scholarly journals Unveiling a hidden31P signal coresonating with extracellular inorganic phosphate by outer-volume-suppression and localized31P MRS in the human brain at 7T

2018 ◽  
Vol 80 (4) ◽  
pp. 1289-1297 ◽  
Author(s):  
Jimin Ren ◽  
Ty Shang ◽  
A. Dean Sherry ◽  
Craig R. Malloy
2010 ◽  
Vol 63 (3) ◽  
pp. 592-600 ◽  
Author(s):  
Manel Martínez-Ramón ◽  
Ascensión Gallardo-Antolín ◽  
Jesús Cid-Sueiro ◽  
Gregory L. Heileman ◽  
Kaung-Ti Yung ◽  
...  

2011 ◽  
Vol 66 (4) ◽  
pp. 911-922 ◽  
Author(s):  
Kaung-Ti Yung ◽  
Weili Zheng ◽  
Chenguang Zhao ◽  
Manel Martínez-Ramón ◽  
André van der Kouwe ◽  
...  

2017 ◽  
Vol 80 (1) ◽  
pp. 29-35 ◽  
Author(s):  
Wybe J.M. van der Kemp ◽  
Dennis W.J. Klomp ◽  
Jannie P. Wijnen

2019 ◽  
Vol 83 (5) ◽  
pp. 1539-1552 ◽  
Author(s):  
Chathura Kumaragamage ◽  
Henk M. De Feyter ◽  
Peter Brown ◽  
Scott McIntyre ◽  
Terence W. Nixon ◽  
...  

2021 ◽  
Author(s):  
Johanna Dorst ◽  
Tamas Borbath ◽  
Loreen Ruhm ◽  
Anke Henning

A method to estimate phosphorus (31P) transversal relaxation times (T2) of coupled spin systems is demonstrated. Additionally, intracellular and extracellular pH (pHext, pHint) and relaxation corrected metabolite concentrations are reported. Echo time (TE) series of 31P metabolite spectra were acquired using STEAM localization. Spectra were fitted using LCModel with accurately modeled Vespa basis sets accounting for J−evolution of the coupled spin systems. T2s were estimated by fitting a single exponential two−parameter model across the TE series. Fitted inorganic phosphate frequencies were used to calculate pH, and relaxation times were used to determine the brain metabolite concentrations. The method was demonstrated in the healthy human brain at a field strength of 9.4T. T2 relaxation times of ATP and NAD are the shortest between 8 ms and 20 ms, followed by T2s of inorganic phosphate between 25 ms and 50 ms, and PCr with a T2 of 100 ms. Phosphomonoesters and −diesters have the longest T2s of about 130 ms. Measured T2s are comparable to literature values and fit in a decreasing trend with increasing field strengths. Calculated pHs and metabolite concentrations are also comparable to literature values


2009 ◽  
Vol 22 (7) ◽  
pp. 683-696 ◽  
Author(s):  
Anke Henning ◽  
Alexander Fuchs ◽  
James B. Murdoch ◽  
Peter Boesiger

2002 ◽  
Vol 66 (6) ◽  
pp. 2227-2238 ◽  
Author(s):  
Binhui Ni ◽  
Yansheng Du ◽  
Xin Wu ◽  
Bradley S. DeHoff ◽  
Paul R. Rosteck ◽  
...  

2016 ◽  
Vol 39 ◽  
Author(s):  
Giosuè Baggio ◽  
Carmelo M. Vicario

AbstractWe agree with Christiansen & Chater (C&C) that language processing and acquisition are tightly constrained by the limits of sensory and memory systems. However, the human brain supports a range of cognitive functions that mitigate the effects of information processing bottlenecks. The language system is partly organised around these moderating factors, not just around restrictions on storage and computation.


Author(s):  
F. B. P. Wooding ◽  
K. Pedley ◽  
N. Freinkel ◽  
R. M. C. Dawson

Freinkel et al (1974) demonstrated that isolated perifused rat pancreatic islets reproduceably release up to 50% of their total inorganic phosphate when the concentration of glucose in the perifusion medium is raised.Using a slight modification of the Libanati and Tandler (1969) method for localising inorganic phosphate by fixation-precipitation with glutaraldehyde-lead acetate we can demonstrate there is a significant deposition of lead phosphate (identified by energy dispersive electron microscope microanalysis) at or on the plasmalemma of the B cell of the islets (Fig 1, 3). Islets after incubation in high glucose show very little precipitate at this or any other site (Fig 2). At higher magnification the precipitate seems to be intracellular (Fig 4) but since any use of osmium or uranyl acetate to increase membrane contrast removes the precipitate of lead phosphate it has not been possible to verify this as yet.


Author(s):  
K.S. Kosik ◽  
L.K. Duffy ◽  
S. Bakalis ◽  
C. Abraham ◽  
D.J. Selkoe

The major structural lesions of the human brain during aging and in Alzheimer disease (AD) are the neurofibrillary tangles (NFT) and the senile (neuritic) plaque. Although these fibrous alterations have been recognized by light microscopists for almost a century, detailed biochemical and morphological analysis of the lesions has been undertaken only recently. Because the intraneuronal deposits in the NFT and the plaque neurites and the extraneuronal amyloid cores of the plaques have a filamentous ultrastructure, the neuronal cytoskeleton has played a prominent role in most pathogenetic hypotheses.The approach of our laboratory toward elucidating the origin of plaques and tangles in AD has been two-fold: the use of analytical protein chemistry to purify and then characterize the pathological fibers comprising the tangles and plaques, and the use of certain monoclonal antibodies to neuronal cytoskeletal proteins that, despite high specificity, cross-react with NFT and thus implicate epitopes of these proteins as constituents of the tangles.


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