Comprehensive Investigation of Constant Voltage Stress Time-Dependent Breakdown and Cycle-to-Breakdown Reliability in Y-Doped and Si-Doped HfO2 Metal-Ferroelectric-Metal Memory.

In this study, we comprehensively investigate the constant voltage stress (CVS) time-dependent breakdown and cycle-to-breakdown while considering metal-ferroelectric-metal (MFM) memory, which has distinct domain sizes induced by different doping species, i.e., Yttrium (Y) (Sample A) and Silicon (Si) (Sample B). Firstly, Y-doped and Si-doped HfO2 MFM devices exhibit domain sizes of 5.64 nm and 12.47 nm, respectively. Secondly, Si-doped HfO2 MFM devices (Sample B) have better CVS time-dependent breakdown and cycle-to-breakdown stability than Y-doped HfO2 MFM devices (Sample A). Therefore, a larger domain size showing higher extrapolated voltage under CVS time-dependent breakdown and cycle-to-breakdown evaluations was observed, indicating that the domain size crucially impacts the stability of MFM memory.

Missing Piece in Colloidal Stability─Morphological Factor of Hydrophobic Nanoparticles.

Hydrophobic nanoparticles (NPs) in water were considered unstable because they lack the repulsive electrostatic interaction and steric effect to prevent aggregation. In this study, porous hydrophobic NPs of two star-shaped giant molecules, POSS-(R)8, were found to be stable in water and able to retain their kinetic stability in a wide range of temperatures, pH values, and ionic strengths. Unlike the solid hydrophobic NPs that aggregate even with the negative zeta potential (ζ) induced by surface-structured hydrogen-bonded (SHB) water, the porous morphology of POSS-(R)8 NPs reduces the entropically driven hydrophobic effect to prevent aggregation. With the porous morphology, the hydrophobic NPs are stable without the hydrophilic or charged surface functional groups and demonstrate good encapsulation capability. The morphological factor of colloids is thus one of the missing pieces in the theory of colloidal stability that extends our understanding of colloidal science.

Adaptive molecular quaternary clips made with pyrene functionalized polyhedral oligomeric silsesquioxane.

Evolving synthetic molecules toward complex structures is a major goal in supramolecular chemistry. Increasing the number of clips in a unimolecular multi-clip (UMC), although vital to elevate the complexity of supramolecular architectures, often prevents the UMC from forming host-guest complexes in the bulk phase. To overcome this difficulty, adaptive chemistry was applied to develop a novel adaptive unimolecular quaternary clip (Q-clip). The Q-clip is intrinsically amorphous, but self-organizes with exclusively 4 eq. of allosteric activators (NDI) to form the Q-clip : NDI4 complexes and a supramolecular lamellar structure in the bulk. The adaptive assembly is fast and allows us to locate the adaptive assembly area of Q-clip : NDI4 complexes in the amorphous Q-clip film. Our results provide new insights into the design of adaptive UMCs for the evolution toward complex structures and supramolecular functional materials.

Retinol dehydrogenase 10 promotes metastasis of glioma cells via the transforming growth factor-ß/SMAD signaling pathway.

BACKGROUND: Glioma is the most common primary malignant tumor in the central nervous system. Because of the resistance of glioma to chemoradiotherapy and its aggressive growth, the survival rate of patients with glioma has not improved. This study aimed to disclose the effect of retinol dehydrogenase 10 (RDH10) on the migration and invasion of glioma cells, and to explore the potential mechanism. METHODS: Reverse transcription-polymerase chain reaction (RT-PCR) was used to determine the expression levels of RDH10 in healthy glial cells and glioma cells. Human glioma cell strains, U87 and U251, were infected with negative control or RDH10-interfering lentiviruses. RT-PCR and Western blotting were performed to determine the knockdown efficiency. Scratch and transwell assays were used to assess cell migration and invasion after RDH10 knockdown. Finally, changes in transforming growth factor-ß (TGF-ß)/SMAD signaling pathway-related expression were examined by Western blotting. Differences between groups were analyzed by one-way analysis of variance. RESULTS: RDH10 was highly expressed in glioma cells. Compared with the control group, RDH10 knockdown significantly reduced RDH10 messenger RNA and protein expression levels in U87 and U251 glioma cells (U87: 1.00 ±â€Š0.08 vs. 0.22 ±â€Š0.02, t = 16.55, P < 0.001; U251: 1.00 ±â€Š0.17 vs. 0.39 ±â€Š0.01, t = 6.30, P < 0.001). The scratch assay indicated that compared with the control group, RDH10 knockdown significantly inhibited the migration of glioma cells (U87: 1.00% ±â€Š0.04% vs. 2.00% ±â€Š0.25%, t = 6.08, P < 0.01; U251: 1.00% ±â€Š0.11% vs. 2.48% ±â€Š0.31%, t = 5.79, P < 0.01). Furthermore, RDH10 knockdown significantly inhibited the invasive capacity of glioma cells (U87: 97.30 ±â€Š7.01 vs. 13.70 ±â€Š0.58, t = 20.36, P < 0.001; U251: 96.20 ±â€Š7.10 vs. 18.30 ±â€Š2.08, t = 18.51, P < 0.001). Finally, Western blotting demonstrated that compared with the control group, downregulation of RDH10 significantly inhibited TGF-ß expression, phosphorylated SMAD2, and phosphorylated SMAD3 (TGF-ß: 1.00 ±â€Š0.10 vs. 0.53 ±â€Š0.06, t = 7.05, P < 0.01; phosphorylated SMAD2: 1.00 ±â€Š0.20 vs. 0.42 ±â€Š0.17, t = 4.01, P < 0.01; phosphorylated SMAD3: 1.00 ±â€Š0.18 vs. 0.41 ±â€Š0.12, t = 4.12, P < 0.01). CONCLUSION: RDH10 knockdown might inhibit metastasis of glioma cells via the TGF-ß/SMAD signaling pathway.

Application of neuroendoscopic surgical techniques in the assessment and treatment of cerebral ventricular infection.

Cerebral ventricular infection (CVI) is one of the most dangerous complications in neurosurgery because of its high mortality and disability rates. Few studies have examined the application of neuroendoscopic surgical techniques (NESTs) to assess and treat CVI. This multicenter, retrospective study was conducted using clinical data of 32 patients with CVI who were assessed and treated by NESTs in China. The patients included 20 men and 12 women with a mean age of 42.97 years. NESTs were used to obliterate intraventricular debris and pus, fenestrate or incise the intraventricular compartment and reconstruct cerebrospinal fluid circulation, and remove artificial material. Intraventricular irrigation with antibiotic saline was applied after neuroendoscopic surgery (NES). Secondary hydrocephalus was treated by endoscopic third ventriculostomy or a ventriculoperitoneal shunt. Neuroendoscopic findings of CVI were used to classify patients into Grade I (n = 3), Grade II (n = 13), Grade III (n = 10), and Grade IV (n = 6) CVI. The three patients with grade I CVI underwent one NES, the 23 patients with grade II/III CVI underwent two NESs, and patients with grade IV CVI underwent two (n = 3) or three (n = 3) NESs. The imaging features and grades of neuroendoscopy results were positively related to the number of neurosurgical endoscopic procedures. Two patients died of multiple organ failure and the other 30 patients fully recovered. Among the 26 patients with secondary hydrocephalus, 18 received ventriculoperitoneal shunt and 8 underwent endoscopic third ventriculostomy. There were no recurrences of CVI during the 6- to 76-month follow-up after NES. Application of NESTs is an innovative method to assess and treat CVI, and its neuroendoscopic classification provides an objective, comprehensive assessment of CVI. The study trial was approved by the Institutional Review Board of Beijing Shijitan Hospital, Capital Medical University, China.

KLF7 promotes polyamine biosynthesis and glioma development through transcriptionally activating ASL.

Krüppel-like factors (KLFs) are zinc-finger transcriptional factors that regulate target gene expression. Recent studies have shown that KLFs play essential roles in cancer development, whereas the function of KLF7 in glioma remains unclear. In this study, we showed that KLF7 was up-regulated in glioma tissues and its expression was inversely correlated with the patients' survival. Functional experiments demonstrated that KLF7 promoted the proliferation, migration and tumorigenesis of glioma cells. Mechanistically, KLF7 transcriptionally activated argininosuccinate lyase (ASL), which was observed highly expressed in glioma tissues. The biosynthesis of polyamine, a urea cycle metabolite, was enhanced by KLF7 in glioma cells. In addition, ASL contributed to the growth of glioma cells triggered by KLF7. Our findings demonstrate KLF7 as an oncogene and link KLF7 to ASL-mediated polyamine metabolism in glioma.