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Introduction: Spontaneous cerebrospinal fluid rhinorrhea (SCSFR) is the most common type of cerebrospinal fluid leakage and may cause serious cerebral complications. The aim of this research was to investigate the relationship between the degree of pneumatization variants of the paranasal sinus and skull base and the incidence of SCSFR. Methods: In total, 131 patients with SCSFR were analyzed, and 50 patients suffering from the nasal septal deviation were selected as controls. The pneumatization of the paranasal sinus and skull base was observed by CT scan. Results: Among the 137 fistulas, 55 (40.15%) were found in the ethmoid sinus. The incidences of Onodi cells (27.27 vs. 8%) and type 3 lateral recess of the sphenoid sinus (LRSS, 70.37 vs. 22%) in the SCSFR subgroups were significantly higher than those in the control group (p < 0.05). Moreover, the occurrence of SCSFR was linearly correlated with the classification of Onodi cells and LRSS (p < 0.05). There was no significant difference in the incidence of frontal cells, anterior clinoid process pneumatization, and posterior clinoid process pneumatization between the SCSFR patients and the controls. Conclusion: The most common site of SCSFR is the ethmoid sinus. The excessive pneumatization of the Onodi cell and LRSS increases the risk for the occurrence of SCSFR in the ethmoid sinus and sphenoid sinus, respectively. The possible association between the paranasal sinus ontogeny and SCSFR pathophysiology needs further studies.

Due to the high scalability of deep learning and its ability to manipulate large-scale hyperparameters, it has achieved great success in many fields. However, encoding such a large-scale data set is ultimately at the cost of expensive computing power and storage resources, which has also prompted model compression and model acceleration to become a hot topic in recent years. Model pruning, weight decomposition, reduction of model accuracy, weight sharing, etc. are all currently popular solutions, but they have a common problem that they cannot ensure that the compressed model is as good as the original model, and they are all based on the original model. to modify. This paper draws on the method based on knowledge distillation, introduces the concept of Renyi-divergence popularized by KL-divergence, and proposes a loss function that has been based on Renyi-divergence distance metric, and uses the rigor of the student network as a hyperparameter. A student network model that minimizes the loss function under rigor. We validated our results on ResNets using the cifar-10, cifar-100, and imagenet datasets. It improved the basic model by 0.6%, and the absolute gain of Top-l accuracy exceeded 1.6%.

Nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome is an important inflammasome in mammals, which is of great significance to eliminate pathogens. However, the research of the NLRP3 inflammasome in teleost is limited. Tetraodon nigroviridis has the characteristics of small genome and easy feeding, which can be used as a model for the study of fish immune function. In present study, three NLRP3 inflammasome component genes (NLRP3, ASC and caspase-1) in T. nigroviridis has been cloned. Real-time fluorescence quantitative PCR showed that TnNLRP3 (T. nigroviridis NLRP3), TnASC (T. nigroviridis ASC) and Tncaspase-1 (T. nigroviridis caspase-1) mRNA in various tissues from health T. nigroviridis were highly expressed in immune-related tissues, such as spleen, gill, head kidney and intestine. After Vibrio parahemolyticus infection, the expression of TnNLRP3, TnASC and Tncaspase-1 mRNA in spleen, gill, head kidney reached a peak at 24 h, and the expression levels of these genes in intestine were the highest at 48 h. After the transfection of TnASC-pAcGFP-N1 monomer GFP plasmid into cos-7 cells, ASC specks, the activation marker of NLRP3 inflammasome, were observed. Bimolecular fluorescence complementarity and fluorescence colocation experiment showed that TnASC and Tncaspase-1 of TnNLRP3 inflammasome were co-located near the cell nucleus, and potentially interacted with each other. NLRP3 inflammasome inducer nigericin and agonist ATP could significantly induce the expression of TnNLRP3, TnASC and Tncaspase-1 mRNA, and activation of NLRP3 inflammasome could promote the generation of mature TnIL-1β (T. nigroviridis IL-1β). These results uncover that T. nigroviridis NLRP3 inflammasome could participate in the antibacterial immune response and the generation of mature TnIL-1β after activation.

BACKGROUND Classifying brain tumors preoperatively provides essential information for guiding treatment plans. However, existing classification methods require manual intervention which often suffer from efficiency and accuracy issues. OBJECTIVE The objective of our study was to Improve the accuracy and efficiency of brain tumor grading or classification. This shows that our method is to help clinicians diagnose brain tumor and formulate treatment plans. METHODS Our proposed method uses a DenseNet-ResNet based U-Net framework to optimize the task of extracting features from brain tumor MRI image data. It also adopts a CRNN model to classify brain tumors from sequence data. The characteristic of our method is that it needs only one sequence-level label, instead of many frame-level labels for each patient. RESULTS We proposed an automated MRI classification method for brain tumor, with an average accuracy of 90.72% for glioma classification, 94.35% for glioma IDH1 mutation classification, and 94.64% for pituitary tumor texture classification. CONCLUSIONS Compared with existing purely auto-encoder based methods, ours has much better efficiency.

Tumor necrosis factor-α (TNF-α) is an important inflammation cytokine without known direct effect on DNA. In this study, we found that TNF-α can cause DNA damages through reactive oxygen species. The mutagenic effect of TNF-α is comparable with that of ionizing radiation. TNF-α treatment in cultured cells resulted in increased gene mutations, gene amplification, micronuclei formation, and chromosomal instability. Antioxidants significantly reduced TNF-α–induced genetic damage. TNF-α also induced oxidative stress and nucleotide damages in mouse tissues in vivo. Moreover, TNF-α treatment alone led to increased malignant transformation of mouse embryo fibroblasts, which could be partially suppressed by antioxidants. As TNF-α is involved in chronic inflammatory diseases, such as chronic hepatitis, ulcerative colitis, and chronic skin ulcers, and these diseases predispose the patients to cancer development, our results suggest a novel pathway through which TNF-α promotes cancer development through induction of gene mutations, in addition to the previously reported mechanisms, in which nuclear factor-κB activation was implicated. (Cancer Res 2006; 66(24): 11565-70)

Supplementary Materials and Figure Legend from Tumor Necrosis Factor-α Is a Potent Endogenous Mutagen that Promotes Cellular Transformation

Supplementary Figure 1 from Tumor Necrosis Factor-α Is a Potent Endogenous Mutagen that Promotes Cellular Transformation

Angiopoietin-2 (Ang-2) is a conditional antagonist and agonist for the endothelium-specific Tie-2 receptor. Although endogenous Ang-2 cooperates with vascular endothelial growth factor (VEGF) to protect tumor endothelial cells, the effect on tumor vasculature of high levels of exogenous Ang-2 with different levels of VEGF has not been studied in detail. Here, we report that systemic overexpression of Ang-2 leads to unexpected massive tumor vessel regression within 24 h, even without concomitant inhibition of VEGF. By impairing pericyte coverage of the tumor vasculature, Ang-2 destabilizes the tumor vascular bed while improving perfusion in surviving tumor vessels. Ang-2 overexpression transiently exacerbates tumor hypoxia without affecting ATP levels. Although sustained systemic Ang-2 overexpression does not affect tumor hypoxia and proliferation, it significantly inhibits tumor angiogenesis, promotes tumor apoptosis, and suppresses tumor growth. The similar antitumoral, antiangiogenic efficacy of systemic overexpression of Ang-2, soluble VEGF receptor-1, and the combination of both suggests that concomitant VEGF inhibition is not required for Ang-2–induced tumor vessel regression and growth delay. This study shows the important roles of Ang-2–induced pericyte dropout during tumor vessel regression. It also reveals that elevated Ang-2 levels have profound pleiotropic effects on tumor vessel structure, perfusion, oxygenation, and apoptosis. [Cancer Res 2007;67(8):3835–44]

Three-dimensional (3D) frameworks have received much attention as an effective modification strategy for next-generation high-energy–density lithium metal batteries. However, the top-growth mode of lithium (Li) on the 3D framework remains a tough challenge. To achieve a uniform bottom-up Li growth, a scheme involving Ag concentration gradient in 3D PVDF framework (C-Ag/PVDF) is proposed. Ag nanoparticles with a concentration gradient induce an interface activity gradient in the 3D framework, and this gradient feature is still maintained during the cycle. As a result, the C-Ag/PVDF framework delivers a long lifespan over 1800 h at a current density of 1 mA cm−2 with a capacity of 1 mAh cm−2, and shows an ultra-long life (>1300 h) even at a high current density of 4 mA cm−2 with a capacity of 4 mAh cm−2. The advantage of concentration gradient provides further insights into the optimal design of the 3D framework for stable Li metal anode.

Background: Staphylococcus aureus biofilms were linked to negative postsurgical outcomes of chronic rhinosinusitis (CRS). This study aims to develop a targeted nanoparticle and characterize its bactericidal effects. Methods: The authors prepared ISMN-loaded poly-lactide-co-glycolide acid (PLGA) and polyethylene glycol (PEG) nanoparticles conjugated with anti- S. aureus α-toxin (AA; ISMN-PLGA-PEG-AA), and determined its bactericidal and toxic effects. The antibiofilm propriety of ISMN-PLGA-PEG-AA was further investigated in a sheep CRS model. Results: ISMN-PLGA-PEG-AA had no toxic effect, while ISMN, ISMN-PLGA-PEG and ISMN-PLGA-PEG-AA had significantly anti- S. aureus effects. The blood concentrations and mRNA levels in sinus tissues of IL-4, IL-8 and IFN-γ in the sheep CRS model were significantly low. Conclusion: ISMN-PLGA-PEG-AA can effectively inhibit S. aureus biofilm, and is a promising drug for CRS treatment.

In this paper, we consider the following critical p-biharmonic equation involving Hardy potential $$\begin{aligned} \begin{aligned} \Delta _p^2u-\Delta _qu-\mu \frac{|u|^{p-2}u}{|x|^{2p}}=|u|^{p_{*}-2}u,\quad {{x\in \mathbb {R}^{N}}}, \end{aligned} \end{aligned}$$ where $$2\leqslant p

Emerging studies have revealed that non-coding RNAs contribute to regulating intervertebral disc degeneration (IVDD). Here, we intended to probe into the function of miR-19b-3p in IVDD evolvement. The miR-19b-3p level in the intervertebral disc (IVD) tissues of IVDD patients and IL-1β/TNF-α/hydrogen peroxide-treated human nucleus pulposus cells (HNPCs) was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Also, qRT-PCR was conducted to examine the profiles of MMP-3, MMP-9, MMP-13, ADAMTS-4 and ADAMTS-5. The PTEN/PI3K/Akt/mTOR pathway was examined by Western blot (WB). The miR-19b-3p overexpression assay was carried out, and HNPC proliferation and apoptosis were compared by the cell counting kit-8 (CCK-8) assay and flow cytometry (FCM). In addition, the mechanism of action of miR-19b-3p was clarified using the PTEN inhibitor (VO-Ohpic triphosphate) or the mTOR inhibitor (Rapamycin) on the basis of IL-1β intervention and miR-19b-3p mimics transfection. Our results testified that miR-19b-3p expression was curbed in IVD tissues of the IVDD patients (vs. normal IVD tissues) and IL-1β-, TNF-α, or hydrogen peroxide-treated HNPCs. Up-regulating miR-19b-3p enhanced HNPC proliferation and hampered its apoptosis. Moreover, miR-19b-3p dampened the PTEN profile and activated the PI3K/Akt/mTOR pathway. Interestingly, attenuating PTEN reduced IL-1β-, TNF-α-, or hydrogen peroxide-mediated HNPC apoptosis and up-regulated PI3K/Akt/mTOR, while inhibiting the mTOR pathway offset the protective function of miR-19b-3p. Further mechanism studies illustrated that miR-19b-3p targeted the 3'untranslated region (UTR) of PTEN and abated the PTEN level. This research confirmed that miR-19b-3p suppressed HNPC apoptosis in the in-vitro model of IVDD by regulating PTEN/PI3K/Akt/mTOR pathway.

Children’s programming is widely aroused people’s concern, is a hotspot of research on education, the children’s programming attention to promoting the development of children’s programming education has important significance. Using Baidu index, elastic coefficient, Gini index and geographic concentration coefficient, this paper analyzes the evolution of spatial and temporal distribution and influencing factors of children’s programming attention in China, and establishes the model through panel data model and carries out empirical analysis. The results show that: the public’s attention to children’s programming continues to rise, and is in a gentle stage of development at the present stage. Spatial difference of children’s programming attention is opposite bigger, the eastern region is the most popular children’s programming in the three regions, followed by the, the western region, the internal unbalance in east and west region, the central region in balance, and the central region difference is small, to strengthen the development of the western region to close the gap and balanced development. Regional economic development level and education level have a significant impact on children’s programming attention on the Internet, while educational funds and education level have a significant impact on children’s programming attention in eastern and central China. To improve the development space of children’s programming, we can start from two aspects: strengthening the creation of characteristic learning fields for primary school children’s programming, and improving the wide application of online learning.