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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Superintendent: China Association for Science and Technology Sponsored by: Chinese Society for Anatomical Sciences Start Publication: Started in 1964(Bimonthly) ISSN 1001-1633 CN 31-1285/R