1.Purification of Polysaccharide Peptide of Coriolus Versicolor in Affinity Chromatography
Yinlin LEI ; Xiaodong WANG ; Zuozhen LIU ; Xingyan WU ;
Chinese Traditional Patent Medicine 1992;0(01):-
Objective: To study a new purification method of Polysaccharide Peptide of Coriolus versicolor in affinity chromatography. Methods: Isotherm and kinetics in absorption and the optimal conditions of absorption and elution were studied through static experiments. The static absorption capacity q m and absorption constant K d were calculated according to Chase model. Results: q m =55.57mg/g wet resin, K d =5.312g/L, the dynamic absorption capacity is 43.1mg, polysaccharide/g wet resin and 10.3mg protein/g wet resin.Conclusion: Affinity chromatography can be used to purify PSP preliminarily.
2.Effect ofGuizhi-Fulingcapsule on expression of AngⅡ, eNOS in rats with UUO-induced tubulointerstitial fibrosis
Shujun LI ; Jianjun LIU ; Yan ZHANG ; Xiyan JIA ; Zuozhen CHAI ; Dasheng YANG
International Journal of Traditional Chinese Medicine 2015;(8):724-727
Objectives To observe the effect ofGuizhi-Fuling capsule on the expression of AngⅡand eNOS.Methods 72 male Sprague-Dawley(SD) rats, aged three months, were randomly divided into three groups: a sham-operated group(n=24),a model group (n=24) and a treatment group (n=24). Renal tubulointerstitial fibrosis model was established via unilateral ureteral obstruction(UUO). Rats in the treatment group were treated withGuizhi-Fulingcapsule (125mg/kg),and the same volume of normal saline were given to the rats in the sham -operated group and the model group at the same time. Rats were put to death at day 7, 14, 21 Immunohisto-chemistry staining was performed to investigate both the expression of AngⅡ, eNOS in TIF. Results 1 Renal interstitium injury was seen in the model group and the treatment group rats at day 7. The degree of renal interstitium fibrosis in rats from the treatment group was lighter than that of the model group at day 7, 14, 21 (P< 0.01).2 At day 7,14 and 21, the expression of AngⅡin rats from the model group and the treatment group were higher than that of the sham-operated group (P<0.01), but those of the treatment group was lower than those of the model group (P< 0.01). The expression of AngⅡ in rats from the model and the treatment groups were increasing,the highest in the 21th day (P<0.01).3 At day 7, 14 and 21, the expression of eNOS in rats from the model group and the treatment group were lower than that of the sham-operated group (P<0.01).ConclusionsGuizhi-Fuling capsule can alleviate the lesion of renal tissue in obstructive kidney and delay the development of TIF.
3.Genetic analysis of a child with Charlevoix-Saguenay spastic ataxia due to variant of SACS gene.
Huan LUO ; Xiaolu CHEN ; Xueyi RAO ; Yajun SHEN ; Jinfeng LIU ; Zuozhen YANG ; Jing GAN
Chinese Journal of Medical Genetics 2023;40(5):558-562
OBJECTIVE:
To explore the clinical feature and genetic variant of a child with autosomal recessive Charlevoix-Saguenay type spastic ataxia (ARSACS).
METHODS:
Clinical data of a child who was admitted to the West China Second Hospital of Sichuan University on April 30, 2021 was collected. Whole exome sequencing (WES) was carried out for the child and his parents. Candidate variants were verified by Sanger sequencing and bioinformatic analysis based on the guidelines from the American College of Medical Genetics and Genomics (ACMG).
RESULTS:
The child, a 3-year-and-3-month-old female, had a complain of "walking instability for over a year". Physical and laboratory examination revealed progressive and aggravated gait instability, increased muscle tone of the right limbs, peripheral neuropathy of the lower limbs, and thickening of retinal nerve fiber layer. The results of WES revealed that she has harbored a maternally derived heterozygous deletion of exons 1 to 10 of the SACS gene, in addition with a de novo heterozygous c.3328dupA variant in exon 10 of the SACS gene. Based on the ACMG guidelines, the exons 1-10 deletion was rated as likely pathogenic (PVS1+PM2_Supporting), and the c.3328dupA was rated as a pathogenic variant (PVS1_Strong+PS2+PM2_Supporting). Neither variant was recorded in the human population databases.
CONCLUSION
The c.3328dupA variant and the deletion of exons 1-10 of the SACS gene probably underlay the ARSACS in this patient.
Female
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Humans
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Heat-Shock Proteins/genetics*
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Muscle Spasticity/genetics*
;
Mutation
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Spinocerebellar Ataxias/pathology*
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Child, Preschool