1.Cost-Effectiveness Analysis of Two Therapeutic Schemes for Chronic Abacterial Prostatitis
Hangshan LI ; Meixing HUANG ; Xiao YANG ; Siying XIANG
China Pharmacy 1991;0(05):-
0.05).CONCLUSION:Scheme B has better compliance and is more economical as compared with scheme A.
2.Prenatal diagnosis and genetic analysis of a family with hypertrophic cardiomyopathy
Xiaokang ZHANG ; Jialing RONG ; Siying HE ; Guohua YANG ; Bin LIANG ; Yang XIANG ; Jing LUO ; Menglan LI ; Jianhong MA
Chinese Journal of Clinical Laboratory Science 2019;37(11):865-870
Objective:
To explore the relationship between HCM pathogenic gene mutations and clinical phenotypes by analyzing the prenatal diagnosis and genetic characteristics of a pregnant woman from a family with hypertrophic cardiomyopathy (HCM).
Methods:
The clinical data of the proband and her family members was collected. The DNA was extracted from the peripheral blood, amniotic fluid cells and cultured amniotic fluid cells of proband. Next generation sequencing (NGS) was utilized for screening pathogenetic loci of the proband. The suspected mutation sequences of HCM pathogenic candidate genes MYH7 and MYBPC3 were directly sequenced after PCR. Pathogenicity prediction of amniotic fluid cells was performed by using genetic data and bioinformatics software, such as Mutation taster, PolyPhen-2 and ANTHEPROT.
Results:
The sequencing results showed that heterozygous mutations of MYH7 c.1988G>A (p.Arg663His) and MYBPC3 c.151G>A (p.Ala51Thr) were found in the proband. The phenotype of her father was normal, and no abnormal mutations were detectable. Her mother also showed normal phenotype but carried MYBPC3 c.151G>A heterozygous mutation. Only MYH7 c.1988G>A heterozygous mutation was found in the fetus and no abnormal variation of MYBPC3 was showed. The prediction of mutation effect and analysis of protein structure and function revealed that the two missense mutations could affect the hydrophobicity and antigenicity of the protein. The genetic data demonstrated MYH7 c.1988G>A was defined as a pathogenic mutation.
Conclusion
MYH7 c.1988G>A should be a newly generated pathogenic mutation in the proband, or caused by reproductive chimerism of her parents. MYBPC3 c.151G>A mutation may promote the occurrence of HCM. Although the fetus only carries MYH7 c.1988G>A, her phenotype may still display as HCM.
3.SBC (Sanhuang Xiexin Tang combined with Baihu Tang plus Cangzhu) alleviates NAFLD by enhancing mitochondrial biogenesis and ameliorating inflammation in obese patients and mice.
Zhitao REN ; Gemin XIAO ; Yixin CHEN ; Linli WANG ; Xiaoxin XIANG ; Yi YANG ; Siying WEN ; Zhiyong XIE ; Wenhui LUO ; Guowei LI ; Wenhua ZHENG ; Xiaoxian QIAN ; Rihan HAI ; Liansheng YANG ; Yanhua ZHU ; Mengyin CAI ; Yinong YE ; Guojun SHI ; Yanming CHEN
Chinese Journal of Natural Medicines (English Ed.) 2023;21(11):830-841
In the context of non-alcoholic fatty liver disease (NAFLD), characterized by dysregulated lipid metabolism in hepatocytes, the quest for safe and effective therapeutics targeting lipid metabolism has gained paramount importance. Sanhuang Xiexin Tang (SXT) and Baihu Tang (BHT) have emerged as prominent candidates for treating metabolic disorders. SXT combined with BHT plus Cangzhu (SBC) has been used clinically for Weihuochisheng obese patients. This retrospective analysis focused on assessing the anti-obesity effects of SBC in Weihuochisheng obese patients. We observed significant reductions in body weight and hepatic lipid content among obese patients following SBC treatment. To gain further insights, we investigated the effects and underlying mechanisms of SBC in HFD-fed mice. The results demonstrated that SBC treatment mitigated body weight gain and hepatic lipid accumulation in HFD-fed mice. Pharmacological network analysis suggested that SBC may affect lipid metabolism, mitochondria, inflammation, and apoptosis-a hypothesis supported by the hepatic transcriptomic analysis in HFD-fed mice treated with SBC. Notably, SBC treatment was associated with enhanced hepatic mitochondrial biogenesis and the inhibition of the c-Jun N-terminal kinase (JNK)/nuclear factor-kappa B (NF-κB) and extracellular signal-regulated kinase (ERK)/NF-κB pathways. In conclusion, SBC treatment alleviates NAFLD in both obese patients and mouse models by improving lipid metabolism, potentially through enhancing mitochondrial biogenesis. These effects, in turn, ameliorate inflammation in hepatocytes.
Humans
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Mice
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Animals
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Non-alcoholic Fatty Liver Disease/metabolism*
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NF-kappa B/metabolism*
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Organelle Biogenesis
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Retrospective Studies
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Mice, Inbred C57BL
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Obesity/metabolism*
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Liver
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Inflammation/metabolism*
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Body Weight
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Lipid Metabolism
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Lipids
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Diet, High-Fat/adverse effects*