Osteosarcoma, a highly invasive and metastatic malignant bone tumor, has a poor prognosis primarily because of early pulmonary metastasis and resistance to conventional treatments. The malignant progression of osteosarcoma cells significantly depends on glycometabolic reprogramming, a process characterized by enhanced aerobic glycolysis. This review begins by mapping the multi-dimensional networks driving sugar metabolism reprogramming, which revealed that functional abnormalities in core glycolytic enzymes, including hexokinase 2, pyruvate kinase M2, and lactate dehydrogenase A (LDHA), are driven by a multi-level regulatory network that includes altered transcription factor activity, epigenetic modifications, and interactions mediated by non-coding RNAs. Mitochondrial dysfunction leads to succinate and reactive oxygen species accumulation, synergistically promoting the remodeling of metabolic pathways. Furthermore, the synergistic interaction between the pentose phosphate pathway and glutamine metabolism accelerates the energy supply and biosynthesis, whereas lactate accumulation shapes the immunosuppressive microenvironment by inhibiting immune cell function. This review focuses on dissecting the core mechanisms of glucose metabolism reprogramming in osteosarcoma pathogenesis, including promoting proliferation, inhibiting apoptosis, enhancing invasion and metastasis, regulating immune metabolism, and mediating chemotherapy resistance. Additionally, it evaluates novel therapeutic strategies targeting key nodes of glucose metabolism in osteosarcoma, including advances in preclinical research on specific small-molecule inhibitors and gene regulatory approaches. Finally, it delves into the major challenges in translational research, such as metabolic heterogeneity, targeting selectivity, and compensatory resistance, as well as prospects for future research, including multi-omics analysis, smart delivery systems, organoid models, and combination immunotherapy. This study offers novel insights into overcoming the therapeutic bottlenecks in osteosarcoma treatment.

Introduction: The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway is a critical sensor in the innate immune response to intracellular pathogens, yet its therapeutic potential for augmenting macrophage-mediated control of Mycobacterium tuberculosis (Mtb) remains incompletely understood. This study investigated whether pharmacological activation of the STING pathway could enhance autophagy to promote Mtb clearance in human macrophages. Methods: Human THP-1 monocytes were differentiated into macrophages and infected with Mtb. The effects of the STING agonist MIW815 (ADU-S100) on Mtb phagocytosis, intracellular bacterial survival, and autophagic flux were assessed using a combination of molecular and cellular techniques, including quantitative real-time polymerase chain reaction, Western blotting, colony-forming unit (CFU) assays, and confocal immunofluorescence microscopy. The dependency on the cGAS-STING pathway was confirmed using small interfering RNA-mediated gene silencing. Results: Pharmacological activation of STING with ADU-S100 significantly enhanced Mtb phagocytosis and subsequent intracellular clearance. This enhanced bactericidal activity was mechanistically linked to an increase in autophagic flux, as evidenced by elevated LC3-II protein levels and significantly increased colocalization of Mtb with lysosomal compartments. Importantly, treatment with the autophagy inhibitor hydroxychloroquine or silencing of cGAS significantly reversed these phenotypes, confirming the pivotal role of the STING-autophagy axis. Conclusion: Activating the STING pathway with ADU-S100 is a potent host-directed strategy to bolster macrophage autophagy and enhance the elimination of intracellular Mtb. This provides a strong rationale for exploring STING agonists as a novel therapeutic intervention for tuberculosis, addressing a significant and clinically relevant challenge in infectious disease.

BACKGROUND:Spinal tuberculosis, a destructive extrapulmonary form, often causes severe deformity and neurological deficits. Surgical intervention aims to debride lesions, reconstruct stability, and correct deformities. This study evaluates a combined posterior fixation and minimally invasive anterior approach for lumbar tuberculosis. AIM:To evaluate the clinical outcomes and radiological parameters of posterior internal fixation combined with minimally invasive anterior lesion clearance and bone graft fusion for the treatment of lumbar tuberculosis. METHODS:Clinical data from 24 patients with lumbar tuberculosis who underwent posterior pedicle screw fixation combined with minimally invasive anterior lesion clearance were analyzed. The Cobb angle, visual analog scale (VAS) score, and Frankel classification were statistically assessed preoperatively and postoperatively. Complications and bone graft fusion were also recorded. RESULTS:Wounds healed in the first stage in 22 patients; one patient developed a posterior incisional sinus tract, and one experienced postoperative tuberculosis recurrence. At the final follow-up, according to the Frankel classification, there were 1, 2, and 21 cases classified as grade C, grade D, and grade E, respectively. By the last follow-up, the Cobb angle, VAS score, and erythrocyte sedimentation rate had all decreased. Both X-ray and computed tomography images confirmed bone healing. The fusion time ranged from 3 to 9 months, with an average of 5.2 months. CONCLUSION:Posterior pedicle screw fixation combined with minimally invasive anterior lesion clearance is an effective and safe treatment for lumbar tuberculosis.

Autophagy is a widespread physiological process in the body, which also protects the host by degrading invading pathogens and harmful substances during pathological conditions. Nevertheless, Mycobacterium tuberculosis (MTB), the causative agent of tuberculosis, has evolved strategies to subvert autophagy by modulating microRNA (miRNA) expression, enabling its escape from host defenses. In this study, we established an in vitro model using the human macrophage cell line infected with the highly virulent MTB strain H37Rv. Through RNA sequencing and bioinformatic analysis post H37Rv infection, we screened 14 differentially expressed miRNAs. We predicted and demonstrated that miR-30c-1-3p inhibits autophagy and promotes MTB survival by targeting ATG4B and ATG9B during the infection process. The results showed that miR-30c-1-3p expression was gradually increased before 12 h of H37Rv infection, followed by a decrease. Overexpression of miR-30c-1-3p suppressed autophagic activity. We also identified the targeting of miR-30c-1-3p to ATG4B and ATG9B for the first time, and overexpression of both ATG4B and ATG9B, alone or together, on the basis with upregulation of miR-30c-1-3p reversed the inhibition of autophagy. Autophagy levels were analyzed at different levels by western blot, immunofluorescence, and transmission electron microscopy, all of which showed that upregulation of miR-30c-1-3p inhibited autophagy during H37Rv infection. Additionally, the intervention of miR-30c-1-3p mimics resulted in an increased bacterial load in macrophages, suggesting that MTB achieves immune evasion by upregulating miR-30c-1-3p during infection. In conclusion, our study provides a valuable target for the development of host-directed anti-tuberculosis therapy as well as a new diagnostic marker.

This study aimed to investigate the differential expression levels of the cGAS-STING pathway in peripheral blood mononuclear cells (PBMCs) of spinal tuberculosis (TB) patients with different progression and its feasibility as a diagnostic marker. Peripheral blood and medical records of 25 patients with spinal TB and 10 healthy individuals, were prospectively collected and analyzed. PBMCs and serum were extracted from peripheral blood and the expression levels of the cGAS-STING pathway in PBMCs were measured by real-time PCR (RT-PCR) and serum interferon β (IFN-β) expression levels were measured by enzyme-linked immunosorbent assay (ELISA). The expression of Interferon regulatory Factor 3 (IRF3) in PBMCs was measured using western blot. Statistical analysis was performed using the SPSS 26.0 statistical package. The results showed that the expression level of the TANK-binding kinase 1 (TBK1) and IRF3 was significantly higher in PBMCs (P < 0.05), in patients with active lesions than in patients with stable lesions. The serum concentration of IFN-β was significantly higher in patients with active lesions (P = 0.028). Compared with healthy individuals, the expression level of the cGAS-STING pathway was elevated in PBMCs of TB patients (P < 0.05), and the difference in the expression level of IFN-β was not statistically significant (P > 0.05), and the serum IFN-β concentration was elevated (P < 0.05). The calculated AUC values for TBK1 and IRF3 in PBMCs, IFN-β in serum and erythrocyte sedimentation rate (ESR) to distinguish between patients with active and stable lesions were 0.732, 0.714, 0.839, and 0.714 respectively. The expression level of TBK1 and IRF3 in PBMCs, and IFN-β in the serum of patients with spinal TB is positively correlated with disease activity. TBK1 has higher specificity and IFN-β in serum has higher sensitivity when used to differentiate between patients with active and stable lesions.

Osteosarcoma (OS), frequently observed in children and adolescents, is one of the most common primary malignant tumors of the bone known to be associated with a high capacity for invasion and metastasis. The incidence of osteosarcoma in children and adolescents is growing annually, although improvements in survival remain limited. With the clinical application of neoadjuvant chemotherapy, chemotherapy combined with limb-preserving surgery has gained momentum as a major intervention. However, certain patients with OS experience treatment failure owing to chemoradiotherapy resistance or metastasis. Nuclear factor E2-related factor 2 (Nrf2), a key antioxidant factor in organisms, plays a crucial role in maintaining cellular physiological homeostasis; however, its overactivation in cancer cells restricts reactive oxygen species production, promotes DNA repair and drug efflux, and ultimately leads to chemoradiotherapy resistance. Recent studies have also identified the functions of Nrf2 beyond its antioxidative function, including the promotion of proliferation, metastasis, and regulation of metabolism. The current review describes the multiple mechanisms of chemoradiotherapy resistance in OS and the substantial role of Nrf2 in the signaling regulatory network to elucidate the function of Nrf2 in promoting OS chemoradiotherapy resistance and formulating relevant therapeutic strategies.

OBJECTIVE: To evaluate the efficacy and safety of Shengmai Yin ((sic), SMY) on visual analogue scale (VAS) for cardiopulmonary symptoms in coronavirus disease 2019 (COVID-19) convalescent patients. METHODS: In this randomized, double blind and multicenter controlled trial, a total of 200 COVID-19 convalescent patients who with cardiopulmonary symptoms were enrolled from three medical centers in Hubei, China. These patients were randomized divided into trial group and the control group, 100 patients in each one, SMY and its placebo were applied to respectively, for two weeks. VAS of clinical symptoms included shortness of breath, hidrosis, chest distress, palpitation, and dry cough was performed at 0, 1, 2 weeks. Decrease in VAS of 30% or more was defined as effective, and a reduction in VAS of 0 was defined as curative. RESULTS: A total of 192 completed the study. The VAS of TCM symptoms showed there was no difference in baseline between the two groups. The VAS in both groups was down-regulated, and there was no significant difference in VAS and cure rates at the first and second week between the two groups. There was no significant difference in breath, hidrosis, palpitation, and dry cough between the two groups but SMY treatment for two weeks has remarkable therapeutic effects in chest distress than placebo. CONCLUSIONS: SMY could effectively ameliorate the symptoms of chest distress, and improve the quality of life of the COVID-19 convalescent patients. (c) 2023 JTCM. All rights reserved.

Introduction:As a mediator of inflammation resolution, lipoxin A4 (LXA4) mainly plays an anti-inflammatory role and promotes inflammation resolution. LXA4 plays an inhibiting inflammatory role in a variety of diseases, tissues and cells, including keratinocytes. Psoriasis is a chronic inflammatory skin disease mediated by dysregulation of inflammation of immune cells and keratinocytes. However, the expression and role of LXA4 in psoriasis-like mouse models are still unclear.Methods:Imiquimod (IMQ) topical treatment of dorsal skin induces psoriasis-like dermatitis in BALB/c mice, pretreated intraperitoneally with or without LXA4 prior to IMQ application. Severity of dorsal lesions is assessed by using a modified human scoring system and histopathology. The concentration of LXA4 and the expression of ALOX15 (a key gene in LXA4 metabolic synthesis) in lesional skins were detected by ELISA and Western blot. Quantitative PCR and ELISA were conducted to detect the mRNA and secretion levels of inflammatory cytokines. The proportion of IL-17A-producing γδT cells in skin and skin draining cervical lymph nodes and helper (Th) 17 cells in spleens was evaluated by flow cytometry. Western blotting was used to analyze the expressions of p-STAT3 and TRAF6.Results:The concentration of LXA4 and the expression of ALOX15 were decreased in IMQ-induced lesional skin. LXA4 significantly relieved psoriasis-like lesions in IMQ-induced mouse models. Furthermore, LXA4 decreased IMQ-induced systemic inflammation, including reduced the proportion of IL-17A-producing gdT cells in skin and skin draining cervical lymph nodes and Th17 cells in spleens, the secretion and expression of CCL20, IL-17A, IL-1β, and TNF-α in skin and serum. LXA4 markedly inhibited IMQ-induced expression of TRAF6 and p-STAT3.Conclusion:LXA4 significantly ameliorates IMQ-induced psoriasis-like inflammation, and LXA4 can be used as a target for psoriasis treatment.

OBJECTIVE: To evaluate the effectiveness and safety of Jinshuibao capsules (kzI M theta Sc ), a Traditional Chinese Medicine (TCM), in the treatment of residual cardiopulmonary symptoms in convalescent corona virus disease 2019 (COVID-19) patients.METHODS: A total of 200 participants with COVID-19 in convalescence phase were randomly assigned into two groups at a 1:1 ratio in this multicenter randomized, double-blind, placebo-controlled trial. One group received Jinshuibao capsules, and the other received placebo. The patients were followed up at one and two weeks of treatment. Five symptoms (dry cough, shortness of breath, sweating, chest tightness and palpitation) improvement rates and full recovery rates were compared.RESULTS: All baseline characteristics were comparable between the two groups. After two weeks of treatment, symptom improvement rates for dry cough (74.00% vs 50.00%, P = 0.015), shortness of breath (78.95% vs 46.15%, P < 0.001), sweating (80.00% vs 57.75%, P = 0.004), chest tightness (87.06% vs 60.47%, P < 0.001) and palpitation (82.50% vs 64.56%, P = 0.010) were significantly higher in the Jinshuibao group compared with the control group. Meanwhile, Jinshuibao capsules treatment also displayed more satisfactory full recovery rates of all five symptoms (dry cough 58.00% vs 19.57%, shortness of breath 18.95% vs 7.69%, sweating 36.00% vs 19.72%, chest tightness 32.94% vs 13.95%, and palpitation 48.75% vs 29.11%) in participants with COVID-19 in convalescence phase compared with the control group (P < 0.05). No severe adverse events were reported in either group.CONCLUSIONS: Jinshuibao capsules have the potential to improve residual cardiopulmonary symptoms in convalescent COVID-19 patients, with few adverse events.(c) 2023 JTCM. All rights reserved.

Objective:To explore the effect of the deletion of the icl1 gene and icl2 gene on the growth rate of Mycobacterium tuberculosis (Mtb) and the specific regulatory mechanism involved.Methods:H37Rv was purchased from the Tuberculosis Prevention and Control Institute, and H37Rv was grown in Middlebrook 7H9 broth. Macrophages THP-1 cells were purchased by our researchers from the Cell Bank of the Chinese Academy of Sciences, which were maintained in Roswell Park Memorial Institute (RPMI) 1640 medium supplemented with 10% fetal bovine serum (FBS), at 37°C and 5% CO2. The experiment was divided into 3 groups: the control group (H37Rv infected with THP-1 cells), the icl1/2 deletion group (H37Rv infected with icl1/2 deleted THP-1 cells) and the icl1/2 complementation group (H37Rv infected with icl1/2 deletion, icl1/2 complementary THP-1 cells). Absorbance was measured with a microplate spectrophotometer and the bacterial growth rate was calculated. The colony-forming units (CFU) obtained from the dilution was used to calculate the total number of CFU per milliliter and the percentage of survival of mycobacteria. The protein levels of isocitrate lyase 1 (ICL1), ICL2, p-mTOR and p-Akt were analyzed by Western blot. The CD4+ level was analyzed by flow cytometry. The mRNA expression levels of CCL20, CXCL2, CXCL8, interferon gamma (IFN-γ), interleukin (IL)-17 and IL-22 were analyzed using the quantitative reverse transcription polymerase chain reaction (RT-qPCR) method. Stably transformed monomeric red fluorescent protein (mRFP)-green fluorescent protein (GFP)-LC3 reporter THP-1 cells were used to monitor the aggregation of LC3B in autophagosomes and autophagolysosomes.Results:The Mtb growth rate and CFU of the icl1/2 deletion group were decreased in comparison with the control group (P < .05). When compared with the icl1/2 deletion group, however, the Mtb growth rate and CFU of the icl1/2 complementation group were associated with increased results (P < .05). The protein levels of ICL1 and ICL2 in the icl1/2 deletion group were significantly decreased compared with the control group (P < .05), which were evidently increased in the icl1/2 complementation group when compared with the icl1/2 deletion group (P < .05). In addition, compared with the control group (25.16 ± 2.18), the level of CD4+ appeared to be increased in the icl1/2 deletion group (62.37 ± 5.46) (P < .05), while it was decreased in the icl1/2 complementation group compared with the icl1/2 deletion group (28.33 ± 1.32) (P < .05). The expression levels of chemokine (C-C motif) ligand 20 (CCL20), chemokine (C-X-C motif) ligand 2 (CXCL2), chemokine (C-X-C motif) ligand 8 (CXCL8), IL-17, IFN-γ, and IL-22 mRNA were increased in the icl1/2 deletion group compared with the control group (P < .05), which were significantly decreased in the icl1/2 complementary group compared with the icl1/2 deletion group (P < .05). A comparison between the control group and the icl1/2 deletion group showed that the latter increased the formation of autophagosomes and autophagolysosomes in H37Rv-infected cells (P < .05). However, compared with the icl1/2 deletion group, the icl1/2 complementation group decreased the formation of autophagosomes and autolysosomes in H37Rv-infected cells (P < .05). Moreover, the expression levels of phosphor-mammalian target of rapamycin (p-mTOR) and p-Akt in the icl1/2 deletion group were significantly reduced compared with the control group (P < .05), and were increased in the icl1/2 complementation group compared with the icl1/2 deletion group (P < .05).Conclusion:Loss of icl1/2 was believed to increase the expression of CD4 and CCL20, CXCL8 as well as CXCL2 in the immune system, which increased autophagy. Furthermore, it exerted potential in inhibiting the growth of intracellular Mtb in macrophages.

EDITORIAL article Front. Oncol., 15 August 2023Sec. Surgical Oncology Volume 13 - 2023 | https://doi.org/10.3389/fonc.2023.1247231

颈椎后纵韧带骨化症是后纵韧带发生病理性异位骨化,缓慢进展的骨化物压迫脊髓、神经根,继而出现一系列神经功能损害的症候群.临床中通过症状体征和影像学检查可明确诊断,其治疗方式的选择依赖于症状的严重性.对于无症状或症状较轻的患者,多采取保守治疗并结合影像学随访;对于出现脊髓或神经病变的患者,则必须采取手术减压治疗.该病的手术入路方式目前主要有前路、后路和前后联合入路3种,不同的手术入路和方式各有其优缺点.颈椎前路椎体骨化物复合体可控前移融合技术是一种治疗颈椎后纵韧带骨化症的新兴术式,经过近几年的推广应用,取得了良好的临床效果.该文结合国内外的临床研究进展,对颈椎前路椎体骨化物复合体可控前移融合技术治疗颈椎后纵韧带骨化症的现状及进展进行综述,为临床工作提供参考.

Dear Editor, Vulvar lichen sclerosus (VLS) is not rare in paediatric dermatology.1 Although histopathology is gold standard, the diagnosis of VLS is primarily based on clinical findings rather than histopathology,2 which is may not always be practical or necessary in children.3 There are no sufficient researches about using noninvasive tools in the diagnosis of VLS,4 only few case report available on dermoscopy Received: 24 April 2022 | Accepted: 22 November 2022

Transient acantholytic dermatosis (TAD, Grover disease) is a benign skin disease with a nonspecific rash that may present as a reddish-brown, dermatomal edematous papule or herpetiform rash with a partially central horny plug. This disease is usually self-limiting and can subside within weeks or months, but it may also have a chronic progression with a trend towards long-term recurrence. The patient is an 80-year-old male who visited the clinic due to recurring erythema and blisters all over his body that had been present for over 2 years. Based on the patient’s course, laboratory tests and histopathological findings were consistent with the diagnosis. The final diagnosis was transient acantholytic dermatosis. The patient has a long course of the disease, a wide range of skin lesions and he has the different subtypes of pathological manifestations. This case and corresponding literature review help us have a clear understanding of Grover’s disease, which has received reference value for the diagnosis and treatment of this disease in clinical work.

Chronic refractory wound (CRW) is one of the most challengeable issues in clinic due to complex pathogenesis, long course of disease and poor prognosis. Experts need to conduct systematic summary for the diagnosis and treatment of CRW due to complex pathogenesis and poor prognosis, and standard guidelines for the diagnosis and treatment of CRW should be created. The Guideline forthe diagnosis and treatment of chronic refractory wounds in orthopedic trauma patients ( version 2023) was created by the expert group organized by the Chinese Association of Orthopedic Surgeons, Chinese Orthopedic Association, Chinese Society of Traumatology, and Trauma Orthopedics and Multiple Traumatology Group of Emergency Resuscitation Committee of Chinese Medical Doctor Association after the clinical problems were chosen based on demand-driven principles and principles of evidence-based medicine. The guideline systematically elaborated CRW from aspects of the epidemiology, diagnosis, treatment, postoperative management, complication prevention and comorbidity management, and rehabilitation and health education, and 9 recommendations were finally proposed to provide a reliable clinical reference for the diagnosis and treatment of CRW.

Abstract Background This study aimed to analyze the clinical efficacy of one-stage anterior debridement of lower cervical tuberculosis using iliac crest bone graft fusion and internal fixation. Materials and methods A retrospective analysis was performed on 48 patients with lower cervical tuberculosis admitted to multiple medical centers from June 2018 to June 2021. Among them, 36 patients had lesions involving two vertebrae and 12 patients had lesions involving more than three vertebrae. All patients were treated with quadruple antituberculosis drugs for more than 2 weeks before the operation, and then treated with one-stage anterior debridement and autogenous iliac bone graft fusion combined with titanium plate internal fixation. After the operation, antituberculosis drugs were continued for 12–18 months. The patients were followed-up to observe the improvement in clinical symptoms, bone graft fusion, Cobb angle, visual analog score (VAS), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), wound healing, and neurological function. Results The patients were followed-up for 13–43 months, with an average of 21.46 ± 1.52 months. The clinical symptoms significantly improved after the operation. The bone graft was completely fused in all patients, and the bone fusion time was 3–6 months, with an average of 4.16 ± 0.47 months. At the last follow-up, the Cobb angle, VAS, ESR, and CRP level were significantly lower than those before surgery (P < 0.05). None of the patients had loosening, detachment, or rupture of the internal fixation, and no recurrence occurred. All surgical incisions healed in one stage without infection or sinus formation. The preoperative Frankel neurological function classification was grade B in 7 cases, grade C in 13, grade D in 18, and grade E in 10. At the last follow-up, 8 cases recovered to grade D and 40 recovered to grade E. Conclusions For patients with lower cervical tuberculosis, based on oral treatment with quadruple antituberculosis drugs, direct decompression through anterior debridement, followed by autologous iliac bone graft fusion combined with internal fixation can completely remove tuberculosis foci, rebuild the stability of the cervical spine, and obtain good clinical efficacy. Level of evidence Level 3.

[目的]介绍带线锚钉"8"字缝合固定髌骨下极骨折的手术技术和初步临床应用效果.[方法] 2017年6月-2019年12月采用上述技术固定髌骨下极骨折38例.行膝前正中切口,暴露骨折端.于近髌骨置入1枚5.0 mm带线锚钉.锚钉旁使用2-0克氏针自髌骨前方分别斜向两侧钻孔至髌骨后方关节面,出针点在骨折断端上方约0.1 mm,使用硬膜外导针将锚钉上两股缝线的单边分别自上述钻孔中引出,锚钉线分别从髌骨下极两侧缝合编织在髌韧带上,自行打结收紧.然后将两股缝线上的另一单边自髌骨一侧锚钉处为起点,连续缝合至同侧髌韧带近端,绕髌韧带缝合至对侧,再缝合至起点处自行收紧打结.[结果] 38例患者均顺利完成手术.骨折愈合时间14～16周,无内固定失效病例,膝关节稳定性良好.术后12个月Bostman髌骨骨折评级标准,优30例,良7例,优良率97.37％.[结论]带线锚钉治疗髌骨下极骨折,修复了伸膝装置,操作简单安全,术后膝关节功能恢复优良,且无需二次手术取出,疗效满意.

目的 探讨单核细胞/高密度脂蛋白胆固醇比值(MHR)与2型糖尿病(T2DM)合并骨质疏松的相关性.方法 选取2019年9月至2021年11月于华中科技大学同济医学院附属武汉市中西医结合医院脊柱外科住院的患者158例,按骨密度及血糖测量结果将其分为骨密度正常组(40例)、骨质疏松组(62例)、T2DM合并骨质疏松组(56例).比较3组患者一般资料、白细胞、单核细胞、淋巴细胞、中性粒细胞、C反应蛋白(CRP)、红细胞沉降率、血清总蛋白(TP)、电解质、总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、肌酐、尿酸、25羟基维生素D[25(OH)D]、骨密度、骨转换标志物等指标,计算MHR值.结果 T2DM合并骨质疏松组的单核细胞、血糖、MHR较骨密度正常组、骨质疏松组明显升高,年龄、CRP、碱性磷酸酶(ALP)、中性粒细胞、甲状旁腺素(PTH)较骨密度正常组明显升高;T2DM合并骨质疏松组的25(OH)D较骨密度正常组、骨质疏松组明显下降,淋巴细胞、BMI、骨钙素较骨密度正常组明显下降,差异均有统计学意义(P＜0.05).多因素logistic回归分析结果显示,MHR、ALP升高及25(OH)D、BMI、骨钙素降低是T2DM合并骨质疏松的独立危险因素(P＜0.05,P＜0.01).ROC曲线显示,对T2DM合并骨质疏松的诊断,MHR的ROC曲线下面积(AUC)为0.771(95％CI:0.670～0.871),最佳截断值为0.347,灵敏度和特异度分别是0.893、0.625,其AUC仅次于25(OH)D.结论 外周血MHR对T2DM合并骨质疏松的诊断有较高参考意义.

Spinal tuberculosis, as one of the most serious forms of extrapulmonary tuberculosis, is one of the primary causes of spinal deformity and paralysis in developing countries. It immensely affects people's quality of life with high incidences of deformity and disability. The onset of spinal tuberculosis is related to many factors such as gender, age, environment, habits and hereditary factor. As a genetic factor, gene polymorphism plays an important role in the occurrence and development of tuberculosis. This article reviews the research progress of the susceptibility of spinal tuberculosis and its related gene polymorphisms, in order to provide reference for early prevention and treatment of spinal tuberculosis.