1.Effect of Acupuncture on Insulin Resistance in Non-insulin Dependent Diabetes Mellitus
Zhicheng LIU ; Fengmin SUN ; Miaohua ZHU ; Xinzheng WANG
Journal of Acupuncture and Tuina Science 2004;2(6):8-11
The fasting blood sugar (FBS), blood insulin (INS), insulin sensitivity index (ISI) and resistant hormone of INS in 46 patients with NIDDM were observed before and after the treatment. It was showed that the good effect was achieved in the cases by acupuncture and moxibustion, while the contents of FBS and INS in plasma were all decreased and ISI was increased in the cases treated by acupuncture and moxibustion, the degree of decrease of FBS and INS, and increase of ISI being closely related to therapeutic effect. The level of resistant hormone of INS and lipid in patients tend to normal level. Acupuncture and moxibustion had a good regulatory effect on the function of endocrine,sugar and lipid metabolism. It suggests that IR can be corrected by acupuncture and moxibustion,which is a key to therapeutic effect.
2.Research on the Function of Regulating Lipid by Moxibustion for Hyperlipidemia
Zhongchao WU ; Lingling WANG ; Lanfeng XU ; Yaoguang LIU ; Yizheng WANG ; Miaohua ZHU
Journal of Acupuncture and Tuina Science 2005;3(1):21-22
One hundred and seventy-one cases of hyperlipidemia were treated by moxibustion on Shenque (CV 8) and bilateral Zusanli (ST 36). After moxibustion, the blood-lipid contents of the patients with hyperlipidemia of various types were all lower than those before moxibustion.There was a significant difference between them. It is indicated that moxibustion on Shenque (CV 8) and bilateral Zusanli (ST 36) had the functions of reinforcing the spleen and kidney,warning yang, removing the stasis and treating both the principal and the secondary aspects of a disease for hyperlipidemia, which embodied the advantage of the function of regulating organism of moxibustion. The treatment by regulating can mobilize the regulating function of self to get the benign and bi-directional regulating effect for the various indexes of lipid metabolism and reach the intention of lowering blood-lipid.
3.Arf6 regulates endometriotic epithelial-mesenchymal transition and mitochondrial distribution
Yichen CHEN ; Qiming WANG ; Liang CHEN ; Miaohua ZHU ; Jing ZHANG
Chinese Journal of Obstetrics and Gynecology 2022;57(6):442-448
Objective:To investigate the role of adenosine diphosphate ribosylation factor 6 (Arf6) in the pathogenesis of endometriosis.Methods:Endometrial tissues were sampled from women who were hospitalized in the Affiliated Hospital of Medical School of Ningbo University and Ningbo Women and Children′s Hospital from November 2020 to May 2021 with endometriosis ( n=44, endometriosis group) and without endometriosis ( n=17, control group). The expression of Arf6 protein in the endometrial tissues was detected by western blot. Endometrial epithelial cells from both groups were primary cultured and the distribution of intracellular mitochondria was detected by immunofluorescence. The expression of Arf6 protein was down-regulated by small interference RNA (siRNA), the distribution of mitochondria in cells with decreased Arf6 protein expression was observed, and the expression of mitochondria-related proteins development and differentiation enhancing factor 1 (DDEF1, also called AMAP1), reactive oxygen species 1 (ROS1) and epithelial-mesenchymal transition (EMT)-related proteins E-cadherin, vimentin were detected. Transwell assay was used to detect the changes in the migration ability of the cells. Results:Compared with the control group, ectopic endometrial tissue of endometriosis group showed high expression of Arf6 protein (0.174±0.019 vs 0.423±0.033; t=29.630, P<0.01); and in ectopic endometrial epithelial cells, mitochondria were distributed near the edge of the cell membrane. While Arf6 expression was down-regulated by siRNA, the distribution of mitochondria in ectopic cells returned to natural, close to the control level. In addition, the expression levels of AMAP1 and ROS1 in ectopic cells after Arf6 protein knockdown were significantly decreased. Transwell assay results indicated that knockdown of Arf6 could reduce the migration ability of ectopic epithelial cells [migration cell count: (34.3±7.5) cells]; and immunofluorescence verified low expression of E-cadherin but high expression of vimentin in ectopic epithelial cells, whereas knockdown of Arf6 protein E-cadherin expression increased but vimentin expression decreased. Conclusions:High expression of Arf6 protein in ectopic endometrial epithelial cells leads to the distribution of mitochondria tending to membrane marginalization, while inducing EMT, which are involved in the mechanism of endoheterosis pathogenesis.
4.Genetic analysis of a Chinese pedigree with 6q26q27 microduplication and 15q26.3 microdeletion.
Dan WANG ; Chaosheng LU ; Jiamin SHI ; Yuan CHEN ; Mianmian ZHU ; Qiu WANG ; Miaohua RUAN
Chinese Journal of Medical Genetics 2023;40(6):733-736
OBJECTIVE:
To explore the genetic basis for a Chinese pedigree with 6q26q27 microduplication and 15q26.3 microdeletion.
METHODS:
A fetus with a 6q26q27 microduplication and a 15q26.3 microdeletion diagnosed at the First Affiliated Hospital of Wenzhou Medical University in January 2021 and members of its pedigree were selected as the study subject. Clinical data of the fetus was collected. The fetus and its parents were analyzed by G-banding karyotyping and chromosomal microarray analysis (CMA), and its maternal grandparents were also subjected to G-banding karyotype analysis.
RESULTS:
Prenatal ultrasound had indicated intrauterine growth retardation of the fetus, though no karyotypic abnormality was found with the amniotic fluid sample and blood samples from its pedigree members. CMA revealed that the fetus has carried a 6.6 Mb microduplication in 6q26q27 and a 1.9 Mb microdeletion in 15q26.3, and his mother also carried a 6.49 duplication and a 1.867 deletion in the same region. No anomaly was found with its father.
CONCLUSION
The 6q26q27 microduplication and 15q26.3 microdeletion probably underlay the intrauterine growth retardation in this fetus.
Female
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Humans
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Pregnancy
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East Asian People
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Fetal Growth Retardation/genetics*
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Karyotype
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Pedigree
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Prenatal Diagnosis
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Sequence Deletion
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Chromosome Duplication