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25 February 2025, Volume 48 Issue 1
  
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    With the advent of the digital information age, human anatomy has entered the stage of digital anatomy. Traditional methods of demonstrating anatomy through cadaver and models are gradually being replaced by mathematical models. Digital anatomy has changed the methods and content of anatomy education, scientific research and clinical applications. This paper reviews the development history, advantages, model construction of digital anatomy, as well as its applications in 3D visualization, new discoveries in medical morphology, medical 3D printing, digital virtual simulation, and medical education. It also offers an outlook on the future development of digital anatomy.
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    Objective: To investigate the expression of tumor necrosis factor-alpha (TNF-α) and interleukin-10 (IL- 10) in the placenta under high-altitude hypoxic conditions, and the effects on reproductive function and offspring development. Methods: A total of 20 female rats and 10 male rats were randomly divided into hypoxic group (simulated 6 000 m altitude in a hypobaric oxygen chamber) and normoxia group (Xining city, Qinghai province, with an average altitude of 2 200 m) with a female-to-male ratio of 2:1 per cage. The pregnancy rate of female rats in each group was recorded. On the 20th day of gestation, after a 12-hour fast, blood samples were collected from the tails of the pregnant rats to measure their fasting glucose. Blood was also taken from the abdominal aorta, and the entire uterus was excised to isolate the placenta and fetuses. The uterine weight and number of fetal rats were recorded, and the offspring malformation rate was calculated for both groups. ELISA was used to detect the serum fasting insulin level of pregnant rats, and H-E staining was used to observe the alteration of placental tissues in hypoxia. Immunohistochemistry was utilized to detect the positive expression of TNF-α and IL-10 in the placental tissues of pregnant rats. RT-qPCR and Western blotting were employed to detect the mRNA and protein expression of TNF-α and IL-10 in placental tissues of pregnant rats. Results: Compared with the normoxia group, the hypoxia group showed significantly lower uterine weight in pregnant rats during late pregnancy, reduced fasting blood glucose and increased fasting insulin levels, lower conception rates, fewer fetuses, and a higher rate of fetal malformations. The placenta of pregnant rats in the hypoxia group was structurally incomplete, with increased distribution of blood vessels, thickened vessel wall, slow development and reduced number of chorionic villi, densely distributed intervillous blood vessels,thickened basement membrane, a small number of inflammatory cells, and blurred boundaries of thickened syncytial trophoblast. Compared with the normoxia group, the expression of TNF-α and IL-10 mRNA and protein were upregulated in the placental tissues of the hypoxia group. Conclusion: Under hypoxic conditions, the expression of TNF-α and IL-10 in the placental tissue is upregulated, which may be related to impaired reproductive function and adverse pregnancy outcomes in female rats.
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    Objective: To explore the regulatory effect of progesterone on the expression of interleukin-8 (IL-8) in decidual stromal cells (DSCs) through transcription factor activator protein 1 (AP-1). Methods: Immunohistochemical staining and western blotting (WB) were used to detect the expression level of AP-1 protein in decidual tissue of the abortion group and the control group. Early pregnancy human DSCs were isolated and cultured in vitro, and cells were treated with different concentrations of progesterone (0.01 μmol/L, 0.1 μmol/L, and 1 μmol/L). WB was used to detect the expression of AP-1 and p-AP-1 in DSCs. After AP-1 inhibitor SR-11302 treatment, the expression of IL-8 in the inhibitor group, progesterone group, and control group was detected by using RT-qPCR and WB. Results: The expression level of p-AP-1 protein in decidual tissue of the abortion group was higher than that of the control group; the relative expression levels of p-AP-1 protein in the 0.1 μmol/L and 1 μmol/L progesterone group were significantly lower than that in the control group; IL-8 mRNA levels were significantly lower in the progesterone group compared with the control group, and were further reduced in the progesterone+SR-11302 group compared with the progesterone group; compared with the control group, the relative expression levels of IL-8 and p-AP-1 proteins in the progesterone group were reduced, and compared with the progesterone group, the relative expression levels of IL-8 and p-AP-1 proteins in the progesterone+SR-11302 group were also reduced. Conclusions: Progesterone downregulates the expression of IL-8 in DSCs via AP-1, offering a theoretical basis for its use in preventing and treating early spontaneous abortion induced by abnormal expression of proinflammatory cytokines.
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    Objective : To investigate the protective effect and mechanism of Wogonoside (WO) on hepatic injury induced by high-fat diet in diabetic rats. Methods : A total of 50 male Wistar rats were randomly divided into control group, model group (DM) and three drug administration groups (DM+WO 2, 4 and 8 mg/kg). The diabetic rat model was established by intraperitoneal injection of 30 mg/kg streptozotocin. Total cholesterol (TC), alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), superoxide dismutase (SOD), and malondialdehyde (MDA) were detected by ELISA. The expression levels of apoptosis-related proteins and lipid metabolism-related proteins in liver tissues were determined by Western blotting. H-E staining was used to observe the histopathological changes of liver. Apoptosis of hepatocytes was assessed by TUNEL staining. Results : Compared with the control group, the rats in the DM group showed typical symptoms of diabetes (frequent urination, thirst, hunger, and weight loss) and hepatic pathological injury. Compared with the DM group, the levels of biochemical indicators such as AST, ALT, TC, TG, LDL-C and MDA were obviously decreased in the drug administration groups, while the levels of HDL-C and SOD were obviously increased. The Bax/Bcl-2 ratio and acetyl-CoA carboxylase expression in liver tissue were significantly reduced, while the expression levels of c-Myc and carnitine palmitoyltransferase 1 were significantly elevated in the drug administration groups. The histopathological morphology of the liver was improved and the apoptosis of liver cells was reduced in the three WO treatment group, among which only a small number of apoptotic cells were observed in DM+WO 8 mg/kg group. Conclusion : WO has a certain protective effect on liver injury induced by high-fat diet in diabetic rats.
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    Objective: To investigate the effect and mechanism of betulinic acid (BA) on epithelial-mesenchymal transition (EMT) in A2780 ovarian cancer cells. Methods: The viability of A2780 cells treated with different concentrations of betulinic acid (5–80 μmol/L) for 24 hours was assessed by using the CCK-8 assay. The effects of BA on epithelial-mesenchymal transformation were detected under treatment with 0, 5, 10, 20 μmol/L of BA for 24 h. The transforming growth factor-β (TGF-β) subtype involved in ovarian cancer was predicted by Oncomine, and the mRNA levels of TGF-β2 in A2780 cells treated with BA (0, 5, 10, 20 μmol/L) for 24 hours were measured. A2780 cells were divided into control group, 10 μmol/L BA group, and 10 μmol/L BA+2 ng/mL TGF-β2 group to determine whether TGF-β2 could reverse the effect of BA on epithelial mesenchymal transformation, invasion, migration and drug resistance in A2780 cells. Results: BA decreased the cell viability of A2780 with an IC50 of 37.8 μmol/L. Compared with 0 μmol/L BA group, the expression of E-cadherin was increased, while N-cadherin, Vimentin were significantly decreased in the 10 μmol/L and 20 μmol/L BA groups. Oncomine prediction results showed significant differences in both DNA copy numbers and mRNA expression levels of TGF-β2 between ovarian cancer and normal tissue. Compared with 0 μmol/L BA group, the expression of TGF-β2 were significantly decreased in the 5, 10, 20 μmol/L BA groups. Compared with the 10 μmol/L BA group, the 10 μmol/L BA +2 ng/mL TGF- β2 group had decreased E-cadherin, increased protein expression of N-cadherin, Vimentin, MMP-2, MMP-9, Smad2, Smad3, along with increased numbe r of invaded cells, enhanced wound healing rate, and improved viability of cisplatin-treated cells. Conclusion: BA may exert its anti-tumor effects by inhibiting the TGF-β2-associated EMT signaling, thereby reducing the invasion, migration, and drug resistance of A2780 ovarian cancer cells.
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    Objective: To investigate the effects of puerarin on the growth, proliferation, apoptosis and invasion of ovarian cancer Caov3 cells by regulating tumor immune microenvironment. Methods: Caov3 cells were treated with supernatants from THP-1 cells treated with different concentrations of puerarin. CCK8 assay was used to detect the growth of ovarian cancer cells. ELISA was utilized to detect the content of interleukin (IL) 4, IL-10, and IL-6. RTPCR was adopted to detect the mRNA expression of IL-4, IL-10, and IL-6. Colony formation assay was adopted to detect the number of cell colonies. Flow cytometry was applied to detect cell apoptosis. Western blotting was adopted detect the expression of apoptosis marker proteins (caspase-3, caspase-9). Transwell chamber was employed detect cell invasion. Western blotting was used to detect the expression of invasion-related proteins (vascular endothelial growth factor, fibronectin, vimentin). Results: Compared with the control group, when the puerarin concentration was 10 μmol/L, the viability of ovarian cancer Caov3 cells was significantly inhibited. Compared with the 0 μmol/L group, the levels and mRNA expression of IL-6, as well as the apoptosis rate, were significantly increased, while clone formation rate, number of invasion cells, and invasion-re lated protein expression were all significantly reduced. The results for IL-4 and IL-10 were opposite. Conclusion: Puerarin modulates tumor immune microenvironment to inhibit the growth and invasion of ovarian cancer Caov3 cells and to promote their apoptosis, thereby alleviating the occurrence and development of ovarian cancer tumors.
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    Objective: To investigate the effect of long non-coding RNA (LncRNA) Down syndrome cell adhesion molecule antisense 1 (DSCAM-AS1) on liver cancer activity and chemotherapy resistance by regulating the miR- 431-5p/sex determining gene box 9 (SOX9) axis. Methods: qRT-PCR was applied to detect the expression levels of DSCAM-AS1, miR-431-5p, and SOX9 mRNA in liver cancer tissue, liver cancer cells, and HepG2/CDDP resistant cells. Western blotting was utilized to detect the expression of multidrug resistance associated protein 1 (MRP1), proliferating cell nuclear antigen (PCNA), Bcl-2, Bax, SOX9. Functional assays included MTT for cell viability, flow cytometry for apoptosis. Bioinformatics, dual luciferase assay, pull down assay, and RIP assay were applied to validate the targeting relationship between DSCAM-AS1, SOX9, and miR-431-5p. Results: DSCAM-AS1 and SOX9 were highly expressed in liver cancer tissues and cells, while miR-431-5p was low expressed. compared with HepG2 cells, the expression of DSCAM-AS1 and SOX9, and the cell viability in HepG2/CDDP cells were significantly increased, while the expression of miR-431-5p was reduced. Silencing DSCAM-AS1 inhibited the proliferation of HepG2 and HepG2/CDDP cells, induced apoptosis, and reduced drug resistance of HepG2/CDDP cells, while inhibiting miR-431-5p weakened the inhibitory effect of silencing DSCAM-AS1 on HepG2 and HepG2/CDDP cell proliferation, promoted apoptosis, and promoted drug resistance in HepG2/CDDP cells. Bioinformatics, dual luciferase assay, pull down assay, and RIP assay confirmed the targeting relationship between DSCAM-AS1, SOX9, and miR-431-5p. Conclusion: Silencing DSCAMAS1 may inhibit HepG2 cell proliferation, promote apoptosis, and reduce drug resistance in HepG2/CDDPcells by regulating the miR-431-5p/SOX9 axis.
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    Objective: To investigate whether forkhead box A1 (FoxA1) could promote high expression of Yesassociated protein (YAP) in esophageal cancer and subsequently promote cancer progression by activating cAMP response element-binding protein (CREB) via the Src homology 2 domain-containing tyrosine phosphatase (SHP2) pathway. Methods: A total of 10 cases of esophageal cancer tissues and corresponding adjacent normal tissues with complete clinical data from May 2021 to September 2021 were collected from Yancheng Tinghu People’s Hospital were collected. H-E staining was used to determine the pathological changes of esophageal carcinoma and adjacent normal tissues. Immunofluorescence staining was employed to evaluate the expressions of FoxA1 and YAP in esophageal carcinoma and adjacent normal tissues. KYSE150 cells were cultured in vitro and divided into four groups: FoxA1-NC group (control group for FoxA1 interference), FoxA1-siRNA group (FoxA1 interference group), DMSO solvent group (DMSO added to the culture medium), and PH PS1 inhibitor group (SHP2 inhibitor PHPS1 added to the culture medium). Western blotting was to measure the expression levels of FoxA1, p-SHP2, p-CREB and YAP protein in KYSE150 cells. Cell scratch assay, Transwell assay, and monoclonal proliferation assay were used to detect the proliferation, migration and invasion ability of KYSE150 cells, respectively. Results: Compared with the adjacent normal tissues, esophageal cancer tissues exhibited pathological changes such as mucosal hyperemia, dark color, disrupted epithelial tissue structure, and increased cell number. In addition, the levels of FoxA1, p-SHP2, p-CREB and YAP proteins in the esophageal cancer tissues were significantly increased. The results of in vitro experiments showed that, in in vitro experiments, both FoxA1-siRNA and the PHPS1 inhibitor significantly reduced the levels of p-SHP2, p-CREB, and YAP proteins in KYSE150 cells, as well asthe cells’ abilities to proliferate, migrate, and invade. However, only FoxA1-siRNA was able to significantly decrease the FoxA1 protein level. Conclusion: FoxA1 promotes the progression of esophageal cancer by activating CREB via the SHP2 pathway, leading to high expression of YAP.
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    目的:系统分析精神分裂症及孤独症患者利手的分布特点,探讨利手左移现象与精神发育异常的相关性。 方法:检索中国知网、万方医学数据库、维普期刊服务平台、PubMed 数据库等公开发表的利手与精神分裂症和 孤独症相关文献(1976 年—2022 年)。利用Stata 14 软件对纳入的研究做异质性检验及合并后结果分析,漏斗图和 Egger 检验评估发表偏倚,敏感性分析评估研究的稳定性,Meta 回归检验影响文章异质性的来源。SPSS 26.0 进 行聚类分析和χ2 检验,探索不同人群非右利手分布可能的遗传学差异。结果: 共纳入符合要求的29 项研究,包含 5 950 例精神分裂症患者及其对照24 725 人;孤独症患者94 人及其对照331 人。荟萃分析结果显示,精神分裂症 组及孤独症组非右利手比率均显著高于对照组;男性精神分裂症患者非右利手比率显著高于对照组;孤独症组非 右利手比率显著高于精神分裂症组及对照组,对照组非右利手比率最低。结论:利手在精神分裂症和孤独症中均 出现明显左移现象,在精神分裂症中男性较女性更为明显,有望成为筛选精神发育异常类疾病的宏观生物学标记。
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    Protein arginine methyltransferase 6 (PRMT6) is one of the type Ⅰ PRMT family members which catalyzes the monomethylation and asymmetric dimethylation of arginine residues on protein substrates. It has a catalytic structure that is not completely identical to other type Ⅰ PRMT family members, and exhibits differences in catalytic substrates. An increasing number of studies have reported that PRMT6 not only plays an important role in the tumor process, but also serves as a regulator in the inflammatory process. This article aims to review the catalytic structure and function of PRMT6, as well as the research progress on its role in both anti-inflammatory and pro-inflammatory responses in organs.
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    Vitamin D deficiency is becoming increasingly common and has emerged as a globally concerned public health issue, especially among people living in high-altitude areas and among Caucasians. Vitamin D is an essential fat-soluble vitamin for the human body, primarily obtained through two main sources. Most of the vitamin D is synthesized in the skin after ultraviolet irradiation, and the other part can be obtained from the diet. Vitamin D itself is not biologically active. After two hydroxylation processes in the body, it produces bioactive calcitriol (1, 25 (OH)2D3), which acts on target organs or tissues and participates in a variety of biological reactions in the body. The reactions include the regulation of calcium and phosphorus metabolism, immune response, cell differentiation, and apoptosis. In recent years, more and more scholars in China and beyond have found that vitamin D is closely related to human fertility, pregnancy, and lactation. This article reviews the recent advances in research on the role of vitamin D in fertility and pregnancy.
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