Although the precise regulatory mechanisms underlying diabetic foot (DF) remain incompletely understood, increasing evidence suggests that mitochondrial metabolism may be involved in DF progression. The study aimed to identify and validate candidate biomarkers associated with mitochondrial metabolism in DF. Transcriptome sequencing data from 12 DF and 18 control tissue samples were analyzed together with 1,234 mitochondrial metabolism-related genes (MMRGs), which were obtained from MSigDB by integrating curated gene sets directly associated with mitochondrial metabolic processes. First, overlapping genes between MMRGs and DEGs between DF and control samples were used as candidate genes. Then, candidate biomarkers were identified using PPI network construction, two machine learning algorithms, and ROC curve analysis. Next, based on the candidate biomarkers, functional enrichment, immune infiltration, regulatory network, compound prediction, as well as molecular docking analyses were undertaken. Finally, to explore the expression of candidate biomarkers in clinical samples, the reverse transcription quantitative polymerase chain reaction (RT-qPCR) was performed. GPAT3 and PTGS2 were identified as mitochondrial metabolism-associated candidate biomarkers for DF, with area under the curve values of 0.963 and 0.958, respectively. Functional enrichment analysis showed that multiple pathways were significantly enriched by both GPAT3 and PTGS2, such as ribosome and Leishmania infection. GPAT3 had the strongest positive and negative correlations with neutrophils and resting CD4 memory T cells, respectively. In contrast, PTGS2 exhibited the strongest negative connection with M1 macrophages and the strongest positive correlation with neutrophils. Subsequently, multiple transcription factors (TFs) were found to co-target GPAT3 and PTGS2, such as BRD4 and NR0B1. Moreover, compound prediction analysis identified several compounds potentially associated with these biomarkers, such as lipopolysaccharides and cisplatin. The binding free energy between PTGS2 and tetradecanoylphorbol acetate was − 8.2 kcal/mol, while the binding free energy between GPAT3 and cyclosporine was − 10.4 kcal/mol, according to molecular docking data. Finally, the expression levels of GPAT3 and PTGS2 were significantly different in clinical samples. GPAT3 and PTGS2 were identified as candidate biomarkers associated with mitochondrial metabolism in DF, providing molecular clues for further investigation of DF pathogenesis and potential intervention strategies.

Peripheral nerve injury, a prevalent clinical issue, typically contributes to extended recovery times and is often associated with muscle atrophy caused by denervation.Denervation in atrophic muscles presents a significant challenge for clinical treatment. Currently, no effective treatment exists to postpone skeletal muscle atrophy resulting from denervation. Mitochondrial autophagy plays a crucial role in counteracting damage related to oxidative stress and inflammation, with many studies suggesting its involvement in alleviating the advancement of skeletal muscle atrophy due to denervation. Mitochondrial transcription factor A (TFAM) is essential for the regulation of mitochondrial autophagy; nevertheless, experimental evidence supporting the therapeutic role of TFAM in muscle atrophy resulting from denervation is lacking. This research assessed how TFAM impacts muscle atrophy resulting from denervation using both cellular and animal models, and investigated the consequences of TFAM inhibition and overexpression. The findings demonstrated that the expression of TFAM can significantly inhibit reactive oxygen species (ROS) generation, modulate the morphology and functionality of mitochondria, enhance mitochondrial autophagy, and postpone skeletal muscle atrophy induced by denervation. Additionally, this research explored the mechanisms through which TFAM exerts its effects, revealing that the attenuation of skeletal muscle atrophy by TFAM may be associated with the cyclic GMP-AMP synthase-stimulator of interferon genes signaling pathway. These findings provided significant insights for the clinical treatment of muscle atrophy due to denervation.

Deep vein thrombosis (DVT) is a serious condition that can lead to complications such as pulmonary embolism (PE) and post-thrombotic syndrome (PTS). This study aimed to compare the Straub-Rotarex thrombectomy system and catheter-directed thrombolytic therapy (CDT) for lower limb DVT. This retrospective study analyzed patients with DVT treated at The Second Hospital of Shanxi Medical University between August 2017 and October 2021. The patients were grouped according to the CDT group or the Straub-Rotarex thrombectomy system (Straub-Rotarex group). This study included 100 patients, with 50 in the Straub-Rotarex group (27 males, mean age of 61.61 ± 3.35 years) and 50 in the CDT group (28 males, mean age 61.12 ± 3.12 years). The Straub-Rotarex thrombectomy group achieved a higher total effective rate (96.00

BACKGROUND:Current guidelines recommend retrievable inferior vena cava filters (RIVCFs) placement prior to endovascular intervention (EI) for deep vein thrombosis (DVT), yet the impact of EI on RIVCF-related thrombosis/trapped embolus (T/TE) remains controversial. METHODS:In this prospective registry-based study (ChiCTR1800014252), 2,773 patients undergoing RIVCF placement across 103 Chinese centers (2018-2019) were stratified into EI (n = 1,472) and no-EI (n = 1,301) groups. Propensity score matching (1:1) balanced 23 baseline variables (e.g., DVT acuity and anticoagulation). The primary end point was RIVCF T/TE (defined as inferior vena cava obstruction or thrombus >5 cm above the filter), validated by core-lab adjudicated imaging (computed tomography/angiography). All treating physicians from the 103 participating centers received unified standardized training on the clinical selection criteria for EI and non-EI therapy prior to the study initiation, ensuring consistent intercenter decision-making. The selection of therapeutic modalities was further based on individualized clinical characteristics, including the anatomical location of DVT, thrombus burden, presence of procedural contraindications, and patient's informed consent after full risk-benefit explanation. RESULTS:After matching (n = 1,007 per group), EI was associated with a 46% lower risk of RIVCF T/TE (8.9% vs. 14.0%, P < 0.001; odds ratio = 0.54, 95% confidence interval: 0.41-0.71). Symptomatic pulmonary embolism rates were comparable (1.2% vs. 2.8%, P = 0.07). No brand-specific differences in T/TE incidence were observed (P = 0.32). CONCLUSION:This study challenges the necessity of routine RIVCF placement before EI, demonstrating that EI itself reduces thrombosis risk. These findings advocate for selective filter use, potentially sparing patients from device-related complications.

The Finkel-Biskis-Jinkins Osteosarcoma (c-Fos; encoded by FOS ) plays an important role in several cardiovascular diseases, including atherosclerosis and stroke. However, the relationship between FOS and venous thromboembolism (VTE) remains unknown. We identified differentially expressed genes in Gene Expression Omnibus dataset, GSE48000, comprising VTE patients and healthy individuals, and analysed them using CIBERSORT and weighted co-expression network analysis (WGCNA). FOS and CD46 expressions were significantly downregulated (FOS p  = 2.26E-05, CD64 p  = 8.83E-05) and strongly linked to neutrophil activity in VTE. We used GSE19151 and performed PCR to confirm that FOS and CD46 had diagnostic potential for VTE; however, only FOS showed differential expression by PCR and ELISA in whole blood samples. Moreover, we found that hsa-miR-144 which regulates FOS expression was significantly upregulated in VTE. Furthermore, FOS expression was significantly downregulated in neutrophils of VTE patients ( p  = 0.03). RNA sequencing performed on whole blood samples of VTE patients showed that FOS exerted its effects in VTE via the leptin-mediated adipokine signalling pathway. Our results suggest that FOS and related genes or proteins can outperform traditional clinical markers and may be used as diagnostic biomarkers for VTE.

BackgroundPrevious research has hinted at a crucial link between gut microbiota and arterial embolism and thrombosis, yet the causal relationship remains enigmatic. To gain a deeper understanding, we aimed to comprehensively explore the causal relationship and elucidate the impact of the gut microbiota on the risk through a two-sample Mendelian randomization (MR) study.MethodsGenetic instrumental variables for gut microbiota were identified from a genome-wide association study (GWAS) of 18,340 participants. Summary statistics for IBS were drawn from a GWAS including 1,076 cases and 381,997 controls. We used the inverse-variance weighted (IVW) method as the primary analysis. To test the robustness of our results, we further performed the weighted median method, MR-Egger regression, and MR pleiotropy residual sum and outlier test.ResultsWe identified three bacterial traits that were associated with the risk of arterial embolism and thrombosis: odds ratio (OR): 1.58, 95% confidence interval (CI): 1.08–2.31, p = 0.017 for genus Catenibacterium; OR: 0.64, 95% CI: 0.42–0.96, p = 0.031 for genus Dialister; and OR: 2.08, 95% CI: 1.25–3.47, p = 0.005 for genus Odoribacter. The results of sensitivity analyses for these bacterial traits were consistent (P<0.05).ConclusionOur systematic analyses provided evidence to support a potential causal relationship between several gut microbiota taxa and the risk of arterial embolism and thrombosis. More studies are required to show how the gut microbiota affects the development of arterial embolism and thrombosis.

Objective:This study aimed to summarize the causes, staging, and treatment of aseptic necrosis of the lunate bone.Methods:The keywords “月骨” “缺血坏死” “临床分期” “治疗” “lunate bone” “avascular necrosis” “clinical stages” and “treatment” were searched in Chinese and English databases such as CNKI, Wanfang, PubMed, and SinoMed. A total of 1 004 articles on aseptic necrosis of the lunate bone published before January 2023 were retrieved. After excluding articles with repeated retrieval, low content correlation, an inability to obtain full text, low quality, and poor innovation, 61 articles were finally included to summarize and analyze the causes, clinical stages, and treatment methods of aseptic necrosis of the lunate bone.Results:Aseptic necrosis of the lunate bone is a common osteonecrosis, which can be induced by anatomical and non-anatomical factors. The anatomical factors include lunate blood supply, lunate bone morphology, lunate bone biomechanics, radial anatomical parameters, and ulna variation. The non-anatomical factors include fracture and genetic factors. The Lichtman staging system is the widely used staging system for aseptic necrosis of the lunate bone. The Schmitt MRI staging system and Bain arthroscopic staging system are also used for the classification of the disease. The new Lichtman classification can guide orthopedic surgeons to treat patients with aseptic necrosis of the lunate bone. Conservative treatment is the main treatment for children and elderly patients with aseptic necrosis of the lunate bone. Adult patients should be treated conservatively for 3 to 6 months before surgery. In the selection of surgical methods, lunate decompression should be considered for the lunate with an intact articular surface and good blood supply prognosis. If there is a partial articular surface injury of the lunate bone, then lunate bone reconstruction should be performed. If the lunate has collapsed and shown no potential for revascularization, then the lunate should be resected. In addition, limited wrist arthrodesis should be performed if the radiolunate articular surface or middle carpal articular surface is injured. If the radioscaphoid joint is also injured, then total wrist arthrodesis should be performed.Conclusion:The occurrence of aseptic necrosis of the lunate bone results from the interaction of various risk factors. Therefore, accurately determining the stage of the disease is the key to its treatment. The new Lichtman classification follows the principle of individualized treatment, which can be used to accurately stage the disease. The treatment of aseptic necrosis of the lunate bone can be divided into conservative treatment and surgical treatment, which should be determined in accordance with the stage of the patient and the degree of disease progression.

舟状骨骨折是最常见的腕骨骨折.舟状骨体积小且形状不规则,加之其血供匮乏和几乎无骨膜覆盖,所以治疗比较棘手.A型或其他稳定性舟状骨骨折的治疗存在很大争议.不同手术方式各有利弊,通常由手术医生根据骨折部位及移位程度,结合治疗经验决定手术方案.该文就近年来舟状骨骨折治疗方法进行综述.

腱鞘巨细胞瘤(GCTTS)是一类起源于关节、滑囊和腱鞘滑膜的增生性炎症性疾病,根据其生长方式分为局限型和弥漫型,通常表现为独立、无痛、生长缓慢的肿块.GCTTS首选治疗方法是手术切除,术后有较高的复发率.目前对GCTTS病因、治疗及术后复发危险因素仍存在争议.该文就GCTTS研究进展进行综述.

腓总神经卡压综合征是下肢最常见的卡压性周围神经疾病,病因复杂.该病治疗方法尚不一致,发病早期及症状较轻时可先行保守治疗,对于保守治疗无效、病情较重或赘生物压迫者需手术治疗,目前常用的手术方法有腓总神经松解、神经端端吻合、神经移植或移位、胫后肌腱移位和踝关节融合术等,而手术时机以及采取何种术式仍有争议.该文就腓总神经卡压综合征诊疗进展进行综述.

目的:探讨掌板前移术治疗陈旧性近指间关节骨折脱位的疗效。方法:自2005年1月至2020年12月我们对8例陈旧性近指间关节骨折脱位患者，采用掌板前移克氏针内固定术治疗。结果:术后所有患者均获得随访，时间为3~23个月，平均14个月。所有患者均无切口感染、克氏针松动。影像学检查发现7例近指间关节无半脱位，1例在术后3个月复查时近指间关节出现半脱位。末次随访时，患手平均握力为健侧的92%。手功能恢复按手指关节总活动度(total active motion，TAM)评定标准评价：优5例，良3例。结论:掌板前移克氏针内固定术可以重建陈旧性近指间关节骨折脱位的稳定性，术后早期功能锻炼可以较大程度恢复患指屈伸功能，是治疗陈旧性近指间关节骨折脱位的有效方法之一。

肘管综合征是常见的周围神经卡压性疾病,发病率仅次于腕管综合征,病因复杂,治疗方法尚不统一.肘管综合征早期可试行保守治疗,保守治疗无效或中重度患者需手术干预,手术方法包括尺神经原位松解术、肱骨内上髁切除术、尺神经前置术及微创治疗等.目前最佳术式以及术式选择标准仍存在争议.该文就相关应用解剖、发病机制、诊断、分型及治疗研究进展作一综述.

内生软骨瘤是手部最常见的骨肿瘤,其症状主要为病变部位的肿胀、疼痛和畸形.内生软骨瘤与软骨肉瘤的鉴别诊断较困难.内生软骨瘤的治疗方法可分为保守治疗和手术治疗.目前,对于手术辅助物使用、术后空洞的处理以及合并病理性骨折患者手术时机选择仍存在争议.该文就手部内生软骨瘤的治疗进展进行综述.

回顾性分析山西医科大学第二医院血管外科收治的合并对侧狭窄的30例颈动脉狭窄患者及合并对侧闭塞的24例颈动脉狭窄患者的临床资料。行颈动脉支架植入30例，颈动脉内膜剥脱24例。所有手术均成功施行。对侧闭塞组1例患者因消化道出血1个月后死亡。术中短暂性脑缺血发作（TIA）对侧闭塞组9例，对侧狭窄组1例（ P=0.03）。6例对侧闭塞患者出现术后并发症，包括术后TIA、脑卒中、心肌梗死、低血压、颈动脉再狭窄和高灌注综合征。笔者认为合并对侧闭塞的颈动脉狭窄患者由于侧支循环代偿较差和血流动力学不稳定，其并发症发生率较高。围手术期应严格监测患者状态，术后应进行定期随访。

Objective:To study the role and mechanism of miRNA-222 in denervated skeletal muscle atrophy.Methods:Forty adult male SD rats were randomly divided into four groups: sham operated group, denervated skeletal muscle atrophy group, denervated skeletal muscle atrophy+ miRNA-222 injection group and denervated skeletal muscle atrophy+ anti-miRNA-222 injection group. The animal model of denervated skeletal muscle atrophy in the right lower limb was established in SD rats. HE staining, detection of gastrocnemius muscle wet mass ratio and diameter of myocytes were performed 4 weeks after operation. The expression level of miRNA-222 was detected by real-time quantitative PCR, and the mRNA and protein expression of MyOD and Rbm24 were detected by real-time quantitative PCR and Western blot.Results:Four weeks after operation, the expression of miRNA-222 in the denervated skeletal muscle atrophy group was significantly increased. Compared with the sham operation group, the denervated skeletal muscle atrophy group appeared obvious atrophy, exogenous injection of miRNA-222 could further aggravate the atrophy, exogenous injection of anti-miRNA-222 could effectively reduce the atrophy. Compared with sham operation group, the MyOD and Rbm24 mRNA in denervated skeletal muscle atrophy group decreased significantly, and the MyOD and Rbm24 mRNA further decreased after exogenous injection of miRNA-222. On the contrary, the MyOD and Rbm24 mRNA after exogenous injection of anti-miRNA-222 was lower than that in sham operation group, but the MyOD and Rbm24 mRNA were significantly higher than those in the denervated skeletal muscle atrophy group and miRNA-222 injection group. The result of protein detection was consistent with that of mRNA.Conclusion:Exogenous miRNA-222 can inhibit the mRNA and protein expression level of MyOD and Rbm24, and aggravate the atrophy degree of denervated skeletal muscle; on the contrary, exogenous anti-miRNA-222 can effectively resist the effect of miRNA-222, and reduce the atrophy degree of denervated skeletal muscle.

肘管综合征是常见的上肢周围神经卡压性疾病,多由尺神经在肘部受压所致,常表现为尺神经所支配区域的感觉障碍(疼痛、麻木、两点辨别觉减退)、所支配肌肉功能减退(肌肉萎缩、运动能力丧失).目前对于中重度及保守治疗无效的轻度肘管综合征,均建议手术治疗.主要目的是解除尺神经压迫,为尺神经的修复提供良好的环境,以期待感觉及运动功能的改善.然而,无论哪种手术方式,均有失败的可能.据文献报道[1],手术失败率为10％～25％.本文就肘管综合征术后翻修的原因及治疗进行综述.

Homeobox A9 (HOXA9), the expression of which is promoted by mixed lineage leukemia 1 (MLL1) and WD-40 repeat protein 5 (WDR5), is a homeodomain-containing transcription factor that plays an essential role in regulating stem cell activity. HOXA9 has been found to inhibit skeletal muscle regeneration and delay recovery after muscle wounding in aged mice, but little is known about its role in denervated/reinnervated muscles. We performed detailed time-dependent expression analyses of HOXA9 and its promoters, MLL1 and WDR5, in rat gastrocnemius muscles after the following three types of sciatic nerve surgeries: nerve transection (denervation), end-to-end repair (repair), and sham operation (sham). Then, the specific mechanisms of HOXA9 were detected in vitro by transfecting primary satellite cells with empty pIRES2-DsRed2, pIRES2-DsRed2-HOXA9, empty pPLK/GFP-Puro, and pPLK/GFP-Puro-HOXA9 small hairpin RNA (shRNA) plasmids. We found, for the first time, that HOXA9 protein expression simultaneously increased with increasing denervated muscle atrophy severity and that upregulated MLL1 and WDR5 expression was partly associated with denervation. Indeed, in vitro experiments revealed that HOXA9 inhibited myogenic differentiation, affected the best known atrophic signaling pathways, and promoted apoptosis but did not eliminate the differentiation potential of primary satellite cells. HOXA9 may promote denervated muscle atrophy by regulating the activity of satellite cells.

周围神经内囊肿是一种良性的、非肿瘤性质的黏液囊肿[1],生长于周围神经外膜内,由厚厚的黏液积聚而成,包裹在致密的纤维囊内.法国解剖学家和外科医生Beauchêne fils于1810年首次描述了一位肘部尺神经内囊肿的病人,他称之为“肘部浆液囊肿”[2].周围神经内囊肿可以发生在全身各处,如颈、肩、肘、腕、髋、膝、踝,直至掌指处[3-4],最常见于膝关节,约占68％,主要累及腓总神经,其次为肘关节,约占10％,主要累及尺神经[5].近年来,上肢神经内囊肿病例报道越来越多[6-11],这些囊肿会压迫邻近神经束,引起周围神经压迫性病变,导致受神经支配的肢体发生疼痛、无力、肌肉失神经和萎缩[12].神经内囊肿多见于中老年人群,男性多于女性,在青少年、儿童中很少见[13].

掌骨骨折后常因短缩、旋转、成角等因素影响手部正常外观及功能,常需行切开复位内固定治疗.克氏针、金属螺钉及钢板等是掌骨骨折治疗的常用内固定材料,但均存在骨折愈合后需二次手术取出的缺点.可吸收材料经逐代发展,多种性能得以优化,能以针棒、钉板等形式用于掌骨骨折治疗,随后在体内经代谢可完全降解,避免了二次手术内植物取出,是金属材料的替代产品.可吸收针棒系统(垂直骨折线固定技术、髓内固定技术)和可吸收钉板固定技术是运用于掌骨骨折治疗的主要技术,可提供足够的稳定性以确保骨折愈合.