Abstract: Objective 　This study aimed to investigate the tumorigenic properties of MMTV-PyMT breast cancer transgenic mice at different ages (in weeks) and the changes in the composition of immune cells in the tumor microenvironment. Methods　Eight groups of 4, 6, 8, 10, 12, 14, 16 and 18 weeks of age MMTV-PyMT female mice (FVB mice as the background) and one group of 8 weeks of FVB female mice were prepared for routine blood testing, the pathological changes of the mammary gland and lung metastases were observed by histopathological sections, and the immune cells in blood, spleen, and tumor were analyzed by flow cytometry. Results　MMTV-PyMT mice showed adenular ductal lesions at 4 ~ 6 weeks of age; the ductal portion expanded to the growth boundary at 8 ~ 9 weeks of age, and then gradually broke through the glandular boundary to form early breast cancer at 8 ~ 12 weeks of age, and advanced breast cancer at 10 ~ 14 weeks of age. At 12 weeks of age, metastases were visible in the lungs of some mice, and at 14 weeks of age, the number of metastases in the lungs increased significantly. As the age of the mice increased, the number of white blood cells, neutrophils, and platelets in their blood increased gradually, while the lymphocytes and erythrocytes showed a gradual downward trend. Flow cytometry showed that with the increase in age, the proportion of T cells in the spleen and tumor gradually decreased, the MDSCs in the blood, spleen, and tumor gradually increased, and the NK cells in the tumor also gradually increased. Conclusions 　This study analyzed routine blood tests, pathology, and immune cells in the tissues of MMTV-PyMT mouse models of different weeks of age, providing a novel perspective on the dynamic alterations of the tumor immune microenvironment during the malignant progression of breast cancer.

Abstract: Objective 　To establish a rat model of ovarian endometriosis (EMS) using the horn reversion method, to provide an ideal animal model for exploring the pathogenesis and treatment of EMS. Methods　Fifty SPFgrade female SD rats were divided randomly into five groups: a sham group, and 1, 2, 3, and 4 weeks after surgery groups, respectively (n=10 rats per group). Apart from the sham group, an ovarian-type EMS model was established in the other groups by the uterine horn refracture method, and the modeling success rate, and ectopic foci volume and mass were observed in each group. The morphology of ectopic foci was observed by hematoxylin-eosin (HE), and expression of proliferating cell nuclear antigen (PCNA), Ki67, epithelial cadherin (E-cadherin), and neural cadherin (N-cadherin) in the uterus and ectopic foci tissues were detected by immunohistochemistry. The model was further evaluated and the degree of cell proliferation and epithelial mesenchymal transformation at different times after modeling were analyzed. Results　The modeling success rates in the 1, 2, 3, and 4 weeks after surgery groups were 80%, 90%, 100%, and 100%, respectively (P>0.05). The volume and mass of the ectopic foci were significantly greater in the 3 and 4 weeks after surgery groups compared with the 1 and 2 weeks after surgery groups (P<0.01). HE staining showed endometrial epithelial cells, mesenchymal cells and a few glands in the ectopic foci tissues. Immunohistochemical staining showed that expression levels of Ki67, PCNA, and N-cadherin in uterus tissues were significantly higher (P<0.05, P<0.01) in all the model groups compared with the sham group, while expression levels of E-cadherin were significantly lower (P<0.05, P<0.01). Expression levels of Ki67, PCNA, and N-cadherin in the uterus and ectopic foci tissues were significantly higher (P<0.05, P<0.01) in the 2, 3, and 4 weeks after surgery groups compared with the 1 week after surgery group, while expression levels of E-cadherin were significantly lower (P<0.05, P<0.01). Conclusions　The uterine horn reversion method can be used to establish an ovarian EMS model in rats. Ectopic lesions can be observed 1 week after surgery. The success rate of modeling increases with modeling time, stabilizing at 3 weeks postoperatively. Ki67, PCNA, and N-cadherin were significantly expressed in the uterus and ectopic foci tissues, and their expression levels increased with modeling time, while E-cadherin expression in the uterus and ectopic foci tissues decreased with modeling time. These Results showed good modeling success of the EMS rat model, suggesting that it could be used as a stable EMS modeling method.

Abstract: Objective 　This study sought to establish a diarrhea-predominant irritable bowel syndrome (IBSD) mouse model by gavage different mass concentrations sennae folium combined with chronic restraint stress, and to determine the appropriate mass concentration of sennae folium to establish IBS-D mouse model. Methods　The mass concentration of sennae folium used for the IBS-D mouse model followed suggested amounts in the literature and on that basis, the mass concentration gradient was established prior to conducting the experiment. Female C57BL/6 mice were divided into a normal group (Group N), a low-dose group (Group L; 0.25 g/mL sennae solution), a medium dose group (Group M; 0.50 g/mL sennae solution), and a high-dose group (Group H; 1.0 g/mL sennae solution), with 10 mice per group. After 14 days, the defecation, diarrhea index, visceral sensitivity, and morphological changes in the colonic tissue in each group were observed and recorded to compare the differences among models established with varying mass concentrations of sennae folium. Results　Compared with Group N (42.90 ± 11.90)%, Group L (80.30 ± 5.77)%, Group M (80.50 ± 3.44)%, and Group H (81.90 ± 2.68)% had significantly higher 6 h fecal water content (P<0.01). Compared with Group N (0.00 ± 0.00), the diarrhea index of mice in Group L (0.57 ± 0.16), Group M (0.62 ± 0.23), and Group H (0.60, 0.23) also increased significantly (P<0.01). Compared with Group N (0.65 (0.60, 0.65)), Group M (0.32 (0.24, 0.39)) and Group H (0.34 (0.27, 0.47)) had significantly lower visceral pain threshold and higher visceral sensitivity (P<0.01). Additionally, the first blue stool time in Group M (98.15 (93.41, 100.44) min) was significantly shorter than that in Group N (186.81 (109.28, 192.05) min) (P<0.01), and the total number of stools in Group M (22.4 ± 3.73) was significantly higher than that in Group N (17.90 ± 4.48) (P<0.05). Conclusions 　Compared with 0.25 and 1.0 g/mL, 0.50 g/mL sennae folium gavage, combined with chronic restraint stress, can better simulate the clinical symptoms of IBS-D.

Abstract: Objective 　To establish a transgenic mouse model of facioscapulohumeral muscular dystrophy (FSHD) using tamoxifen induction and Myf6-CreERT2 and FLExDUX4 mice. Methods　Dual transgenic (M6D4/+) mice were generated by crossbreeding Myf6-CreERT2 hemizygous and FLExDUX4 hemizygous mice. Full length DUX4 (DUX4-fl) expression was induced by tamoxifen starting at 3 weeks old. The disease model was evaluated at 9 weeks old by assessing changes in body mass, four-limb strength, inverted screen test, skeletal muscle weight ratio, hematoxylin/eosin, Picrosirius Red, and immunofluorescent staining of skeletal muscle paraffin sections, quantitative real-time polymerase chain reaction (RT-PCR), and RNA-sequencing (RNA-seq) of skeletal muscle. Results Dual transgenic heterozygous mice (M6D4/+) were successfully obtained. These mice exhibited significant physiological and pathological changes at 9 weeks, including delayed weight gain, reduced four-limb strength and endurance, decreased skeletal muscle weight ratio, and increases in centrally nucleated muscle fibers and fibrosis. Expression levels of DUX4 and its targeted genes were significantly up-regulated in skeletal muscle, as demonstrated by RT-PCR. RNA-seq revealed up-regulation of immune regulation-, interleukin-6, and tumor necrosis factor-related genes and down-regulation of skeletal muscle development- and differentiation-related genes. Conclusions M6D4/+ mice effectively simulated the skeletal muscle phenotype of FSHD and thus provide a good animal model for research into the pathogenesis, intervention, and treatment of FSHD.

Abstract: Objective 　To investigate the effects of different doses of 3,3’-iminodipropionitrile (IDPN) in mice with Tourette syndrome (TS) to optimize the dosage and establish a stable TS model. Methods　Thirty-two male C57BL/6J mice were divided randomly into a control group and a model group. The model group was further subdivided and administered low-dose (300 mg/kg), medium-dose (350 mg/kg), and high-dose (400 mg/kg) IDPN, respectively, while the control group received an equal volume of saline by intraperitoneal injection for 7 days. Modeling effectiveness was assessed on days 0 and 7 using stereotypy scoring, the number of head and body twitches, and open-field testing. Dopamine and tumor necrosis factor (TNF-α) levels in serum and brain tissue were measured by enzyme-linked immunosorbent assay. The morphology of striatum and hippocampus tissues were observed by hematoxylin/eosin (HE) staining. Results　The stereotypy scores indicated successful modeling of TS in the medium- and high-dose groups. Significant behavioral changes in the open-field test were only detected in the highdose IDPN group (P<0.05). Serum dopamine levels were significantly increased (P<0.05) in the model group, and TNF-α levels were significantly elevated in the medium- and high-dose groups (P<0.05), but there was no significant difference in brain-tissue levels (P>0.05). HE staining showed that the neurons and glial cells in the striatum and hippocampus were morphologically normal in the control group, but there were some neurodegenerative changes and a few swollen neuronal cell bodies in the striatum and hippocampus in the model group, and obvious lymphocyte infiltration in the striatum and hippocampus in the high-dose group. Conclusions 　Through systematic comparison of varying IDPN dosages in establishing a TS model, this study identified 400 mg/kg as the optimal dosage for effective model induction. These findings provide data to support dose optimization in the TS model and offer valuable references for ensuring the smooth progress of early-stage experiments, which could aid the evaluation of the therapeutic effects of subsequent drug interventions.

Abstract: Objective 　To simulate modern social stress using a pre-pregnancy chronic mild stress (CMS) model and to explore the mechanisms of emotional, behavioral, and neurodevelopmental changes in male offspring of pre-pregnancy liver qi stagnation female mice through corticosterone (CORT)-brain-derived neurotrophic factor (BDNF) extracellular signal-regulated kinase (ERK) 1/2 signaling cascade-mediated hippocampal injury. This study aimed to elucidate the impact of negative life events on offspring and the interventional mechanism of Shuyu Capsules. Methods　CMS stress was used to induce pre-pregnancy depression in female rats (liver qi stagnation state), followed by intervention with Shuyu and fluoxetine capsules. After screening, male rats were mated and 12 male offspring from each group were selected for behavioral testing and detection of serum CORT levels by enzyme-linked immunosorbent assay. BDNF, ERK1/2, phospho (p)-ERK1/2, cAMP-response element binding protein (CREB), and p-CREB protein levels in the hippocampus were detected by Western Blot, and BDNF, ERK1, ERK2, and CREB mRNA levels in the hippocampus were detected by reverse transcription-polymerase chain reaction(RT-PCR), to verify the effects of pre-pregnancy CMS on the BDNF-ERK1/2-CREB signaling pathway and to investigate the key micro-mechanisms of Shuyu Capsules on emotional and learning memory-related behaviors of male offspring of females with pre-pregnancy liver qi stagnation syndrome. Results　The distance, number of entries, and duration of stay in the central area in open-field experiments were significantly reduced in offspring in the model group (all P<0.05). The escape latency during the exploration period of the water-maze experiment was significantly prolonged (P<0.05) and the swimming distance, duration of the target quadrant, and number of platform crossings were significantly reduced (P<0.05, P<0.05, P<0.01), the suspension time and frequency in the forced-swimming experiment were increased (P<0.05, P<0.01), and the incubation period was shortened (P<0.05) in offspring in the model group. Prophylactic treatment with Shuyu Capsules and fluoxetine improved the depression-like behavior and cognitive impairment in the offspring in the model group. Biochemical tests showed that CORT levels were increased in the CMS model group (P<0.05), BDNF, p-ERK1/2, and p-CREB protein levels in the hippocampus were decreased (all P<0.05), and BDNF, ERK1, ERK2, and CREB mRNA levels were significantly reduced (P<0.01, P<0.05, P<0.01, P<0.05). Treatment with Shuyu Capsules and fluoxetine increased the CORT content and BDNF, ERK1/2, and CREB protein and mRNA levels in male offspring to varying degrees. Conclusions 　High levels of CORT in offspring act selectively on the hippocampus, exerting adverse effects on the emotional and learning memory functions of rats by downregulating the BDNF-ERK1/2 signaling cascade. The Chinese medicine Shuyu Capsules can reduce the impact of an adverse intrauterine environment on offspring development by correcting abnormal levels and pathways of glucocorticoids.

Abstract: Objective 　This study sought to establish a non-alcoholic fatty liver disease (NAFLD)model in Wistar-SD hypercholesterolemia (WSHc)rats induced by a high-fat diet and to reveal the pathogenesis of NAFLD in these rats through the Srebp-1 gene. Methods　After 2 weeks of dietary treatment, thirty 6-week-old WSHc rats were divided into High-fat control group, HFD + AAV no load group, and HFD + AAV group, with 10 rats in each group. The HFD + AAV no load group and HFD +AAV group were intravenously injected with a vector virus and an shRNA containing virus, respectively. WSHc rats were fed with a normal fat diet as a normal control group. Serum levels of ALT, AST, TBIL, ALP, TBA, GLU, CHOL, and TG were measured every 2 weeks. After a further 8 weeks of feeding, the rats were euthanized and livers were excised for HE staining, Oil Red O staining, Masson staining, and Sirius red staining to observe the morphology, lipid deposition, and fibrosis of the liver tissues. RT-qPCR was performed to detect the expression of lipid metabolism-related genes namely Srebp-1, Aacs, FASN and LDLR in the livers. Furthermore, hepatocytes were isolated, cultured, and divided into a normal control group and a high-fat control group. Next, expression of the Srebp-1 gene was detected by RT-qPCR. Srebp-1 knockout (KO)hepatocytes were constructed, then TG content was detected and the lipid accumulation was observed by Oil Red O staining. Results　After 10 weeks of high-fat diet treatment, serum ALT (P<0.001), ALP (P<0.001), TBA (P<0.05), GLU (P<0.001), and CHOL (P<0.001)significantly increased in WSHc rats. Abnormal lipid deposition with formation of large vacuolar lipid droplets and fibrotic lesions in livers were observed. The mRNA expression of Srebp-1 noticeably increased in WSHc rats (P<0.001). Moreover, compared with the high-fat control group, the ALT (P<0.05)and GLU (P<0.01)in the HFD + AAV group decreased, and liver lipid deposition and the formation of large vacuolar lipid droplets were alleviated. Expressions of genes such as FASN (P<0.05)and LDLR (P<0.01)were significantly upregulated. Additionally, there was a significant increase in the expression of Srebp-1 in hepatocytes of the high-fat control group (P<0.001), while after Srebp-1 gene knockout, cellular TG levels decreased and the degree of lipid droplet aggregation was reduced. Conclusions 　The Srebp-1 gene plays a regulatory role in hepatic lipid metabolism and deposition, modulating the expression of lipid metabolism-related genes in WSHc rats with NAFLD. In vitro experiments demonstrated that downregulation of Srebp-1 alleviates lipotoxic injury in hepatocytes, suggesting that the development of NAFLD in WSHc rats is closely associated with abnormally high expressions of the Srebp-1 gene.

Abstract: Objective 　This study aimed to observe the effects of Yin-Yang balancing acupotomy intervention on knee-joint function and lower limb biomechanics in a rat model of knee osteoarthritis (KOA), and to explore the mechanisms of acupotomy when treating KOA. Methods　Forty SD rats were randomly divided into a blank group, a model group, an acupotomy group, and a medication group. Except for the blank group, KOA models were established by injecting a mixed solution of 4% papain and 0.03 mol/L L-cysteine into the left knee-joint cavity. The acupotomy group received Yin-Yang balancing acupotomy interventions targeting the medial/lateral collateral ligaments and patellar ligament. The medication group received daily oral celecoxib (10 mg/(kg·d)). Interventions began on day 7 post-modeling, and occurred once weekly for 4 weeks. All rats were assessed pre- and post-intervention using the modified Lequesne MG knee-joint grading system and rotarod fatigue test. Post-intervention, in vivo DR imaging was used to measure joint space width. Cartilage morphology was evaluated via HE and safranin O-fast green staining. Ligament biomechanical tensile testing was performed. Serum and cartilage tissues were analyzed by ELISA and Western Blot for matrix metalloproteinase-13 (MMP-13) expression. Results　(1)Compared with the blank group, the model group showed increased modified Lequesne MG scores, reduced rotarod endurance time, and narrowed joint space (P<0.01). (2)Compared with the model and medication groups, the acupotomy group exhibited lower Lequesne MG scores, prolonged rotarod endurance time (P<0.05), and expanded joint space (P<0.05). (3) The elastic modulus of ligaments in the acupotomy group showed no significant difference from those in the model group but was higher than those in the medication group. Yield strength, maximum strain, and yield-to-tensile strength ratio in the acupotomy group were higher than those in the model and medication groups (P<0.05). (4)HE and Safranin O-Fast green staining revealed minimal inflammatory infiltration in the acupotomy group compared with the model group. Cartilage surfaces in the acupotomy group were smoother than those in the medication group. (5)ELISA showed reduced serum MMP-13 levels in the acupotomy group versus the model group (P<0.01), and no significant differences between levels in the drug and acupotomy groups. (6)Cartilage MMP-13 expression in the acupotomy group was significantly lower than that in the model group (P<0.01) and lower than that in the medication group (P<0.05). Conclusions 　Acupotomy intervention enhances knee joint stability, improves lower limb mechanical alignment, and suppresses MMP-13 expression in KOA rats.

Abstract: Objective 　To explore the mechanism of GS-9620 in improving imiquimod (IMQ)-induced psoriasis-like inflammation by regulating the Th1/Th17-related immune response, and to investigate its regulatory effect on the gut microbiota in mice. Methods　An IMQ-induced psoriasis-like inflammation model was established in BALB/c mice. The severity of the skin lesions was evaluated by psoriasis area and severity index (PASI) score. The proportions of CD4⁺ interleukin (IL)-17⁺ and CD4⁺ interferon (IFN)-γ⁺ cells in spleen tissue were detected by flow cytometry. Levels of the inflammatory factors tumor necrosis factor (TNF)-α, IL-1β, and IL-6 in skin tissues were determined by enzyme-linked immunosorbent assay, and pathological analysis was performed by hematoxylin/eosin staining. The effects of GS-9620 on the structure of the gut microbiota in control, IMQ model, and GS-9620-treated mice were detected by 16S rRNA sequencing. Results　GS-9620 significantly reduced the PASI score in IMQinduced mice and effectively reduced the proportions of CD4⁺ IL-17⁺ and CD4⁺ IFN-γ⁺ cells in the spleen. GS-9620 also significantly down-regulated the expression levels of TNF-α, IL-1β, and IL-6 in skin tissues. 16S rRNA sequencing showed that GS-9620 significantly regulated the abundance of gut microbiota related to inflammation, including the relative abundances of bacteria such as Lachnospiraceae_NK4A136_group, Lachnospiraceae_UCG-008, Alloprevotella, Desulfovibrio, Prevotellaceae_UCG-001, and Alistipes. Conclusions 　GS-9620 effectively alleviates IMQ-induced psoriasis-like skin inflammation in mice by regulating the expression of Th1/Th17-related inflammatory factors. It may also improve IMQ-induced clinical symptoms by regulating the structure of the gut microbiota, thus providing a new theoretical basis for the treatment of psoriasis. The result of this study provide important experimental evidence to support further investigations into the application of GS-9620 for the treatment of psoriasis.

Abstract: Objective 　Using different concentrations of Coxsackievirus B3 (CVB3) to infect young SD rats. To investigate the distribution of coxsackievirus B3 (CVB3) in rat tissues and the immune response and inflammatory factors, to clarify the immunopathological mechanism of viral infection and provide an experimental basis for drug screening and efficacy evaluation. Methods　Young SD rats (7 days old) were injected intraperitoneally with different doses of CVB3 (TCID₅₀=10^-3.34 /100 μL) and the proportions of lymphocyte subsets (CD4⁺, CD8⁺ ) in whole blood at days 4 and 8 were detected by flow cytometry. The CVB3 loads in the heart, liver, spleen, brain, kidney, and gastrointestinal tissues were detected by real-time fluorescence quantitative polymerase chain reaction, TNF-α and IFN-γ levels were detected by enzyme-linked immunosorbent assay, and histomorphologic changes were observed by hematoxylin and eosin staining. Results　Different doses of CVB3 caused different degrees of diarrhea and decreased body mass in young rats. CVB3 was mainly distributed in the stomach, small intestine, large intestine, and stools, with the highest load in the large intestine and stools. The stock solution group (TCID₅₀=10^-3.34 /100 μL) increased the proportion of CD8⁺ T cells in the whole blood in young rats and decreased the CD4⁺ /CD8⁺ ratio (P<0.05, P<0.01).Compared with the nomal group high TNF-α and low IFN-γ expression were observed in the large intestine of young rats in the concentrate group (P<0.05, P<0.01), and submucosal edema and inflammatory cell infiltration were observed in the large intestine (cecum and rectum). There were no significant differences in the proportion of lymphocyte subsets, TNF-α and IFN-γ levels, and morphological changes in whole blood of young rats in the group 10^-1, 10^-2, and 10^-3 (P>0.05). Conclusions 　Different doses of CVB3 can induce infections in young SD rats. CVB3 (TCID₅₀ = 10^-3.34 /100 μL) causes pathological changes in the large intestine (cecum and rectum) in young rats, and high virus replication can increase levels of inflammatory factors and cause an imbalance of immune cells. CVB3 may have a unique pathogenic mechanism in young rats, providing a theoretical basis for developing evaluation strategies for drugs against CVB3 virus infections.

Abstract: Objective 　To explore the change trend and related mechanism of resting metabolic rate induced by corticosterone in mice, and observe the intervention effects of Zhibai Dihuang Pill and Jinkui Shenqi pill. Methods Sixty-four mice were randomly divided into short-term and long-term groups, and each group was randomly divided into four groups. Mice in CORT group, ZBDH group and JKSQ group were given sterile drinking water containing corticosterone, and mice in Ctrl group were given sterile drinking water containing 1% anhydrous ethanol. Mice in ZBDH group and JKSQ group were given Chinese medicine by gavage. RMR of mice in each group was dynamically monitored during modeling and Chinese medicine intervention. The morphology of mitochondria in liver and muscle were observed by transmission electron microscope. The TR expression level in liver and muscle tissues of each group was observed by immunofluorescence, and MDA and ATP levels were detected in liver and muscle tissues of each group. levels of ACTH, TSH, INS, T3, T4, FT3, FT4, 8-OHdG, FGF-21, GDF-15, L-lactic acid and pyruvic acid in serum were also detected. Results　Compared with Ctrl group, the mitochondrial morphology of liver and muscle tissues in CORT group was damaged, and the expression of TR was decreased. In short-term (Day 8), RMR, ATP in liver, serum T4, ACTH and INS levels were significantly increased in the CORT group, while serum FGF-21, TSH levels and MDA in liver were significantly decreased. In long term (Day 56), RMR, serum 8-OhdG, INS, and ATP in liver and muscle were significantly decreased in the CORT group, serum FGF-21, GDF-15, T3, T4, FT3, FT4, MDA in liver and muscle were significantly increased. Compared with CORT group, in short term, RMR, serum L (+)-lactate in ZBDH group were significantly decreased, while serum 8-OHdG and the expression of TRα in muscle significantly increased. In JKSQ group, the mitochondrial morphology of muscle tissue was improved, the expression of TRα and serum FGF-21 were significantly increased, while serum L(+)-lactic acid, FT4 and ATP in liver were significantly decreased. In long term, serum FGF-21 was significantly lower in ZBDH group, and in JKSQ group, RMR, ATP in liver tissue and TRα expression in muscle were significantly increased, while the levels of FGF21, GDF-15, T3, FT4 in serum and MDA in muscle tissue were significantly decreased. Conclusions　CORT induced RMR to increase first and then decrease with the intervention time. In the short term, Zhibai Dihuang Pill significantly decreased RMR in mice, while in the long term, Jinkui Shenqi Pill significantly increased RMR. The mechanism may be related to mitochondrial injury, thyroxine secretion and thyroxine receptor expression.

Abstract:Mice are a core model organism in neuroscience and are undergoing a technological transition in whole-brain atlas construction, as researchers shift from traditional anatomical approaches to multidimensional molecular-level analysis. This marks a new phase in brain research method ology, characterized by higher resolution and systemic integration. Spatial transcriptomics technologies have significantly advanced the biological depth of neuroscience studies, offering novel paradigms for exploring dynamic neural circuit evolution and cellular diversity in the brain. By combining traditional anatomical localization, single-cell molecular connectomics, and functional imaging for macroscopic dynamic tracking, brain atlas research achieves “molecule-circuit-behavior” tri-level integration, thereby constructing molecular regulatory networks underlying dynamic neural circuit remodeling. However, current challenges persist in technical integration. Reference brain atlases hold great promise for elucidating brain homeostasis mechanisms, identifying abnormal circuit metabolic features in neurological disorders (e. g., anxiety), and screening therapeutic targets. Future brain atlas research must advance multimodal technology fusion and cross-dimensional data integration to achieve precise mapping from static structures to dynamic functional networks, and thus provide revolutionary tools for neuroscience.

Abstract:Chronic pain causes physical suffering and can have major psychological impacts in patients. Chronic pain can induce depressive disorder, and clinical studies have consistently shown that chronic pain and depression frequently co-occur, suggesting the possibility of shared pathogenic mechanisms underlying these conditions. Acupuncture, as an alternative therapy, has been widely used for analgesia and to treat depression, with demonstrated clinical efficacy. The therapeutic mechanism of acupuncture is related to neural and endocrine regulation. This review considers the mechanism of chronic pain accompanied by depression, in relation to the brain regions and neural circuits affected by acupuncture treatment. This review provides a new approach for the treatment of depression caused by chronic pain.

Abstract:Planarians have strong regenerative abilities and play an important role in evolution. Planarians are ideal model animals for experimental research, and have reportedly been used in regenerative medicine, toxicology, immunology, and genetics, among other fields. This article summarizes the progress of research on planarians as model animals, and provides a reference for future research on these animals.

Abstract:Perimenopausal depression seriously affects women’s physical and mental health. It is caused primarily by gonadal function decline, which is typically characterized by low mood, anxiety, slow thinking, and loss of interest, and is accompanied by autonomic dysfunction and endocrine dysfunction. The pathogenesis of perimenopausal depression remains unclear and controversial. Many scholars have conducted scientific research that is based on animal models of perimenopausal depression. Indeed, a good animal model of perimenopausal depression is the basic premise for studying its pathophysiological mechanisms and for facilitating reliability of the scientific result. Therefore, this paper combines the modern research mechanisms of perimenopausal depression and the current status of animal models in China, and provides an overview, evaluation, and generalization of the modeling method, principles and result, to provide a scientific basis and reference for the selection of suitable animal models for scientific research experiments.