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1.
Int Wound J ; 21(4): e14605, 2024 Apr.
Article in English | MEDLINE | ID: mdl-38149500

ABSTRACT

The objective of this study was to investigate the risk factors associated with surgical site infection (SSI) after percutaneous endoscopic lumbar discectomy (PELD) in patients with lumbar disc herniation (LDH). A retrospective analysis was performed on a cohort of 335 patients who underwent PELD between January 2016 and January 2023. Data were derived from the Hospital Information System (HIS), and a comprehensive statistical assessment was performed using IBM SPSS Statistics version 25.0. Both univariate and multivariate logistic regression analyses assessed a range of risk determinants, such as age, body mass index (BMI), comorbidities, laboratory test parameters and surgery-related variables. The incidence of SSI after PELD was 2.7% (9/335). Univariate analysis highlighted BMI, diabetes mellitus, long-term corticosteroid consumption, surgical time and cerebrospinal fluid leakage as significant predictors of SSI. Multivariate logistic regression identified BMI, diabetes mellitus, long-term corticosteroid consumption, surgical time and cerebrospinal fluid leakage as significant risk factors for SSI after PELD. High BMI, diabetes mellitus, long-term corticosteroid consumption, long surgical time and postoperative cerebrospinal fluid leakage are predisposing factors for SSI in patients undergoing PELD. Precise interventions focused on such risk components, including careful preoperative assessment and strategic postoperative care, are essential to reduce the incidence of SSI and improve surgical efficacy.


Subject(s)
Diabetes Mellitus , Diskectomy, Percutaneous , Intervertebral Disc Displacement , Humans , Retrospective Studies , Intervertebral Disc Displacement/epidemiology , Intervertebral Disc Displacement/etiology , Intervertebral Disc Displacement/surgery , Surgical Wound Infection/epidemiology , Surgical Wound Infection/etiology , Surgical Wound Infection/surgery , Diskectomy, Percutaneous/adverse effects , Lumbar Vertebrae/surgery , Risk Factors , Adrenal Cortex Hormones , Cerebrospinal Fluid Leak/etiology , Cerebrospinal Fluid Leak/surgery , Treatment Outcome
2.
Cell Death Dis ; 14(11): 757, 2023 11 20.
Article in English | MEDLINE | ID: mdl-37985768

ABSTRACT

Aggressiveness and drug resistance are major challenges in the clinical treatment of glioblastoma (GBM). Our previously research reported a novel candidate oncogene ribosomal protein L22 like 1 (RPL22L1). The aim of this study was to elucidate the potential role and mechanism of RPL22L1 in progression and temozolomide (TMZ) resistance of GBM. Online database, tissue microarrays and clinical tissue specimens were used to evaluate the expression and clinical implication of RPL22L1 in GBM. We performed cell function assays, orthotopic and subcutaneous xenograft tumor models to evaluate the effects and molecular mechanisms of RPL22L1 on GBM. RPL22L1 expression was significantly upregulated in GBM and associated with poorer prognosis. RPL22L1 overexpression enhanced GBM cell proliferation, migration, invasion, TMZ resistance and tumorigenicity, which could be reduced by RPL22L1 knockdown. Further, we found RPL22L1 promoted mesenchymal phenotype of GBM and the impact of these effects was closely related to EGFR/STAT3 pathway. Importantly, we observed that STAT3 specific inhibitor (Stattic) significantly inhibited the malignant functions of RPL22L1, especially on TMZ resistance. RPL22L1 overexpressed increased combination drug sensitive of Stattic and TMZ both in vitro and in vivo. Moreover, Stattic effectively restored the sensitive of RPL22L1 induced TMZ resistance in vitro and in vivo. Our study identified a novel candidate oncogene RPL22L1 which promoted the GBM malignancy through STAT3 pathway. And we highlighted that Stattic combined with TMZ therapy might be an effective treatment strategy in RPL22L1 high-expressed GBM patients.


Subject(s)
Brain Neoplasms , Glioblastoma , Humans , Temozolomide/therapeutic use , Glioblastoma/drug therapy , Glioblastoma/genetics , Glioblastoma/pathology , Cell Line, Tumor , Brain Neoplasms/drug therapy , Brain Neoplasms/genetics , Brain Neoplasms/pathology , Oncogenes , Drug Resistance, Neoplasm/genetics , Antineoplastic Agents, Alkylating/pharmacology , Antineoplastic Agents, Alkylating/therapeutic use , Xenograft Model Antitumor Assays , STAT3 Transcription Factor/genetics , STAT3 Transcription Factor/metabolism , Ribosomal Proteins/genetics , Ribosomal Proteins/metabolism
3.
Sci Rep ; 12(1): 18868, 2022 11 07.
Article in English | MEDLINE | ID: mdl-36344575

ABSTRACT

This study introduced a novel point "O" puncture approach for percutaneous kyphoplasty (PKP) in patients with L4 or L5 osteoporotic vertebral compression fracture (OVCF) and evaluated its clinical and radiographic outcomes. Between September 2019 and December 2020, we compared the clinical and radiographic outcomes in 31 cases (36 vertebrae) using the "O" entry point PKP intervention (O-PKP) and 31 cases (37 vertebrae) using transverse the process-pedicle approach PKP intervention (T-PKP). No serious postoperative complications were observed in any of the participants. Only two T-PKP patients experienced intervertebral disc space leakage. Compared with the T-PKP patients, the O-PKP patients showed shorter operative time and fluoroscopy times (P < 0.05), comparable blood loss and cement volume (P > 0.05), improved VAS and ODI scores at the final follow-up (P < 0.05), better increases in the vertebral compression ratio (P < 0.05), comparable Cobb angle (P > 0.05), comparable anteroposterior bone cement distribution, enhanced bilateral bone cement distribution (P < 0.05), and larger sagittal and transverse angles (P < 0.05). Herein, O-PKP was indicated for patients with L4 or L5 OVCF. This puncture approach showed significant advantages over T-PKP not only in terms of pain relief, surgery and fluoroscopy times but also in the puncture angle, vertebral reconstruction, and symmetrical cement distribution.


Subject(s)
Fractures, Compression , Kyphoplasty , Osteoporotic Fractures , Spinal Fractures , Humans , Kyphoplasty/adverse effects , Fractures, Compression/diagnostic imaging , Fractures, Compression/surgery , Fractures, Compression/complications , Bone Cements/therapeutic use , Spinal Fractures/diagnostic imaging , Spinal Fractures/surgery , Spinal Fractures/complications , Retrospective Studies , Treatment Outcome , Osteoporotic Fractures/diagnostic imaging , Osteoporotic Fractures/surgery , Osteoporotic Fractures/etiology , Spine , Punctures/adverse effects
4.
Oxid Med Cell Longev ; 2016: 6929306, 2016.
Article in English | MEDLINE | ID: mdl-26798426

ABSTRACT

We show that hypercholesterolemia contributes to oxidative stress injury progression in brain and simvastatin counteracts the cholesterol-induced peroxidation injury in rabbit hippocampus, and we demonstrate for the first time that the simvastatin is a critical role in brain protection and identify HO-1 and other related antioxidant enzymes as molecular target for active redox compounds. Second, our experiments have pointed out an association between statin treatment and a decrease in the risk of having peroxidation damage of brain. The balance effects of simvastatin to ROS and antioxidants enzymes network are most probably due to improved SOD functional activity, increase in GSH-Px, increase in HO-1 expression, and decrease of MDA generation.


Subject(s)
Antioxidants/pharmacology , Aorta/drug effects , Hippocampus/drug effects , Simvastatin/pharmacology , Animals , Antioxidants/metabolism , Aorta/pathology , Atherosclerosis/pathology , Diet, High-Fat , Disease Models, Animal , Heme Oxygenase-1/genetics , Heme Oxygenase-1/metabolism , Hippocampus/enzymology , Hippocampus/pathology , Immunohistochemistry , Male , Oxidative Stress/drug effects , RNA, Messenger/genetics , RNA, Messenger/metabolism , Rabbits
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