In a literature survey, Chernoff et al. (
2017
) dismissed the hypothesis that chronic exposure to β-
N
-methylamino-L-alanine (BMAA) may be a risk factor for progressive neurodegenerative disease. ...They question the growing scientific literature that suggests the following: (1) BMAA exposure causes ALS/PDC among the indigenous Chamorro people of Guam; (2) Guamanian ALS/PDC shares clinical and neuropathological features with Alzheimer’s disease, Parkinson’s disease, and ALS; (3) one possible mechanism for protein misfolds is misincorporation of BMAA into proteins as a substitute for L-serine; and (4) chronic exposure to BMAA through diet or environmental exposures to cyanobacterial blooms can cause neurodegenerative disease. We here identify multiple errors in their critique including the following: (1) their review selectively cites the published literature; (2) the authors reported favorably on HILIC methods of BMAA detection while the literature shows significant matrix effects and peak coelution in HILIC that may prevent detection and quantification of BMAA in cyanobacteria; (3) the authors build alternative arguments to the BMAA hypothesis, rather than explain the published literature which, to date, has been unable to refute the BMAA hypothesis; and (4) the authors erroneously attribute methods to incorrect studies, indicative of a failure to carefully consider all relevant publications. The lack of attention to BMAA research begins with the review’s title which incorrectly refers to BMAA as a “non-essential” amino acid. Research regarding chronic exposure to BMAA as a cause of human neurodegenerative diseases is emerging and requires additional resources, validation, and research. Here, we propose strategies for improvement in the execution and reporting of analytical methods and the need for additional and well-executed inter-lab comparisons for BMAA quantitation. We emphasize the need for optimization and validation of analytical methods to ensure that they are fit-for-purpose. Although there remain gaps in the literature, an increasingly large body of data from multiple independent labs using orthogonal methods provides increasing evidence that chronic exposure to BMAA may be a risk factor for neurological illness.
Ceramic Bi0.86Nd0.14Fe1-xTixO3 (0.02 ≤ x ≤ 0.1) compounds were prepared to study the structural evolution, microstructure, and magnetic properties. The structural analysis by X-ray diffraction and ...Rietveld refinement revealed a coexistence of the polar rhombohedral (R3c symmetry) and antipolar orthorhombic (Pbam symmetry) structures over the entire composition range, while Raman scattering spectroscopy detected not only the phonon vibrations of the R3c and Pbam but also the Pbnm symmetries. The microstructure investigation showed the small and large grain size regions corresponding to the R3c and Pbam/Pbnm phases, respectively. The dependence of magnetization on the Ti concentration suggested that the weak ferromagnetism observed in the compounds arised from the intrinsic collapse of cycloidal order rather than defect-induced magnetism. The magnetic aging observed at room temperature was explained on the basic of phase switching and spin frustration at the phase boundary. The influence of phase switching induced by an external electric field on the magnetic properties was also studied to reveal the contribution of phase boundary spins to the net magnetization.
•Bi0.86Nd0.14Fe1-xTixO3 samples were synthesized by solid-state reaction method.•A complex phase mixture of the rhombohedral and double orthorhombic structures was observed.•The magnetic aging was induced by the phase switching and spin frustration at the phase boundary.•The intimate connection of electric field-induced phase switching and magnetic properties was studied.
The study of multinuclear NMR spectroscopies, ES-MS and HPLC suggested that the reactions of
cis-Pt(NH
3)
2(Am)Cl
+ with 5′-GMP proceed via direct nucleophilic attack and no loss of ammonia.
...cis-Pt(NH
3)
2(Am)Cl
+ binds to the N7 nitrogen of the guanine residue of 5′-GMP to form a coordinate bond with the Pt metal centre.
The multinuclear (
1H,
15N,
31P and
195Pt) NMR spectroscopies, ES-MS and HPLC have been employed to investigate the structure–activity relationship for the reactions between guanosine 5′-monophosphate (5′-GMP) and the platinum(II)–triamine complexes of the general formulation
cis-Pt(NH
3)
2(Am)ClNO
3 (where Am represents a substituted pyridine). The order of reaction rate of the reactions was found to be: 3-phpy
>
4-phpy
>
py
>
4-mepy
>
3-mepy
>
2-mepy. The two basic factors, steric and electronic, were attributed to the order of the binding rate constants. A possible mechanism of the reaction of
cis-Pt(NH
3)
2(Am)Cl
+ with 5′-GMP suggested that the reactions proceed via direct nucleophilic attack and no loss of ammonia.
cis-Pt(NH
3)
2(Am)Cl
+ binds to the N7 nitrogen of the guanine residue of 5′-GMP to form a coordinate bond with the Pt metal centre. This mechanism is apparently different from that of cisplatin. The p
K
a value of
cis-Pt(NH
3)
2(4-mepy)(H
2O)(NO
3)
2 (5.63) has been determined at 298 K by the use of distortionless enhancement by polarization transfer (DEPT)
15N NMR spectroscopy and compared to the p
K
a value of
cis-PtCl(H
2O)(NH
3)
2
+.
PDF
