol during workup procedures and analysis of sterols and oxysterols from biological samples.

Levels of 7-oxocholesterol in cerebrospinal fluid are more than one thousand times lower than reported in multiple sclerosis.

There is evidence that increased blood concentrations of homocysteine may be a risk factor for Alzheimer's disease. (E)-4-hydroxy-2-nonenal (HNE) is a neurotoxic product of lipid peroxidation that is increased in the ventricular fluid and brains of patients with Alzheimer's disease. We measured the concentrations of homocysteine, HNE, vitamin B(12) and folate in the plasma of 27 patients with Alzheimer's disease and 25 control subjects. There was a statistically significant increase in the plasma concentration of homocysteine (P < 0.001) and HNE (P < 0.001) in the Alzheimer's disease patients compared to the control group. There was a significant decrease in the plasma concentration of vitamin B(12) (P < 0.001) and folate (P = 0.002) in the Alzheimer's group compared to the controls. There was a significant positive correlation between the plasma concentrations of homocysteine and HNE in the patients with Alzheimer's disease (r = 0.661, P < 0.001). A significant negative correlation was found between the plasma concentration of homocysteine and the plasma concentrations of vitamin B(12) (r = -0.605, P = 0.0006) and folate (r = 0.586, P = 0.001). We also measured the concentrations of homocysteine, HNE, vitamin B(12) and folate in the cerebrospinal fluid (CSF) of 8 patients with Alzheimer's disease compared to 6 control subjects. The concentrations of homocysteine (P = 0.032) and HNE (P = 0.001) were significantly higher in the CSF of Alzheimer's patients than in the control subjects. There were significant positive correlations between the CSF concentrations of homocysteine and HNE (r = 0.924, P = 0.001). There was also a significant positive correlation between the plasma concentration of homocysteine and the CSF concentrations of homocysteine (r = 0.850, P = 0.007) and HNE (r = 0.092, P = 0.002). These results demonstrate that there is a relationship between increased homocysteine concentrations and increased HNE concentrations in Alzheimer's disease.

The effect of increased concentrations of homocysteine on the concentration of (E)-4-hydroxy-2-nonenal in the plasma and cerebrospinal fluid of patients with Alzheimer's disease.

Markers of oxidative stress are increased in cerebrospinal fluid (CSF) of patients with Alzheimer disease (AD), although none of those reported are appropriate diagnostic markers because of the overlap between patients with AD and control subjects. To determine the ratio of 8-hydroxyguanine (8-OHG) levels in intact DNA to free 8-OHG in the ventricular CSF of patients with AD and age-matched control subjects. The most prominent marker of DNA oxidation is 8-OHG. Free 8-hydroxy-2'-deoxyguanosine (8-OHdG) was isolated from ventricular CSF taken at autopsy from 18 subjects with AD and 7 control subjects using solid-phase extraction columns. Levels were measured as the hydrolysis product, 8-OHG, using gas chromatography/mass spectrometry with selective ion monitoring. Intact DNA was isolated from the same CSF and the levels of 8-OHG were determined in the intact structures. Stable-labeled 8-OHG was used for quantification. A statistically significant (P<.05) 108-fold increase in the ratio of 8-OHG in intact DNA to free 8-OHG was observed in patients with AD. Analysis of the data distribution indicated that the lowest AD ratio was 3.5 times higher than the highest control ratio; there was no overlap of the 2 populations. Although the data for each individual measurement demonstrates overlap between patients with AD and control subjects, the ratio of 8-OHG intact in DNA to free 8-OHG demonstrates a delineation between patients with AD and control 8-OHG subjects and may be useful as a marker of disease progression or the efficacy of therapeutic antioxidant intervention.

Ratio of 8-hydroxyguanine in intact DNA to free 8-hydroxyguanine is increased in Alzheimer disease ventricular cerebrospinal fluid.

The cobalamin status was evaluated in Alzheimer dementia (n = 26), other dementias (n = 24), various gerontopsychiatric disorders (n = 25), and in neuro-psychiatrically healthy controls (n = 20). Supplementing serum cobalamin we measured methylmalonic acid (MMA), a metabolite accumulating early in cobalamin deficiency. Subnormal cobalamin and/or clearly elevated MMA concentrations were found in 11 cases: 7 Alzheimer patients (27%), 2 with other dementias (8%), one psychiatric patient (4%), and one control (5%). None presented the typical neurologic features of cobalamin deficiency and macrocytosis was found in only one. The mean cobalamin concentration was significantly lower in Alzheimer patients (179 +/- 18 pmol/l) than in the age-matched controls (256 +/- 23 pmol/l) (p = 0.013) and the other patient groups. Correspondingly, the mean MMA level was higher in the Alzheimer group (0.480 +/- 0.062 mumol/l) than in any other diagnostic group (controls: 0.347 +/- 0.040 mumol/l). Comparing the Alzheimer group to the other groups as a whole, the elevation was significant (p = 0.0097). Our findings indicate that Alzheimer patients are particularly prone to cobalamin deficiency, and even subtle biochemical signs of deficiency seem to justify treatment.

Serum cobalamin and methylmalonic acid in Alzheimer dementia.

24S-Hydroxycholesterol (24OHC) and 27-hydroxycholesterol (27OHC) are two structurally similar oxysterols of different origins--the former almost exclusively formed in the brain and the latter formed to a lesser extent in the brain than in most other organs. HYPOTHESIS TO BE TESTED: Neuronal damage and/or demyelination causes increased flux of 24OHC from the brain into the cerebrospinal fluid (CSF), whereas a defect blood-brain barrier causes increased flux of 27OHC from the circulation into the CSF. Isotope dilution-mass spectrometry was used to assay the two oxysterols in CSF and plasma from more than 250 patients with different neurological and geriatric diseases. The CSF-levels of the two oxysterols were much more affected by the different diseases than the plasma levels. Patients with active demyelinating diseases had increased levels of 24OHC in CSF with a relatively high 24OHC/27OHC ratio. Patients with meningitis in general had high levels of both steroids with a low 24OHC/27OHC ratio. Patients with Alzheimer's disease had slightly increased levels of 24OHC in CSF with less increase in 27OHC. Patients with multiple sclerosis had a tendency to have higher levels of 24OHC during active periods with a high 24OHC/ 27OHC ratio. Measurements of the two oxysterols in CSF and plasma may add significantly to existing biochemical methods for evaluation of neurological diseases.

Aluminum

powder, ≥91% (complexometric)

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