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Abstract Background Zfx is a zinc finger protein of the Zfy family, whose members are highly conserved in vertebrates. Zfx is a shared transcriptional regulator of both embryonic stem cells (ESC) and hematopoietic stem cells (HSC), which suggests a common genetic basis of self-renewal in embryonic and adult stem cells. The level of Zfx expression correlates with aggressiveness and severity in many cancer types, including prostate cancer, breast cancer, and leukemia. However, the importance of Zfx in human glioma is largely unknown. In the present study, we examined the role of Zfx in human glioma. Methods We detected expression levels of Zfx mRNA in U251 cells, U87 cells, U373 cells, and A172 cells by semi-quantitative RT-PCR. To analyze the expression of Zfx mRNA in glioma tissues, we performed real-time quantitative PCR on 35 pathologically confirmed glioma samples (Grade I-4cases, Grade II-13cases, Grade III-11cases, and Grade IV-7cases) and on 5 noncancerous brain tissue samples. We used lentivirus-mediated small interfering RNAs (siRNAs) to knock down Zfx expression in the human malignant glioma cell line U251. Changes in Zfx target gene expression were determined by real-time RT-PCR. Cell proliferation was examined by a High Content Screening assay. DNA synthesis in proliferating cells was determined by BrdU incorporation. Cell cycle distribution and apoptosis were detected by flowcytometric analysis. Results We discovered that Zfx mRNA was expressed in U251 cells, U87 cells, U373 cells, and A172 cells. The expression level of Zfx is significantly higher in gliomas compared to noncancerous brain tissue. Using a lentivirus-based RNAi approach, Zfx expression was significantly inhibited in human glioblastoma U251 cells. The effects of Zfx knockdown on cell proliferation, cell cycle distribution, and apoptosis were assessed. Inhibition of Zfx expression in U251 cells by RNAi significantly impaired cell proliferation, increased apoptosis, and arrested cells in S phase. Conclusions The results of our study demonstrate that the Zfx gene is highly expressed in glioma tissue and in glioma cell lines. Furthermore, Zfx may play a critical role in cell proliferation, cell cycle distribution, and apoptosis of human malignant glioma cells.

Long noncoding RNAs (lncRNAs) have been proven to exert important functions in the various biological processes of human cancers. It has been reported that lncRNA HNF1 homeobox A antisense RNA 1 (HNF1A‐AS1) was abnormally expressed and played a role in the initiation and development of various human cancers. In this study, we confirmed that the expression level of HNF1A‐AS1 was increased in glioma tissues and cells. Knockdown of HNF1A‐AS1 inhibited cell proliferation and promoted cell apoptosis in glioma. Then, we disclosed the downregulation of miR‐363‐3p in glioma tissues and cell lines. The interaction between HNF1A‐AS1 and miR‐363‐3p was identified in glioma cells. Furthermore, an inverse correlation between HNF1A‐AS1 and miR‐363‐3p was observed in glioma tissues. Afterwards, we recognized that MAP2K4 was a direct target of miR‐363‐3p. The expression of MAP2K4 was negatively correlated with miR‐363‐3p while positively related to HNF1A‐AS1 in glioma tissues. We also found the regulatory effect of HNF1A‐AS1 on the MAP2K4‐dependent JNK signaling pathway. All findings indicated that HNF1A‐AS1 induces the upregulation of MAP2K4 to activate the JNK signaling pathway to promote glioma cell growth by acting as a miR‐363‐3p sponge. [ABSTRACT FROM AUTHOR]

Glioblastoma (GBM) is the most universal and invasive brain tumor among adults. Increasing studies have reported that long noncoding RNAs play vital roles in regulating downstream molecules at the transcriptional or posttranscriptional level in tumor progression. The purpose of the current research was to inquire the modulation mechanism by which homeobox B cluster antisense RNA 1 (HOXB‐AS1) functioned in GBM. Our study first discovered the lifted expression of HOXB‐AS1 and its nearby genes HOXB2 and HOXB3 in GBM and the positive relationship between HOXB‐AS1 and HOXB2 or HOXB3. Loss‐of‐function assays and in vivo study detected that silencing of HOXB‐AS1, HOXB2, or HOXB3 restrained the proliferation and induced the apoptosis in GBM. In addition, mechanism experiments demonstrated that HOXB‐AS1 recruited interleukin enhancer‐binding factor 3 (ILF3) to regulate HOXB2 and HOXB3 expression at the transcriptional level, and HOXB‐AS1 sponged miR‐186‐5p to modulate HOXB2 and HOXB3 expression at posttranscriptional level. Finally, the regulatory mechanism of HOXB‐AS1 in GBM was certified through rescue experiments. Our results indicated that HOXB‐AS1 boost the HOXB2 or HOXB3 expression at the transcriptional and posttranscriptional levels. We detected the HOXB‐AS1‐ILF3‐HOXB2/HOXB3 axis and HOXB‐AS1‐miR‐186‐5p‐HOXB2/HOXB3 axis driving the GBM progression, which might generate more effective diagnostic biomarkers and therapeutic targets for patients with GBM. [ABSTRACT FROM AUTHOR]

Abstract: Generally, cBN crystals exhibit many colors from white, yellow to black due to different impurities and defects present in them. In this paper, black cBN crystals with relatively integrated octahedral morphology were obtained in hBN–Li3N–B system under high temperature and high pressure. The color, morphology and property of the synthesized cBN crystals were extensively studied. X-ray diffraction (XRD) and Raman spectroscopy were used to characterize the synthesized cBN single crystals. We found that boron entered into the synthesized black cBN crystals through the way of substituting N vacancy and resulted in a change in color and morphology. We brought out a different coloration mechanism compared with a previous study according to the results in this system. The residual stress in the synthesized cBN crystals, which was calculated by the results of Raman spectroscopy, decreased markedly with the increase in the content of additive boron. [Copyright &y& Elsevier]

Abstract The metastatic potential of malignant tumor has been shown to be correlated with the increased expression of tri- and tetra-antennary β1,6- N -acetylglucosamine (β1,6-GlcNAc) N -glycans. In this study, We found that GnT-V expression was negatively correlated with receptor protein tyrosine phosphatase type μ(RPTPμ) in human glioma tissues. To study whether RPTPμ is a novel substance of GnT-V which further affect RPTPμ′s downstream dephosphorylation function, we preform lentiviral infection with GnT-V gene to construct stably transfected GnT-V glial cell lines. We found RPTPμ undergone severer cleavage in GnT-V transfected glioma cells compare to Mock cells. RPTPμ intracellular domain fragments increased while β1,6-GlcNAc-branched N -glycans increased, in consistent with the decrease of RPTPμ′s catalytic activity. The results showed that abnormal glycosylation could decrease the phosphorylation activity of PTP μ, and affect PLCγ-PKC pathways. Both protease inhibitor Furin and N -glycan biosynthesis inhibitor swainsonine could decrease cell mobility in GnT-V-U87 transfectants and other glioma cell lines. All results above suggest increased post-translational modification of RPTPμ N -glycans by GnT-V attenuates its tyrosine phosphatase activity and promotes glioma cell migration through PLCγ-PKC pathways, and that the β1,6-GlcNAc-branched N -glycans of RPTPμ play a crucial role in glioma invasivity. [ABSTRACT FROM AUTHOR]

Background:To assessed the significance of thoracic injury on the 30-day mortality and outcome of traumatic brain injury (TBI). Methods:TBI patients admitted to our department were retrospectively evaluated. We developed two prognostic models based on admission predictors with logistic regression analysis to assess the significance of thoracic injuries in determining the 30-day mortality and outcome. The internal validity of the models was evaluated with the bootstrap re-sampling technique. We also validated the models in an external series of 165 patients that collected from our center. Discriminative ability was evaluated with C statistic. Calibrative ability was assessed with the Hosmer-Lemeshow test (H-L test). Results:Among 505 TBI patients admitted, 102 (20.2%) had thoracic injuries. Patients with a PCS ≥6 had a 3.142 and 8.065 times higher odds of mortality and poor outcome compared with patients with a PCS <6, respectively. Any one-score increase of the TTS had a 1.193 times higher odds of a poor outcome (p = 0.017). The predictive model for mortality and 30-day functional outcome both had good accuracy (AUC: 0.875; 95% confidence interval [CI], 0.841–0.910 and AUC: 0.888; 95%CI, 0.860–0.916, respectively). Internal validation showed no over optimism in any of the two models’ predictive C statistics (C statistic 0.872 for 30-day mortality and C statistic 0.884 for the 30-day neurological outcome). The external validation confirmed the discriminatory ability of these models (C statistic 0.949 (95%CI: 0.919–0.980) for 30-day mortality and C statistic 0.915 (95%CI: 0.868–0.963) for the 30-day neurological outcome). The calibration was also good for patients from the validation population (H-L test p>0.05). Conclusion:Thoracic injury diagnosed by CT has a negative impact on the 30-day mortality and functional outcome of TBI patients. The extent of PC and the TTS are the predictors for TBI outcome. [ABSTRACT FROM AUTHOR]

Abstract: In this paper, the influence of hBN crystallinity and additive Lithium hydride (LiH) on cBN synthesis with Lithium nitride (Li3N) as catalyst was investigated under the pressure of 4.5–5 GPa and the temperature of 1500–1700 °C. hBN with different crystallinities was obtained by the same hBN. Some were explored to high pressure and high temperature, and others were subjected to heat treatment with alkali. X-ray diffraction (XRD), Raman spectroscopy and X-ray photoelectronic spectroscopy (XPS) were used to characterize the property of the starting materials. The synthesized samples were observed by optical microscopy (OM). The results indicated that besides the crystallinity of hBN, which is a general parameter for controlling the structural quality of hBN powders, some other factors such as the content of B+ at the surface of hBN and additive LiH all strongly influence the synthesis of cBN. [Copyright &y& Elsevier]

Background: As antioxidant and anti-inflammatory agents, carbonic anhydrase inhibitors can exert potentially useful therapeutic effects following central nervous system trauma, including intracerebral hemorrhage (ICH). However, the therapeutic efficacy of ethoxyzolamide (ETZ) as a novel carbonic anhydrase inhibitor for ICH has not yet been determined., Methods: An autologous blood injection method was used to establish ICH models, which were then used to establish the effects of intraperitoneal injection of ETZ on ICH. Neuronal damage, apoptotic protein expression, oxidative and inflammatory factor content, microglia marker Iba-1 positivity, hepatic and renal pathological changes, and serum concentrations of hepatic and renal function indices were assessed by Nissl staining, western blotting, enzyme-linked immunosorbent assay (ELISA), immunohistochemistry, hematoxylin and eosin (HE) staining, and automatic biochemical analysis in brain tissues., Results: The ICH group showed massive hemorrhagic foci; significant increases in brain water content, modified mouse neurological deficit scoring (mNSS) score, pro-apoptotic protein expression, oxidative factors, pro-inflammatory factors, and Iba-1 positivity; and significant reductions in Nissl body size, anti-apoptotic protein expression, and antioxidant factors, all of which were reversed by ETZ in a dose-dependent manner. ETZ has a good biosafety profile with no significant burden on the human liver or kidneys. The Kelch-like ECH-associated protein 1 (Keap1)/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway was mildly activated in ICH mice, and was further increased after ETZ injection. Molecular docking experiments revealed that ETZ could dock onto the Nrf2-binding domain of keap1., Conclusions: ETZ, as a novel carbonic anhydrase inhibitor, further activated the Keap1/Nrf2 pathway by docking with the Nrf2-binding domain of keap1, thereby exerting antioxidant, anti-inflammatory, anti-apoptotic, and cerebral neuroprotective effects in ICH mice., (© 2024 The Author(s). Published by IMR Press.)

Zinc-finger protein X-linked (ZFX) has been demonstrated to play an important role in the development of human malignancies. However, its prognostic significance in cancer patients remains unclear and less is known about its role in colorectal cancer (CRC). In this study, we found that the expression of ZFX in CRC tissues was significantly higher than that in corresponding normal tissues by quantitative real-time polymerase chain reaction and Western blot. Using immunohistochemistry, we explored the associations between protein expression of ZFX and clinicopathological parameters in 120 CRC cases. The results showed that ZFX expression was significantly associated with tumor differentiation (P = 0.022), tumor size (P = 0.037), tumor invasion (P = 0.027), lymph node metastasis (P = 0.042), distant metastasis (P = 0.011), and Dukes' classification (P = 0.028). Moreover, according to Kaplan-Meier model, patients with high expression of ZFX had a significantly poorer prognosis compared to those with low expression of ZFX. Multivariate analysis suggested that high expression of ZFX was an independent prognostic factor for CRC patients. In conclusion, our findings for the first time demonstrated that ZFX expression may be associated with the progress of CRC and suggested that ZFX has the potential value to be an effective prognostic predictor for CRC patients.