Search

Brain glymphatic dysfunction is critical in neurodegenerative processes. While animal studies have provided substantial insights, understandings in humans remains limited. Recent attention has focused on the non‐invasive evaluation of brain glymphatic function. However, its association with brain parenchymal lesions in large‐scale population remains under‐investigated. In this cross‐sectional analysis of 1030 participants (57.14 ± 9.34 years, 37.18% males) from the Shunyi cohort, we developed an automated pipeline to calculate diffusion‐weighted image analysis along the perivascular space (ALPS), with a lower ALPS value indicating worse glymphatic function. The automated ALPS showed high consistency with the manual calculation of this index (ICC = 0.81, 95% CI: 0.662–0.898). We found that those with older age and male sex had lower automated ALPS values (β = −0.051, SE = 0.004, p <.001, per 10 years, and β = −0.036, SE = 0.008, p <.001, respectively). White matter hyperintensity (β = −2.458, SE = 0.175, p <.001) and presence of lacunes (OR = 0.004, 95% CI < 0.002–0.016, p <.001) were significantly correlated with decreased ALPS. The brain parenchymal and hippocampal fractions were significantly associated with decreased ALPS (β = 0.067, SE = 0.007, p <.001 and β = 0.040, SE = 0.014, p =.006, respectively) independent of white matter hyperintensity. Our research implies that the automated ALPS index is potentially a valuable imaging marker for the glymphatic system, deepening our understanding of glymphatic dysfunction. [ABSTRACT FROM AUTHOR]

An optical type touch‐input flat panel is designed. The driving system is based on the passive pixel sensor (PPS) array with amorphous silicon (a‐Si) TFT technology. The embedded sensing structure of the optical sensor is using the a‐Si TFT phototransistor and four‐mask process architecture technology. This paper presents a primary optical pixel sensor circuit that utilizes hydrogenated amorphous silicon photo‐transistor sensor. The a‐Si TFT phototransistor sensor is high reliability by using Multi‐N+ layer in the a‐Si TFT structure. [ABSTRACT FROM AUTHOR]

We have developed a new AMLCD with multiple ambient light sensors (ALSs) for reducing backlight (BL) power consumption, and false sensing of ambient illuminance. ALSs perform well in showing BL control for power‐saving, even though one of the sensors is covered by a finger shadow. Architecture of integrated ALS with a‐Si technologies are presented. We fabricate the in‐cell and wide‐dynamic‐sensing ALSs display using a‐Si photo‐transistor sensor technology. Photo‐electrical characteristics with well linearity and reliability under long‐term operation were observed. [ABSTRACT FROM AUTHOR]

Objective. Glioblastoma is one of the most common malignant tumors in the brain, and these glioblastoma patients have very poor prognosis. Ferroptosis is involved in the progression of various tumors, including the glioblastoma. This study aims to determine the involvement of microRNA (miR)-147a in regulating ferroptosis of glioblastoma in vitro. Methods. Human glioblastoma cell lines were transfected with the inhibitor, mimic and matched negative controls of miR-147a in the presence or absence of ferroptotic inducers. To knock down the endogenous solute carrier family 40 member 1 (SLC40A1), cells were transfected with the small interfering RNA against SLC40A1. In addition, cells with or without the miR-147a mimic treatment were also incubated with temozolomide (TMZ) to investigate whether miR-147a overexpression could sensitize human glioblastoma cells to TMZ chemotherapy in vitro. Results. We found that miR-147a level was decreased in human glioblastoma tissues and cell lines and that the miR-147a mimic significantly suppressed the growth of glioblastoma cells in vitro. In addition, miR-147a expression was elevated in human glioblastoma cells upon erastin or RSL3 stimulation. Treatment with the miR-147a mimic significantly induced ferroptosis of glioblastoma cells, and the ferroptotic inhibitors could block the miR-147a mimic-mediated tumor suppression in vitro. Conversely, the miR-147a inhibitor prevented erastin- or RSL3-induced ferroptosis and increased the viability of glioblastoma cells in vitro. Mechanistically, we determined that miR-147a directly bound to the 3 ′ -untranslated region of SLC40A1 and inhibited SLC40A1-mediated iron export, thereby facilitating iron overload, lipid peroxidation, and ferroptosis. Furthermore, miR-147a mimic-treated human glioblastoma cells exhibited higher sensitivity to TMZ chemotherapy than those treated with the mimic control in vitro. Conclusion. We for the first time determine that miR-147a targets SLC40A1 to induce ferroptosis in human glioblastoma in vitro. [ABSTRACT FROM AUTHOR]

Lignin depolymerization into aromatic monomers with high yields and selectivity is essential for the economic feasibility of biorefinery. However, the relationship between lignin structure and its reactivity for upgradeability is still poorly understood, in large part owing to the difficulty in quantitative characterization of lignin structural properties. To overcome these shortcomings, advanced NMR technologies [2D HSQC (heteronuclear single quantum coherence) and 31P] were used to accurately quantify lignin functionalities. Diverse lignin samples prepared from Eucalyptus grandis with varying β‐O‐4 linkages were subjected to Pd/C‐catalyzed hydrogenolysis for efficient C−O bond cleavage to achieve theoretical monomer yields. Strong correlations were observed between the yield of monomeric aromatic compounds and the structural features of lignin, including the contents of β‐O‐4 linkages and phenolic hydroxyl groups. Notably, a combined yield of up to 44.1 wt % was obtained from β‐aryl ether rich in native lignin, whereas much lower yields were obtained from technical lignins low in β‐aryl ether content. This work quantitatively demonstrates that the lignin reactivity for acquiring aromatic monomer yields varies depending on the lignin fractionation processes. [ABSTRACT FROM AUTHOR]

Zinc finger proteins (ZNF) play important roles in various physiological processes. Here we report that ZNF300, a novel zinc finger protein, identified specifically in humans, promotes tumour development by modulating the NF-κB pathway. Inflammatory factors were found to induce ZNF300 expression in HeLa cell line, and ZNF300 expression further enhanced NF-κB signalling by activating TRAF2 and physically interacting with IKKβ. Furthermore, ZNF300 overexpression increased ERK1/2 phosphorylation and the expression of c-myc, IL-6, and IL-8 but decreased the expression of p21waf-1 and p27Kip1; whose down-regulation led to the opposite effect. Most importantly, ZNF300 overexpression stimulated cancer cell proliferation in vitro and significantly enhanced tumour development and metastasis in mouse xenograft model, while knocking down ZNF300 led to the opposite effects. We have identified a novel function for ZNF300 in tumour development that may uniquely link inflammation and NF-κB to tumourigenesis in humans but not in mice. [ABSTRACT FROM AUTHOR]

Nearly one-third of Krupple-type C2H2 zinc finger proteins have a krupple-associated box (KRAB) domain, which may act as a transcriptional repressor. ZNF268, which was novelty isolated from early human embryo, is a typical krupple-type C2H2 zinc finger protein with a conserved KRAB domain. In this report, the KRAB domain of ZNF268 is identified to localize in the nucleus and has transcriptional repressor activity. [ABSTRACT FROM AUTHOR]

From a cDNA library of Chinese scorpion Buthus martensii Karsch, full-length cDNAs of 351 nucleotides encoding precursors (named BmKIM) that contain signal peptides of 21 amino acid residues, a mature toxin of 61 residues with four disulfide bridges, and an extra Gly-Lys-Lys tail, were isolated. The genomic sequence of BmKIM was cloned and sequenced; it consisted of two exons disrupted by an intron of 1622 bp, the largest known in scorpion toxin genomes, inserted in the region encoding the signal peptide. The cDNA was expressed in Escherichia coli . The recombinant BmKIM was toxic to both mammal and insects. This is the first report that a toxin with such high sequence homology with an insect-specific depressant toxin group exhibits toxicity to mammals. Using whole cell patch-clamp recording, it was discovered that the recombinant BmKIM inhibited thesodium current in rat dorsal root ganglion neurons andventricular myocytes and protected against aconitine- induced cardiac arrhythmia. [ABSTRACT FROM AUTHOR]

A full-length cDNA sequence encoding the precursor of a novel venom peptide (named BmKn1) with no disulfide bridge was first isolated from the venom gland cDNA library of Chinese scorpion Buthus martensii Karsch. The encoded precursor consisted of 70 amino acid residues including two parts: a signal peptide of 23 residues, and a putative mature venom peptide (BmKn1) of 47 residues. The sequence of BmKn1 showed no similarity to those of other scorpion venom peptides. BmKn1 may be the first member of a new venom peptide family from scorpion. Future research will be interesting to unravel further the pharmacological function of this novel scorpion venom peptide. [ABSTRACT FROM AUTHOR]

Based on the amino acid sequence of a bradykinin-potentiating peptide (Bpp) (peptide K-12) from scorpion Buthus occitanus, a full-length cDNA sequence encoding the precursor of a novel venom peptide (named BmKbpp) related to this Bpp, has been isolated and analyzed. The cDNA encodes a precursor of 72 amino acid residues, including a signal peptide of 22 residues and an extra Arg-ArgArg tail at the C-terminal end of the precursor, which have to be removed in the processing step. The C-terminal region (21 residues) of the precursor is homologous (57% identical) with the sequence of peptide K-12. Thus, according to the primary structure of the BmKbpp precursor, there may be a propeptide between the signal peptide and the putative mature BmKbpp at the C-terminal region of the precursor. [ABSTRACT FROM AUTHOR]