ObjectiveTo explore the effects and mechanism of the modified Danggui Yinzi on "itch-anxiety" model rats of chronic urticaria （CU）. MethodsThe 36 SPF-grade 6-8-week-old female SD rats were randomly divided into a blank control group，a model group，a positive control group，a low-dose modified Danggui Yinzi group，a medium-dose modified Danggui Yinzi group，and a high-dose modified Danggui Yinzi group. A "itch-anxiety" model was established by intraperitoneal injection of a suspension of sodium chloride and aluminum hydroxide and ovalbumin，combined with chronic unpredictable emotional stress stimulation. After successful modeling，rats in each group were administered drugs by gavage. The positive control group was given intragastric administration of the drug solutions of cetirizine and fluoxetine （2.08 mg·kg^-1·d^-1 fluoxetine， 2 mg·kg^-1·d^-1 cetirizine）， the low-，medium-，and high-dose modified Danggui Yinzi groups were administered traditional Chinese medicine at 1.44，2.88， 5.76 g·kg^-1， respectively，while the blank control group and model group were given an equal volume of normal saline. All interventions lasted for 15 days. Behavioral changes were evaluated by the elevated plus-maze test （detecting the percentage of entries into the open arms （OE%），the percentage of time spent in the open arms （OT%），and the total number of entries into the open and closed arms （TNE）），the open-field test （detecting total activity，average movement speed，and latency to enter the central area），and scratching behavior observation. Pathological changes of skin tissues were observed by hematoxylin-eosin （HE） staining and toluidine blue staining，while those of amygdala tissues were observed by HE staining，Nissl staining，and immunofluorescence detection of ionized calcium-binding adapter molecule-1 （Iba-1）. The content of immunoglobulin E （IgE），interleukin-33 （IL-33），histamine in serum and glutamate in the amygdala was detected by enzyme-linked immunosorbent assay （ELISA）. Western blot was used to detect the protein expression of striatal-enriched protein tyrosine phosphatase （STEP），N-methyl-D-aspartate receptor subunit 2B （NR2B）， calmodulin-dependent protein kinase Ⅱ （CaMKⅡ），phosphorylated CaMKⅡ （p-CaMKⅡ），mitogen-activated protein kinase （MAPK），phosphorylated MAPK （p-MAPK），nuclear factor kappa-light-chain-enhancer of activated B cells （NF-κB），phosphorylated NF-κB （p-NF-κB），and postsynaptic density protein-95 （PSD-95） in the amygdala. ResultsCompared with the blank control group，the model group rats showed obvious anxiety-like behaviors （decreased OE%，OT%，and TNE，reduced total activity，slower average movement speed，and prolonged latency to enter the central area），increased scratching times，obvious skin inflammation and mast cell degranulation，severe amygdala tissue damage，increased glutamate content in the amygdala，and elevated levels of IgE and IL-33 in serum. The expression of STEP，NF-κB，p-NF-κB，NR2B，MAPK，p-MAPK，CaMKⅡ，and p-CaMKⅡ proteins in the amygdala increased，while the expression of PSD-95 protein decreased （P<0.05）. Compared with the model group，the modified Danggui Yinzi group of each dose had increased OE%，OT%，TNE，total activity，and average movement speed，shortened latency to enter the central area， reduced scratching times，alleviated skin inflammation and mast cell degranulation，relieved amygdala tissue damage，decreased glutamate content in the amygdala，and reduced levels of IgE and IL-33 in serum. Moreover，compared with the model group，the low -，medium-，and high-dose modified Danggui Yinzi groups showed decreased expression levels of STEP，NF-κB，p-NF-κB，NR2B，MAPK，p-MAPK，CaMKⅡ，and p-CaMKⅡ proteins in the amygdala，and increased expression of PSD-95 protein. There was a significant dose-effect relationship，with the high-dose group showing the most significant regulatory effect （P<0.05）. ConclusionThe modified Danggui Yinzi has a therapeutic effect on "itch-anxiety" model rats of CU. Its mechanism may be related to regulating glutamate metabolism in the amygdala，modulating the STEP/NR2B/CaMKⅡ/MAPK/NF-κB pathway，and regulating the expression of PSD-95.

OBJECTIVE: To review the research progress on the lower limb biomechanical characteristics of patients with discoid lateral meniscus (DLM) injury after surgery. METHODS: By searching relevant domestic and international research literature on DLM, the postoperative characteristics of knee joint movement biomechanics, tibiofemoral joint stress distribution, lower extremity force line, and patellofemoral joint changes in patients with DLM injury were summarized. RESULTS: Surgical treatment can lead to varying degrees of changes in the lower limb biomechanical characteristics of patients with DLM injury. Specifically, the kinematic biomechanics of the knee joint can significantly improve, but there are still problems such as extension deficits in the affected knee joint. The peak stress of the tibiofemoral joint decreases with the increase of the residual meniscus volume, and the degree of change is closely related to the residual meniscus volume. Preserving a larger volume of the meniscus, especially the anterior horn volume, helps to reduce stress concentration. The lower extremity force line will deviate outward after surgery, and the more meniscus is removed during surgery, the greater the change in the lower extremity force line after surgery. There are conditions such as cartilage degeneration, position and angle changes in the patellofemoral joint after surgery. CONCLUSION The changes in the lower limb biomechanical characteristics after DLM injury are closely related to the choice of surgical methods and rehabilitation programs. However, the mechanisms of biomechanical changes in multiple lower limb joints and individual differences still need to be further studied and clarified.
Humans ; Biomechanical Phenomena ; Tibial Meniscus Injuries/physiopathology* ; Menisci, Tibial/physiopathology* ; Knee Joint/surgery* ; Lower Extremity/physiopathology* ; Patellofemoral Joint/physiopathology* ; Range of Motion, Articular ; Knee Injuries/physiopathology*

Diabetic nephropathy(DN)ranks as a frequent and serious complication in diabetes mellitus,and it's a key factor in chronic kidney disease and end-stage renal disease(ESRD),greatly diminishing the life quality of patients.Presently,the conventional treatment approaches for DN mainly involve strict regulation of blood sugar and pressure,in conjunction with the application of renin-angiotensin-aldosterone system inhibitors.While these therapies can slow down the advancement of DN,they are ineffective in stopping its final development into ESRD.Lately,the involvement of the gut-kidney axis in the development and advancement of DN has attracted growing interest.Individuals suffering from DN show changes in the variety of gut microbiota,which are crucial in the development and management of DN due to metabolic interactions with the host.The goal of this analysis is to explore the fundamental processes of gut microbiota's role in DN and explore treatment approaches focusing on gut microbiota,aiming to offer new perspectives for the clinical handling of DN.

Objective:Through microscopic and ultrastructural observations,to explore the origin of the cartilage of the anteroposterior pseudocyst.Staging for the auricular pseudocyst according to the different pathological changes and exploring its clinical significance.Methods:48 cases(51 ears)of the auricular pseudocyst were collected as the observation objects(46 males, 2 females, 15-76 years old) and 45 patients(45 ears)chronic suppurative otitis media hospitalized patients who underwent tympanic membrane repair as a normal control group(43 males, 2 females, 12-74 years old).The outer wall of the cyst was surgically resected and the residual auricular cartilage was retained in the control group for HE staining or transmission electron microscopy specimens, and the specimens were observed and analyzed under light microscope and transmission electron microscopy.Results:According to the data of this study, auricular pseudocyst was relatively common in people aged 21-60 years. The disease course of 4 ears was ≤ 10 days,the course of 16 ears was > 10 days yet ≤ 30 days, the course of 20 ears was > 1 month but ≤ 2 months,the course of 6 ears was > 2 months yet ≤ 1 year, the course of 3 ears was > one year but ≤ two years,and the course of 2 ears was > 2 years. The observation of microstructure and ultrastructure of the different course of outer walls of the auricle pseudocyst was shown:due to various causes of cartilage fluid that separated perichondrium and cartilage tissue, when the perichondrium was stimulated, the bone progenitor cells from the quiescence phase came to the activities period. With the extension of the course, the periosteum was thickening gradually, cartilage the bone progenitor cells idifferentiated into chondroblasts, which idifferentiated into chondrocytes last, from native to mature, from thin to thick. It was stable a period of time when the cartilage mature. The outer wall of the cyst was new cartilage, which reflected additional growth. The nucleus of the chondrocytes evolved into nucleolysis, and necrosis, when the lesions was stimulated.The control group had a thin layer of cartilage and periosteum, containing a small amount of osteoprogenitor cells; the cartilage layer was thick, the cartilage cells were small near the periosteum, and the deep cartilage cells were large, all of which were mature chondrocytes.Conclusions:The outer cartilage of auricle pseudocyst is newborn cartilage. The pathological staging is divided into early stage(cartilage formation), middle stage(cartilage maturity) and late stage(cartilage necrosis).This stage can provide a reference for exploring the pathogenesis of pseudocysts of the auricle and formulating surgical treatment principles.

Objective To investigate the effect of knockdown PRTN3 on polarization phenotype and anti-tumor function of macrophages in breast cancer.Methods A mouse monocyte/macrophage cell line(RAW264.7)with knockdown of PRTN3 was constructed.The mRNA and protein levels of PRTN3 were detected by RT-qPCR and flow cytometry.Macrophages were co-cultured with tumor cells,and the polarization phenotypes of macrophages were detected by flow cytometry,and the mRNA levels of polarization and cytokines related genes were detected by RT-qPCR.The tumor phagocytosis and tumor killing ability of macrophages were determined by in vitro phagocytosis assay and tumor killing assay.The effect of macrophages with PRTN3 knockdown on tumor progression and metasta-sis was compared in an orthotopic transplantation model of mouse breast cancer.Results The mRNA and protein levels of PRTN3 in the RAW264.7 cell line with stable knockdown of PRTN3 were significantly decreased(P＜0.01).Knockdown of PRTN3 in RAW264.7 cells upregulated the expression of M1 phenotype-related genes(CD80,CD86,iNOS,IL-1β,IL-6 and TNF-α)(P＜0.05).After macrophages co-culture with tumor cells,macrophages with knockdown of PRTN3 upregulated the expression of M1 phenotype-related genes(CD80,CD86,iNOS,IL-1β,IL-6 and TNF-α)(P＜0.01).Knockdown of PRTN3 enhanced the phagocyto-sis(P＜0.05)and tumor killing ability(P＜0.05)of macrophages in vitro.Adoptive transfusion of PRTN3-knockdown macrophages into tumor-bearing mice inhibited the growth of in situ breast cancer and reduced lung metastasis(P＜0.05).Conclusions PRTN3 regulates phenotypic polarization of macrophages,and knockdown of PRTN3 enhances the anti-tumor function of macrophages.

Trauma can disrupt the body′s internal environment, resulting in organ dysfunction. This may manifest as symptoms such as acute respiratory distress, liver and kidney dysfunction, circulatory disorders and neurological damage. Mitochondrial quality control (MQC), encompassing processes like autophagy, dynamic changes, and biogenesis, plays an essential role in maintaining mitochondrial function. Stress responses following trauma can cause mitochondrial dysfunction and MQC imbalance, thereby exacerbating organ injury. Correcting MQC imbalance can improve organ function. Current researches on MQC in post-traumatic organ dysfunction mainly focuses on imbalance in specific MQC mechanism, lacking a systemic understanding of its incidence and progression. To this end, the authors reviewed the progress in researches on the impact of MQC imbalance on post-traumatic organ dysfunction, aiming to provide insights for clinical treatment.

Diabetic nephropathy(DN)ranks as a frequent and serious complication in diabetes mellitus,and it's a key factor in chronic kidney disease and end-stage renal disease(ESRD),greatly diminishing the life quality of patients.Presently,the conventional treatment approaches for DN mainly involve strict regulation of blood sugar and pressure,in conjunction with the application of renin-angiotensin-aldosterone system inhibitors.While these therapies can slow down the advancement of DN,they are ineffective in stopping its final development into ESRD.Lately,the involvement of the gut-kidney axis in the development and advancement of DN has attracted growing interest.Individuals suffering from DN show changes in the variety of gut microbiota,which are crucial in the development and management of DN due to metabolic interactions with the host.The goal of this analysis is to explore the fundamental processes of gut microbiota's role in DN and explore treatment approaches focusing on gut microbiota,aiming to offer new perspectives for the clinical handling of DN.

Trauma can disrupt the body′s internal environment, resulting in organ dysfunction. This may manifest as symptoms such as acute respiratory distress, liver and kidney dysfunction, circulatory disorders and neurological damage. Mitochondrial quality control (MQC), encompassing processes like autophagy, dynamic changes, and biogenesis, plays an essential role in maintaining mitochondrial function. Stress responses following trauma can cause mitochondrial dysfunction and MQC imbalance, thereby exacerbating organ injury. Correcting MQC imbalance can improve organ function. Current researches on MQC in post-traumatic organ dysfunction mainly focuses on imbalance in specific MQC mechanism, lacking a systemic understanding of its incidence and progression. To this end, the authors reviewed the progress in researches on the impact of MQC imbalance on post-traumatic organ dysfunction, aiming to provide insights for clinical treatment.

Objective:To investigate the effects of the histone deacetylase(HDAC)inhibitor panobinostat on melanoma growth,tumor immunity,and the underlying mechanisms.Methods:B16F0 melanoma cells were cultured and treated with different concentrations of panobinostat.The effect of panobinostat on HDAC expression in B16F0 cells was detected by WB.The effects of panobinostat on the proliferation,migration,invasion,apoptosis and cell cycle of B16F0 cells were detected by CCK-8 assay,wound-healing assay,Transwell assay and flow cytometry,respectively.The effect of panobinostat on gene expression in B16F0 cells was detected using transcriptome analysis and verified by qPCR.Flow cytometry was used to detect the effect of panobinostat on the expression of MHCⅠ/Ⅱ in B16F0 cells.B16F0 cells and bone marrow-derived dendritic cells(BMDC)were co-cultured to assess the effects of panobinostat on the expression of CD11c,CD80 and CD86 in BMDC cells.A xenograft mouse model was used to evaluate the effects of panobinostat on tumor growth and host immune function.Results:panobinostat promoted the acetylation of H3 and α-tubulin proteins in B16F0 cells(P<0.01 or P<0.001 or P<0.000 1),inhibited cell proliferation,migration,and invasion,promoted apoptosis,and induced G1-phase cell cycle arrest(P<0.05 or P<0.001 or P<0.000 1).Additionally,panobinostat enhanced surface expression of MHC Ⅰ/Ⅱ on B16F0 cells and promoted BMDC maturation(all P<0.01).Transcriptomic analysis showed that panobinostat upregulated the expression of E-cadherin and antigen presentation related genes in B16F0 cells,and inhibited the expression of N-cadherin,vimentin,c-Myc and CDK1,which was confirmed by qPCR.In vivo,panobinostat suppressed xenograft tumor growth and enhanced immune function in tumor-bearing nude mice(P<0.05,P<0.000 1).Conclusion:panobinostat can inhibit the malignant biological behavior of B16F0 cells,promote apoptosis,regulate tumor immunity,and enhance immune function of tumor-bearing nude mice.

Objective:Through microscopic and ultrastructural observations,to explore the origin of the cartilage of the anteroposterior pseudocyst.Staging for the auricular pseudocyst according to the different pathological changes and exploring its clinical significance.Methods:48 cases(51 ears)of the auricular pseudocyst were collected as the observation objects(46 males, 2 females, 15-76 years old) and 45 patients(45 ears)chronic suppurative otitis media hospitalized patients who underwent tympanic membrane repair as a normal control group(43 males, 2 females, 12-74 years old).The outer wall of the cyst was surgically resected and the residual auricular cartilage was retained in the control group for HE staining or transmission electron microscopy specimens, and the specimens were observed and analyzed under light microscope and transmission electron microscopy.Results:According to the data of this study, auricular pseudocyst was relatively common in people aged 21-60 years. The disease course of 4 ears was ≤ 10 days,the course of 16 ears was > 10 days yet ≤ 30 days, the course of 20 ears was > 1 month but ≤ 2 months,the course of 6 ears was > 2 months yet ≤ 1 year, the course of 3 ears was > one year but ≤ two years,and the course of 2 ears was > 2 years. The observation of microstructure and ultrastructure of the different course of outer walls of the auricle pseudocyst was shown:due to various causes of cartilage fluid that separated perichondrium and cartilage tissue, when the perichondrium was stimulated, the bone progenitor cells from the quiescence phase came to the activities period. With the extension of the course, the periosteum was thickening gradually, cartilage the bone progenitor cells idifferentiated into chondroblasts, which idifferentiated into chondrocytes last, from native to mature, from thin to thick. It was stable a period of time when the cartilage mature. The outer wall of the cyst was new cartilage, which reflected additional growth. The nucleus of the chondrocytes evolved into nucleolysis, and necrosis, when the lesions was stimulated.The control group had a thin layer of cartilage and periosteum, containing a small amount of osteoprogenitor cells; the cartilage layer was thick, the cartilage cells were small near the periosteum, and the deep cartilage cells were large, all of which were mature chondrocytes.Conclusions:The outer cartilage of auricle pseudocyst is newborn cartilage. The pathological staging is divided into early stage(cartilage formation), middle stage(cartilage maturity) and late stage(cartilage necrosis).This stage can provide a reference for exploring the pathogenesis of pseudocysts of the auricle and formulating surgical treatment principles.