Effect of Yogurt Intake Frequency on Blood Pressure: A Cross-Sectional Study.

Yogurt consumption is a significant factor in reducing the risk of hypertension and preventing cardiovascular diseases. Although increasing evidence has emerged regarding the potential benefits of probiotics in hypertension, there is a lack of large, cross-sectional studies assessing the association between yogurt intake and blood pressure parameters. We aimed to evaluate the association between yogurt intake frequency and blood pressure. A cross-sectional study was designed using data from the National Health and Nutrition Examination Survey from 2003 to 2004 and 2005 to 2006. We included 3, 068 adults with blood pressure data and yogurt intake data. Multivariate regression analyses revealed significant inverse associations between yogurt and systolic blood pressure (P < 0.05), diastolic blood pressure (P < 0.05), and mean arterial pressure (P < 0.05) in nonhypertensive participants (n = 1 822) but not in hypertensive participants (n = 1 246). Furthermore, a high frequency of yogurt intake prevented hypertension; however, no additional antihypertensive effects were observed in patients already diagnosed with hypertension.

Insights into the oral microbiota in human systemic cancers.

The oral cavity stands as one of the pivotal interfaces facilitating the intricate interaction between the human body and the external environment. The impact of diverse oral microorganisms on the emergence and progression of various systemic cancers, typified by oral cancer, has garnered increasing attention. The potential pathogenicity of oral bacteria, notably the anaerobic Porphyromonas gingivalis and Fusobacterium nucleatum, has been extensively studied and exhibits obvious correlation with different carcinoma types. Furthermore, oral fungi and viruses are closely linked to oropharyngeal carcinoma. Multiple potential mechanisms of oral microbiota-induced carcinogenesis have been investigated, including heightened inflammatory responses, suppression of the host immune system, influence on the tumor microenvironment, anti-apoptotic activity, and promotion of malignant transformation. The disturbance of microbial equilibrium and the migration of oral microbiota play a pivotal role in facilitating oncogenic functions. This review aims to comprehensively outline the pathogenic mechanisms by which oral microbiota participate in carcinogenesis. Additionally, this review delves into their potential applications in cancer prevention, screening, and treatment. It proves to be a valuable resource for researchers investigating the intricate connection between oral microbiota and systemic cancers.

Allergens induce upregulated IL-18 and IL-18Rα expression in blood Th2 and Th17 cells of patients with allergic asthma.

Allergic asthma (AA) is closely associated with the polarization of T helper (Th)2 and Th17 cells. Interleukin (IL)-18 acts as an inducer of Th2 and Th17 cell responses. However, expressions of IL-18 and IL-18 receptor alpha (IL-18Rα) in blood Th2 and Th17 cells of patients with AA remain unclear. We therefore investigated their expressions in Th2 and Th17 cells using flow cytometric analysis, qPCR and murine AA model. We observed increased proportions of Th2, Th17, IL-18+, IL-18+ Th2 and IL-18+ Th17 cells in blood CD4+ T cells of patients with AA. Additionally, house dust mite seemed to upregulate further IL-18 expression in Th2 and Th17, and upregulate IL-18Rα expression in CD4+ T, Th2 and Th17 cells of AA patients. It was also found that the plasma levels of IL-4, IL-17A and IL-18 in AA patients were elevated, and they were correlated between each other. In OVA-induced asthma mouse (AM), we observed that the percentages of blood CD4+ T, Th2 and Th17 cells were increased. Moreover, OVA-induced AM expressed higher level of IL-18Rα in blood Th2 cells, which was downregulated by IL-18. Increased IL-18Rα expression was also observed in blood Th2 cells of OVA-induced FcεRIα-/-mice. Collectively, our findings suggest the involvement of Th2 cells in AA by expressing excessive IL-18 and IL-18Rα in response to allergen, and that IL-18 and IL-18Rα expressing Th2 cells are likely to be the potential targets for AA therapy.

A rational designed multi-epitope vaccine elicited robust protective efficacy against Klebsiella pneumoniae lung infection.

BACKGROUND: The emergence of drug-resistant strains of Klebsiella pneumoniae (K. pneumoniae) has become a significant challenge in the field of infectious diseases, posing an urgent need for the development of highly protective vaccines against this pathogen. METHODS AND RESULTS: In this study, we identified three immunogenic extracellular loops based on the structure of five candidate antigens using sera from K. pneumoniae infected mice. The sequences of these loops were linked to the C-terminal of an alpha-hemolysin mutant (mHla) from Staphylococcus aureus to generate a heptamer, termed mHla-EpiVac. In vivo studies confirmed that fusion with mHla significantly augmented the immunogenicity of EpiVac, and it elicited both humoral and cellular immune responses in mice, which could be further enhanced by formulation with aluminum adjuvant. Furthermore, immunization with mHla-EpiVac demonstrated enhanced protective efficacy against K. pneumoniae channeling compared to EpiVac alone, resulting in reduced bacterial burden, secretion of inflammatory factors, histopathology and lung injury. Moreover, mHla fusion facilitated antigen uptake by mouse bone marrow-derived cells (BMDCs) and provided sustained activation of these cells. CONCLUSIONS: These findings suggest that mHla-EpiVac is a promising vaccine candidate against K. pneumoniae, and further validate the potential of mHla as a versatile carrier protein and adjuvant for antigen design.

Efficient phosphate removal by Mg-La binary layered double hydroxides: synthesis optimization, adsorption performance, and inner mechanism.

Layered double hydroxides (LDH) hold great promise as phosphate adsorbents; however, the conventional binary LDH exhibits low adsorption rate and adsorption capacity. In this study, Mg and La were chosen as binary metals in the synthesis of Mg-La LDH to enhance phosphate efficient adsorption. Different molar ratios of Mg to La (2:1, 3:1, and 4:1) were investigated to further enhance P adsorption. The best performing Mg-La LDH, with Mg to La ratio is 4:1 (LDH-4), presented a larger adsorption capacity and faster adsorption rate than other Mg-La LDH. The maximum adsorption capacity (87.23 mg/g) and the rapid adsorption rate in the initial 25 min of LDH-4 (70 mg/(g·h)) were at least 1.6 times and 1.8 times higher than the others. The kinetics, isotherms, the effect of initial pH and co-existing anions, and the adsorption-desorption cycle experiment were studied. The batch experiment results proved that the chemisorption progress occurred on the single-layered LDH surface and the optimized LDH exhibited strong anti-interference capability. Furthermore, the structural characteristics and adsorption mechanism were further investigated by SEM, BET, FTIR, XRD, and XPS. The characterization results showed that the different metal ratios could lead to changes in the metal hydroxide layer and the main ions inside. At lower Mg/La ratios, distortion occurred in the hydroxide layer, resulting in lower crystallinity and lower performance. The characterization results also proved that the main mechanisms of phosphate adsorption are electrostatic adsorption, ion exchange, and inner-sphere complexation. The results emphasized that the Mg-La LDH was efficient in phosphate removal and could be successfully used for this purpose.

Targeted Drug Delivery to ACE2+ Cells Using Engineered Extracellular Vesicles: A Potential Therapeutic Approach for COVID-19.

BACKGROUND: Extracellular vesicles (EVs) are emerging as potential drug carriers in the fight against COVID-19. This study investigates the ability of EVs as drug carriers to target SARS-CoV-2-infected cells. METHODS: EVs were modified using Xstamp technology to carry the virus's RBD, enhancing targeting ability to hACE2+ cells and improving drug delivery efficiency. Characterization confirmed EVs' suitability as drug carriers. For in vitro tests, A549, Caco-2, and 4T1 cells were used to assess the targeting specificity of EVRs (EVs with membrane-surface enriched RBD). Moreover, we utilized an ex vivo lung tissue model overexpressing hACE2 as an ex vivo model to confirm the targeting capability of EVRs toward lung tissue. The study also evaluated drug loading efficiency and assessed the potential of the anti-inflammatory activity on A549 lung cancer cells exposed to lipopolysaccharide. Results demonstrate the successful construction of RBD-fused EVRs on the membrane-surface. In both in vitro and ex vivo models, EVRs significantly enhance their targeting ability towards hACE2+ cells, rendering them a safe and efficient drug carrier. Furthermore, ultrasound loading efficiently incorporates IL-10 into EVRs, establishing an effective drug delivery system that ameliorates the pro-inflammatory response induced by LPS-stimulated A549 cells. CONCLUSION: These findings indicate promising opportunities for engineered EVs as a novel nanomedicine carrier, offering valuable insights for therapeutic strategies against COVID-19 and other diseases.

Trends in Sexual Harassment Prevalence and Recognition During Intern Year.

This cohort study uses Internal Health Study and Sexual Experiences Questionnaire data to assess changes in sexual harassment prevalence and recognition among training physicians.

Rap1GAP exacerbates myocardial infarction by regulating the AMPK/SIRT1/NF-κB signaling pathway.

Rap1 GTPase-activating protein (Rap1GAP) is an important tumor suppressor. The purpose of this study was to investigate the role of Rap1GAP in myocardial infarction (MI) and its potential mechanism. Left anterior descending coronary artery ligation was performed on cardiac-specific Rap1GAP conditional knockout (Rap1GAP-CKO) mice and control mice with MI. Seven days after MI, Rap1GAP expression in the hearts of control mice peaked, the expression of proapoptotic markers (Bax and cleaved caspase-3) increased, the expression of antiapoptotic factors (Bcl-2) decreased, and the expression of the inflammatory factors IL-6 and TNF-α increased; thus, apoptosis occurred, inflammation, infarct size, and left ventricular dysfunction increased, while the heart changes caused by MI were alleviated in Rap1GAP-CKO mice. Mouse heart tissue was obtained for transcriptome sequencing, and gene set enrichment analysis (GSEA) was used to analyze Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. We found that Rap1GAP was associated with the AMPK and NF-κB signaling pathways and that Rap1GAP inhibited AMPK/SIRT1 and activated the NF-κB signaling pathway in model animals. Similar results were observed in primary rat myocardial cells subjected to oxygen-glucose deprivation (OGD) to induce ischemia and hypoxia. Activating AMPK with the AMPK activator 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) reversed the damage caused by Rap1GAP overexpression in cardiomyocytes. In addition, the coimmunoprecipitation results showed that exogenous Rap1GAP interacted with AMPK. Rap1GAP was verified to regulate the AMPK SIRT1/NF-κB signaling pathway and exacerbate the damage to myocardial cells caused by ischemia and hypoxia. In conclusion, our results suggest that Rap1GAP promotes MI by modulating the AMPK/SIRT1/NF-κB signaling pathway and that Rap1GAP may be a therapeutic target for MI treatment in the future.

Dyslipidemia is associated with sarcopenia of the elderly: a meta-analysis.

PURPOSE: Sarcopenia is a pathological change characterized by muscle loss in older people. According to the reports, there is controversy on the relationship between dyslipidemia and sarcopenia. Therefore, this meta-analysis aimed to explore the association between sarcopenia and dyslipidemia. METHODS: We searched the Cochrane Library, Web of Science, PubMed, China National Knowledge Infrastructure (CNKI), Wan Fang, China Science and Technology Journal Database (VIP Database) for case‒control studies to extract data on the odds ratio (OR) between sarcopenia and dyslipidemia and the MD(mean difference) of TC, LDL-C, HDL-C, TG, and TG/HDL-C between sarcopenia and nonsarcopenia. The JBI(Joanna Briggs) guidelines were used to evaluate the quality. Excel 2021, Review Manager 5.3 and Stata 16.0 were used for the statistical analysis. RESULTS: Twenty studies were included in the meta-analysis, 19 of which were evaluated as good quality. The overall OR of the relationship between sarcopenia and dyslipidemia was 1.47, and the MD values of TC, LDL-C, HDL-C, TG, and TG/HDL-C were 1.10, 1.95, 1.27, 30.13, and 0.16 respectively. In female, compared with the non-sarcopnia, the MD of TC, LDL-C, HDL-C, TG of sarcopenia were - 1.67,2.21,1.02,-3.18 respectively. In male, the MD of TC, LDL-C, HDL-C, TG between sarcopenia and non-sarcopenia were - 0.51, 1.41, 5.77, -0.67. The OR between sarcopenia and dyslipidemia of the non-China region was 4.38, and it was 0.9 in China. In the group(> 60), MD of TC between sarcopenia and non-sarcopenia was 2.63, while it was 1.54 in the group(20-60). CONCLUSION: Dyslipidemia was associated with sarcopenia in the elderly, which was affected by sex, region and age.

Interventing mitochondrial PD-L1 suppressed IFN-γ-induced cancer stemness in hepatocellular carcinoma by sensitizing sorafenib-induced ferroptosis.

Evidence recently showed that pleiotropic cytokine interferon-gamma (IFN-γ) in the tumor microenvironment (TME) plays a positive role in hepatocellular carcinoma (HCC) progression through the regulation of liver cancer stem cells (LCSCs) in HCC. The present study explored the role and potential mechanism of mitochondrial programmed cell death-ligand 1 (PD-L1) and its regulation of ferroptosis in modulating the cancer stemness of LCSCs. It was shown that mimicking TME IFN-γ exposure increased the LCSCs ratio and cancer stemness phenotypes in HCC cells. IFN-γ exposure inhibited sorafenib (Sora)-induced ferroptosis by enhancing glutathione peroxidase 4 (GPX4) expression as well reactive oxygen species (ROS) and lipid peroxidation (LPO) generation in LCSCs. Furthermore, IFN-γ exposure upregulated PD-L1 expression and its mitochondrial translocation, inducing dynamin-related protein 1 (Drp1)-dependent mitochondrial fission and correlating with glycolytic metabolism reprogramming in LCSCs. The genetic intervention of PD-L1 promoted ferroptosis-dependent anti-tumor effects of Sora, reduced glycolytic metabolism reprogramming, and inhibited cancer stemness of HCC in vitro and in vivo. Our results revealed a novel mechanism that IFN-γ exposure-induced mitochondrial translocation of PD-L1 enhanced glycolytic reprogramming to mediate the GPX4-dependent ferroptosis resistance and cancer stemness in LCSCs. This study provided new insights into the role of mitochondrial PD-L1-Drp1-GPX4 signal axis in regulating IFN-γ exposure-associated cancer stemness in LCSCs and verified that PD-L1-targeted intervention in combination with Sora might achieve promising synergistic anti-HCC effects.

Exosome-specific loading Sox10 for the treatment of Cuprizone-induced demyelinating model.

Demyelination is a pathological feature commonly observed in various central nervous system diseases. It is characterized by the aggregation of oligodendrocyte progenitor cells (OPCs) in the lesion area, which face difficulties in differentiating into mature oligodendrocytes (OLGs). The differentiation of OPCs requires the presence of Sox10, but its expression decreases under pathological conditions. Therefore, we propose a therapeutic strategy to regulate OPCs differentiation and achieve myelin repair by endogenously loading Sox10 into exosomes. To accomplish this, we generated a lentivirus-armed Sox10 that could anchor to the inner surface of the exosome membrane. We then infected HEK293 cells to obtain exosomes with high expression of Sox10 (exosomes-Sox10, ExoSs). In vitro, experiments confirmed that both Exos and ExoSs can be uptaken by OPCs, but only ExoSs exhibit a pro-differentiation effect on OPCs. In vivo, we administered PBS, Exos, and ExoSs to cuprizone-induced demyelinating mice. The results demonstrated that ExoSs can regulate the differentiation of PDGFRα+ OPCs into APC+ OLGs and reduce myelin damage in the corpus callosum region of the mouse brain compared to other groups. Further testing suggests that Sox10 may have a reparative effect on the myelin sheath by enhancing the expression of MBP, possibly facilitated by the exosome delivery of the protein into the lesion. This endogenously loaded technology holds promise as a strategy for protein-based drugs in the treatment of demyelinating diseases.

Mapping Cellular Interactions from Spatially Resolved Transcriptomics Data.

Cell-cell communication (CCC) is essential to how life forms and functions. However, accurate, high-throughput mapping of how expression of all genes in one cell affects expression of all genes in another cell is made possible only recently, through the introduction of spatially resolved transcriptomics technologies (SRTs), especially those that achieve single cell resolution. However, significant challenges remain to analyze such highly complex data properly. Here, we introduce a Bayesian multi-instance learning framework, spacia, to detect CCCs from data generated by SRTs, by uniquely exploiting their spatial modality. We highlight spacia's power to overcome fundamental limitations of popular analytical tools for inference of CCCs, including losing single-cell resolution, limited to ligand-receptor relationships and prior interaction databases, high false positive rates, and most importantly the lack of consideration of the multiple-sender-to-one-receiver paradigm. We evaluated the fitness of spacia for all three commercialized single cell resolution ST technologies: MERSCOPE/Vizgen, CosMx/Nanostring, and Xenium/10X. Spacia unveiled how endothelial cells, fibroblasts and B cells in the tumor microenvironment contribute to Epithelial-Mesenchymal Transition and lineage plasticity in prostate cancer cells. We deployed spacia in a set of pan-cancer datasets and showed that B cells also participate in PDL1/PD1 signaling in tumors. We demonstrated that a CD8+ T cell/PDL1 effectiveness signature derived from spacia analyses is associated with patient survival and response to immune checkpoint inhibitor treatments in 3,354 patients. We revealed differential spatial interaction patterns between γδ T cells and liver hepatocytes in healthy and cancerous contexts. Overall, spacia represents a notable step in advancing quantitative theories of cellular communications.

Construction and application of highly efficient waste cooking oil degrading bacteria consortium in oily wastewater.

The treatment of cooking oil wastewater is an urgent issue need to be solved. We aimed to screen for efficient oil-degrading bacteria and develop a new microbial agent for degrading waste cooking oil in oily wastewater. Three extremely effective oil-degrading bacteria, known as YZQ-1, YZQ-3, and YZQ-4, were found by the enrichment and acclimation of samples from various sources and separation using oil degradation plates. The 16S rRNA sequencing analysis and phylogenetic tree construction showed that the three strains were Bacillus tropicus, Pseudomonas multiresinivorans, and Raoultella terrigena. Under optimal degradation conditions, the maximal degradation rates were 67.30 ± 3.69%, 89.65 ± 1.08%, and 79.60 ± 5.30%, respectively, for YZQ-1, YZQ-3, and YZQ-4. Lipase activity was highest for YZQ-3, reaching 94.82 ± 12.89 U/L. The best bacterial alliance was obtained by adding equal numbers of microbial cells from the three strains. Moreover, when this bacterial alliance was applied to oily wastewater, the degradation rate of waste cooking oil was 61.13 ± 7.30% (3.67% ± 2.13% in the control group), and COD removal was 62.4% ± 5.65% (55.60% ± 0.71% in the control group) in 72 h. Microbial community analysis results showed YZQ-1 and YZQ-3 were adaptable to wastewater and could coexist with local bacteria, whereas YZQ-4 could not survive in wastewater. Therefore, the combination of YZQ-1 and YZQ-3 can efficiently degrade oil and shows great potential for oily wastewater treatment.

The impact of COVID-19 on a college freshman sample reveals genetic and nongenetic forms of susceptibility and resilience to stress.

Using a longitudinal approach, we sought to define the interplay between genetic and nongenetic factors in shaping vulnerability or resilience to COVID-19 pandemic stress, as indexed by the emergence of symptoms of depression and/or anxiety. University of Michigan freshmen were characterized at baseline using multiple psychological instruments. Subjects were genotyped, and a polygenic risk score for depression (MDD-PRS) was calculated. Daily physical activity and sleep were captured. Subjects were sampled at multiple time points throughout the freshman year on clinical rating scales, including GAD-7 and PHQ-9 for anxiety and depression, respectively. Two cohorts (2019 to 2021) were compared to a pre-COVID-19 cohort to assess the impact of the pandemic. Across cohorts, 26 to 40% of freshmen developed symptoms of anxiety or depression (N = 331). Depression symptoms significantly increased in the pandemic years and became more chronic, especially in females. Physical activity was reduced, and sleep was increased by the pandemic, and this correlated with the emergence of mood symptoms. While low MDD-PRS predicted lower risk for depression during a typical freshman year, this genetic advantage vanished during the pandemic. Indeed, females with lower genetic risk accounted for the majority of the pandemic-induced rise in depression. We developed a model that explained approximately half of the variance in follow-up depression scores based on psychological trait and state characteristics at baseline and contributed to resilience in genetically vulnerable subjects. We discuss the concept of multiple types of resilience, and the interplay between genetic, sex, and psychological factors in shaping the affective response to different types of stressors.

Rectal malakoplakia mimicking advanced rectal cancer: A case report.

Background: Malakoplakia is a rare acquired chronic infectious granulomatous condition, that is characterized by the accumulation of large granular macrophages containing basophilic inclusion bodies in the cytoplasm termed Michaelis-Gutmann (MG) bodies. Malakoplakia most commonly involves the genitourinary system, and the second most commonly affected site is the gastrointestinal tract. Rectal malakoplakia is an unusual entity that is difficult to diagnose due to its diverse clinical manifestations and radiological findings that are similar to different diseases and advanced cancers. Case description: A 61-year-old male patient presented with difficulty in urination and defecation that started 4 months prior, along with a weight loss of 10 kg. Abdominal computerized tomography (CT) scanning revealed diffuse lesions of the perirectal region with multiple lymphadenopathies and involvement of the bladder, prostate, bilateral seminal vesicles, and left ureter. 18F-FDG PET/CT MIP showed intense FDG uptake in the rectal region, and a diagnosis of an occupying lesion was proposed. Colonoscopy and histological examination of rectal lesion biopsies showed the characteristic features of malakoplakia. Conclusion: Malakoplakia of the rectum with lymph node involvement and adjacent organ extension has been extensively misdiagnosed in clinical practice, and mimics malignancy radiologically. It is of great importance for radiologists to be aware of malakoplakia when making the differential diagnosis of benign and malignant mass lesions of the rectum, although the radiologic findings are nonspecific. Endoscopic evaluation and pathologic examination of a biopsy should be recommended to make the correct diagnosis, which may prevent unnecessary surgical resection.

Metabolomics analysis of amino acid and fatty acids in colorectal cancer patients based on tandem mass spectrometry.

Metabolic differences between colorectal cancer (CRC) and NI (NI) play an important role in early diagnoses and in-time treatments. We investigated the metabolic alterations between CRC patients and NI, and identified some potential biomarkers, and these biomarkers might be used as indicators for diagnosis of CRC. In this study, there were 79 NI, 50 CRC I patients, 52 CRC II patients, 56 CRC III patients, and 52 CRC IV patients. MS-MS was used to measure the metabolic alterations. Univariate and multivariate data analysis and metabolic pathway analysis were applied to analyze metabolic data and determine differential metabolites. These indicators revealed that amino acid and fatty acids could separate these groups. Several metabolites indicated an excellent variables capability in the separation of CRC patients and NI. Ornithine, arginine, octadecanoyl carnitine, palmitoyl carnitine, adipoyl carnitine, and butyryl carnitine/propanoyl carnitine were selected to distinguish the CRC patients and NI. And methionine and propanoyl carnitine, were directly linked to different stages of CRC. Receiver operating characteristics curves and variables importance in projection both represented an excellent performance of these metabolites. In conclusion, we assessed the difference between CRC patients and NI, which supports guidelines for an early diagnosis and effective treatment.

The emerging roles of MARCH8 in viral infections: A double-edged Sword.

The host cell membrane-associated RING-CH 8 protein (MARCH8), a member of the E3 ubiquitin ligase family, regulates intracellular turnover of many transmembrane proteins and shows potent antiviral activities. Generally, 2 antiviral modes are performed by MARCH8. On the one hand, MARCH8 catalyzes viral envelope glycoproteins (VEGs) ubiquitination and thus leads to their intracellular degradation, which is the cytoplasmic tail (CT)-dependent (CTD) mode. On the other hand, MARCH8 traps VEGs at some intracellular compartments (such as the trans-Golgi network, TGN) but without inducing their degradation, which is the cytoplasmic tail-independent (CTI) mode, by which MARCH8 hijacks furin, a cellular proprotein convertase, to block VEGs cleavage. In addition, the MARCH8 C-terminal tyrosine-based motif (TBM) 222YxxL225 also plays a key role in its CTI antiviral effects. In contrast to its antiviral potency, MARCH8 is occasionally hijacked by some viruses and bacteria to enhance their invasion, indicating a duplex role of MARCH8 in host pathogenic infections. This review summarizes MARCH8's antiviral roles and how viruses evade its restriction, shedding light on novel antiviral therapeutic avenues.

[Locking loop stitch with suture-bridge technique in repair of acute closed distal Achilles tendon rupture by using suture anchors].

OBJECTIVE: To explore clinical efficacy of Locking loop stitch with suture-bridge technique in repair of acute closed distal Achilles tendon rupture by using suture anchors. METHODS: From July 2019 to March 2021, 20 patients with acute closed distal Achilles tendon rupture were treated by minimally invasive suture anchor locking suture bridging repair technique. Among them, including 18 males and 2 females, aged from 19 to 52 years old with an average of(40.0±9.0) years old. Complications were observed, and recovery of ankle function was evaluated by American Orthopaedic Foot & Ankle Society(AOFAS) ankle and hindfoot function scoring system before operation and 1 year after operation. RESULTS: All patients followed up from 6 to 18 months with an average of (12.0±3.2) months. The incisions were healed at stageⅠwithout infection and skin necrosis occurred;no gastrocnemius nerve injury and deep vein thrombosis of the lower extremities occurred;and no heel pain and Achilles tendon re-rupture occurred. AOFAS scores of ankle and hindfoot increased from(59.0±4.3) before opertaion to(95.1±2.6) at 1 year after operation (t=-32.1, P<0.05). CONCLUSION: The effect of locking suture bridging with suture anchor nails to repair acute distal Achilles tendon rupture is definite, and it could reduce incidence of complications such as Achilles tendon re-rupture, nerve injury, and skin necrosis, which has advantages of small surgical trauma, reliable anastomosis method and good functional recovery, and is an ideal method for treating acute closed distal Achilles tendon rupture.