ABSTRACT
OBJECTIVE: To establish a method based on HPLC fingerprint, pattern recognition and simultaneous determination of multi-component for quality evaluation of Chrysanthemum indicum, and investigate its feasibility and accuracy. METHODS: HPLC fingerprints of 21 batches of Chrysanthemum indicum were established, similarity analysis, principal component analysis and cluster analysis were performed on fingerprints of Chrysanthemum indicum by TCMYS fingerprint software, and 12 common chromatographic peaks in fingerprints were identified, and 12 components were quantified by external standard method. RESULTS: The HPLC fingerprints of 21 batches of Chrysanthemum indicum were similar, and their classification trend was found. Seventeen common peaks were found and 12 of them were identified as neochlorogenic acid, chlorogenic acid, caffeic acid, 1,3-dicaffeoylquinic acid, cynaroside, isochlorogenic acid C, isochlorogenic acid A, (1S, 3R, 4R, 5R)-3, 4-bis[[(E)-3-(3, 4-dihydroxyphenyl)prop-2-enoyl]oxy]-1, 5-dihydroxycyclohexane-1-carboxylic acid, linarin, luteolin, apigenin and acacetin. Good linear relationship (r≥0.999 6) was shown for the external standard method, the average recoveries were between 95.84% and 102.46%, and the RSDs were all below 2.72%. CONCLUSION: Combination of HPLC fingerprint, pattern recognition and simultaneous determination of multi-component are accurate and reliable for quality evaluation of Chrysanthemum indicum, which can provide important information for the overall quality evaluation of Chrysanthemum indicum.
ABSTRACT
INTRODUCTION: Transmissible spongiform encephalopathies are a group of neurodegenerative diseases of humans and animals. Genetic Creutzfeldt-Jakob diseases, in which mutations in the PRNP gene predispose to disease by causing the expression of abnormal PrP protein, include familial Creutzfeldt-Jakob disease, Gerstmann-Straussler-Scheinker syndrome and fatal familial insomnia. CASE PRESENTATION: A 47-year-old Han-Chinese woman was hospitalized with a 2-year history of progressive dementia, tiredness, lethargy and mild difficulty in falling asleep. On neurological examination, there was severe apathy, spontaneous myoclonus of the lower limbs, generalized hyperreflexia and bilateral Babinski signs. A missense mutation (T to G) was identified at the position of nt 341 in one PRNP allele, leading to a change from glycine (Gly) to valine (Val) at codon 114. PK-resistant PrPSc was detected in brain tissues by Western blotting and immunohistochemical assays. Information on pedigree was collected notably by interviews with family members. A further four suspected patients in five consecutive generations of the family have been identified. One of them was hospitalized for progressive memory impairment at the age of 32. On examination, he had impairment of memory, calculation and comprehension, mild ataxia of the limbs, tremor and a left Babinski sign. He is still alive. CONCLUSION: This family with G114V inherited prion disease is the first to be described in China and represents the second family worldwide in which this mutation has been identified. Three other suspected cases have been retrospectively identified in this family, and a further case with suggestive clinical manifestations has been shown by gene sequencing to have the causal mutation.
