BACKGROUND:With the development of the concept of minimally invasive surgery,lumbar posterior dynamic internal fixation has become the mainstream operation for the treatment of diseases caused by intervertebral disc degeneration.OBJECTIVE:To review the latest progress of lumbar posterior dynamic internal fixation in the treatment of lumbar degenerative diseases and postoperative intervertebral disc rehydration.METHODS:The relevant literature published in CNKI,WanFang,and PubMed databases from 2010 to 2025 was searched with the Chinese and English search terms"lumbar spine,dynamic internal fixation,intervertebral disc degeneration,Coflex system,Dynesys system,In-space system,PercuDyn system,intervertebral disc rehydration,crushing stress."By reading the articles,we eliminated the literature with little relevance to the article topic,poor quality and outdated content,and finally 65 articles were included for summary.RESULTS AND CONCLUSION:(1)Although the main surgical method for the treatment of disc degeneration is still the traditional open surgical method of implantation,posterior lumbar dynamic internal fixation has made great progress.(2)Posterior lumbar dynamic fixation can be divided into open dynamic fixation system and percutaneous dynamic fixation system.Each system can be divided into interspinous dynamic internal fixation system and pedicle dynamic internal fixation system according to the different fixation positions.According to the design of specific instruments and the differences of operation methods in the surgery,different operation methods have been derived.At present,the focus of research at home and abroad is on open dynamic internal fixation system.(3)Under the premise that the clinical effect of posterior lumbar dynamic internal fixation is better than that of traditional interbody fusion surgery,it can cause the rehydration phenomenon of postoperative lumbar intervertebral disc,and further improve the long-term postoperative efficacy of patients.

BACKGROUND:With the development of the concept of minimally invasive surgery,lumbar posterior dynamic internal fixation has become the mainstream operation for the treatment of diseases caused by intervertebral disc degeneration.OBJECTIVE:To review the latest progress of lumbar posterior dynamic internal fixation in the treatment of lumbar degenerative diseases and postoperative intervertebral disc rehydration.METHODS:The relevant literature published in CNKI,WanFang,and PubMed databases from 2010 to 2025 was searched with the Chinese and English search terms"lumbar spine,dynamic internal fixation,intervertebral disc degeneration,Coflex system,Dynesys system,In-space system,PercuDyn system,intervertebral disc rehydration,crushing stress."By reading the articles,we eliminated the literature with little relevance to the article topic,poor quality and outdated content,and finally 65 articles were included for summary.RESULTS AND CONCLUSION:(1)Although the main surgical method for the treatment of disc degeneration is still the traditional open surgical method of implantation,posterior lumbar dynamic internal fixation has made great progress.(2)Posterior lumbar dynamic fixation can be divided into open dynamic fixation system and percutaneous dynamic fixation system.Each system can be divided into interspinous dynamic internal fixation system and pedicle dynamic internal fixation system according to the different fixation positions.According to the design of specific instruments and the differences of operation methods in the surgery,different operation methods have been derived.At present,the focus of research at home and abroad is on open dynamic internal fixation system.(3)Under the premise that the clinical effect of posterior lumbar dynamic internal fixation is better than that of traditional interbody fusion surgery,it can cause the rehydration phenomenon of postoperative lumbar intervertebral disc,and further improve the long-term postoperative efficacy of patients.

N-glycosylation is a crucial posttranslational modification of proteins that can modulate their functions and plays key roles in various biological processes. Current research has revealed that alterations in protein N-glycosylation are closely associated with the pathogenesis and progression of multiple ocular diseases. N-glycosylation detection methods can identify changes in N-glycans on proteins; therefore, understanding these techniques and their application value in ocular diseases is important. This article provides a systematic review of the current state of N-glycosylation detection methods, including techniques such as capillary electrophoresis, liquid chromatography, and mass spectrometry. It also offers a detailed discussion on the specific applications of these technologies in the study of various ocular diseases, including diabetic retinopathy, age-related macular degeneration and vernal keratoconjunctivitis/atopic keratoconjunctivitis.

AIM:To investigate the associations of triglyceride glucose(TyG)index, triglyceride glucose-body mass index(TyG-BMI), and homeostatic model assessment of insulin resistance(HOMA-IR)with diabetic retinopathy(DR), and to evaluate their diagnostic value.METHODS: This study was a single-center retrospective study. Patients with type 2 diabetes mellitus(T2DM)who were hospitalized in the endocrinology department of 3201 Hospital from January 1, 2023 to March 1, 2025 were included. According to the diagnostic criteria for DR, participants were classified into DR group and non-DR(NDR)group. Then the association of TyG index, TyG-BMI, and HOMA-IR index with DR of the two groups of patients were alalyzed.RESULTS:A total of 969 patients with T2DM were enrolled in this study, including 816 patients in the DR group. Among DR group, 271 were males(33.2%)and 545 were females(66.8%), with a mean age of 56.78±11.88 years. The NDR group consisted of 153 patients, including 41 males(26.8%)and 112 females(73.2%), with a mean age of 59.40±10.52 years. Statistically significant differences were observed between the DR group and the NDR group in terms of age, BMI, TyG index, TyG-BMI, HOMA-IR index, fasting blood glucose(FBG), 2-h postprandial blood glucose(2 hPBG), fasting insulin(FINS), 2-h postprandial insulin(2 hPINS), fasting C-peptide(FCP), 2-h postprandial C-peptide(2 hPCP), total cholesterol(CHO), triglyceride(TG), low-density lipoprotein(LDL-C), blood urea nitrogen(BUN), uric acid(UA), direct bilirubin(DBIL), glycated hemoglobin(HbA1c), milligrams per total protein(M-TP), microalbuminuria(MALB), urinary albumin to creatinine ratio(UACR), 24-hour urine protein, white blood cell(WBC), neutrophil(N), and platelets(PLT; all P<0.05), while no significant differences were found in the remaining indicators(all P>0.05). In multivariable Logistic regression, both TyG index(aOR=198.65, 95% CI: 66.73-591.41, P<0.001)and TyG-BMI(aOR=1.03, 95% CI: 1.02-1.04, P<0.001)remained independently positive associated with DR. Quartile analysis indicated a progressive increase in DR risk with ascending quartiles of TyG index and TyG-BMI(all Ptrend<0.001). In contrast, HOMA-IR was not significantly associated with DR. Restricted cubic spline analysis, fully adjusted for confounders, showed a nonlinear upward trend in DR risk with increasing TyG index(Pnonlinearity<0.001), whereas TyG-BMI exhibited a U-shaped association(Pnonlinearity<0.05). No significant association was found between HOMA-IR and DR after propensity score matching. Receiver operating characteristic(ROC)curve demonstrated area under curve(AUC)values of 0.870(95% CI: 0.839-0.901)for TyG index, 0.710(95% CI: 0.665-0.755)for TyG-BMI, and 0.657(95% CI: 0.608-0.706)for HOMA-IR.CONCLUSION:The TyG index and TyG-BMI are risk factors for DR. A dose-dependent increase in DR risk was associated with elevated TyG index values. TyG-BMI exhibited an inverted U-shaped relationship with DR risk. The TyG index had better diagnostic efficiency for DR compared to both TyG-BMI and HOMA-IR index.

ObjectiveTo detect the proportion of splenic follicular helper T （Tfh） cells and their functionally related cytokine expression levels in the incomplete embryo implantation disorder （EID） model mice， and to explore the immunological mechanism of Tfh in infertility caused by embryo implantation disorder. MethodsSixteen female Kunming mice were randomly divided into two groups， with eight mice in each group. On day 4 of pregnancy， an incomplete EID mouse model was established by oral gavage of mifepristone suspension， while an equal volume of saline was administered to the control group. On day 8 of pregnancy， the mice were euthanized. Flow cytometry was used to detect the levels of Tfh cells in the spleen lymphocytes of both incomplete EID mice and normal control mice. qRT-PCR was performed to measure the mRNA levels of B-cell lymphoma 6 （Bcl-6） and C-X-C chemokine receptor type 5 protein （CXCR5） in the spleen lymphocytes of both groups. Western blot was employed to assess the protein expression levels of Bcl-6 and CXCR5 in the spleen lymphocytes of both groups. Serum levels of interleukin-4 （IL-4）， IL-6， and IL-21 were measured by ELISA. Immunohistochemistry （IHC） was used to observe the expression levels of progesterone receptor （PR）， Bcl-6， and CXCR5 proteins in the uterine endometrial tissue of mice in both groups. ResultsIncomplete-type EID mice had a reduced number of embryo implantation points and reduced endometrial PR expression. Flow assay results showed that the proportion of CD4⁺CXCR5⁺Tfh cells in splenic lymphocytes of incomplete-type EID mice was significantly higher than that of normal controls （P<0.05）. Compared with the normal control group， Bcl-6 and CXCR5 mRNA levels and protein levels were elevated in splenic lymphocytes of incomplete EID mice， with statistically significant differences （P<0.05）； serum IL-4， IL-6， and IL-21 levels were elevated in incomplete EID mice， and Bcl-6 and CXCR5 proteins in the endometrium were significantly elevated （P<0.05）. ConclusionThe increase of Tfh cells and their associated cytokines Bcl-6 and CXCR5 is associated with the development of incomplete EID， and may be involved in the development of female immune infertility.

ObjectiveTo investigate the effects of hypoxia-treated mesenchymal stem cell （MSCs） exosomes （Exo） and their loading with curcumin on microglial inflammatory responses， and to explore the enhancing effect of hypoxia treatment on the function of MSCs Exo. MethodsThe supernatants of human umbilical cord （hUC）-MSCs cultured under normal and hypoxic conditions were collected， and Exo were isolated using ultracentrifugation. After identification by transmission electron microscopy and Western blot， curcumin was loaded using the co-incubation method. The lipopolysaccharide （LPS）-induced microglial inflammation model was treated with dimethyl sulfoxide （DMSO）， curcumin， normoxia Exo， hypoxia Exo， normoxic Exo loaded with curcumin， and hypoxic Exo loaded with curcumin， respectively. The expression of the M1-type marker inducible nitric oxide synthase （iNOS） in BV2 cells was detected by immunofluorescence （IF）. Western blot and enzyme-linked immunosorbent assay （ELISA） were used to measure the expression and secretion levels of tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， and IL-6 in the cells and their culture supernatants. ResultsNormoxia Exo， hypoxia Exo， normoxic Exo loaded with curcumin， and hypoxic Exo loaded with curcumin exhibited a "saucer-like" shape with a diameter ranging from 30~150 nm， and the expression of exosomal markers CD9， CD81， and TSG101 were positive. After treating the BV2 cell inflammation model， IF results showed that， compared with the normoxia Exo group， treatment with hypoxic Exo significantly reduced the expression of iNOS. Moreover， when compared with the curcumin group and the normoxic Exo loaded with curcumin group， the expression level of iNOS significantly decreased after treatment with hypoxic Exo loaded with curcumin. The results of Western blot and ELISA indicated that， in comparison with the normoxia Exo group， treatment with hypoxic Exo significantly reduced the expression and secretion of the inflammatory cytokines TNF-α， IL-1β， and IL-6. Additionally， when compared with the curcumin group and the normoxic Exo loaded with curcumin group， both the expression and secretion of TNF-α， IL-1β， and IL-6 significantly decreased after treatment with hypoxic Exo loaded with curcumin. ConclusionHypoxia preconditioning can enhance the ability of hUC-MSCs-Exo in the inhibition of microglial polarization and inflammatory factors’ secretion. Additionally， using Hypoxia-MSCs-Exo as a drug-delivery carrier of curcumin can improve its solubility and stability， facilitating its absorption by cells and exerting the therapeutic effect of combination therapy.

Stroke is the leading cause of death and disability among adults in China， and its common complications include digestive system abnormalities， cognitive impairment， depression， stroke-associated pneumonia， and hemiplegia. The combination of traditional Chinese and Western medicine has great potential in treating post-stroke complications. Xinglou Chengqitang （XLCQT） is a representative prescription of alleviating the disease in the upper part by treating the lower part. It has definite therapeutic effect and high safety. Clinically， XLCQT is often used to treat stroke and its complications. However， the quantity and quality of clinical trials of XLCQT in treating post-stroke complications need to be improved. Additionally， since the basic research is weak， the material basis and multi-target mechanism for the efficacy of this prescription are unknown. This article reviews XLCQT in terms of the pharmacodynamic basis， medicinal properties， safety evaluation， and progress in clinical research and mechanisms in treating post-stroke complications. This article summarizes 22 key active ingredients of XLCQT in treating acute stroke complicated with syndrome of phlegm heat and fu-organ excess. Among these key active ingredients， resveratrol， kaempferol， luteolin， chrysoeriol， apigenin， （+）-catechin， and adenosine have good pharmacokinetic properties and high bioavailability. The mechanisms of XLCQT in treating post-stroke complications are complex， including inflammatory response， brain-gut axis， hypothalamic-pituitary-adrenal （HPA） axis， intestinal flora， neurotrophic factors， autophagy， oxidative stress， and free radical damage. This review helps to deeply understand the pharmacodynamic basis and mechanisms of XLCQT in treating post-stroke complications and provides a theoretical basis for the clinical application of XLCQT against post-stroke complications and the development of drugs.

Objective To investigate the distribution characteristics of pathogens causing infections within 90 days after liver transplantation and the influencing factors of infection. Methods Clinical data of 176 recipients who underwent liver transplantation at the Liver Transplant Center of Beijing Friendship Hospital Affiliated to Capital Medical University from September 2021 to August 2024 were retrospectively analyzed. Patients were divided into the infection group (n=124) and the non-infection group (n=52) based on whether they developed infection within 90 days after transplantation. The distribution characteristics of pathogens in infected patients were analyzed. Univariate and multivariate logistic regression analyses were used to explore the influencing factors of infection. Results Among the 176 liver transplant recipients, 124 cases developed 243 episodes of 518 bacterial, fungal, viral or mycoplasma infections within 90 days after transplantation, with an overall infection rate of 70.5% (124/176). The composition of pathogens was mainly Gram-negative bacteria (38.6%, 200/518), followed by Gram-positive bacteria (32.2%, 167/518) and viruses (15.4%, 80/518), and fungi accounted for 13.1% (68/518). Among Gram-negative bacteria, the main pathogen was Klebsiella pneumoniae (6.8%, 35/518), and among Gram-positive bacteria, the main pathogen was Enterococcus faecalis (8.5%, 44/518). Viruses included Epstein-Barr virus (3.7%, 19/518) and cytomegalovirus (3.7%, 19/518), and fungi were mainly Candida albicans (6.8%, 35/518). The most common infection site among the 243 episodes was pulmonary infection (42.0%, 102/243), followed by abdominal infection (22.6%, 55/243) and bloodstream infection (18.1%, 44/243). The infections mainly occurred within 2 weeks after transplantation (60.9%, 148/243). Multivariate logistic regression analysis indicated that preoperative infection within 2 weeks, a high preoperative model for end-stage liver disease (MELD) score, and preoperative sarcopenia were independent risk factors for infection within 90 days after liver transplantation (all odds ratio>1, P<0.05). After multivariate correction, the levels of CD4⁺T cells and CD8⁺T cells within 90 days after surgery were independently associated with the occurrence of infection. Low levels of CD4⁺T cells and CD8⁺T cells might be related to an increased risk of infection. Conclusions The infection rate after liver transplantation is high, and the pathogens are mainly Gram-negative bacteria. The lungs are the most common infection site. Preoperative MELD score, preoperative sarcopenia and preoperative infection within 2 weeks are independent risk factors for infection within 90 days after liver transplantation. Regular monitoring of immune indicators CD4⁺T cells and CD8⁺T cells levels after transplantation is helpful to reduce the occurrence of post-transplantation infection.

Gout is a crystal-associated arthropathy caused by the deposition of monosodium urate crystals and is closely related to purine metabolic disorders and impaired uric acid excretion. It is clinically characterized by hyperuricemia， recurrent joint swelling and pain， and tophus formation. The disease course is divided into three stages： The hyperuricemia stage， acute attack stage， and chronic gouty arthritis stage. Modern medicine has reached a consensus on its pathology， but traditional Chinese medicine （TCM） lacks a systematic stage-specific understanding of gout pathogenesis and its underlying mechanisms， making it difficult to guide precise syndrome differentiation and treatment. By integrating classical TCM theory， clinical practice， and modern medical understanding， and drawing upon descriptions of Bi syndrome caused by endogenous dampness and turbidity in classical texts such as Huangdi Neijing·Ling Shu and Synopsis of the Golden Chamber， our team proposes the pathogenic concept of gout as ''endogenous dampness leading to Bi syndrome'' and the core pathogenesis of ''spleen deficiency with internal retention of dampness-turbidity''. We systematically elucidate the evolution of pathogenesis across different stages and corresponding therapeutic strategies. This study posits that metabolic byproducts such as urate fall under the category of ''endogenous pathogenic dampness-turbidity''. When genetic or dietary factors lead to metabolic abnormalities， it manifests as ''spleen deficiency with impaired transport and transformation''， resulting in ''internal retention of pathogenic dampness-turbidity''. When damp-turbidity stagnates in the blood vessels， serum uric acid levels rise. When it stagnates in the viscera and limbs， monosodium urate crystals deposit in the joints. Triggered by precipitating factors， this leads to gout attacks—the core pathological process of ''endogenous dampness leading to Bi syndrome''. Based on this theory， the stage-specific pathogenic characteristics of gout are proposed： The hyperuricemia stage is characterized by ''spleen deficiency with impaired transport and transformation， internal retention of pathogenic dampness-turbidity''， the acute attack stage is primarily marked by ''dampness-turbidity and static heat obstructing the limbs and joints''， while the chronic stage is defined by ''spleen deficiency with internal retention of pathogenic dampness-turbidity， intermingled with phlegm-stasis binding''. The treatment principle centers on ''strengthening the spleen and draining dampness'' throughout all stages. During the hyperuricemia stage， treatment focuses on ''strengthening the spleen， draining dampness， and eliminating turbidity''. In the acute attack stage， the treatment should "strengthen the spleen， drain dampness， clear heat， eliminate turbidity， alleviate swelling， and relieve pain''. In the chronic stage， the treatments emphasizes to ''strengthen the spleen， drain dampness， transform turbidity， clear heat， resolve phlegm， and activate blood circulation''. This approach has yielded favorable therapeutic outcomes in clinical practice. This theoretical system clarifies the nature of gout as ''spleen deficiency being the root， dampness-turbidity being the secondary manifestation'' and systematically analyzes its pathogenesis evolution process and characteristics. The constructed stage-based treatment protocol has been validated through clinical and basic research， providing systematic theoretical guidance and a practical framework for the precise TCM management of gout， thereby promoting the modernization of TCM pathogenesis theory related to gout.

ObjectiveTo evaluate the therapeutic effect of Huazhuo SanJie Chubi presciption （HSCD） on chronic gouty arthritis （CGA） rats with low-grade inflammation and to explore the underlying mechanism with a focus on macrophage polarization. MethodsThe 41 male 6-week-old SD rats were randomly allocated， using the random number table， to a normal group （n=8） and a model group （n =33）. CGA with low-grade inflammation was induced in the model group by daily gavage of potassium oxonate （250 mg·kg^-1·d^-1） and hypoxanthine （300 mg·kg^-1·d^-1）， combined with intra-articular injection of a monosodium urate （MSU） crystal suspension （50 μL， 25 g·L^-¹） into the left ankle twice weekly. After 4 weeks of modeling， 3 rats were randomly selected from each group for model validation. The remaining successfully modeled rats were randomly divided into a model group， an HSCD group （10.35 g·kg^-1·d^-1， gavage once daily）， an M1 polarization agonist group （L-methionine sulfoximine， 300 mg·kg^-1， subcutaneous injection every other day）， an M1 polarization agonist + HSCD group， an M2 polarization inhibitor group （PD0325901， 10 mg·kg^-1·d^-1， gavage once daily）， and M2 polarization inhibitor + HSCD group. The corresponding drug or drug combination was administered according to group assignment， whereas rats in the normal and model groups received 0.5% carboxymethyl cellulose sodium （CMC-Na） vehicle （10.35 g·kg^-1·d^-1， gavage once daily）. All interventions were continued for four weeks. During the intervention period， except for the normal group， potassium oxonate （250 mg·kg⁻¹） and hypoxanthine （300 mg·kg^-1） were co-administered by gavage every other day to maintain the model. At the end of treatment， serum uric acid （SUA）， ankle joint diameter and joint swelling index were measured. The levels of high-sensitivity C-reactive protein （hs-CRP）， interleukin-1β （IL-1β）， interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， chemokine C-C motif ligand 2 （CCL2）， S100 calcium-binding protein A8/A9 （S100A8/A9）， interleukin-10 （IL-10） and arginase-1 （Arg-1） in serum and joint fluid were determined by enzyme-linked immunosorbent assay （ELISA）. High-frequency ultrasound was used to assess MSU deposition in the ankle joint. Hematoxylin-eosin （HE） staining was performed to evaluate synovial histopathological changes. Quantitative Real-time PCR and immunofluorescence were used to detect the mRNA and protein expression of the M1 macrophage polarization markers inducible nitric oxide synthase （iNOS） and the M2 macrophage polarization marker scavenger receptor cysteine-rich type 1 protein M130 （CD163） in synovial tissue. ResultsCompared with the normal group， the model group showed significantly elevated SUA level and joint swelling index， and increased levels of pro-inflammatory cytokines， CCL2， and S100A8/A9 in both serum and joint fluid （P<0.05）， accompanied by MSU deposition and synovial inflammation in the ankle joint. The mRNA and protein expression levels of macrophage polarization M1/M2 markers iNOS and CD163 in synovial tissues were also significantly up-regulated （P<0.05）. Compared with model group， rats in HSCD group had significantly lower SUA levels， attenuated joint swelling， reduced serum levels of pro-inflammatory cytokines， and decreased levels of CCL2 and S100A8/A9 in both serum and joint fluid， accompanied with alleviated MSU deposition and synovial inflammation （P<0.05）. HSCD markedly downregulated the mRNA and protein expression of M1 marker iNOS （P<0.05）， whereas it had no significant effect on the expression of M2 marker CD163. Compared with the M1 polarization agonist group， the M1 polarization agonist + HSCD group showed significantly reduced joint swelling， lower serum levels of pro-inflammatory cytokines， and decreased levels of CCL2 and S100A8/A9 in joint fluid （P<0.05）. In addition， synovial inflammatory cell infiltration and angiogenesis were attenuated， and iNOS mRNA and protein expression levels were significantly reduced （P<0.05）. Compared with the M2 polarization inhibitor group， the M2 polarization inhibitor + HSCD group exhibited reduced joint swelling， decreased levels of CCL2 and S100A8/A9 in joint fluid and ameliorated synovial inflammation （P<0.05）， whereas the levels of anti-inflammatory mediators （IL-10， Arg-1） and CD163 mRNA and protein expression were not significantly increased. ConclusionHSCD alleviates low-grade inflammation in CGA rats， at least in part， by inhibiting macrophage polarization toward the M1 phenotype.