Peripheral nerve injury (PNI) and the subsequent regeneration, and functional reconstruction remain oneof the pressing challenges in neurosurgery. The clinical outcomes of its treatment have not met expectations and haveresulted in significant social and economic burdens. As a traditional Chinese medicine therapy， Acupuncture plays apositive role in the treatment of PNI. This article reviews the animal selection， Acupuncture acupoints， Acupunctureparameters， and therapeutic effects of Acupuncture in the treatment of PNI in recent years， and further summarizesthe mechanism of Acupuncture in PNI， to provide a theoretical basis for seeking better therapeutic targets andAcupuncture approaches.

Objective ： To explore the effect of Canagliflozin on thoracic aorta remodeling in spontaneoushypertension rats （SHR） by regulating vascular smooth muscle cell proliferation， migration， and the reninangiotensin-aldosterone system （RAAS）/ transforming growth factor β1（TGF-β1） signaling pathway. Methods ：The rats were divided into normal blood pressure control group （WKY group）， SHR group, and SHR+Canagliflozingroup. Tail-cuff sphygmomanometer was used to monitor the rats tail artery blood pressure （BP）. H-E stainingwas used to evaluate the media thickness of thoracic aortic wall and the ratio of media thickness to lumen diameter.Masson staining was used to detect the degree of vascular wall fibrosis. Vascular smooth muscle cells（VSMCs）were isolated and cultured from thoracic aorta of WKY and SHR. Cells were divided into WKY group， WKY+Canagliflozin group， SHR group, and SHR+Canagliflozin group. Scratch assay was conducted to evaluate cellmigration， while CCK-8 assay was performed to assess cell proliferation. The expressions of alpha-smooth muscleactin（α-SMA）， secreted phosphoprotein 1 （SPP1），collagen type Ⅰ alpha （Col1a）， collagen type Ⅲ alpha（Col3a）， angiotensinogen （AGT）， angiotensin Ⅱreceptor 1 （AGTR1） and TGF-β1 were detected byreal-time quantitative polymerase chain reaction and Western blotting. Results ： After eight weeks of canagliflozinadministration， compared with the SHR group， the blood pressure， thoracic aortic media thickness， mediathickness/lumen diameter ratio， and collagen deposition degree in the SHR+Canagliflozin group were decreased.The proliferation and migration ability of VSMCs in SHR group was significantly enhanced compared with that inWKY group， the expression of α-SMA was decreased， and the expression of SPP1， Col1a， Col3a， AGT， AGTR1and TGF-β1 were increased. Compared with SHR group， SHR+Canagliflozin group significantly reduced theproliferation and migration capacity of VSMCs， and the expression of α-SMA was increased， and the expressionsof SPP1， Colla， Col3a， AGT， AGTR1, and TGF-β1 were decreased. Conclusion ： Canagliflozin may inhibit theproliferation and migration of hypertensive vascular smooth muscle cells by inhibiting RAAS/TGF-β1 signalingpathway， thereby improving aortic vascular remodeling in SHR.

Objective： To compare the differential expression of endogenous competitive long-chain non-codingribonucleic acid （lncRNA） with messenger ribonucleic acid （mRNA） before and after partial injury of the anteriorcruciate ligament （ACL） and medial collateral ligament （MCL） in knee joint of rabbits and to explore the possiblemolecular mechanisms impeding the endogenous repair of the ACL. Methods： RNA after partial injury of ACL andMCL in rabbits was sequenced to obtain differentially expressed lncRNAs and differentially expressed mRNAs andverified by qRT-PCR， followed by Kyoto Encyclopaedia of Genes and Genomes （KEGG） and Gene Ontology （GO）analyses for theconstruction of a ceRNA network. Results： A total of 853 differential lncRNAs and 994 differentialmRNAs were obtained. GO and KEGG analyses showed that the differential lncRNAs differed significantly ininflammatory responses， extracellular matrix-receptor interactions， and cell proliferation， and thedifferentialmRNAs differed significantly in cytokine activation and cell adhesion. Significant differences in core genes werefound between the ACL and the MCL after partial injury.Conclusion： Significant differences in lncRNAs andmRNAs between partially injured ACL and MCL in rabbits provide more theoretical basis for the molecular levelstudy of the mechanism of endogenous repair disorders in ACL injury.

Objective ： To reveal the interaction between endogenous competitive circular RNAs （circRNAs） withmicroRNAs（ miRNAs） and messenger RNAs（ mRNAs） after partial damage to the anterior cruciate ligament（ ACL）and medial collateral ligament （MCL） in rabbits， in order to explore the molecular mechanisms that may hinderendogenous repair of the ACL. Methods ： Normal and partially injured ACL and MCL tissues of rabbits were stainedwith H-E staining for morphological observation. Whole transcriptome libraries were sequenced and differentiallyexpressed genes were identified by differential analysis. Functional analysis and protein interaction networkwas constructed. Core genes were identified and endogenous competitive circRNA-miRNA-mRNA network wasestablished. Results ： ACL and MCL differed significantly ininflammatory response， cell proliferation， and collagendeposition. Sixteen core genes were obtained， and circRNA-miRNA-mRNA networks were obtained from six ofthem. Conclusion ： The differentially expressed genes in ACL and MCL show significant differences in enrichmentpathways and core gene expression trends， providing new insights for further investigation into the mechanismsunderlying endogenous repair obstacles in ACL injuries.

Objective ： To analyze the expression of glucose transporter 1 （GLUT1） in placental tissues of pregnantrats under plateau hypoxia and its effect on the growth and development of fetal rats. Methods ： Twenty pregnant ratswere randomly divided into normoxic group and hypoxic group. On the 9th day of pregnancy， the normoxic groupwas housed in Xining city， Qinghai province （average altitude 2 200 m）， while the hypoxic group was housed in ahypobaric oxygen chamber （simulated altitude 5 000 m）. The two groups of pregnant rats were kept until day 21 ofgestation. Blood samples were collected from the abdominal aorta and tail vein to determine fasting blood glucose（FBG）. The serum insulin concentration of pregnant rats was measured by ELISA method. Placentas and embryoswere collected for the comparisons of the weights of the placentas and fetal rats， as well as the length of fetal ratsbetween the two groups. The placental structure of the pregnant rats in the two groups was observed under lightmicroscopy after H-E staining， and the expression levels of GLUT1 mRNA and protein in placental tissues weredetected by RT-qPCR and immunohistochemistry， respectively. The correlation between fetal rat weight and lengthwith the FBG level and the relative expression of placental GLUT1 protein in pregnant rats was analyzed. Results ：Compared with the normoxic group， the FBG level of pregnant rats in the hypoxic group was decreased and theserum insulin concentration was increased. The placental weight of the hypoxic group did not change， and the weightand length of fetal rats in the hypoxic group were decreased. Under the light microscopy， disordered arrangementof trophoblasts， widened intercellular space， and dilated capillaries with a large number of red blood cells wereobserved in the hypoxic group. The expression of GLUT1 mRNA in placental tissues of pregnant rats in the hypoxicgroup was up-regulated. The GLUT1-positive cells were distributed in trophoblasts and erythrocytes， mainly in thecell membrane， and the expression level of GLUT1protein in the hypoxic group was increased. Pearsoncorrelation analysis showed that fetal rat weight waspositively correlated with FBG level in pregnantrats， while fetal rat length was negatively correlated with the relative expression of placental GLUT1protein.Conclusion ： The expression of GLUT1 in placental tissues of pregnant rats is up-regulated under plateau hypoxia，which subsequently affects the growth of fetal rats.

Objective ： To investigate the effects of Honeysuckle extract （HFE）combined with Octreotide onacinar cell injury repair， immune indices and p38MAPK/ATF2 levels in rats with severe pancreatitis. Methods ：Forty rats were divided into healthy group， model groupHFE+Octreotide group， and Octreotide group. Severepancreatitis models were established in all groups except the healthy group. The healthy group and model groupwere intraperitoneally injected with 1 mL/kg saline ； the HFE+Octreotide group was injected with 120 mg/kg HFEand 10 μg/kg Octreotide via the tail vein ； and the Octreotide group was injected with 10 μg/kg Octreotide via thetail vein. All injections were administered once daily for a total of four weeks. Immunoglobulins （IgA， IgG， IgM）were detected by enzyme-linked immunosorbent assay （ELISA）.Immunohistochemistry was used to detect the p38mitogen-activated protein kinase （p38MAPK） and activating transcription factor 2 （ATF2） in rat pancreatic tissue.H-E staining was used to observe the pathological changes of pancreatic tissue. Protease and amylase activities weremeasured within acinar cells by using colorimetric method. Results ： Compared with healthy group， the model groupshowed a decrease in serum levels of IgA， IgG and IgM， an increase in p38MAPK， ATF2， protease andamylaseactivities within acinar cells. Compared with the model group， the Octreotide group exhibited an increase in serumlevels of IgA， IgG， IgM， a decrease in p38MAPK， ATF2， protease and amylase activities within acinar cells.Compared with the Octreotide group， the HFE+Octreotide group showed an increase in serum levels of IgA， IgG，IgM， and a decrease in p38MAPK， ATF2， protease and amylase activities within acinar cells. The model groupexhibited more severe tissue damage and acinar cellinjury. The Octreotide group showed improvements inlesion severity， cell quantity， and morphology， butstructural damage was still present. In HFE+Octreotidegroup， cell degeneration and swelling were decreased， with gradual restoration of pancreatic tissue. Conclusion ：Honeysuckle extract combined with Octreotide can treat severe pancreatitis in rats by repairing acinar cell damageand improving immune indices， the mechanism of which is related to the regulation of p38MAPK and ATF2 levels.

Objective： To explore the mechanism of Resveratrol （RSV） improving lipopolysaccharide （LPS）-inducedacute lung injury （ALI） by weakened migration and infiltration of neutrophils. Methods ： BALB/c mice wererandomly divided into control group， RSV group， model group， and model+RSV group （LPS+RSV）. In the modelgroup and LPS+RSV group， ALI mice were induced by LPS， while mice in the RSV group and LPS+RSV groupwere intragastrically administered with 40 mg/kg of RSV for 7 d. After the last administration， bronchoalveolarlavage fluid （BALF） was collected to detect levels of white blood cells， neutrophils and proteins. The activity ofmyeloperoxidase（ MPO） in lung tissues was evaluated. The pathological damage of lung tissues was observed byH-E staining. The expressions of inflammatory cytokines and chemokines in lung tissues and BALF were detected.Neutrophils were cultured in vitro and treated with 1 μg/mL of LPS and RSV， respectively. Neutrophils apoptosisand expression of chemokines receptors （CXCR2， Mac-1） were detected by flow cytometry. The level of reactiveoxygen species （ROS） in cells was detected by dichlorodihydrofluorescein diacetate （DCFH-DA） probe to evaluatechemotaxis and migration ability of neutrophils. The phosphorylation level of nuclear factor （NF-κB p65） wasdetected by Western blotting. Results ： Compared with the modelgroup， the total count of cells， the count ofneutrophils， expression level of proteins， expression levels of TNF-α，IL-6 and CXCL2 in BALF were decreased inthe LPS+RSV group， and MPO activity in lung tissues， expression levels of TNF-α， IL-1β， IL-6， CXCL2 mRNAand protein were decreased. Compared with the control group， the apoptosis rate of neutrophils was decreased in themodel group and the LPS+RSV group， but there was nosignificant difference in neutrophils apoptosis betweenthe model group and the LPS+RSV group. Comparedwith the mode group， ROS activity in neutrophils wasdeclined after 10 and 30 minutes of treatment in the LPS+RSV group， but there was no significant difference in ROSactivity between the two groups at the other time points. Compared with the mode group， chemotaxis and migrationability of neutrophils， the number of neutrophils expressing CXCL2 and Mac-1 on the surface， expression of CXCL2mRNA and protein， and p-NF-κB p65 were decreased in the LPS+RSV group. Conclusion ： RSV can improve LPSinducedALI， which may be related to the migration and infiltration of neutrophils inhibited by RSV.

Objective ： To investigate the effect of dendritic cell associated C-type lectin-1（Dectin-1） ongalactomannan （GM）， thymocyte apoptosis and lung injury in invasive pulmonary aspergillosis rats. Methods ：Thirty rats were randomly divided into control group， Ad-EGFP group and Ad-Dectin-1-EGFP group. The lungfunction of rats（ transformation of lung volume and resting breath） was detected. The contents of interferon-γ（ IFN-γ）and interleukin-4（IL-4） in bronchoalveolar lavage fluid and the content of GM in serum were detected by ELISA.The pathological changes of lung tissue were detected by H-E staining. Thymus index was examined. TUNEL wasused to detect thymocyte apoptosis. Western blotting was used to detect the expression of Dectin-1， T-bet， andGATA-3 protein in lung tissue. Results ： Compared with in the control group， the IFN-γ content， thymus index，lung volume change and resting ventilation volume were significantly decreased， while the IL-4 content， GM valueand apoptotic index， the thymus index were significantly increased in the Ad-EGFP group. Compared with the Ad-EGFP group， the content of IFN-γ， the thymus index， the lung volume change and the resting ventilation volumewere significantly increased in the Ad-Dectin-1-EGFP group， while the content of IL-4， GM value and apoptosisindex were decreased significantly. Compared with the control group， the expressions of Dectin-1 and T-bet proteinsin the lung tissue of the Ad-EGFP group were significantly decreased， and the expression of GATA-3 protein wassignificantly increased. Compared with the Ad-EGFP group. The expressions of Dectin-1 and T-bet proteins in lungtissue of rats in the Ad-Dectin-1-EGFP group were significantly increased， and the expression of GATA-3 proteinwas significantly decreased. Conclusion ：Dectin-1recombinant plasmid can alleviate lung injury ininvasive pulmonary aspergillosis rats， reduce serumGM value， and maintain the balance of immunefunction by inhibiting thymocyte apoptosis. Themechanism may be related to the expression of T-bet and GATA-3 proteins

Objective ： To investigate effect of miR-222-3p on the activity and glycolysis of positive cervical cancercells infected with human papillomavirus and related mechanism. Methods ： Siha cells were divided into cervicalcancer group （untransfected HPV infected Siha cells）， miR-222-3p-NC group （HPV infected Siha cells weretransfected with miR-222-3p-NC）， lactate dehydrogenase A group （HPV infected Siha cells were transfected withmiR-222-3p mimics and miR-222-3p siRNA group （HPV infected Siha cells transfected with miR-222-3p siRNA）.qPCR was used to detect the relative expression of miR-222-3p in Siha cells of each group. Siha cell activity wasdetected by CCK-8. The apoptosis rate of Siha cells was detected by flow cytometry. The invasion number of Sihacells in each group was detected by Transwell chamber. The migration distance of Siha cells in each group wasdetected by scratch test. Glucose and lactic acid levels of Siha cells were detected by kit. The protein expressionsof pyruvate kinase M2（PKM2）， lactate dehydrogenase A（LDHA）， phosphatidylinositol 3-kinase（PI3K） andprotein kinase B（AKT） were detected by Western blotting. Luciferase was used confirmed the regulation of miR-222-3p on PI3K and AKT. Results ： The relative expression of miR-222-3p in Siha cells of cervical cancer group，miR-222-3p-NC group， miR-222-3p mimics group and miR-222-3p siRNA group were 1.00±0.00， 0.96±0.02，1.33±0.09 and 0.60±0.04， respectively. Compared with the miR-222-3p-NC group， cell proliferation， invasionand migration， lactic acid， glucose， PKM2， LDHA，PI3K and AKT were increased in the miR-222-3pmimics group， and the apoptosis rate was decreased.Proliferation， invasion， migration， lactic acid，glucose， PKM2， LDHA， PI3K and AKT were decreased in miR-222-3p siRNA group， and apoptosis was increased.Luciferase confirmed that inhibition of miR-222-3 could inhibit the expression of wild-type PI3K and AKT.Conclusion ： Inhibition of miR-222-3p can significantly reduce the proliferation， migration and malignant invasionof HPV-infected cervical cancer cells， promote apoptosis， and inhibit the glycolysis of tumor cells. The mechanismof action may be related to the decrease of PI3K/AKT activity.

Objective： To enrich the anatomical data of the bony nasolacrimal duct and its surrounding structures toprovide anatomical reference for clinical surgery. Methods： The positions of various anatomical structures on 26 adultdry skulls were identified and marked by dental faculty members by using measuring tools such as vernier caliperand compass. The data were recorded and statistically analyzed. Results： There were three types of upper openingfor the bony nasolacrimal duct ： round 48.08%， oval 42.31%， and elliptic 9.61%. The transverse diameter of upperopening for the nasolacrimal duct was （5.28±0.78） mm， the anteroposterior diameter was （5.26±0.94） mm， andthe distance from the lateral point of the upper opening to the highest point of the lacrimal sac fossa was （17.17±1.56）mm. The distances from the lateral point of the upper opening for the bony nasolacrimal duct， or the distancesfrom the highest point of the lacrimal sac fossa to the following positions were as follows ： to the intersection ofthe frontal process of the maxilla and the anteromedial point of the nasolacrimal suture were （25.77±2.13） mm，（32.13±2.54） mm ； to the midpoint of the nasofrontal suture were（ 22.88±2.06） mm，（ 13.50±1.91） mm ； to theexternal venous foramen of the ipsilateral nasal bone were（ 10.59±1.93） mm，（ 36.52±1.31） mm ； to the innerupper margin of the ipsilateral infraorbital foramen were（ 34.58±1.86） mm，（ 26.13±1.79） mm； to the intersectionof the zygomaticomaxillary suture with the inferior orbital margin were（ 40.10±1.61） mm，（ 40.46±1.99） mm ； tothe anterolateral point of the infraorbital fissure were（ 10.04±1.68） mm，（ 16.41±1.51） mm ； to the intersection

of the zygomaticofrontal suture and lateral orbital margin were（14.23±2.05） mm， （29.91±2.41） mm ； to thesuperior lateral point of the supraorbital fissure were（ 24.75±2.39） mm，（ 37.75±2.11） mm ； to the superior lateralpoint of the optic foramen were （23.27±1.79） mm，（37.27±2.17） mm ； and to the supraorbital notchwere （38.64±1.88） mm， （39.24±1.95） mm. Afterstatistical analysis， the difference was not statisticallysignificant. Conclusions： The measurement of thedistances between the bony nasolacrimal duct and its surrounding structures can provide an anatomical basis forclinical-related operations.

Human liver is an important metabolic organ， which has important functions such as digestion，absorption， and detoxification. At present， the gross anatomy of the liver has been studied thoroughly， but thestudy of microanatomy of the liver and the hepatic functional unit are stillinsufficient and controversial. This articleprovides a comprehensive review of the research progress on liver microanatomy and its functions, combiningadvancements in microanatomical techniques,livermicroanatomicalmorphology, as well as the application of 3Dprinting and virtual simulation in the field.

Ferroptosis is a newly discovered form of regulated cell death in recent years. It is characterized by ironoverload， lipid peroxidation， and reactive oxygen species accumulation. Ferroptosis is regulated by various metabolicpathways such as iron metabolism， lipid metabolism， and amino acid metabolism. Ferroptosis plays an importantregulatory role in cardiovascular diseases such as acute myocardial infarction， myocardial ischemia-reperfusion injury，heart failure， and atherosclerosis， which is closely related to myocardial cell injury. In this review， we discussed therole of ferroptosis in cardiovascular diseases to explore new targets for the treatment of cardiovascular diseases.