BACKGROUND:Traditional treatments for corneal alkali burns are limited,especially in controlling inflammation,preventing neovascularization,and inhibiting corneal scarring.Natural,synthetic,or composite materials provide a wide range of treatment options.However,the mechanism by which biomaterials promote corneal alkali burn repair has not yet been systematically understood. OBJECTIVE:To summarize the current research on biomaterials in promoting corneal alkali burn repair in and outside China,and review the mechanism and application of biomaterials in repairing corneal alkali burn. METHODS:The first author searched"cornea,alkali burn,amniotic membrane,hyaluronic acid,collagen,chitosan,polymer materials"as Chinese keywords and"amniotic membrane,hyaluronic acid,collagen,chitosan,polymer,cornea,alkali burn"as English keywords in PubMed,Web of Science,CNKI,and WanFang databases.According to inclusion and exclusion criteria,76 eligible articles were finally included for review. RESULTS AND CONCLUSION:(1)In the field of corneal alkali burn repair,biomaterials such as amniotic membrane,hyaluronic acid,collagen,chitosan,and degradable polymer materials have been widely studied and applied.Each of these biomaterials has its own characteristics,advantages,and disadvantages,and stands out in different aspects.(2)First and foremost,amniotic membranes are considered one of the most promising biomaterials due to their abundance of bioactive factors.They are biocompatible and can regulate the corneal inflammatory response.However,there are issues with donor shortages and susceptibility to infectious diseases.(3)Hyaluronic acid has good moisturizing properties and biocompatibility,and is able to improve the survival rate of corneal cells and increase corneal transparency.(4)The good biocompatibility and scaffold structure of collagen enable the promotion of corneal cell adhesion and proliferation,as well as the reconstruction of corneal tissue structure.(5)Chitosan is recognized for its good biocompatibility and degradability,making it suitable as a carrier for drug delivery and cell transplantation.(6)Degradable polymer materials have good controllability over degradation and can provide a good support and delivery platform for the repair of corneal alkali burns,but further research is needed on their stability and biocompatibility.(7)Overall,there is currently no single biomaterial that can completely address the repair problem of corneal alkali burns,and each biomaterial has its own specific application scenarios and limitations.(8)Future research directions should focus on further improving the properties and structure of biomaterials,exploring more effective combination applications,and deeply understanding the interaction mechanism between biomaterials and corneal tissue,in order to enhance the therapeutic effect of corneal alkali burns and the quality of life of patients.

The paper introduces Professor SUN Shentian's experience in clinical practice of Ningshen (tranquilizing the mind) point. This point is an empirical point discovered by Professor SUN on the basis of meridian differentiation, nerve function and anatomic location, and in association with the years of clinical practice. The point is located in the prefrontal area, jointed with the distribution of the governor vessel, and responded to the body surface projection area of the frontal pole. It works on regulating the mind, regaining consciousness, improving cognition, alleviating depression, mutually treating physical and mental disorders, as well as unblocking collaterals, regulating the tendons and relieving spasm. This point is widely used in treatment of mental disorders, stroke and extrapyramidal diseases and obtains the reliable therapeutic effect in clinical practice.
Humans ; Acupuncture Points ; Acupuncture Therapy/history* ; China ; Meridians ; History, 20th Century

OBJECTIVES: To investigate the clinical significance of SLC1A5 overexpression in pan-cancer and its mechanism for promoting hepatocellular carcinoma (HCC) progression. METHODS: We analyzed the correlation of SLC1A5 expression with clinical stage, lymph node metastasis and prognosis in pan-cancer using TCGA and ICGC datasets and explored its association with immune cell infiltration using EPIC, CIBERSORT, and TIMER algorithms. In HCC cell lines, the effects of lentivirus-mediated SLC1A5 overexpression or RNA interference on cell proliferation were examined using CCK-8 assay, and the growth of HCC cell xenografts overexpressing SLC1A5 was observed in nude mice. The effects of SLC1A5 overexpression or silencing in HCC cells on macrophage polarization were evaluated in a cell co-culture system. RESULTS: SLC1A5 was mainly localized on cell membrane and was highly expressed in most cancers in association with clinical stage, lymph node metastasis and poor prognosis. SLC1A5 expression was positively correlated with immunity score in 13 cancer types, especially in low-grade glioma (LGG), LIHC and thyroid cancer. SLC1A5 was positively correlated with macrophage infiltration level in LGG and LIHC but negatively correlated with macrophage infiltration in 5 cancers including lung squamous carcinoma, pancreatic carcinoma, and gastric carcinoma. Patients with SLC1A5 overexpression and high level of M2 macrophage infiltration had the worst survival outcomes. SLC1A5 was correlated with immunosuppression-related genes, cytokines, and cytokine receptors, which was the most obvious in LGG and LIHC. SLC1A5 was highly expressed in different HCC cell lines, and its overexpression promoted HCC cell proliferation both in vitro and in nude mice. In the cell co-culture experiment, SLC1A5 was positively correlated with the molecular markers of M2 polarization of macrophages, and its overexpression strongly promoted M2 polarization of the macrophages and inhibited T cell secretion of IFN-γ. CONCLUSIONS SLC1A5 expression level is correlated with clinical stage, lymph node metastasis, prognosis, and immune cell infiltration in most cancers, and its overexpression promotes HCC progression by inhibiting T-cell function via promoting M2 polarization of macrophages.
Humans ; Carcinoma, Hepatocellular/metabolism* ; Liver Neoplasms/metabolism* ; Animals ; Macrophages/cytology* ; Disease Progression ; Cell Line, Tumor ; Mice ; Amino Acid Transport System ASC/genetics* ; Cell Proliferation ; Lymphatic Metastasis ; Mice, Nude ; Prognosis ; Minor Histocompatibility Antigens

Objective:To explore the changes in the functional connectivity (FC) of hippocampal subregions in nicotine addicts after repetitive transcranial magnetic stimulation (rTMS) using resting-state FC.Methods:This study was a cross-sectional study. The clinical and imaging data from 20 male nicotine addicts at Zhejiang Hospital between 2022 and 2024 were analyzed prospectively. All participants received rTMS treatment and were assessed with nicotine-related clinical scales and resting-state FC analysis before and after treatment. The clinical scale evaluations included the Fagerstr?m test for nicotine dependence (FTND), smoking severity index, Minnesota nicotine withdrawal scale (MNWS), short tobacco craving questionnaire (sTCQ), and visual analog scale (VAS). Paired t-tests and Wilcoxon signed-rank tests were used to compare the differences in clinical scale scores before and after treatment. Ten subregions of the bilateral hippocampus (including the hippocampus, dentate gyrus, entorhinal cortex, hippocampus-amygdala transition area, and subiculum) were used as seed points, and paired t-tests were conducted to compare the FC differences in these subregions before and after treatment. Pearson and Spearman correlation analyses were used to assess the correlation between changes in resting-state FC in the rTMS group and clinical scale scores. Results:Compared to pre-treatment, the scores on the FTND, smoking severity index, MNWS, sTCQ, and VAS all significantly decreased after rTMS treatment in nicotine addicts (all P<0.05). Compared to pre-treatment, post-treatment FC was reduced between the left dentate gyrus subregion and the bilateral supplementary motor area and left middle cingulate gyrus, while it increased between the left entorhinal cortex subregion and the right middle and superior temporal gyri, and between the left hippocampus-amygdala transition area subregion and the bilateral calcarine cortex and cuneus (Gaussian random field correction, voxel-level P<0.01, cluster-level P<0.05). Negative correlations were observed between the FC difference in the left hippocampus-amygdala transition area subregion and the right calcarine cortex and the difference in sTCQ-impulse score before and after treatment ( r=-0.447, P=0.048). Negative correlations were observed between the FC difference in the left hippocampus-amygdala transition area subregion and the right cuneus and the difference in the sTCQ-expectation score ( r=-0.559, P=0.010). Negative correlations were observed between the FC difference in the left hippocampus-amygdala transition area subregion and the left calcarine cortex and the differences in sTCQ-emotion and sTCQ-expectation scores ( r=-0.516, P=0.020; r=-0.466, P=0.038, respectively). Negative correlations were observed between the FC difference in the left hippocampus-amygdala transition area subregion and the left cuneus and the differences in sTCQ-emotion and sTCQ-expectation scores ( r=-0.459, P=0.042; r=-0.501, P=0.024, respectively). Conclusion:Changes in FC in certain hippocampal regions are observed in nicotine addicts following rTMS treatment, suggesting that hippocampal subregions may serve as potential biomarkers for nicotine addiction withdrawal to some extent.

Pancreatic metastases originating in colon cancer are very rare clinically, and there are few reports on their imaging manifestations. In this paper, it improves the diagnosis of the disease by reporting a case of pancreatic head metastases and focusing on the appearance of contrast-enhanced ultrasound.

Objective:The phenotype and genotype of a pedigree with Glanzmann thrombasthenia caused by compound heterozygous mutation in the ITGA2B gene and its molecular pathogenesis were explored.Methods:The platelet aggregation rate of the proband and his family was detected by using a platelet aggregation test with adenosine diphosphate, collagen, epinephrine, arachidonic acid, and ristocetin. The expression levels of CD41 (αⅡb), CD61 (β3), and CD42b (GPⅠb) on the platelet surface was detected by flow cytometry. Gene sequencing technology was used for the genetic identification of the family. RT-PCR was used in the detection of mRNA splicing, and qRT-PCR was used in detecting the relative mRNA level of the ITGA2B gene. Bioinformatics analysis was used to evaluate the pathogenicity of mutation sites and their effects on protein structure and function. The expressions of total αⅡb and β3 in platelets were analyzed by Western blot.Results:Except ristocetin, the other four inducers could not induce platelet aggregation in the proband. Flow cytometry showed that the expression levels of αⅡb and β3 were only 0.25% and 9.76%, respectively, on the platelet surface of the proband, whereas GPⅠb expression was relatively normal. The expression levels of glycoproteins in the other family members were almost normal. c.480C>G and c.2929C>T mutations were detected in the proband through gene sequencing. The c.480C>G mutation was inherited from his mother, and the c.2929C>T mutation was inherited from his father. The RT-PCR and sequencing results showed that the c.480C>G mutation caused mRNA splicing in the proband and his mother, resulting in the deletion of 99 bases in c.476G-574A (p.S160-S192). qRT-PCR showed that the c.2929C>T variant reduced the mRNA level of the ITGA2B gene in the proband and his father. Bioinformatics analysis suggested that the c.480C>G mutation might form a binding sequence with hnRNP A1 protein and generate the 5′SS splice site. The three-dimensional structural model of the αⅡb subunit showed that the β-propeller domain of the p.S160-S192 deletion lost two β-strands and one α-helix in blade 2. The c.2929C>T nonsense mutation caused premature translation termination and produced a truncated protein with the deletion of p.R977-E1039, including the cytoplasmic domain, transmembrane domain, and a β chain of the extracellular Calf-2 domain. The total αⅡb expression of the proband was absent, and the relative expression of β3 was 11.36% of the normal level.Conclusion:The compound heterozygous mutation c.480C>G in exon 4 and c.2929C>T in exon 28 of the ITGA2B gene probably underlies Glanzmann thrombasthenia in this pedigree.

Objective:To analyze the F10 gene mutations in a Chinese pedigree affected with the deficiency of the hereditary coagulation factor X (FX), resulting from a new deletion mutation, and to study the associated molecular pathogenesis.Methods:Next generation sequencing (NGS) was performed to screen the genetic mutations in the proband which were then verified by Sanger sequencing. The FX activity (FX∶C) of probands and their family members was detected using the blood clotting method, and the mutation sites of the family members were analyzed using Sanger sequencing. The pathogenicity of the mutation site was predicted by using the online bioinformatics software, Mutation Taster. The SWISS-MODEL software was used for stimulating the three-dimensional models of the wild-type and mutant proteins for analyzing the influence of the mutation site on the structure and function of the proteins, and for analyzing the difference between the catalytic residues of the wild-type and the mutant proteins. The level of the F10 gene mRNA was quantitatively analyzed by qRT-PCR (quantitative reverse transcription polymerase chain reaction) method by constructing plasmids, transfecting human embryonic kidney 293T cells (HEK 293T), and analyzing the splicing of the mutated site by RT-PCR method. The levels of FⅩ∶Ag in cell lysates and cell culture media (both inside and outside the cells) were detected by the ELISA (enzyme linked immunosorbent assay) method.Results:A medium-grade factor X deficiency with a 36.42% FⅩ∶C ratio was detected in the proband by the coagulation method. NGS analysis demonstrated a heterozygous deletion mutation in exon 8:c.902_919del (p.Ala301_Glu306del) in the proband. Sanger sequencing analysis indicated that some members of the family (mother and grandfather) were also carriers of the corresponding deletion mutation. Online bioinformatics software predicted the pathogenic nature of the c.902_919del mutation, with a pathogenic score of 0.999. The 3D protein structure model analysis indicated that the c.902_919del mutation resulted in the disappearance of a segment of β-fold in the protein structure, thereby shortening the preceding segment of the β-fold and a subsequent loss of hydrogen bonds between adjacent amino acids with no significant difference in the side chain conformation of the key catalytic residues compared to the wild-type. mRNA splicing analysis indicated the absence of alternative splicing changes in the mutation, and qRT-PCR results indicated the absence of a statistically significant difference between the mRNA levels of F10 gene and wild-type mRNA in cells expressing c.902_919del mutant. The ELISA results indicated that there was no statistically significant difference in the FX∶Ag levels of the mutant cell culture medium and the lysate.Conclusions:In this pedigree, the heterozygous mutation in exon 8 of F10 gene (c.902_919del, p.Ala301_Glu306del) caused the hereditary factor Ⅹ deficiency.

Objective The aim of this study was to explore the correlation between the methylation status of microRNA let-7a-3 in esophageal squamous cell carcinoma(ESCC)and the expression of insulin-like growth factor 2(IGF-Ⅱ).Methods The methylation specific PCR(qMSP)was used to detect the methylation status of let-7a-3 in 83 cases of esophageal cancer and corre-sponding adjacent normal tissues.The enzyme linked immunosorbent assay(ELISA)was used to detect the expression of IGF-Ⅱ in plasma.Results The degree of let-7a-3 methylation in cancer tissues of 83 patients with ESCC was significantly higher than that in normal tissues adjacent to cancer(P<0.001).The expression of IGF-Ⅱ in the plasma of 83 patients with ESCC was positively corre-lated with the methylation degree of let-7a-3,which was statistically significant(r=0.600,P<0.001).Conclusion microRNAlet-7a-3 may participate in the occurrence and progression of ESCC by regulating the methylation of downstream molecules,which is of great significance for understanding the mechanisms of ESCC development and providing a basis for the diagnosis and prognosis of ESCC.

Public hospitals bear the responsibility of ensuring people's health and promoting their healthy lives.New media have emerged as a pivotal platform for health science popularization in public hospitals.Under these contexts,the Science Popularization Base for Health and Chronic Disease Prevention of the First Hospital of Lanzhou University established a multidisci-plinary team model for science popularization,mainly relying on the WeChat official account to disseminate health knowledge and dispel rumors.This article explored the experiences and practices of health science popularization under this model,focusing on the"meticulous selection for science popularization"strategy employed on their WeChat official account.

ObjectiveTo observe the possible mechanism of Dihuang Yinzi Decoction （地黄饮子） for improving cognitive dysfunction in Alzheimer's disease （AD） from the perspective of retina. MethodsForty-five APP/PS1 mice （AD model mice） were randomly divided into model group， Dihuang Yinzi Decoction group， and memantine group， with 15 mice in each group， while 15 wild-type C57BL/6J mice from the same litter were used as blank group. Mice in Dihuang Yinzi Decoction group were given Dihuang Yinzi Decoction 30.03 g/（kg·d） by gavage， mice in the memantine group were given memantine hydrochloride 6.1 mg/（kg·d） by gavage， and mice in the blank group and the model group were given normal saline 2 ml/（kg·d） by gavage for 4 consecutive weeks. Fasting blood glucose was measured weekly. After 4 weeks of intervention， oral glucose tolerance test （OGTT） and insulin tolerance test （ITT） were performed； Morris water maze was used to detect the changes in spatial memory ability of mice； glucose oxidase method was used to detect retinal glucose content of mice； enzyme-linked immunosorbent assay （ELISA） was used to detect serum and retinal insulin content of mice， and Homeostatic Model Assessment of insulin resistance （HOMA-IR） was calculated. Hematoxylin-eosin （HE） staining was performed to observe the histopathological changes in the retina， and the retinal thickness and ganglion cell number were counted； protein immunoblotting was performed to detect the retinal pathway-associated proteins ［insulin receptor substrate 1 （IRS1）， phosphorylated insulin receptor substrate 1 （pIRS1）， phosphatidylinositol-3-hydroxykinase （PI3K）， protein kinase B （Akt1）， phosphorylated protein kinase B （pAkt1）］ expression； retinal glucose transporter protein 4 （GLUT4） expression was detected by immunohistochemistry. ResultsCompared with the blank group， fasting blood glucose of mice in the model group at weeks 1， 2， 3， and 4， blood glucose and area under the curve （AUC） at different time point of OGTT and ITT test， fasting serum insulin， and HOMA-IR increased （P＜0.05， P＜0.01）； in the Morris water maze experiment， the escape latency increased from day 3 to day 5， and the number of crossing platforms， the percentage of target quadrant distance， and the percentage of target quadrant time decreased （P＜0.05， P＜0.01）； the outer nuclear layer of the retina became sparse， thinner， and the number of ganglion cells decreases （P＜0.01）； the expression level of retinal glucose increased， while the expression levels of insulin， pIRS1/IRS1， PI3K/β-Actin， pAkt1/Akt1， and GLUT4 proteins decreased （P＜0.01）. Compared with the model group， fasting blood glucose at week 4， blood glucose at each time point of the OGTT and ITT tests AUC decreased （P＜0.05， P＜0.01）， and fasting serum insulin and HOMA-IR decreased （P＜0.05） in Dihuang Yinzi Decoction group； In the Morris water maze test， the escape latency shortened on day 4 and day 5， number of platform crossings， target quadrant distance as a proportion of total distance， and target quadrant movement time as a proportion of total time decreased （P＜0.05， P＜0.01）； retinal pathological changes alleviated， and retinal thickness and ganglion cell number increased （P＜0.01）； retinal glucose content decreased， and retinal pIRS1/IRS1， PI3K/β-Actin， and GLUT4 protein expression elevated （P＜0.05 or P＜0.01）. ConclusionsDihuang Yinzi Decoction can improve cognitive dysfunction of Alzheimer's disease， which may be related to regulating retinal insulin content and insulin signaling pathway.