Purpose: To report complications after epilepsy surgery, grade the severity of complications, investigate risk factors, and develop a nomogram for risk prediction of complications. Methods: Patients with epilepsy surgery performed by a single surgeon at a single center between October 1, 2003 and April 30, 2019 were retrospectively analyzed. Study outcomes included severity grading of complications occurring during the 3-month period after surgery, risk factors, and a prediction model of these complications. Multivariable logistic regression analysis was used to calculate odds ratio and 95% confidence interval to identify risk factors. Results: In total, 2,026 surgical procedures were eligible. There were 380 patients with mild complications, 23 with moderate complications, and 82 with severe complications. Being male (odds ratio 1.29, 95% confidence interval 1.02-1.64), age at surgery (>40 years: 2.58, 1.55-4.31; ≤ 40: 2.25, 1.39-3.65; ≤ 30: 1.83, 1.18-2.84; ≤ 20: 1.71, 1.11-2.63), intracranial hemorrhage in infancy (2.28, 1.14-4.57), serial number of surgery ( ≤ 1,000: 1.41, 1.01-1.97; ≤ 1,500: 1.63, 1.18-2.25), type of surgical procedure (extratemporal resections: 2.04, 1.55-2.70; extratemporal plus temporal resections: 2.56, 1.80-3.65), surgery duration (>6 h: 1.94, 1.25-3.00; ≤ 6: 1.92, 1.39-2.65), and acute postoperative seizure (1.44, 1.06-1.97) were independent risk factors of complications. A nomogram including age at surgery, type of surgical procedure, and surgery duration was developed to predict the probability of complications. Conclusions: Although epilepsy surgery has a potential adverse effect on the patients, most complications are mild and severe complications are few. Risk factors should be considered during the perioperative period. Patients with the above risk factors should be closely monitored to identify and treat complications timely. The prediction model is very useful for surgeons to improve postoperative management.
Circular RNAs are involved in the pathogenesis of various diseases, although its expression pattern and role in polycystic ovary syndrome (PCOS), characterised by hyperandrogenism, are not very clear. This article assessed the circRNAs expression profile in the ovaries of PCOS mice by circRNAs high-throughput sequencing and explored the role of circEpha5 in hyperandrogenism. The results showed that the overexpression of circEpha5 in mouse preantral follicles could increase the expression of Cyp17a1, an androgen synthesis-related gene, which resulted in a higher serum level of testosterone. Dual-luciferase reporter gene studies identified miR-758-5p as a direct target of circEpha5. Consequently, miR-758-5p expression was downregulated upon circEpha5 overexpression. Ectopically expressed miR-758-5p reversed the stimulation effects of circEpha5 on steroidogenesis-related gene expression and testosterone release. Therefore, circEpha5 could sponge miR-758-5p to regulate the expression of Cyp17a1, thereby promoting the synthesis and secretion of androgen in the preantral follicles. This work is contributed to the understanding of the pathogenesis of hyperandrogenemia and lays the foundation for the development of therapeutic targets of PCOS hyperandrogenism. What is already known on this subject? PCOS is a complex endocrine and metabolic disorders with hyperandrogenism as the main clinical manifestation. There are a variety of abnormal expression circRNAs in PCOS, however, the relationship between circEpha5 and hyperandrogenism has yet to be fully elucidated. What do the results of this study add? We first found that expression levels of serum circEpha5 were significantly higher in PCOS than in a normal group. Using mouse preantral follicle culture model and the letrozole-induced PCOS mouse model, the mechanism of CircEpha5 regulating androgen secretion was studied. What the implications are of these findings for clinical practice and/or further research? It was revealed that CircEpha5 can absorb miR-758-5p in the sponge to regulate the expression of Cyp17a1, thereby promoting the synthesis and secretion of androgen in preantral follicles, which may become a key target for the screening and treatment of PCOS hyperandrogenism.
Street is believed as one of most important public spaces in a city, which carries the commuting, shopping, recreation, and communication functions of citizens' daily life.However, during the rapid urban expansions, street spaces in cities have also encountered many troubles, such as decreased street space quality, diminished suitability for street-walking, insufficient street security, and low street vitality.Therefore, how to enhance the street walkability through human scale and how to build a healthy and sustainable city development model become core arguments in the relevant fields.Most of the previous research usually focuses on the transportation aspect of streets, addressing their accessibility and permeability, whereas the human-scale aspects of street space quality has been largely ignored.Therefore, this article selects street walkability as the research object, looking into a city's central district area in specific.A multi-source database is established, based on urban 3D morphology big data, POIs data, and street image data for the quantitative analysis of this research.The results depict a fanshaped circular distribution pattern for the street walkability-measured into accessibility, convenience, comfort, and safety-in the central area of Nanjing city, consisting of a multi-core connected central area and scattered fringe areas.In addition, the interactive mechanism between street walkability and the influencers, such as urban 3D morphology, natural environment, landscape, and urban function distribution and POIs is found.Based on that, strategies with an aim of walkability optimization are further provided.
<p>Supplementary Figure 1. Hedgehog pathway is not activated in U251 cells. Supplementary Figure 2. Colony formation from passaged U251 cells after Nestin knockdown. Supplementary Figure 3. GBM cells from PDX undergo apoptosis after Nestin knockdown. Supplementary Figure 4. Nestin deletion causes G2/M arrest and apoptosis in U251 cells. Supplementary Figure 5. Colony formation from U87 cells after transduction with Nestin shRNA. Supplementary Figure 6. No alterations in the mRNA expression of TUBB2A and TUBB2B in U251 cells after Nestin manipulation. Supplementary Figure 7. No alterations in the expression of Nestin mRNA and protein in U251 cells after βII-tubulin knockdown.</p>
Multiple myeloma (MM) is incurable once osteocytic lesions have seeded at skeletal sites, but factors mediating this deadly pathogenic advance remain poorly understood. Here we report evidence of a major role for the cell adhesion molecule CD166, which we discovered to be highly expressed in MM cell lines and primary bone marrow (BM) cells from patients. CD166+ MM cells homed more efficiently than CD166- cells to the BM of engrafted immunodeficient NSG mice. CD166 silencing in MM cells enabled longer survival, a smaller tumor burden and less osteolytic lesions, as compared to mice bearing control cells. CD166 deficiency in MM cell lines or CD138+ BM cells from MM patients compromised their ability to induce bone resorption in an ex vivo organ culture system. Further, CD166 deficiency in MM cells also reduced formation of osteolytic disease in vivo after intra-tibial engraftment. Mechanistic investigation revealed that CD166 expression in MM cells inhibited osteoblastogenesis of BM-derived osteoblast progenitors by suppressing RUNX2 gene expression. Conversely, CD166 expression in MM cells promoted osteoclastogenesis by activating TRAF6-dependent signaling pathways in osteoclast progenitors. Overall, our results define CD166 as a pivotal director in MM cell homing to the BM and MM progression, rationalizing its further study as a candidate therapeutic target for MM treatment.
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