Evaluation and analysis of risk factors for adverse events of the fractured vertebra post-percutaneous kyphoplasty: a retrospective cohort study using multiple machine learning models.

BACKGROUND: Adverse events of the fractured vertebra (AEFV) post-percutaneous kyphoplasty (PKP) can lead to recurrent pain and neurological damage, which considerably affect the prognosis of patients and the quality of life. This study aimed to analyze the risk factors of AEFV and develop and select the optimal risk prediction model for AEFV to provide guidance for the prevention of this condition and enhancement of clinical outcomes. METHODS: This work included 383 patients with primary osteoporotic vertebral compression fracture (OVCF) who underwent PKP. The patients were grouped based on the occurrence of AEFV postsurgery, and data were collected. Group comparisons and correlation analysis were conducted to identify potential risk factors, which were then included in the five prediction models. The performance indicators served as basis for the selection of the best model. RESULTS: Multivariate logistic regression analysis revealed the following independent risk factors for AEFV: kissing spine (odds ratio (OR) = 8.47, 95% confidence interval (CI) 1.46-49.02), high paravertebral muscle fat infiltration grade (OR = 29.19, 95% CI 4.83-176.04), vertebral body computed tomography value (OR = 0.02, 95% CI 0.003-0.13, P < 0.001), and large Cobb change (OR = 5.31, 95% CI 1.77-15.77). The support vector machine (SVM) model exhibited the best performance in the prediction of the risk of AEFV. CONCLUSION: Four independent risk factors were identified of AEFV, and five risk prediction models that can aid clinicians in the accurate identification of high-risk patients and prediction of the occurrence of AEFV were developed.

Deep learning-driven diagnosis of multi-type vertebra diseases based on computed tomography images.

Background: Osteoporotic vertebral compression fractures (OVCFs) are the most common type of fragility fracture. Distinguishing between OVCFs and other types of vertebra diseases, such as old fractures (OFs), Schmorl's node (SN), Kummell's disease (KD), and previous surgery (PS), is critical for subsequent surgery and treatment. Combining with advanced deep learning (DL) technologies, this study plans to develop a DL-driven diagnostic system for diagnosing multi-type vertebra diseases. Methods: We established a large-scale dataset based on the computed tomography (CT) images of 1,051 patients with OVCFs from Luhe Hospital and used data of 46 patients from Xuanwu Hospital as alternative hospital validation dataset. Each patient underwent one examination. The dataset contained 11,417 CT slices and 19,718 manually annotated vertebrae with diseases. A two-stage DL-based system was developed to diagnose five vertebra diseases. The proposed system consisted of a vertebra detection module (VDModule) and a vertebra classification module (VCModule). Results: The training and testing dataset for the VDModule consisted of 9,135 and 3,212 vertebrae, respectively. The VDModule using the ResNet18-based Faster region-based convolutional neural network (R-CNN) model achieved an area under the curve (AUC), false-positive (FP) rate, and false-negative (FN) rate of 0.982, 1.52%, and 1.33%, respectively, in the testing dataset. The training dataset for VCModule consisted of 14,584 and 47,604 diseased and normal vertebrae, respectively. The testing dataset consisted of 4,489 and 15,122 diseased and normal vertebrae, respectively. The ResNet50-based VCModule achieved an average sensitivity and specificity of 0.919 and 0.995, respectively, in diagnosing four kinds of vertebra diseases except for SN in the testing dataset. In the alternative hospital validation dataset, the ResNet50-based VCModule achieved an average sensitivity and specificity of 0.891 and 0.989, respectively, in diagnosing four kinds of vertebra diseases except for SN. Conclusions: Our proposed DL system can accurately diagnose four vertebra diseases and has strong potential to facilitate the accurate and rapid diagnosis of vertebral diseases.

Plasmonic distributed feedback lasing in an anodic aluminum oxide/silver/polymer hybrid membrane.

A hybrid membrane is employed as a high-order plasmonic distributed feedback (DFB) cavity to reduce the lasing threshold of polymer lasers. The hybrid membrane consists of an anodic aluminum oxide (AAO) membrane, a 25 nm thick silver layer and a free-standing polymer membrane. The AAO membrane is fabricated by a low-cost, single chemical etching method. Then, a layer of silver with a thickness of 25 nm is sputtered on the surface of the AAO. Subsequently, a polymer membrane is directly attached to the silver-plated AAO membrane, forming an AAO/silver/polymer hybrid membrane. Under optical pumping conditions, low-threshold, three-order DFB lasing is observed. The proposed laser device exhibited a dual-threshold characteristic because of the evolution from amplified spontaneous emission to DFB lasing. And a significant shift from omnidirectional emission to directional emission lasing can be observed while the pump energy density is beyond the second threshold. Furthermore, the plasmonic enhancement sourced from silver corrugation reveals important improvement effects to the DFB lasing of AAO/silver/polymer hybrid membrane for decreasing threshold, narrowing full width at half maximum (FWHM), and an increasing Q factor. This work may promote the design and production of low-cost and large-area high-order plasmonic DFB polymer lasers.

Sorafenib promotes sensory conduction function recovery via miR-142-3p/AC9/cAMP axis post dorsal column injury.

Spinal cord injury results in sensation dysfunction. This study explored miR-142-3p, which acts a critical role in sciatic nerve conditioning injury (SNCI) promoting the repair of the dorsal column injury and validated its function on primary sensory neuron(DRG). miR-142-3p expression increased greatly in the spinal cord dorsal column lesion (SDCL) group and increased slightly in the SNCI group. Subsequently, the expression of adenylate cyclase 9 (AC9), the target gene of miR-142-3p, declined sharply in the SDCL group and declined limitedly in the SNCI group. The expression trend of cAMP was opposite to that of miR-142-3p. MiR-142-3p inhibitor improved the axon length, upregulated the expression of AC9, cAMP, p-CREB, IL-6, and GAP43, and downregulated the expression of GTP-RhoA. miR-142-3p inhibitor combined with AC9 siRNA showed shorter axon length, the expression of AC9, cAMP, p-CREB, IL-6, and GAP43 was decreased, and the expression of GTP-RhoA was increased. H89 and AG490, inhibitors of cAMP/PKA pathway and IL6/STAT3/GAP43 axis, respectively, declined the enhanced axonal growth by miR-142-3p inhibitor and altered the expression level of the corresponding proteins. Thus, a substitution therapy using Sorafenib that downregulates the miR-142-3p expression for SNCI was investigated. The results showed the effect of Sorafenib was similar to that of miR-142-3p inhibitor and SNCI on both axon growth in vitro and sensory conduction function recovery in vivo. In conclusion, miR-142-3p acts a pivotal role in SNCI promoting the repair of dorsal column injury. Sorafenib mimics the treatment effect of SNCI via downregulation of miR-142-3p, subsequently, promoting sensory conduction function recovery post dorsal column injury.

[Radiological characteristics and clinical manifestation of isolated lumbar foraminal stenosis].

OBJECTIVE: To discuss radiological characteristics and clinical manifestation of isolated lumbar foraminal stenosis. METHODS: From March 2011 to March 2014, 21 patients with isolated degenerative lumbar foraminal stenosis accepted lumbar decompression and fusion in Beijing Luhe Hospital. Intervertebral disc space was evaluated by measuring the position of joint-body line on preoperative X-ray. Bilateral foraminal area of the corresponding segment in CT (sagittal view of 2D reconstruction) and MRI (T2W1 sagittal view) were measured by Surgimap software. For patients with unilateral symptoms, foraminal area of the affected side was compared with that of the contralateral side. Foraminal area of the same segment on CT was also compared with that on MRI. Preoperatively and at the final follow-up, visual analogue score (VAS) and Oswestry Disability Index (ODI) were used to evaluate clinical outcomes. RESULTS: All patients had a follow-up over 6 months and the average follow-up was 16.8 months (7-42 months). Of the 21 patients (26 segments), 12 segments showed gross narrowing and 14 segments showed slight narrowing. After preoperative measurement on MRI, 6 patients had foraminal stenosis of grade 2, and 15 patients had foraminal stenosis of grade 3, showing no significant difference in clinical outcomes. Compared with the foraminal area of the unaffected side, the affected side showed a decrease of 16% on CT and 28% on MRI, and the difference was statistically significant (t = 3.453, P < 0.05). The foraminal area measured on CT was larger than that measured on MRI (P < 0.05). Compared with that preoperatively, VAS (back pain), VAS (leg pain) and ODI showed significant improvement at the final follow-up (P < 0.05). CONCLUSIONS: Radiological examinations as X-ray, CT, MRI and intervertebral foramen block technique play an important role in the diagnosis of foraminal stenosis. Soft oppression caused by hyperplasia and hypertrophy of transforaminal ligment or joint capsule may be important promoters of degenerative lumbar foraminal stenosis. Lumbar foraminal decompression and interbody fusion can satisfactorily improve preoperative symptoms.

Zinc depletion reduced Egr-1 and HNF-3beta expression and apolipoprotein A-I promoter activity in Hep G2 cells.

We examined the influence of zinc status on expression of certain transcription factors involved in regulation of apolipoprotein A-I (apoAI) expression in human hepatoblastoma Hep G2 cells. A low zinc basal medium (zinc deficient, ZD) consisting of DMEM and 10% Chelex100-treated fetal bovine serum was used to deplete cellular zinc over one passage. Cells were also cultured for one passage in medium supplemented with 0.4 (ZD0.4), 4.0 (zinc normal, ZN), 16.0 (zinc adequate, ZA), or 32.0 microM zinc (zinc supplemented, ZS). Compared with ZN cells, cellular zinc levels were 43 and 31% lower in ZD and ZD0.4 cells but 70 and 146% higher in ZA and ZS cells, respectively. Supplementation of 0.4 microM zinc significantly increased DNA contents per plate, from 65% in ZD cells to 83% in ZD0.4 cells compared with ZN cells. Addition of >4 microM zinc in medium did not further increase DNA contents. The proportion of cells in G(1)/S and S phase was about fourfold higher and threefold lower, respectively, in ZD cells compared with ZN and other groups. Nuclear Egr-1 protein was markedly decreased in ZD and ZD0.4 cells. Moreover, hepatocyte nuclear factor (HNF)-3beta was severely degraded in ZD and ZD0.4 cells. In contrast, HNF-4alpha remained stable in all groups and was not significantly lower in ZD and ZD0.4 cells. Furthermore, downregulation of trans-acting factor Egr-1 and cleavage of HNF-3beta were associated with reduction of apoAI promoter activity in zinc-deficient Hep G2 cells. Thus zinc is critical in transcriptional regulation of apoAI gene expression in hepatocytes.

p53 protein and p21 mRNA levels and caspase-3 activity are altered by zinc status in aortic endothelial cells.

The influence of zinc status on the levels of p53, as well as downstream targets of p53 in cell repair and survival, was examined in human aortic endothelial cells (HAECs). A serum-reduced low-zinc medium (ZD) was used to deplete zinc over one passage. Other treatments included zinc-normal control (ZN), zinc-adequate (ZA), and zinc-supplemented (ZS) treatment with 3.0, 16.0, and 32.0 microM zinc, respectively. Cellular zinc levels in the ZD cells were 64% of ZN controls; levels in the ZA cells were not different, but levels in ZS cells were significantly higher (40%) than in ZN cells. No difference in p53 mRNA abundance was detected among all treatments; however, p53 nuclear protein levels were >100% higher in the ZD and ZS cells and almost 200% higher in the ZA cells than in ZN controls. In addition, p21 mRNA abundance, a downstream target of p53 protein, was increased in the ZS cells compared with both the ZN control and ZD cells. In the ZS cells, bax and mcl-1 were also approximately 50% higher compared with ZN controls, whereas bcl-2 mRNA was increased compared with ZA cells. Moreover, caspase-3 activity of ZD cells was not different from that of ZN controls but was reduced to 83 and 69% of ZN controls in ZA and ZS cells, respectively. Thus p53 protein and p53 downstream target genes appeared to be modulated by intracellular zinc status in HAECs.