Leakage and Thermal Reliability Optimization of Stacked Nanosheet Field-Effect Transistors with SiC Layers.

In this work, we propose a SiC-NSFET structure that uses a PTS scheme only under the gate, with SiC layers under the source and drain, to improve the leakage current and thermal reliability. Punch-through stopper (PTS) doping is widely used to suppress the leakage current, but aggressively high PTS doping will cause additional band-to-band (BTBT) current. Therefore, the bottom oxide isolation nanosheet field-effect transistor (BOX-NSFET) can further reduce the leakage current and become an alternative to conventional structures with PTS. However, thermal reliability issues, like bias temperature instability (BTI), hot carrier injection (HCI), and time-dependent dielectric breakdown (TDDB), induced by the self-heating effect (SHE) of BOX-NSFET, become more profound due to the lower thermal conductivity of SiO2 than silicon. Moreover, the bottom oxide will reduce the stress along the channel due to the challenges associated with growing high-quality SiGe material on SiO2. Therefore, this method faces difficulties in enhancing the mobility of p-type devices. The comprehensive TCAD simulation results show that SiC-NSFET significantly suppresses the substrate leakage current compared to the conventional structure with PTS. In addition, compared to the BOX-NSFET, the stress reduction caused by the bottom oxide is avoided, and the SHE is mitigated. This work provides significant design guidelines for leakage and thermal reliability optimization of next-generation advanced nodes.

Interaction of Negative Bias Instability and Self-Heating Effect on Threshold Voltage and SRAM (Static Random-Access Memory) Stability of Nanosheet Field-Effect Transistors.

In this paper, we investigate the effects of negative bias instability (NBTI) and self-heating effect (SHE) on threshold voltage in NSFETs. To explore accurately the interaction between SHE and NBTI, we established an NBTI simulation framework based on trap microdynamics and considered the influence of the self-heating effect. The results show that NBTI weakens the SHE effect, while SHE exacerbates the NBTI effect. Since the width of the nanosheet in NSFET has a significant control effect on the electric field distribution, we also studied the effect of the width of the nanosheet on the NBTI and self-heating effect. The results show that increasing the width of the nanosheet will reduce the NBTI effect but will enhance the SHE effect. In addition, we extended our research to the SRAM cell circuit, and the results show that the NBTI effect will reduce the static noise margin (SNM) of the SRAM cell, and the NBTI effect affected by self-heating will make the SNM decrease more significantly. In addition, our research results also indicate that increasing the nanosheet width can help slow down the NBTI effect and the negative impact of NBTI on SRAM performance affected by the self-heating effect.

Triphenyl phosphate induces cardiotoxicity through myocardial fibrosis mediated by apoptosis and mitophagy of cardiomyocyte in mice.

Triphenyl phosphate (TPHP) is an organophosphorus flame retardant, but its cardiac toxicity has not been adequately investigated. Therefore, in the current study, the effect of TPHP on the heart and the underlying mechanism involved was evaluated. C57BL/6 J mice were administered TPHP (0, 5, and 50 mg/kg/day) for 30 days. In addition, H9c2 cells were treated with three various concentrations (0, 50, and 150 µM) of TPHP, with and without the reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine or the mitochondrial fusion promoter M1. TPHP caused cardiac fibrosis and increased the levels of CK-MB and LDH in the serum. TPHP increased the levels of ROS, malondialdehyde (MDA), and decreased the level of superoxide dismutase (SOD) and Glutathione peroxidase (GSH-Px). Furthermore, TPHP caused mitochondrial damage, and induced fusion and fission disorders that contributed to mitophagy in both the heart of C57BL/6 J mice and H9c2 cells. Transcriptome analysis showed that TPHP induced up- or down-regulated expression of various genes in myocardial tissue and revealed enriched apoptosis pathways. It was also found that TPHP could remarkably increase the expression levels of Bax, cleaved Caspase-9, cleaved Caspase-3, and decreased Bcl-2, thereby causing apoptosis in H9c2 cells. Taken together, the results suggested that TPHP promoted mitophagy through mitochondria fusion dysfunction resulting from oxidative stress, leading to fibrosis by inducing myocardial apoptosis.

Thermodynamic evaluation on chemical looping conversion of Cd- and Zn-contained phytoremediation plant with different CaO pathways.

With the development of phytoremediation for soil contamination, disposal of phytoremediation plant becomes a serious problem. Thermochemical conversion of phytoremediation plant can greatly reduce the volume and mass, meanwhile the clean and reusable utilization is realized. As one of the thermochemical conversion technologies, chemical looping (CL) offers a carbon negative way for clean utilization of biomass. In this technology, CaO has binary roles of heavy metal solidification and CO2 sorption for gasification enhancement. To assess the CaO pathway in CL of phytoremediation plant, two different CL processes are constructed and comparatively studied based on thermodynamic evaluation. The effects of different operating parameters on the products of gasifier (GR) and reduction reactor (RR) are compared and discussed. Results demonstrated that the CaO addition in GR is beneficial to the production of pure combustible gases. Increasing RR temperature can promote the chemical looping reactions in RR. Under lower temperature, CaO in RR can consume more CO2 leading to CO2 free environment. When it is higher than 850 °C, there is no effect of CaO in RR. Increasing the amount of OC in system can enhance the conversion of combustible gases. When αOC is higher than 0.3, the OC is reduced to a mixed state of Fe3O4 and FeO. When the CaO circulates only between GR and calciner, pure CO2 can be captured at the outlet of calciner. Existence of CaO is beneficial to retain Cd and Zn in solid phases. When the gasification temperature increases from 500 °C to 800 °C, the Cd(g) increases while Cd decreases in both CL1 and CL2. For a long lifetime of OC, CaO is suggested to circulates between GR and calciner.

Lignocellulose-Based Superabsorbent Polymer Gel Crosslinked with Magnesium Aluminum Silicate for Highly Removal of Zn (II) from Aqueous Solution.

Lignocellulose (LCE) was ultrasonically treated and intercalated into magnesium aluminum silicate (MOT) clay to prepare a nano-lignocellulose magnesium aluminum silicate polymer gel (nano-LCE-MOT) for the removal of Zn (II) from aqueous solution. The product was characterised using nitrogen adsorption/desorption isotherm measurements, Fourier-transform infrared spectroscopy, scanning electron microscopy and energy-dispersive X-ray spectroscopy. The conditions for the adsorption of Zn (II) on nano-LCE-MOT were screened, and adsorption kinetics and isotherm model analysis were carried out to explore the adsorption mechanism and achieve the optimal adsorption of Zn (II). Optimal adsorption was achieved at an initial Zn (II) concentration of 800 mg/L at 60 °C in 160 min at a pH of 4.52. The adsorption kinetics were explored using a pseudo-second-order model, with the isotherm adsorption equilibrium found to conform to the Langmuir model. The maximum adsorption capacity of the nano-LCE-MOT polymer gel toward Zn (II) is 513.48 mg/g. The materials with adsorbed Zn (II) were desorbed using different media, with HCl found to be the most ideal medium to desorb Zn (II). The optimal desorption of Zn (II) was achieved in 0.08 mol/L HCl solution at 65 °C in 60 min. Under these conditions, Zn (II) was almost completely desorbed from the adsorbents, with the adsorption effect after cycling being slightly different from that of the initial adsorption.

Catalpol Enhances Neurogenesis And Inhibits Apoptosis Of New Neurons Via BDNF, But Not The BDNF/Trkb Pathway.

BACKGROUND: The role of catalpol in brain neurogenesis and newborn neuron survival has not been previously determined in permanent middle cerebral artery occlusion (pMCAO). METHODS: Fifty-four rats were divided into 6 groups: pMCAO (model, n=9); sham operation (NS, n=9); catalpol treatment (5 mg/kg and 10 mg/kg subgroups, n=9 each); K252a (n=9); and K252a+catalpol 5 mg/kg (n=9) with stroke. The effects of catalpol on behavior, neurogenesis surrounding the infarction ipsilateral to pMCAO, and the expression of brain-derived neurotrophic factor (BDNF) and its receptor (TrkB) were evaluated. Vehicle or, K252a (i.p.), an inhibitor of TrkB phosphorylase. RESULTS: Repeated administration of catalpol reduced neurological deficits and significantly improved neurogenesis. Catalpol increased the number of newborn immature neurons, as determined by BrdU+-Nestin+ and BrdU+-Tuj-1+ staining, and downregulated cleaved caspase 3 in Tuj-1+ cells at day 7 following stroke. Moreover, catalpol increased the protein expression of Tuj-1, MAP2, and the Bcl-2/Bax ratio, as determined using Western blot. Catalpol also significantly increased brain levels of BDNF, but not TrkB, resulting in enhanced survival of newborn neurons via inhibition of apoptosis. CONCLUSION: Catalpol may contribute to neurogenesis in infarcted brain regions and help promote the survival of newborn neurons by activating BDNF, but not BDNF/TrkB signaling.

Catalpol may improve axonal growth via regulating miR-124 regulated PI3K/AKT/mTOR pathway in neurons after ischemia.

BACKGROUND: MicroRNA-124 (miR-124) is a brain-specific miRNA molecule, the highest expression in the cortex and is associated with neuronal protection after stroke. This study aimed to investigate whether catalpol could affect miR-124 to regulate PI3K/AKT/mTOR pathway, promoting axonal growth in stroke rats. METHODS: Cells were divided into three groups: control group, miRNA124 agomir group, and miRNA124 antagomir group. To explore the mechanism, cells were divided into seven groups: control group, OGD group (OGD/R), miRNA124 agomir group, miRNA124 agomir plus catalpol group, miRNA124 antagomir group, miRNA124 antagomir plus catalpol group, and catalpol group. Before OGD/R, miRNA124 antagomir and microRNA124 agomir were transfected into neurons for 6 h by using ribo FECT nd Consumablesn/reper transfection kit. Cell survival and cell death were detected by MTT and LDH assay. Axonal growth was assessed by MAP-2 immunofluorescence staining. Western blotting and qPCR were used to detect the expression of molecules in the PI3K/AKT/mTOR pathway. RESULTS: Inhibition of miR-124 activated PI3K/AKT/mTOR pathway and promoted neuronal survival and axonal growth. The expression of miR-124 increased after OGD/R, and catalpol could inhibit miR-124 to activate PI3K/AKT/mTOR pathway to further promote axonal growth. CONCLUSIONS: It is concluded that catalpol may inhibit miR-124 to activate PI3K/AKT/mTOR pathway, promoting axonal growth.

Catalpol prevents denervated muscular atrophy related to the inhibition of autophagy and reduces BAX/BCL2 ratio via mTOR pathway.

AIM: To investigate the effects of catalpol on muscular atrophy induced by sciatic nerve crush injury (SNCI). METHODS: Seventy male Kunming mice were randomized into five groups (n=10): model, sham, catalpol (Cat), rapamycin (Rapa), and catalpol+rapamycin (Rapa+Cat). The ratio of gastrocnemius muscle wet weight (right/left, R/L) between the operated leg (right) and the normal leg (left) was calculated, and acetylcholinesterase (AChE) immunohistochemistry assays were performed to observe the change of motor end plate (MEP), along with the sizes of denervated and innervated muscle fibers. The expression levels of LC3II, TUNEL, BAX/BCL-2, LC3II/LC3I and P62, Beclin1, mTOR, and p-mTOR (ser2448) proteins in muscle were examined by fluorescence immunohistochemistry or Western blotting. RESULTS: Results show that catalpol improved the results of the grid walking tests by reducing the percentage of foot slips, which increased the gastrocnemius muscle wet weight (R/L), enhanced AChE expression at the MEP, and enlarged the section area of the muscle. The expression of LC3II and TUNEL was significantly inhibited by catalpol. The BAX/BCL-2 ratio was significantly increased in muscles of denervated and control groups. Lower LC3II/LC3I and BAX/BCL-2 ratios in denervated muscles were also detected after catalpol treatment. CONCLUSION: These results indicated that apoptosis and autophagy play a role in the regulation of denervation-induced muscle atrophy after SNCI, and catalpol alleviates muscle atrophy through the regulation of muscle apoptosis and autophagy via the mTOR signaling pathway.