Explore the vast range of titles available.

Objective The reported date in the repeat surgical intervention for adolescent lumbar disc herniation (ALDH) after percutaneous endoscopic lumbar discectomy (PELD) was quite scarce. This study aims to introduce cases of repeat surgeries after PELD for ALDH and assess the incidence, chief causes, repeat surgery methods, and surgical outcomes of repeat surgeries after PELD for ALDH. Methods A retrospective multicenter observational study was conducted on patients undergoing repeat surgeries after PELD for ALDH at four tertiary referral hospitals from January 2014 through August 2022. The incidence of repeat surgeries, chief causes, strategies for repeat surgeries, and timing of repeat surgeries were recorded and analyzed. The clinical outcomes were evaluated by the Numeric Rating Scales (NRS) scores and the modified MacNab criteria. Statistical analyses were performed with the Wilcoxon signed‐rank test. Results A total of 23 patients who underwent repeat surgeries after PELD for ALDH were included. The chief causes were re‐herniation (homo‐lateral re‐herniation at the same level, new disc herniation of adjacent level). The repeat surgery methods were revision PELD, micro‐endoscopic discectomy (MED), open discectomy and instrumented lumbar inter‐body fusion. The NRS scores decreased significantly in follow‐up evaluations and these scores demonstrated significant improvement at the last follow‐up (p < 0.002). For the modified MacNab criteria, at the last follow‐up, 18 patients (78.26%) had an excellent outcome, and the overall success rate was 86.95%. Conclusion This study's data suggest that young patients who underwent repeat surgery improved significantly compared to baseline. The chief cause was re‐herniation. Revision PELD was the main surgical procedure, which provides satisfactory clinical results in young patients who underwent repeat surgeries. An 18‐year‐old male who underwent revision PELD surgery for homolateral re‐herniation at the same level due to radiating pain and neurologic symptoms resistant to nonoperative treatment.

Study Design Retrospective study. Objectives Our objective is to create comprehensible machine learning (ML) models that can forecast bone cement leakage in percutaneous vertebral augmentation (PVA) for individuals with osteoporotic vertebral compression fracture (OVCF) while also identifying the associated risk factors. Methods We incorporated data from patients (n = 425) which underwent PVA. To predict cement leakage, we devised six models based on a variety of parameters. Evaluate and juxtapose the predictive performances relied on measures of discrimination, calibration, and clinical utility. SHapley Additive exPlanations (SHAP) methodology was used to interpret model and evaluate the risk factors associated with cement leakage. Results The occurrence rate of cement leakage was established at 50.4%. A binary logistic regression analysis identified cortical disruption (OR 6.880, 95% CI 4.209-11.246), the basivertebral foramen sign (OR 2.142, 95% CI 1.303-3.521), the fracture type (OR 1.683, 95% CI 1.083-2.617), and the volume of bone cement (OR 1.198, 95% CI 1.070-1.341) as independent predictors of cement leakage. The XGBoost model outperformed all others in predicting cement leakage in the testing set, with AUC of .8819, accuracy of .8025, recall score of .7872, F1 score of .8315, and a precision score of .881. Several important factors related to cement leakage were drawn based on the analysis of SHAP values and their clinical significance. Conclusion The ML based predictive model demonstrated significant accuracy in forecasting bone cement leakage for patients with OVCF undergoing PVA. When combined with SHAP, ML facilitated a personalized prediction and offered a visual interpretation of feature importance.

Objectives Tumour necrosis factor alpha (TNF‐α) expressed by nucleus pulposus cells (NPCs) plays a critical role in intervertebral disc (IVD) degeneration. A key unfolded protein response (UPR) component, X‐box binding protein 1 (XBP1) and nuclear factor‐kappa B (NF‐κB) are essential for cell survival and proliferation. The aim of our study was to elucidate the roles of XBP1 and NF‐κB in IVD degeneration (IDD). Materials and methods Rat NPCs were cultured with TNF‐α in the presence or absence of XBP1 and NF‐κB‐p65 small interfering RNA. The associated genes and proteins were evaluated through quantitative real‐time PCR, Western blot analyses and immunofluorescence staining to monitor UPR and NF‐κB signalling and identify the regulatory mechanism of p65 by XBP1. Cell counting kit‐8 assay, cell cycle analysis and related gene and protein expression were performed to examine the proliferation of NPCs. Results The acute exposure of TNF‐α accelerated the proliferation of rat NPCs by activating the UPR/XBP1 pathway. XBP1 signalling favoured the phosphorylation and nuclear translocation of p65 subunit of NF‐κB. The activation of NF‐κB in the later phase also enhanced NPC proliferation. Conclusions Unfolded protein response reinforces the survival and proliferation of NPCs under TNF‐α stimulation by activating the XBP1 pathway, and NF‐κB serves as a vital mediator in these events. The XBP1 signalling of UPR can be a novel therapeutic target in IDD.

PurposeTo elucidate the natural history of intervertebral disk (IVD) and characterize its embryonic beginnings and age-related degeneration.MethodsCoronal sections of embryonic (E13.5-neonatal) and postnatal (4–60-week-old) Sprague–Dawley rat IVD were stained by a series of histological stainings (hematoxylin and eosin, Alcian blue, Picrosirius red, Masson, Periodic acid–Schiff). Growth kinetics within embryonic IVD were evaluated by immunohistochemical staining of Ki67 and proliferating cell nuclear antigen. Postnatal maturation and degeneration of IVD were visualized on radiology by X-ray, CT, and MR imaging.ResultsDuring the formation of rat IVD, inner annulus fibrosus (AF) and cartilaginous endplate (CEP) shared similar cell density, extracellular matrix, and potential of growth kinetics; notochord provided increased and enlarged cytoplasmic vacuoles to generate nucleus pulposus (NP), part of which was retained within CEP. Postnatally, vacuolated notochord cells were reduced by devacuolation, while chondrocytic NP cells increased; cartilaginous layers of CEP were narrowed by vertebrae growth and secondary ossification; fibrotic portion of AF decreased as cartilaginous matrix accumulated and infiltrated outward. In aged and degenerated IVD, large longitudinal fissures were detected near the boundaries between inner and outer AF, whereas both reduced cellularity and accumulated cell clusters were evident within the dehydrated NP; only part of these histocytological changes could be reported on radiology.ConclusionsBy showing that the natural history of IVD is orchestrated by a dynamic histocytological regulation, our study may facilitate better understanding of the developmental defects, cellular heterogeneity, age-related degenerative mechanisms, and biological regeneration of IVD.Graphical abstractThese slides can be retrieved under Electronic Supplementary Material.

Study Design: Case-control study. Objectives: To compare the outcomes of 2 different criteria (time driven and output driven) for wound drain removal and identify which one is better. Methods: 743 patients who underwent posterior lumbar fusion with instrumentation involving 1 or 2 motion segments were enrolled in this study. Based on the different criteria for drain removal, the patients were divided into 2 groups. The drains were discontinued by time driven (postoperative day 2) in group I and output driven (<50 ml per day) in group II. Demographic characteristics, perioperative parameters and clinical outcomes were compared between the 2 groups. Results: The demographic characteristics in both groups were comparable. The postoperative drain output, total blood loss, postoperative timing of ambulation, and postoperative duration of hospital stay in group I were lower than those in group II (P < 0.001). There was a higher proportion of patients requiring postoperative blood transfusion in group II, but not to a level of statistical significance (P = 0.054). There was no statistical significant difference in the incidence of surgical site infection (SSI) or symptomatic spinal epidural hematoma (SEH) between the 2 groups (P > 0.05). Conclusions: This study reveals that there are more benefits of wound drain removal by time driven than that by output driven for patients undergoing posterior 1-level or 2-level lumbar fusion with instrumentation, including less postoperative drain output, less total blood loss, earlier postoperative timing of ambulation and less postoperative duration of hospital stay without increasing the incidence of postoperative SSI or symptomatic SEH.

The dorsal horn (DH) of the spinal cord is the integrative center that processes and transmits pain sensation. Abnormal changes in ion channel expression can enhance the excitability of pain-related DH neurons. Sodium-activated potassium (K ) channels are highly expressed particularly in the central nervous system; however, information about whether rat DH neurons express the SLICK channel protein is lacking, and the direct effects on SLICK in response to inflammation and the potential signaling pathway mediating such effects are yet to be elucidated. Here, using cultured DH neurons, we have shown that tumor necrosis factor-α inhibits the total outward potassium current I and the K current predominantly as well as induces a progressive loss of firing accommodation. However, we found that this change in channel activity is offset by the p38 inhibitor SB202190, thereby suggesting the modulation of SLICK channel activity via the p38 MAPK pathway. Furthermore, we have demonstrated that the tumor necrosis factor-α modulation of K channels does not occur at the level of SLICK channel gating but arises from possible posttranslational modification.

Purpose We conducted a systematic review and meta-analysis to compare the clinical outcomes of percutaneous endoscopic lumbar discectomy (PELD) and microendoscopic discectomy (MED) for the treatment of lumbar disc herniation (LDH), and to clarify whether PELD is more superior to MED. Methods We performed a comprehensive search in the databases of MEDLINE, EMBASE, PubMed, Web of Science, Cochrane database, CNKI, and Wanfang Data to acquire all relevant studies up to July 2018. The searched literatures were then screened according to the strict inclusion and exclusion criteria. The critical data were extracted and analyzed utilizing Review Manager software. The pooled effects were calculated by mean difference (MD) or odds ratio (OR) with 95% confidence intervals (CI) on the basis of data attributes. Results A total of 18 studies (2161 patients, 1093 in the PELD group and 1068 in the MED group) were included in this systematic review and meta-analysis. At last follow-up, the results revealed that no significant difference was found between PELD group and MED group with respect to ODI (MD − 0.30; 95% CI − 1.02 to 0.42; P  = 0.41), VAS-leg pain (MD − 0.18; 95% CI − 0.45 to 0.09; P  = 0.19), VAS-unspecified (MD − 0.00; 95% CI − 0.05 to 0.04; P  = 0.94), excellent & good rate (OR, 1.04; 95% CI 0.68 to 1.59; P  = 0.86), total complication rate (OR, 0.96; 95% CI 0.65 to 1.43; P  = 0.85), dural tear rate (OR, 0.39; 95% CI 0.10 to 1.55; P  = 0.18), and residue or recurrence rate (OR, 2.22; 95% CI 1.02 to 4.83; P  = 0.05). When compared to MED group, the PELD group showed significantly better results with regard to shorter length of incision (MD − 1.18; 95% CI − 1.39 to − 0.97; P  < 0.00001), less blood loss (MD − 45.17; 95% CI − 64.74 to − 25.60; P  < 0.00001), shorter post-operative in-bed time (MD − 59.11; 95% CI − 71.19 to − 47.04; P  < 0.00001), shorter post-operative hospital stay (MD − 3.07; 95% CI − 4.81 to − 1.33; P  < 0.00001), shorter total hospital stay (MD − 2.29; 95% CI − 3.03 to − 1.55; P  < 0.00001), and lower VAS-back pain at last follow-up (MD − 0.77; 95% CI − 1.31 to − 0.24; P  = 0.005), but with significantly worse results such as more fluoroscopy (MD 7.63; 95% CI 5.25 to 10.01; P  < 0.00001) and higher re-operation rate (OR, 2.67; 95% CI 1.07 to 6.67; P  = 0.04). Although no significant difference was found between the two groups in terms of duration of operation (MD 6.27; 95% CI − 2.44 to 14.98; P  = 0.16) and total hospital cost (MD − 0.69; 95% CI − 12.60 to 11.23; P  = 0.91), further subgroup analysis revealed that the duration of operation was significantly longer in the PELD group compared with the MED group in “Years before 2016” (MD 24.97; 95% CI 7.07 to 42.87; P  = 0.006) and “Year 2016 to 2017” (MD 6.57; 95% CI 0.58 to 12.55; P  = 0.03) subgroups but not in the subgroup “Year 2018” (MD − 5.66; 95% CI − 18.84 to 7.53; P  = 0.40), and that the total hospital cost was significantly more in the PELD group compared with the MED group in the subgroup “Southeast of China” (MD 6.67; 95% CI 3.23 to 10.28; P  = 0.0002) but not in the subgroup “Midwest of China” (MD − 8.09; 95% CI − 17.99 to 1.80; P  = 0.11). Conclusions For the treatment of LDH, both of PELD and MED can reach excellent results and no superiority was found between the two minimally invasive procedures with regard to duration of operation, ODI, VAS-leg pain, VAS-unspecified, excellent & good rate, total complication rate, dural tear rate, and residue or recurrence rate. While PELD can achieve better outcomes with respect to the length of incision, blood loss, post-operative in-bed time, post-operative hospital stay, total hospital stay, and VAS-back pain at last follow-up, however, MED showed certain advantages of less fluoroscopic times and lower re-operation rate. More practice and development are needed to make up for the deficiencies of PELD. Besides, the economic factor should also be considered according to different regions before making the treatment strategies. Well-defined randomized controlled trials with large samples are needed to further confirm these results.

Activation of acid-sensing ion channel 1a (ASIC1a) is responsible for tissue injury caused by acidosis in nervous systems. But its physiological and pathological roles in nucleus pulposus cells (NPCs) are unclear. The aim of this study is to investigate whether ASIC1a regulates the survival of NPCs in the acidic environment of degenerated discs. NPCs were isolated and cultured followed by immunofluorescent staining and Western-blot analysis for ASIC1a. Intracellular calcium ([Ca ] ) was determined by Ca -imaging using Fura-2-AM. Cell necrosis, apoptosis, and senescence following acid exposure were determined using lactate dehydrogenase (LDH) release assay, annexin V-fluorescein isothiocyanate/propidium iodide dual-staining and cell cycle analysis, respectively, followed by Western-blot analysis for apoptosis-related proteins (Bax, Bcl-2, and caspase-3) and senescence-related proteins (p53, p21, and p16). Effects of treatment with psalmotoxin-1 (PcTX1, blocker of ASIC1a) on [Ca ] and cell survival were investigated. ASIC1a was detected in healthy NPCs, and its expression was significantly higher in degenerated cells. When NPCs were treated with PcTX1, acid-induced increases in [Ca ] were significantly inhibited. PcTX1 treatment also resulted in decreased LDH release, cell apoptosis and cell cycle arrest in acid condition. Acid exposure decreased the expression of Bcl-2 and increased the expression of Bax, cleaved caspase-3 and senescence-related proteins (p53, p21, and p16), which was inhibited by PcTX1. The present findings suggest that further understanding of ASIC1a functionality may provide not only a novel insight into intervertebral disc biology but also a novel therapeutic target for intervertebral disc degeneration.

Acid-sensing ion channel 1a (ASIC1a) participates in human intervertebral disc degeneration (IVDD) and regulates the destiny of nucleus pulposus cells (NPCs) in acid stimulus. However, the mechanism of ASIC1a activation and its downstream pathway remain unclear. Endoplasmic reticulum (ER) stress also participates in the acid-induced apoptosis of NPCs. The main purpose of this study was to investigate whether there is any connection between ASIC1a and ER stress in an acid-induced nucleus pulposus degeneration model. The IVDs of Sprague-Dawley rats were stained by immunohistochemical staining to evaluate the expression of ASIC1a in normal and degenerated rat nucleus pulposus. ASIC1a expression was also quantified by quantitative real-time-polymerase chain reaction and Western blotting analysis. NPCs were exposed to the culture media with acidity at pH 7.2 and 6.5 for 24 h, with or without 4-phenylbutyrate (4-PBA, a blocker of the ER stress pathway). Cell apoptosis was examined by Annexin V/Propidium Iodide (PI) staining and was quantified using flow cytometry analysis. ASIC1a-mediated intracellular calcium was determined by Ca imaging using Fura-2-AM. Acidity-induced changes in ER stress markers were studied using Western blotting analysis. , ASIC1a expression was upregulated in natural degeneration. , acid stimulus increased intracellular calcium levels, but this effect was blocked by knockdown of ASIC1a, and this reversal was partly inhibited by 4-PBA. In addition, blockade of ASIC1a reduced expression of ER stress markers, especially the proapoptotic markers. ASIC1a partly regulates ER stress and promotes apoptosis of NPCs under acid stimulus and may be a novel therapeutic target in IVDD.