With economic development， diabetes has become one of the most common chronic diseases globally，and liver insulin resistance is one of the key factors for the occurrence and development of type 2 diabetes mellitus.This paper reviews the studies on the direct effects of fructose on insulin pathway and the indirect blocking of insulinpathway through increasing de novo synthesis of liver lipids， weakening fatty acid oxidation in hepatocytes， activating oxidative stress in hepatocytes， and enhancing hepatic inflammatory responses. It provides a new perspective for thediagnosis and treatment of obesity ， type 2 diabetes and other diseases closely related to hepatic insulin resistance.

Objective ： To explore the susceptibility of amacrine cell（ AC） types to N-methyl-D-aspartate（ NMDA）excitotoxicity in the rat retina. Methods ： H-E staining was used to observe the pathological changes in retinal tissueafter NMDA injury， while immunofluorescence staining was used to observe the changes in the quantity of Brn3a（the marker of retinal ganglion cell） and syntaxin（ the marker of AC）. In the study of the dose-effect relationshipand time-effect relationship of NMDA-induced AC injury， immunofluorescence staining was used to detect themorphological and numerical changes of GAD65/67+ （the marker of GABAergic AC）， GlyT1+（the marker ofglycinergic AC）， ChAT+（the marker of cholinergic AC）， TH+（ the marker of dopaminergic AC）， and PV+ cells（the marker of AⅡ AC） in the rat retina. Propidium iodide （PI） and cleaved caspase-3 staining were employed to determine the subtypes of dead AC. Results ： NMDA can damage both retinal ganglion cells and displaced ACs in the retinal ganglion cell layer（ GCL）， as well as ACs in the inner nuclear layer（ INL）. In the dose-effectrelationship of AC damage induced by NMDA， all ACs significantly decreased with the increase of NMDA dose，and the cholinergic ACs in the INL and dopaminergic ACs （DAC） did not show their cell somas in 100 nmol NMDA.In the time-effect relationship of AC damage induced by NMDA， the number of GAD65/67+ in INL， GlyT1+， ChAT+ and TH+ cells began to decrease at 6 h after injury， while the number of GAD65/67+ cells in GCL， the total numberof GAD65/67+ cells in the retina， and PV+ cells all began to decrease at 12 h after injury and continued to decreasewith the progression of NMDA-induced damage.Conclusion ： The GABAergic ACs and glycinergicACs in the retina both show damage under the influenceof NMDA， with cholinergic ACs in the INL and DACsbeing particularly sensitive to NMDA-induced damage.

Objective ： To investigate the mechanism of hepatitis B virus（ HBV） on myeloid-derived suppressor cells （MDSCs）. Methods ： C57BL/6 mice were allocated into normal and HBV groups. The chronic HBV infection model was established within the HBV group， with subsequent assessment of miR-21-5p levels in mice. Additionally， C57BL/6mice were distributed across control， miR-21-5p negative control， miR-21-5p overexpression， and miR-21-5p knockdown groups. All mice， except those in the control group， were subjected to miR-21-5p lentiviral intervention， followed by theestablishment of a chronic HBV infection mouse model. Levels of miR-21-5p and MDSCs were measured in mice. Mouse MDSCs were transfected with miR-21-5p lentivirus， exposed to HBV， and subsequent levels of p-STAT3（ Ser727），Arginase-1， IL-10， and p-STAT3 proteins were assessed. Stattic was introduced into the culture medium to evaluate levels of p-STAT3， Arginase-1， and IL-10 proteins. Results ： The HBV group exhibited a higher miR-21-5p expression level compared to the normal group. Compared with the control group， miR-21-5p expression levels and MDSC counts increased in the miR-21-5p negative control group， whereas both increased in the miR-21-5p overexpression group compared with the miR-21-5p knockdown group. Following the HBV infection of mouse MDSCs， there was a marked elevation in the expression of p-STAT3 （Ser727）， Arginase-1， IL-10， and p-STAT3 proteins. Similarly， miR-21-5p overexpression led to increased expression of p-STAT3（ Ser727）， Arginase-1， IL-10， and p-STAT3 proteins. Notably， upon Stattic administration， there was no discernible difference in the expression of p-STAT3， Arginase-1， and IL-10 proteins. Conclusion ： HBV potentially fosters the proliferation and functional activity of MDSCs through the modulation of the miR-21-5p/STAT3 pathway.

Objective ： To explore the role of long chain non-coding RNA（ lncRNA） colon cancer-relatedtranscription factor 1 （CCAT1） targeting miR-375-3p in inducing the apoptosis of human oral cancer SAS cellsthrough mitochondrial pathway. Methods ： Human oral cancer cell line SAS cells were randomly divided intoblank group， CCAT1 down-regulated group， CCAT1 up-regulated group， CCAT1 down-regulated control group，CCAT1 up-regulated control group， miR-375-3p down-regulated group， miR-375-3p up-regulated group， miR-375-3p down-regulated control group， and miR-375-3p up-regulated control group. After 48 hours of transfection， theapoptosis was detected by flow cytometry. RT-qPCR was used to detect the expression of miR-375-3p and the mRNAexpressions of genes related to mitochondrial apoptosis pathway， such as caspase-3， caspase-9， Bcl-2， and Bcl-2-related X protein （Bax）. The protein expressions of caspase-3， caspase-9， Bcl-2 and Bax were detected by Westernblotting. The targeting relationship between CCAT1 and miR-375-3p was analyzed by dual luciferase reporter assay.Results ： Compared with the blank group and the CCAT1 down-regulated control group， the apoptosis rate， miR-375-3p expression， and mRNA and protein expressions of caspase-3， caspase-9， and Bax in the CCAT1 downregulatedgroup were increased， while the Bcl-2 mRNAand protein expressions were decreased. Compared withthe blank group and CCAT1 down-regulated controlgroup， the apoptosis rate， miR-375-3p expression， andmRNA and protein exprssions of caspase-3， caspase-9， and Bax in the CCAT1 up-regulated group weredecreased，while the Bcl-2 mRNA and protein expressions were increased. Compared with the blank group and the miR-375-3pdown-regulated control group， the apoptosis rate， the expression of miR-375-3p， and mRNA and protein expressionsof caspase-3， caspase-9， and Bax in the miR-375-3p down-regulated group were decreased， while Bcl-2 mRNA andprotein expressions were increased. Compared with the blank group and the miR-375-3p up-regulated control group，the apoptosis rate， the expression of miR-375-3p， the mRNA and protein expressions of caspase-3， caspase-9， Baxwere increased in the miR-375-3p up-regulated group， while the Bcl-2 mRNA and protein expressions were decreased. The dual luciferase reporter assay confirmed that CCAT1 could target miR-375-3p. Conclusion ： CCAT1 can inhibit theapoptosis of human oral cancer SAS cells， which is speculated to be achieved by targeting the expression of miR-375-3p and regulating the expressions of genes and proteins related to the mitochondrial apoptosis pathway.

Objective ： To investigate the molecular mechanism of hypoxia-inducible factor-1α（ HIF-1α） promotingrenal fibrosis in mice with chronic kidney disease by inducing miR-126/JAK2-STAT3 axis. Methods ： MaleC57/BL6 mice at 8 weeks old were divided into sham operation, model, HIF-1α mimic, miR-126 mimic, HIF-1α+miR mimic, WP1066, and miR-126 mimic+WP1066 groups. Using a fully automated biochemical analyzer, 24-hour urinary protein, bloorea nitrogen (BUN), and serum creatinine (SCr) levels were measured in the mousekidneys. MiR-126 expression in kidney tissues was assessed via qRT-PCR, and HIF-α expression, along with renalfibrosis-related proteins (fibronectin, collagen-Ⅰ, α-SMA), and key proteins in the JAK2/STAT3 signaling pathwaywere detected through immunoblotting. Masson staining aided in the analysis of renal pathology and interstitialfibrosis in mice. Results ： The expression of miR-126 was inhibited after UUO model was established， and thedifference was statistically significant. Compared with the sham operation group, mice in the model group exhibitedelevated levels of 24-hour urinary protein, BUN, and SCr. There was evident disruption in the structure of renaltubules and interstitium, accompanied by marked renal fibrosis. Expression levels of fibronectin, collagen-Ⅰ,α-SMA, p-JAK2, and p-STAT3 were up-regulated.Furthermore, overexpression of HIF-1α further elevatedthe expression of 24-hour urinary protein, BUN,SCr, fibronectin, collagen-Ⅰ, α-SMA, p-JAK2, andp-STAT3. Conversely, overexpression of miR-126 ledto downregulation of these parameters. Additionally, overexpression of HIF-1α could reverse the inhibitory effect ofmiR-126 overexpression on renal fibrosis, with statistical significance. Compared with the model group, blockadeof the JAK2/STAT3 signaling pathway resulted in significant downregulation of p-JAK2, p-STAT3, fibronectin,collagen-Ⅰ, and α-SMA expression. Conclusions ： Mouse renal fibrosis promotes high expression of HIF-1α inrenal tissue， and HIF-1α enhances the activity of JAK2-STAT3 signaling pathway by inhibiting miR-126， ultimatelypromoting the progression of renal fibrosis.

Objective ： To investigate the effect of specific immunotherapy （SIT） on pulmonary inflammation in asthmatic mice and its mechanism. Methods ： Mice were randomly divided into control group， model group， SIT group， and dexamethasone group. Asthmatic mouse models were established in model group， SIT group， and dexamethasone group. After the modeling and stimulation stage， SIT group was injected with 1 mg OVA， dexamethasone group was injected with 0.075 mg/mL dexamethasone solution， and other rats were injected with PBS solution of equal volume， and then entered the atomization stage. Airway response was detected by pulmonary function apparatus. The inflammatory cells of alveolar lavage fluid (BALF) were observed by Reiss-Giemsa staining. The cytokines interleukin (IL)-13， IL-4， IL-5， and interferon-γ (IFNγ) in BALF were detected by enzyme-linked immunosorbent assay (ELISA). The morphology of lung tissue was observed by hematoxylin-eosin (H-E) staining. The activity of pulmonary airway epithelial goblet cells was observed by periodic acid-Schiff (PAS) staining. IFNγ and IL-4 in lung tissue were detected by flow cytometry. Results ： The airway response of model group was higher than that of control group under 6.25， 12.50， 25.00 μg/kg and 50.00 μg/kg acetylcholine， and the airway response of SIT group and dexamethasone group were lower than that of model group， but there was no significant difference between SIT group and dexamethasone group. Compared with the control group， the total number of BALF cells， centriocytes (%)， eosinophils(%)， IL-4， IL-5， IL-13， airway epithelial goblet cells and helper T cells 2（Th2） in the model group were all increased， and IFNγ was decreased. The total number of BALF cells ， centriocytes (%)， eosinophils (%)， IL-4， IL-5， IL-13 and airway epithelial goblet cells were decreased in SIT group， and IFNγ was increased. There was no significant difference between SIT group and dexamethasone group. In the control group， the alveolar and airway structures were organized， the airway walls were thin， and the lumen was not narrow. In the model group， the lung tissue structure was significantly damaged and the airway wall was thicker. The alveolar structure was destroyed， the inflammatory infiltration was obvious， and there was edema around the blood vessels. The inflammatory infiltration of lung tissue was improved， the degree of vascular edema was reduced， and the lumen stenosis was relieved in SIT group and dexamethasone group. Conclusion ： SIT can relieve airway hyperplasia in asthmatic mice， inhibit the activity of inflammatory cells and inflammatory factors in the BALF， and improve ventilation by inhibiting the hyperplasia of airway epithelial goblet cells. The mechanism of improvement is related to correcting the helper T cell 1/helper T cell 2 immune imbalance in lung tissue.

Objective ： To investigate the feasibility of cryopreservation of ICR mouse cleaved embryos and blastocysts with our self-made carrier. Methods ： The vitrification effect of mouse cleavage embryos and blastocyst were compared between our self-made Cryotip and commercial Cryotop. The data of cleavage embryos recovery rate ， blastocyst formation rate， blastocyst recovery rate and hatching rate in the Cryotip grou p and the Cryotop group were analyzed. Results ： There was no significant difference in the cleavage embryos recovery rate， blastocyst formation rate and blastocyst hatching rate of mice cryopreserved in Cryotip and commercial Cryotop groups. The blastocyst hatching rate, recovery rate, and blastocyst formation rate were slightly lower in the Cryotip group compared with the Cryotop group. There was no significant difference in the recovery rate and blastocyst hatching rate in mouse blastocyst cryopreservation. Conclusion ：Our self-made carrier Cryotip shows close effect in cryopreservation of ICR mouse cleavage embryos and blastocysts that are comparable to the commercial carrier Cryotop.

Influence of Baicalein on blood brain barrier in rats with bacterial meningitis by regulating PI3K/Akt/NF-κB signal pathway

Objective ： To investigate the effects of Plantamajoside (PMS) on hippocampal neuron damage in rats with cerebral ischemia/reperfusion (CI/R) and changes in oxidative stress and inflammation. Methods ： The CI/R model of male SD rats was constructed， and the SD rats were randomly divided into five groups ： control group， CI/R group， CI/R+PMS low， medium， and high dose groups (50 mg/kg，100 mg/kg， 200 mg/kg). After 24 h reperfusion， brain function of each group was evaluated. Relevant protein expression was detected by immunoblotting. H-E staining was used to observe the changes of the pathological structure of the hippocampus. N issl staining was used to observe the neuron injury. Superoxide dismutase（ SOD） activity and malondialdehyde（ MDA） content were detected with the kits. Results ： Compared with the control group， the CI/R group of rats showed a significant increase in the number of platform jumping mistakes， brain water content， and neurological scores， while the new arm entries were significantly reduced. The neural cell structure in the hippocampus was significantly damaged， and the number of Nissl bodies was significantly reduced. The expression of caspase-3， caspase-9， and Bax/Bcl-2 was significantly upregulated. The SOD activity was significantly decreased， MDA content and NF- κB p65 phosphorylation level were significantly increased. Compared with CI/R， the PMS medium and high dose groups had significantly reduced number of platform jumping errors， brain water content and neurological scores， while the new arm entries were significantly increased. The damage to the neural cell structure in the hippocampus was weakened， and the number of Nissl bodies was increasesd. The expression of caspase-3， caspase-9， and Bax/ Bcl-2 was significantly downregulated. The SOD activity was significantly enhanced， MDA content and NF-κB p65 phosphorylation level were significantly decreased. Conclusion ： PMS can reduce the neuronalcell damage， reverse damaged brain function in CI/R rats， and the mechanism may be due to the inhibition of NF-κB p65 activation and alleviation of oxidative stress.

Objective ： To observe and measure normal stabilized ligaments around the an kle joint in male and female specimens including anterior talofibular ligament (ATFL)， calcaneofibular ligaments (CFL)， and posterior talofibular ligaments (PTFL)， so as to find out the data differences between males and females， and provide an anatomic foundation for the precaution， diagnosis， and rehabilitation of the ankle injury. Methods ： Anatomical observation was carried on male and female ligaments. Precision measure and statistics were done on the length of anterior and posterior borders， the ligament’s origin and insertion points， the widest distance， and the thickness. MRI scanning were performed to examine the lateral ligaments. Results ： The morphological data differences of ankle ligaments between males and females were statistically significant. In males, CFL and PTFL were longer than in females, while there was no difference in ATFL length. In females, ATFL and CFL were wider than in males, whereas PTFL was the opposite. However, there was no difference in thickness. Conclusions ： The morphology of ankle stabilizing ligaments differs between females and males, emphasizing the need for greater attention to ankle ligament protection and exercises in females. Gender differences should be considered in the diagnosis, treatment, and rehabilitation of ankle joint disorders.

Objective ：To investigate the relationship between digit ratio (2D︰4D) and body mass index (BMI)， waist-hip ratio (WHR) and fat mass in Daur adults from Inner Mongolia. Methods ： Using anthropometric measurements， the mean values of 2D︰4D ratios of the left hand， right hand， both hands， and the difference between the right and left hand（ DR-L）， as well as the mean values of BMI， WHR， and fat mass， in Daur adults from the Daur autonomous banner of Morin Dawa of Inner Mongolia were compared. The correlation between 2D︰ 4D and BMI， WHR， and fat mass were analyzed. Results ： The 2D︰4D ratios in the left hand， right hand， and both hands were significantly higher in females than males. Correlation analysis showed that in females， the 2D︰4D ratios in the right hand， left hand， and both hands were positively correlated with BMI， waist circumference， trunk fat mass， and limb fat mass. Additionally， the 2D︰4D ratios in the right hand and both hands were positively correlated with hip circumference in females. Receiver operating characteristic curve analysis showed a certain effectiveness in screening obesity through the 2D︰4D ratio in the right hand and the average 2D︰4D ratio of both hands， the optimal tangent points of the 2D︰4D ratios in the right hand and average 2D︰4D ratio of both hands were 0.989 and 0.980， sensitivity were 46.5% and 53.5%， and specificity were 78.9% and 68.4% in females. Conclusion ： There is a correlation between the 2D︰4D ratio and fat mass in Daur female adults from Inner Mongolia.

Over the past decade， new technologies such as novel acetabular plates， modified surgical approaches， and 3D printing have enriched the options for treating acetabular fractures. However， challenges persist， including difficulties in fracture exposure and fixation， large surgical incisions， increased intraoperative bleeding， and substantial surgical trauma. As acetabulum is surrounded by a network of blood vessels， nerves and lymph vessels， pelvic organs， and abundant muscles and ligaments， iatrogenic injury can easily occur to the surroundings， even with the use of orthopedic surgical robots in acetabular fracture operation. This article reviews the surgical approach for acetabular fractures， taking into account the adjacent anatomical structures， and aims to explore a safe， fast and precise surgical targeted approach by aligning with the anatomical and physiologica l spaces within the human body.

Anterior cruciate ligament (ACL) injury is one of the common ligament injuries in the field of sports medicine. Due to its limited endogenous repair capacity， reconstruction surgery has become the preferred treatment method. However， postoperative ligament function is difficult to fully restore， and various complications are prone to occur， which can reduce the patient's quality of life. With the accumulation of experience in ligament repair and the development of tissue engineering and regenerative medicine， non-operative reconstruction methods and biological enhancement techniques have become research hotspots ， especially in animal models， to explore treatment approaches that improve the effectiveness of anterior cruciate ligament injury repair. This article reviews the progress of basic research promoting endogenous repair of the anterior cruciate ligament， which can be summarized into six aspects: growth factor therapy， stem cell therapy， gene therapy， bioengineering， pharmacological therapy， and physical therapy.