Protective effects of sinomenine against dextran sulfate sodium-induced ulcerative colitis in rats via alteration of HO-1/Nrf2 and inflammatory pathway.

BACKGROUND: Dextran Sulfate Sodium (DSS) induces ulcerative colitis (UC), a type of inflammatory bowel disease (IBD) that leads to inflammation, swelling, and ulcers in the large intestine. The aim of this experimental study is to examine how sinomenine, a plant-derived alkaloid, can prevent or reduce the damage caused by DSS in the colon and rectum of rats. MATERIAL AND METHODS: Induction of ulcerative colitis (UC) in rats was achieved by orally administering a 2% Dextran Sulfate Sodium (DSS) solution, while the rats concurrently received oral administrations of sinomenine and sulfasalazine. The food, water intake was estimated. The body weight, disease activity index (DAI), colon length and spleen index estimated. Antioxidant, cytokines, inflammatory parameters and mRNA expression were estimated. The composition of gut microbiota was analyzed at both the phylum and genus levels in the fecal samples obtained from all groups of rats. RESULTS: Sinomenine treatment enhanced the body weight, colon length and reduced the DAI, spleen index. Sinomenine treatment remarkably suppressed the level of NO, MPO, ICAM-1, and VCAM-1 along with alteration of antioxidant parameters such as SOD, CAT, GPx, GR and MDA. Sinomenine treatment also decreased the cytokines like TNF-α, IL-1, IL-1ß, IL-6, IL-10, IL-17, IL-18 in the serum and colon tissue; inflammatory parameters viz., PAF, COX-2, PGE2, iNOS, NF-κB; matrix metalloproteinases level such as MMP-1 and MMP-2. Sinomenine significantly (P < 0.001) enhanced the level of HO-1 and Nrf2. Sinomenine altered the mRNA expression of RIP1, RIP3, DRP3, NLRP3, IL-1ß, caspase-1 and IL-18. Sinomenine remarkably altered the relative abundance of gut microbiota like firmicutes, Bacteroidetes, F/B ratio, Verrucomicrobia, and Actinobacteria. CONCLUSION: The results clearly indicate that sinomenine demonstrated a protective effect against DSS-induced inflammation, potentially through the modulation of inflammatory pathways and gut microbiota.

Evaluating glioma-associated microRNA by complementation on a biological nanosensor.

Glioma is a tumor in the brain and spinal cord originating in the glial cells that surround the nerve cells. Among several microRNAs reported, miRNA-363 is associated with human glioma. Based on miRNA-363 levels, the development and progression of glioma can be monitored. The current study used an interdigitated electrode sensor to monitor microRNA-363 levels, which indeed reflects the severity of glioma. The interdigitated electrode was generated using a photolithography technique followed by surface chemical modification carried out to insert miRNA-363 complementary oligo as the probe complexed with gold nanoparticles. The proposed sensor works based on the dipole moment between two electrodes, and when molecular immobilization or interaction occurs, the response by the signal output changes. The changes in the target microRNA-363 sequence were standardized to identify glioma. The limit of detection of miRNA-363 was 10 fM with an R2 value of 0.996 on the linear coefficient regression ranges between 1 fM and 100 pM. Furthermore, unrelated sequences failed to increase the response of the current with the complementary probe, indicating specific miRNA-363 detection on the interdigitated electrode. This study demonstrates the platform to be used for determining the presence of microRNA-363 in glioma and as the basis for other biomarker analyses.

Triptonide inhibits growth and metastasis in HCC by suppressing EGFR/PI3K/AKT signaling.

Liver cancer represents one of the deadliest cancers, with a rising incidence worldwide. Triptonide is found in the traditional Chinese medicinal plant Tripterygium wilfordii Hook. This study aimed to examine the anticancer properties of triptonide in human hepatocellular carcinoma (HCC). HCC cells were administered with triptonide at various levels, and CCK-8 and colony formation assays were carried out for detecting HCC cell proliferation. Then, cell apoptosis and cell cycle distribution were evaluated by flow cytometry. Tumor growth was monitored noninvasively by ultrasound imaging. Cell migration and invasion were quantitated by wound healing and Transwell assays. A metastasis model was established via tail vein injection of HCC cells in nude mice. Immunoblot was performed to quantitate the expression of proteins involved in the EGFR/PI3K/AKT signaling and its downstream effectors. Triptonide repressed cell proliferation and induced cell cycle arrest and apoptosis in cultured HCC cells, and suppressed tumor growth in vivo. In addition, triptonide inhibited EMT, migration and invasion in cultured HCC cells, and lung metastasis in nude mice. Mechanistically, triptonide acted by inhibiting the EGFR/PI3K/AKT signaling and regulated its downstream effectors, e.g., the cell cycle-associated protein cyclin D1, the apoptosis-related protein Bcl-2, the EMT marker E-cadherin, and the invasion-related protein MMP-9. Triptonide suppresses proliferation, EMT, migration and invasion, and promotes apoptosis and cell cycle arrest by repressing the EGFR/PI3K/AKT signaling. Therefore, triptonide might be considered for liver cancer treatment.

SRI-42127, a novel small molecule inhibitor of the RNA regulator HuR, potently attenuates glial activation in a model of lipopolysaccharide-induced neuroinflammation.

Glial activation with the production of pro-inflammatory mediators is a major driver of disease progression in neurological processes ranging from acute traumatic injury to chronic neurodegenerative diseases such as amyotrophic lateral sclerosis and Alzheimer's disease. Posttranscriptional regulation is a major gateway for glial activation as many mRNAs encoding pro-inflammatory mediators contain adenine- and uridine-rich elements (ARE) in the 3' untranslated region which govern their expression. We have previously shown that HuR, an RNA regulator that binds to AREs, plays a major positive role in regulating inflammatory cytokine production in glia. HuR is predominantly nuclear in localization but translocates to the cytoplasm to exert a positive regulatory effect on RNA stability and translational efficiency. Homodimerization of HuR is necessary for translocation and we have developed a small molecule inhibitor, SRI-42127, that blocks this process. Here we show that SRI-42127 suppressed HuR translocation in LPS-activated glia in vitro and in vivo and significantly attenuated the production of pro-inflammatory mediators including IL1ß, IL-6, TNF-α, iNOS, CXCL1, and CCL2. Cytokines typically associated with anti-inflammatory effects including TGF-ß1, IL-10, YM1, and Arg1 were either unaffected or minimally affected. SRI-42127 suppressed microglial activation in vivo and attenuated the recruitment/chemotaxis of neutrophils and monocytes. RNA kinetic studies and luciferase studies indicated that SRI-42127 has inhibitory effects both on mRNA stability and gene promoter activation. In summary, our findings underscore HuR's critical role in promoting glial activation and the potential for SRI-42127 and other HuR inhibitors for treating neurological diseases driven by this activation.

Theoretical study of extremely narrow plasmonic surface lattice resonances observed by MIM nanogratings under normal incidence in asymmetric environments.

Nanoarray structures can support plasmonic surface lattice resonances (SLRs) with extremely narrow linewidths and huge electric field enhancement features, which are attractive applications in nanolasers, biochemical sensors, and nonlinear optics. However, current nanoarray structures located in an asymmetric dielectric environment with a refractive index contrast of 1.00/1.52 of the superstrate/substrate excite much poorer SLRs under normal incidence, which largely limits their application range. In this work, we report extremely narrow SLRs supported by one-dimensional metal-insulator-metal nanograting in asymmetric dielectric environments. The simulation results show that an SLRs with linewidth of 3.26 nm and quality factor of 233.2 can be excited under normal incidence. This high-quality SLRs is attributed to the interference formation between the out-of-plane dipole resonance mode and the out-of-plane quadrupole resonance mode. We also show that the resonance wavelength and quality factor can be tuned by changing the structure geometry and period, and we calculate the normal incidence SLRs quality factor to be up to 248 in 1.33/1.52 and 250 in 1.45/1.52. We expect the SLRs of this work to find potential applications in asymmetric dielectric environments.

The Update Immune-Regulatory Role of Pro- and Anti-Inflammatory Cytokines in Recurrent Pregnancy Losses.

Recurrent pregnancy losses (RPL) is a common reproductive disorder with various underlying etiologies. In recent years, rapid progress has been made in exploring the immunological mechanisms for RPL. A propensity toward Th2 over Th1 and regulatory T (Treg) over Th17 immune responses may be advantageous for reproductive success. In women with RPL and animals prone to abortion, an inordinate expression of cytokines associated with implantation and early embryo development is present in the endometrium or decidua secreted from immune and non-immune cells. Hence, an adverse cytokine milieu at the maternal-fetal interface assaults immunological tolerance, leading to fetal rejection. Similar to T cells, NK cells can be categorized based on the characteristics of cytokines they secrete. Decidual NK (dNK) cells of RPL patients exhibited an increased NK1/NK2 ratio (IFN-γ/IL-4 producing NK cell ratios), leading to pro-inflammatory cytokine milieu and increased NK cell cytotoxicity. Genetic polymorphism may be the underlying etiologies for Th1 and Th17 propensity since it alters cytokine production. In addition, various hormones participate in cytokine regulations, including progesterone and estrogen, controlling cytokine balance in favor of the Th2 type. Consequently, the intricate regulation of cytokines and hormones may prevent the RPL of immune etiologies. Local or systemic administration of cytokines or their antagonists might help maintain adequate cytokine milieu, favoring Th2 over Th1 response or Treg over Th17 immune response in women with RPL. Herein, we provided an updated comprehensive review regarding the immune-regulatory role of pro- and anti-inflammatory cytokines in RPL. Understanding the roles of cytokines involved in RPL might significantly advance the early diagnosis, monitoring, and treatment of RPL.

Homoharringtonine inhibits the progression of hepatocellular carcinoma by suppressing the PI3K/AKT/GSK3ß/Slug signaling pathway.

Homoharringtonine (HHT), was first isolated from the bark of Cephalotaxus harringtonia (Knight ex J. Forbes) K. Koch and Cephalotaxus fortunei Hook trees. The bark extract is used to treat leukemia and in recent years has also been used in traditional Chinese medicine (TCM) to treat solid tumors. However, the inhibitory mechanism of HHT in the progression of hepatocellular carcinoma (HCC) is rarely studied. We aimed to evaluate the antitumor efficacy of HHT on HCC in vitro and in vivo and elucidate the underlying molecular mechanism(s). HCC cell lines, including HCCLM3, HepG2, and Huh7, were used to evaluate the antitumor efficacy of HHT in vitro. Cytotoxicity and proliferative ability were evaluated by MTT and colony formation assays. Cell cycle progression and apoptosis in HHT-treated HCC cells were evaluated by flow cytometry. To determine the migration and invasion abilities of HCC cells, wound-healing and Transwell assays were used. Finally, western blot analysis was used to reveal the proteins involved. We also established a xenograft nude mouse model for in vivo assessments of the preclinical efficacy of HHT, mainly using hematoxylin and eosin staining, immunohistochemistry, ultrasound imaging (USI), and magnetic resonance imaging (MRI). HHT suppressed the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of HCC cells, and induced cell cycle arrest at the G2 phase and apoptosis. In the HCC xenograft model, HHT showed an obvious tumor-suppressive effect. Surprisingly, Slug expression was also decreased by HHT via the PI3K/AKT/GSK3ß signaling pathway at least partially suppressed the growth of HCC via the PI3K/AKT/GSK3ß/Slug signaling pathway.

miR-215-5p decreases migration and invasion of trophoblast cells through regulating CDC6 in preeclampsia.

Preeclampsia (PE) is a serious disease that occurs after 20 weeks during pregnancy. There are some aberrant microRNAs (miRNAs) that are associated with the etiology of PE. As discovered by scholars, there was an increased level of miR-215-5p in plasma of PE patients compared with the control group; nonetheless, there is still no knowledge of the mechanism of miR-215-5p in PE. We carried out the comparison of the expression levels of miR-215-5p, and the supposed target gene cell division cycle 6 (CDC6) in 30 placentas from PE patients as well as 30 placentas from normal pregnant women. The verification of the impacts of miR-215-5p and CDC6 was carried out by functional assays in HTR-8/SVneo cells transfected with the miR-215-5p mimic or siR-CDC6. As indicated by findings, miR-215-5p showed an apparent increase; conversely, CDC6 was inhibited in the experiment group. The upregulation of miR-215-5p inhibited both the migration and invasive potential of trophoblasts, besides decreasing the G1-S transition and downregulating CDC6 in HTR-8/SVneo cells; nonetheless, it did not significantly impact the cell proliferation. Furthermore, siR-CDC6 replicated the functions of the miR-215-5p mimic. Also, the miR-215-5p mimic and siR-CDC6 both decreased the epithelial-mesenchymal transition (EMT) with additional E-cadherin level and decreased the expressions of N-cadherin as well as vimentin in trophoblast cells. To conclude, miR-215-5p decreased not only the migration but also the invasion of trophoblasts through regulating CDC6, which indicated that miR-215-5p might be associated with the etiology of PE. SIGNIFICANCE OF THE STUDY: More and more attention has been paid on the roles of miRNAs in the pathogenesis of PE. However, there is no study of miR-215-5p in the etiology of PE. We first investigated the mechanism of miR-215-5p in placental tissues and HTR-8/SVneo cells. It was suggested that miR-215-5p decreased the abilities of migration and invasion of trophoblasts through regulating CDC6 in PE. miR-215-5p might be used as an target for the early diagnosis and treatment of PE in the future.

The transcription factor Krüppel-like factor 5 promotes cell growth and metastasis via activating PI3K/AKT/Snail signaling in hepatocellular carcinoma.

The transcription factor Krüppel-like factor 5 (KLF5) is highly expressed in many cancers and serves as a prognostic factor. However, the function of KLF5 in hepatocellular carcinoma (HCC) is unclear. In this study, we found that KLF5 was significantly overexpressed in HCC cell lines and specimens, and high KLF5 expression predicted a poor prognosis for HCC patients. Then, we studied the effects of KLF5 on the proliferation, apoptosis, migration and invasion of HCC cells in vitro and vivo. The inhibition of KLF5 markedly inhibited HCC growth and metastasis, while KLF5 overexpression promoted these processes. In addition, we observed that KLF5 could promote the epithelial-mesenchymal transition (EMT) in HCC via the PI3K/AKT/Snail signaling pathway. The silencing of KLF5 in HCC cell lines downregulated the expression of N-cadherin, Vimentin and Snail and increased the expression of the epithelial marker E-cadherin. The expression of MMP2 and MMP9 was also decreased in KLF5-silenced HCC cells. However, opposite results were observed in the KLF5-overexpressing group. These results indicate that KLF5 plays a significant role in HCC progression and metastasis and induces EMT via activating PI3K/AKT/Snail signaling, and the inhibition of KLF5 may be a potential treatment modality for patients with HCC.

Narrow plasmonic surface lattice resonances with preference to asymmetric dielectric environment.

Plasmonic surface lattice resonances (SLRs) supported by metal nanoparticle arrays exhibit narrow linewidths and enhanced localized fields and thus are attractive in diverse applications including nanolasers, biochemical sensors and nonlinear optics. However, it has been shown that these SLRs have much worse performance in a less symmetric environment, hindering their practical applications. Here, we propose a novel type of narrow SLRs that is supported by metal-insulator-metal nanopillar arrays and that has better performance in a less symmetric dielectric environment. When the dielectric environment is as asymmetric as the air/polymer environment with a refractive index contrast of 1.0/1.52, the proposed SLRs have high quality factors of 62 under normalincidence and of 147 under oblique incidence in the visible regime. We attribute these new SLRs to Fano resonance between an in-plane dipole and an out-of-plane quadrupole (or dipole) that are respectively supported by the two metal ridges under normal (or oblique) incidence. We also show that the resonance wavelength can be tuned by varying the geometric sizes or by changing the angle of incidence. By doing this, we clarify the conditions for the formation of the proposed SLRs and illustrate their attractive merits in sensing applications. We expect that this new SLR can open up applications in asymmetric dielectric environments.

Hu antigen R (HuR) multimerization contributes to glioma disease progression.

Among primary brain cancers, gliomas are the most deadly and most refractory to current treatment modalities. Previous reports overwhelmingly support the role of the RNA-binding protein Hu antigen R (HuR) as a positive regulator of glioma disease progression. HuR expression is consistently elevated in tumor tissues, and a cytoplasmic localization appears essential for HuR-dependent oncogenic transformation. Here, we report HuR aggregation (multimerization) in glioma and the analysis of this tumor-specific HuR protein multimerization in clinical brain tumor samples. Using a split luciferase assay, a bioluminescence resonance energy transfer technique, and site-directed mutagenesis, we examined the domains involved in HuR multimerization. Results obtained with the combination of the split HuR luciferase assay with the bioluminescence resonance energy transfer technique suggested that multiple (at least three) HuR molecules come together during HuR multimerization in glioma cells. Using these data, we developed a model of HuR multimerization in glioma cells. We also demonstrate that exposing glioma cells to the HuR inhibitor tanshinone group compound 15,16-dihydrotanshinone-I or to the newly identified compound 5 disrupts HuR multimerization modules and reduces tumor cell survival and proliferation. In summary, our findings provide new insights into HuR multimerization in glioma and highlight possible pharmacological approaches for targeting HuR domains involved in cancer cell-specific multimerization.

Overexpression of circular RNA circ_001569 indicates poor prognosis in hepatocellular carcinoma and promotes cell growth and metastasis by sponging miR-411-5p and miR-432-5p.

Emerging evidence indicated that abnormally expressed circular RNAs (circRNAs) are critically involved in tumorigenesis and development of several cancers. However, the study relevant to the relationship between circRNAs and hepatocellular carcinoma (HCC) is rare. In this study, the expression of circ_001569 in HCC tissue specimens and cells were determined by qRT-PCR. The clinical relevance of circ_001569 was also analyzed. In addition, loss-of-function and gain-of-function assays were conducted to explore the biological functions of circ_001569. Furthermore, tumor formation and lung metastasis studies were induced to confirm the in vitro data. Mechanistically, bioinformatics analysis and luciferase reporter assays were conducted to illustrate the underlying mechanism of circ_001569. The results indicated that circ_001569 was overexpressed in HCC tissue samples and cells. This overexpression is correlated with larger tumor size, advanced TNM stages and unfavorable prognosis in the patients with HCC. Additionally, circ_001569 significantly facilitated HCC cell growth, migration and invasion. The animal studies further confirmed thein vitroresults. More importantly, circ_001569 could directly sponge miR-411-5p and miR-432-5p. The oncogenic functions of circ_001569 is partially dependent on its regulation on miR-411-5p and miR-432-5p. In summary, circ_001569/miR-411-5p/miR-432-5p regulatory signaling might be a rational HCC-related therapeutic target.

MicroRNA Dysregulation Associated with Red Blood Cell Storage.

INTRODUCTION: Stored red blood cells (RBCs) undergo storage lesions involving morphological, physiological and biochemical changes. MicroRNAs (miRNAs) have important functions in cell apoptosis and life processes. Therefore, the aim of this study was to explore potential roles of miRNAs in the damage of stored RBCs. METHODS: Blood samples were collected from 13 healthy male O-type donors, and leuko-reduced RBCs were divided into fresh RBC group and 20-day storage RBC group. RESULTS: Eight predicted miRNAs with modified expressions with an intersection ≥ 3 were found dysregulated in the 20-day storage RBC group and involved in apoptosis and senescence signaling pathway: miR-31-5p, miR-196a-5p, miR-203a, miR-654-3p and miR-769-3p were increased, while miR-96-5P, miR-150-5P and miR-197-3p were decreased. Evidence associating miR-31-5p, miR-203a, miR-654 and miR-769 to RBCs or blood in general are not available. CONCLUSIONS: Dysregulated miRNAs might represent potential biomarkers to identify storage lesions, and their detection might help to evaluate the quality of stored RBCs.

Removal of bromide and bromate from drinking water using granular activated carbon.

Granular activated carbon (GAC) was used to remove bromide (Br⁻) and bromate (BrO(3)(-)) from drinking water in both bench- and pilot-scale experiments. The present study aims to minimize BrO(3)(-) formation and eliminate BrO(3)(-) generated during the ozonation of drinking water, particularly in packaged drinking water. Results show that the Br⁻ and BrO(3)(-) levels in GAC-treated water decreased in both bench- and pilot-scale experiments. In the bench-scale experiments, when the empty bed contact time (EBCT) was 5 min, the highest reduction rates of Br(-) in the mineral and ultrapure water were found to be 74.9% and 91.2%, respectively, and those of BrO(3)(-) were 94.4% and 98.8%, respectively. The GAC capacity for Br⁻ and BrO(3)(-) removal increased with the increase in EBCT. Reduction efficiency was better in ultrapure water than in mineral water. In the pilot-scale experiments, the minimum reduction rates of Br⁻ and BrO(3)(-) were 38.5% and 73.2%, respectively.

[Transrectal ultrasound-guided biopsy for prostate cancer: an update].

The prostate-specific antigen (PSA) test contributes a lot to the diagnosis and treatment of prostate cancer (PCa) and, along with imaging-guided prostate biopsy, has improved the diagnosis rate of lower-risk PCa and the accuracy of its clinical staging. However, many questions and controversies remain as to the choice of optimal biopsy strategies. Scholars differ in views about how to utilize PCa-related biomarkers to optimize the detection of initial and repeat biopsies. This review focuses on the present status of and advances in transrectal ultrasound-guided biopsy for PCa.

Expression of PRMT5 correlates with malignant grade in gliomas and plays a pivotal role in tumor growth in vitro.

Protein arginine methyltransferase 5 (PRMT5) catalyzes the formation of ω-NG,N'G-symmetric dimethylarginine residues on histones as well as other proteins. These modifications play an important role in cell differentiation and tumor cell growth. However, the role of PRMT5 in human glioma cells has not been characterized. In this study, we assessed protein expression profiles of PRMT5 in control brain, WHO grade II astrocytomas, anaplastic astrocytomas, and glioblastoma multiforme (GBM) by immunohistochemistry. PRMT5 was low in glial cells in control brain tissues and low grade astrocytomas. Its expression increased in parallel with malignant progression, and was highly expressed in GBM. Knockdown of PRMT5 by small hairpin RNA caused alterations of p-ERK1/2 and significantly repressed the clonogenic potential and viability of glioma cells. These findings indicate that PRMT5 is a marker of malignant progression in glioma tumors and plays a pivotal role in tumor growth.

Response to Climate Change and GAP Analysis of Thuja koraiensis Nakai.

Due to global warming and increased human activity, the wild population of Thuja koraiensis Nakai (T. koraiensis) has dropped, placing it in danger. An understanding of the response of T. koraiensis to climate change and the determination of priority conservation areas are tremendously critical for proper conservation. Using sixty-nine T. koraiensis distribution points and seven environmental factors, the Maxent model was used to predict potentially suitable areas and spatial variation patterns of T. koraiensis and the Marxan conservation planning model was used to evaluate conservation gap areas. Research shows that the dominant environmental factors affecting the distribution of potentially suitable areas for T. koraiensis included elevation, precipitation of the driest month, isothermality and precipitation of the wettest quarter. Under the current climatic conditions, highly suitable areas for T. koraiensis are mainly distributed in the Changbai Mountains within Samjiyon County and Baishan City, the Hamgyong Mountains within the western part of Hamgyong-Bukto Province, and the T'aeback-Sanmaek Mountains within Gangwon-do, Kumgangsan Special Administrative Region and Kangwon-do. Under future climate conditions, suitable areas for T. koraiensis show a decreasing trend, and the suitable area will be reduced to higher elevations, and the Hamgyong Mountains may become a refuge. Based on GAP analysis, 69.69% of the priority conservation areas of T. koraiensis are located outside of the nature reserve, and these conservation gap areas are primarily in the southern part of the Changbai Mountains and Kangwon-do.

ZSM-5@ceramic foam composite catalyst derived from spent bleaching clay for continuous pyrolysis of waste oil to produce monocyclic aromatic hydrocarbons.

Spent bleaching clay, a solid waste generated during the refining process of vegetable oils, lacks an efficient treatment solution. In this study, spent bleaching clay was innovatively employed to fabricate ceramic foams. The thermal stability analysis, microstructure, and crystal phase composition of the ceramic foams were characterized by TG-DSC, SEM, and XRD. An investigation into the influence of Al2O3 content on the ceramic foams was conducted. Results showed that, as the Al2O3 content increased from 15 wt% to 30 wt%, there was a noticeable decrease in bulk density and linear shrinkage, accompanied by an increase in compressive strength. Additionally, the ceramic foams were used as catalyst supports, to synthesize ZSM-5@ceramic foam composite catalysts for pyrolysis of waste oil. The open pores of the ZSCF catalyst not only reduced diffusion path length but also facilitated the exposure of more acid sites, thereby increasing the utilization efficiency of ZSM-5 zeolite. This, in turn, engendered a significant enhancement in monocyclic aromatic hydrocarbons content from 39.15 % (ZSM-5 powder catalyst) to 78.96 %. Besides, a larger support pore size and a thicker ZSM-5 zeolite coating layer led to an increase in monocyclic aromatic hydrocarbons content. As the time on stream was extended to 56 min, the monocyclic aromatic hydrocarbon content obtained with the composite catalyst remained 12.41 % higher than that of the ZSM-5 powder catalyst. These findings validate the potential of the composite catalyst. In essence, this study advances the utilization of spent bleaching clay and introduces a novel concept for ceramic foam fabrication. Furthermore, it contributes to the scaling up of catalytic pyrolysis technology.

Phosphoregulation of the RNA-binding protein Hu antigen R (HuR) by Cdk5 affects centrosome function.

Hu antigen R (HuR) is an mRNA-binding protein belonging to the ELAV family. It is highly expressed in cancer and involved in cell survival and proliferation. The impact of post-translational regulation of HuR and resulting cellular effects are poorly understood. In the current report, we describe a direct interaction between HuR and Cdk5 in glioma. We determined that Cdk5 specifically phosphorylates HuR at the serine 202 residue in the unique hinge region. The molecular consequences of this interaction are an altered HuR ability to bind, stabilize, and promote translation of mRNAs. At the cellular level, the anomalous HuR phosphorylation at this site evokes robust defects in centrosome duplication and cohesion as well as arrest of cell cycle progression. Subcellular fractionation and immunofluorescence technique confirm a direct integration of HuR and Cdk5 with centrosomes. We propose that HuR stores mRNA in the centrosome and that HuR phosphorylation by Cdk5 controls de novo protein synthesis in near proximity to centrosomes and, thus, impacts centrosome function.