ABSTRACT
A quantitative proton nuclear magnetic resonance(qHNMR) method was established to determine the glucose content in commercially available Massa Medicata Fermentata(MMF) products and explore the variations of glucose content in MMF products during processing. The qHNMR spectrum of MMF in deuterium oxide was obtained with 2,2,3,3-d_4-3-(trimethylsilyl) propionate sodium salt as the internal standard substance. With the doublet peaks of terminal hydrogen of glucose with chemical shift at δ 4.65 and δ 5.24 as quantitative peaks, the content of glucose in MMF samples was determined. The glucose content showed a good linear relationship within the range of 0.10-6.44 mg·mL~(-1). The relative standard deviations(RSDs) of precision, stability, repeatability, and recovery for determination were all less than 2.3%. The glucose content varied in different commercially available MMF samples, which were associated with the different fermentation days, wheat bran-to-flour ratios, and processing methods. The glucose content in MMF first increased and then decreased over the fermentation time. Compared with the MMF products fermented with wheat bran or flour alone, the products fermented with both wheat bran and flour had increased glucose. The glucose content of bran-fried MMF was slightly lower than that of raw MMF, while the glucose content in charred MMF was extremely low. In conclusion, the qHNMR method established in this study is simple, fast, and accurate, serving as a new method for determining the glucose content in MMF. Furthermore, this study clarifies the variations of glucose content in MMF during processing, which can not only indicate the processing degree but also provide a scientific basis for revealing the fermentation mechanism and improving the quality control of MMF.
Subject(s)
Protons , Drugs, Chinese Herbal/chemistry , Dietary Fiber , Magnetic Resonance SpectroscopyABSTRACT
The study of the magnonic thermal Hall effect in magnets with Dzyaloshinskii-Moriya interaction (DMI) has recently drawn attention because of the underlying topology. Topological phase transitions may arise when there exist two or more distinct topological phases, and they are often revealed by a gap-closing phenomenon. In this work, we consider the magnons in honeycomb ferromagnets described by a Heisenberg Hamiltonian containing both an out-of-plane DMI and a Zeeman interaction. We demonstrate that the magnonic system exhibits temperature (or magnetic field) driven topological phase transitions due to magnon-magnon interactions. Specifically, when the temperature increases, the magnonic energy gap at Dirac points closes and reopens at a critical temperature, T_{c}. By showing that the Chern numbers of the magnonic bands are distinct above and below T_{c}, we confirm that the gap-closing phenomenon is indeed a signature for the topological phase transitions. Furthermore, our analysis indicates that the thermal Hall conductivity in the magnonic system exhibits a sign reversal at T_{c}, which can serve as an experimental probe of its topological nature. Our theory predicts that in CrI_{3} such a phenomenon exists and is experimentally accessible.
ABSTRACT
Calcium sensing receptor (CaSR) is implicated in the establishment of neural connections and myelin formation. However, its contribution to brain development remains unclear. We addressed this issue by analyzing brain phenotype in postnatal CaSR null mice, a model of human neonatal severe hyperparathyroidism. One- and 2-week-old CaSR null mice exhibited decreased brain weight and size with a developmental delay in expression of proliferating cell nuclear antigen. Neuronal and glial differentiation markers, neuronal specific nuclear protein, glial fibrillary acidic protein, and myelin basic protein, were also decreased compared with age-matched wild-type littermates. Moreover, deletion of the parathyroid hormone gene that corrects hyperparathyroidism, hypercalcemia, hypophosphatemia, and whole-body growth retardation normalized brain cell proliferation, but not differentiation, in CaSR null mice. Cultured neural stem cells (NSCs) derived from the subventricular zones of CaSR null neonatal mice exhibited normal proliferation capacity but decreased differentiation capacity, compared with wild-type controls. These results demonstrate that direct effects of CaSR absence impair NSC differentiation, while secondary effects of parathyroid hormone-related endocrine abnormalities impair NSC proliferation, both of which contribute to delayed brain development in CaSR null newborn mice.
