Objective:To establish a method to determine the metabolites in rat kidney tissues by gas chromatography-mass spectrometry (GC-MS) combined with chemometric techniques. Methods:Metabolites were separated and identiifed on HP-5MS column (30 m × 0.25 μm × 0.25 mm). The initial column temperature was 100℃lasting 3 min, and then programmed at 8℃/min to 300℃, maintaining at this temperature for 6 min. hTe internal standard was heptadecanoic acid. hTe grinded kidney tissue was exacted by methanol. hTe supernatant was dried by nitrogen. Atfer the oximation and derivation, the supernatant was analyzed by GC-MS. hTe overlapped peaks were resolved into pure chromatogram and mass spectra with chemometric techniques. Qualitative analysis was performed by comparing the obtained pure mass spectra with those in NIST mass spectra database and certiifcated by the standards and the references. hTe internal method was used for semi-quantitation. Results:A total of 53 compounds were identiifed. hTe main constitutions in the kidney tissue were amino acids, saccharides, fatty acids and urea. Conclusion:hTe combination of methods is rapid and accurate for the analysis of metabolites in the kidney tissue, which provides more information for further study of metabonomics in kidney tissues.

Primary age-related tauopathy (PART) is characterized by tau neurofibrillary tangles (NFTs) in the absence of amyloid plaque pathology. In the present study, we analyzed the distribution patterns of phosphorylated 43-kDa TAR DNA-binding protein (pTDP-43) in the brains of patients with PART. Immunohistochemistry and immunofluorescence double-labeling in multiple brain regions was performed on brain tissues from PART, Alzheimer's disease (AD), and aging control cases. We examined the regional distribution patterns of pTDP-43 intraneuronal inclusions in PART with Braak NFT stages > 0 and ≤ IV, and a Thal phase of 0 (no beta-amyloid present). We found four stages which indicated potentially sequential dissemination of pTDP-43 in PART. Stage I was characterized by the presence of pTDP-43 lesions in the amygdala, stage II by such lesions in the hippocampus, stage III by spread of pTDP-43 to the neocortex, and stage IV by pTDP-43 lesions in the putamen, pallidum, and insular cortex. In general, the distribution pattern of pTDP-43 pathology in PART cases was similar to the early TDP-43 stages reported in AD, but tended to be more restricted to the limbic system. However, there were some differences in the distribution patterns of pTDP-43 between PART and AD, especially in the dentate gyrus of the hippocampus. Positive correlations were found in PART between the Braak NFT stage and the pTDP-43 stage and density.
Aged ; Aged, 80 and over ; Aging ; metabolism ; pathology ; Brain ; metabolism ; pathology ; DNA-Binding Proteins ; metabolism ; Disease Progression ; Female ; Humans ; Immunohistochemistry ; Inclusion Bodies ; pathology ; Male ; Middle Aged ; Neurofibrillary Tangles ; metabolism ; pathology ; Neurons ; metabolism ; pathology ; Severity of Illness Index ; Tauopathies ; metabolism ; pathology