Objective To investigate the role and regulatory mechanism of LINC00657 in the progression of cervical cancer. Methods Bioinformatics analysis predicted potential binding sites between LINC00657 and miR-30a-5p and between miR-30a-5p and Skp2. These sites were verified by using RNA immunoprecipitation and dual-luciferase reporter experiments. LINC00657, miR-30a-5p, and Skp2 mRNA expression levels in cervical cancer tissues and cell lines were assessed by utilizing RT-qPCR. Western blot analysis was employed to examine the protein levels of Skp2 in cells and subcutaneous xenograft tumor models in nude mice. Immunohistochemistry was applied to analyze Skp2 expression in animal tissues. The cellular processes of cervical cancer cell lines were evaluated through CCK-8, scratch, and Transwell assays. Results LINC00657 and Skp2 presented binding sites for miR-30a-5p. In cervical cancer, LINC00657 and Skp2 showed high expression levels (P<0.05), whereas miR-30a-5p displayed low expression (P<0.05). Functional experiments demonstrated that linc00657 upregulates Skp2 expression, a process that is dependent on its sequestration of miR-30a-5p. Conclusion LINC00657 promoted the malignant progression of cervical cancer by upregulating Skp2 expression through specifically sequestering miR-30a-5p, thereby relieving its inhibitory effect on the target gene Skp2.

BACKGROUND:Stand-alone oblique lateral interbody fusion has a high rate of complications of fusion segment sink.Oblique lateral interbody fusion with posterior fixation can provide stable support,but intraoperative position changes and double incisions weaken the advantages of this technique.Oblique lateral interbody fusion combined with lateral plate fixation can achieve one-stage decompression in the same incision,while the lateral internal fixation provides stable support. OBJECTIVE:To analyze the short-term efficacy of oblique lateral interbody fusion combined with lateral plate fixation in the treatment of single-level lumbar degenerative disease. METHODS:The clinical data of 34 patients with single-level lumbar degenerative disease treated with oblique lateral interbody fusion combined with lateral plate fixation were collected from May 2020 to October 2022.Among them,14 were males and 20 were females aged from 41 to 72 years at the mean age of(58.6±9.9)years.There were 11 cases of lumbar spondylolisthesis(Ⅰ°),7 cases of lumbar disc herniation with segmental instability,and 16 cases of lumbar spinal stenosis.Operation time,blood loss,and complications were recorded.Visual analog scale scores of lumbago,radiative pain of both lower limbs,and Oswestry disability index scores were evaluated before surgery,3 months after surgery,and the last follow-up.Dural sac cross-sectional area,intervertebral height,and intervertebral fusion were measured and observed. RESULTS AND CONCLUSION:(1)The 34 patients were followed up for 14-36 months,with an average of(21.3±5.2)months.(2)The operation time ranged from 50 to 92 minutes,with an average of(68.5±11.1)minutes.Intraoperative blood loss was 50-170 mL,with an average of(71.6±25.3)mL.(3)Compared with the preoperative results,the visual analog scale scores and Oswestry disability index scores were significantly decreased at 3 months after surgery and at the last follow-up(P<0.001),and the maximum Oswestry disability index scores were improved by nearly 50％.(4)Bone fusion was achieved in all patients during half-year follow-up.The overall complication rate was 21％(7/34),including 1 case of plate displacement,3 cases of cage subsidence,1 case of psoas weakness,and 2 cases of anterior thigh pain.(5)It is concluded that oblique lateral interbody fusion combined with lateral plate fixation for the treatment of lumbar degenerative diseases has the characteristics of less blood loss,short operation time,rapid postoperative recovery,and significant short-term clinical efficacy with the stable support to a certain extent.The long-term curative effect needs further follow-up observation.

Mitochondria, functioning not only as the central hub of cellular energy metabolism but also as semi-autonomous organelles, orchestrate cellular fate decisions through their endogenous mitochondrial DNA (mtDNA), which encodes core components of the electron transport chain. Emerging research has identified microRNAs localized within mitochondria, termed mitochondria-located microRNAs (mitomiRs). Recent studies have revealed that mitomiRs are transcribed from nuclear DNA (nDNA), processed and matured in the cytoplasm, and subsequently transported into mitochondria. mitomiRs regulate mtDNA through diverse mechanisms, including modulation of mtDNA expression at the translational level and direct binding to mtDNA to influence transcription. Aberrant expression of mitomiRs leads to mitochondrial dysfunction and contributes to the pathogenesis of metabolic diseases. Restoring mitomiR expression to physiological levels using mitomiRs mimics or inhibitors has been shown to improve mitochondrial function and alleviate related diseases. Consequently, the regulatory mechanisms of mitomiRs have become a major focus in mitochondrial research. Given that mitomiRs are located in mitochondria, targeted delivery strategies designed for mtDNA can be adapted for the delivery of mitomiRs mimics or inhibitors. However, numerous intracellular and extracellular barriers remain, highlighting the need for more precise and efficient delivery systems in the future. The regulation of mtDNA expression mediated by mitomiRs not only expands our understanding of miRNA functions in post-transcriptional gene regulation but also provides promising molecular targets for the treatment of mitochondrial-related diseases. This review systematically summarizes recent research progress on mitomiRs in regulating mtDNA expression and discusses the underlying mechanisms of mitomiRs-mtDNA interactions. Additionally, it provides new perspectives on precision therapeutic strategies, with a particular emphasis on mitomiRs-based regulation of mitochondrial function in mitochondrial-related diseases.

AIM:To analyze the clinical phenotypes and genotypes of children with incontinentia pigmenti(IP)and enhance clinicians' understanding of the condition.METHODS: A family with IP diagnosed in February 2020 at the ophthalmology department of People's Hospital of Ningxia Hui Autonomous Region was enrolled. The proband and family members underwent comprehensive systemic and ocular examinations. Peripheral venous blood was collected for DNA extraction, followed by whole-exome sequencing and MLPA assay to identify pathogenic variants. Corresponding treatments were administered based on the severity of fundus lesions, and ocular clinical features and therapeutic outcomes were monitored during follow-up.RESULTS: The child in this study was a female, aged 8 years, with typical skin changes and scarring alopecia and dental abnormalities at the time of initial consultation. The results of genetic testing suggested that the child carried a heterozygous deletion of exons 4-10 of the IKBKG gene chrX:153440010-153446570del. The child had asymmetric lesions in both eyes, with severe lesions in the left eye, atrophy of the eyeballs, and ocular B-ultrasound suggesting structural disturbances in the eye, and neovascularization was seen in the peripheral retina of the right eye, and the patient was given laser photocoagulation treatment for the right eye, and no progression of retinopathy was detected during follow-up.CONCLUSION:Children with IP have different ocular clinical phenotypes, and retinal vasculopathy is the main change. Early screening and timely and standardized treatment are crucial for children diagnosed with IP.

OBJECTIVE: To evaluate the clinical efficacy of self-made anatomical tower-shaped pads combined with splint plaster fixation in the treatment of unstable 2nd to 5th metacarpal fractures and to provide a reference for clinical practice. METHODS: A retrospective analysis was conducted on 98 patients with unstable 2nd to 5th metacarpal fractures treated with self-made anatomical tower-shaped pads combined with splint plaster fixation between January 2019 and December 2022. There were 74 males and 24 females, aged from 19 to 63 years old with an average of (41.58±7.23) years old. The total active movement (TAM) score was used to evaluate the metacarpophalangeal joint function. Complications and fracture healing time were recorded. RESULTS: All patients were followed up for a period ranging from 1 to 5 months, with an average duration of (3.45±1.03) months. Among the 98 patients, anatomical alignment was achieved in 75 patients, with 68 patients still maintaining anatomical alignment after fixation removal. Functional alignment was achieved in 23 patients, with 20 patients maintaining functional alignment even after fixation removal. There were 10 patients with displacement after reduction. The average fracture healing time was (5.78±1.14) weeks, and the fracture healed well without any angular or rotational deformities. TAM score was utilized to assess the hand function of patients 3 months post-treatment. The extension range of motion (10.72±1.35)° and flexion range of motion (83.19±4.08)° of the metacarpophalangeal joint were significantly higher than the pre-treatment values of (8.25±0.68)° and (70.35±2.36)°, respectively. These differences were statistically significant (P<0.05). TAM outcomes were excellent in 92 cases, good in 5, fair in 1, and poor in none. CONCLUSION The implementation of self-made anatomical tower-shaped pad combined with splint plaster fixation is effective for the conservative management of unstable 2nd to 5th metacarpal fractures.
Humans ; Male ; Female ; Adult ; Middle Aged ; Metacarpal Bones/surgery* ; Splints ; Retrospective Studies ; Fractures, Bone/therapy* ; Casts, Surgical ; Young Adult ; Fracture Fixation, Internal/instrumentation*

PURPOSE: To investigate the incidence and influencing factors of bone loss in patients with spinal cord injury (SCI). METHODS: A retrospective case-control study was conducted. Patients with SCI in our hospital from January 2019 to March 2023 were collected. According to the correlation between bone mineral density (BMD) at different sites, the patients were divided into the lumbar spine group and the hip joint group. According to the BMD value, the patients were divided into the normal bone mass group (t > -1.0 standard deviation) and the osteopenia group (t ≤ -1.0 standard deviation). The influencing factors accumulated as follows: gender, age, height, weight, cause of injury, injury segment, injury degree, time after injury, start time of rehabilitation, motor score, sensory score, spasticity, serum value of alkaline phosphatase, calcium, and phosphorus. The trend chart was drawn and the influencing factors were analyzed. SPSS 26.0 was used for statistical analysis. Correlation analysis was used to test the correlation between the BMD values of the lumbar spine and bilateral hips. Binary logistic regression analysis was used to explore the influencing factors of osteoporosis after SCI. p < 0.05 was considered statistically significant. RESULTS: The incidence of bone loss in patients with SCI was 66.3%. There was a low concordance between bone loss in the lumbar spine and the hip, and the hip was particularly susceptible to bone loss after SCI, with an upward trend in incidence (36% - 82%). In this study, patients with SCI were divided into the lumbar spine group (n = 100) and the hip group (n = 185) according to the BMD values of different sites. Then, the lumbar spine group was divided into the normal bone mass group (n = 53) and the osteopenia group (n = 47); the hip joint group was divided into the normal bone mass group (n = 83) and the osteopenia group (n = 102). Of these, lumbar bone loss after SCI is correlated with gender and weight (p = 0.032 and < 0.001, respectively), and hip bone loss is correlated with gender, height, weight, and time since injury (p < 0.001, p = 0.015, 0.009, and 0.012, respectively). CONCLUSIONS The incidence of bone loss after SCI was high, especially in the hip. The incidence and influencing factors of bone loss in the lumbar spine and hip were different. Patients with SCI who are male, low height, lightweight, and long time after injury were more likely to have bone loss.
Humans ; Spinal Cord Injuries/complications* ; Male ; Female ; Retrospective Studies ; Incidence ; Adult ; Bone Density ; Middle Aged ; Case-Control Studies ; Osteoporosis/etiology* ; Lumbar Vertebrae ; Bone Diseases, Metabolic/etiology* ; Aged ; Risk Factors

OBJECTIVE: To study the effects and mechanisms of juglone on the proliferation and apoptosis of acute myeloid leukemia (AML) cells. METHODS: Juglone and AML targets were collected from public databases, and the intersecting target clusters were taken for functional enrichment analysis to explore the potential mechanism of juglone in the treatment of AML. Then wet experiments were performed to verify. AML cell lines including KG-1a, MV-411, THP-1 and MOLM-13 were treated with different concentrations of juglone for 24 h. MTT assay was used to detect cell viability and determine the IC₅₀, and the most sensitive cell line was screened for subsequent experiments. Flow cytometry was used to detect the apoptosis of cells treated with different concentrations of juglone. Western blot was performed to check the expression of relevant proteins. RESULTS: Eleven targets were obtained as potential targets for juglone in the treatment of AML, and the top ten significantly enriched pathways were intrinsic pathway of apoptosis, programmed cell death, cytochrome c-mediated apoptotic response, apoptosis, apoptotic factor-mediated response, regulated necrosis, cytokine signaling in immune system, signaling by interleukins, oncogene induced senescence, and signal transduction. The cell viability of KG-1a, MV-411, THP-1 and MOLM-13 was decreased with increasing juglone concentration after 24 h of juglone treatment (r =-0.992, -0.886, -0.956, -0.910). Among them, MOLM-13 was the most sensitive to juglone. The results of flow cytometry showed that the apoptosis rate of MOLM-13 tended to significantly increase with the increasing concentration of juglone (r =0.99). At the same time point, p-RIPK1/RIPK1, p-RIPK3/RIPK3, and p-MLKL/MLK were decreased in each juglone concentration group compared with control group. CONCLUSION Juglone inhibits the viability of KG-1a, MV-411, THP-1 and MOLM-13 cells, and induces apoptosis of MOLM-13 cells, the mechanism of which may be related to the inhibition of RIPK1/RIPK3/MLKL signaling pathway.
Humans ; Naphthoquinones/pharmacology* ; Apoptosis/drug effects* ; Cell Proliferation/drug effects* ; Leukemia, Myeloid, Acute/pathology* ; Cell Line, Tumor ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism* ; Protein Kinases/metabolism* ; Signal Transduction ; Cell Survival/drug effects*