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With the scaling of lateral dimensions in advanced transistors, an increased gate capacitance is desirable both to retain the control of the gate electrode over the channel and to reduce the operating voltage1. This led to a fundamental change in the gate stack in 2008, the incorporation of high-dielectric-constant HfO2 (ref. 2), which remains the material of choice to date. Here we report HfO2-ZrO2 superlattice heterostructures as a gate stack, stabilized with mixed ferroelectric-antiferroelectric order, directly integrated onto Si transistors, and scaled down to approximately 20 ångströms, the same gate oxide thickness required for high-performance transistors. The overall equivalent oxide thickness in metal-oxide-semiconductor capacitors is equivalent to an effective SiO2 thickness of approximately 6.5 ångströms. Such a low effective oxide thickness and the resulting large capacitance cannot be achieved in conventional HfO2-based high-dielectric-constant gate stacks without scavenging the interfacial SiO2, which has adverse effects on the electron transport and gate leakage current3. Accordingly, our gate stacks, which do not require such scavenging, provide substantially lower leakage current and no mobility degradation. This work demonstrates that ultrathin ferroic HfO2-ZrO2 multilayers, stabilized with competing ferroelectric-antiferroelectric order in the two-nanometre-thickness regime, provide a path towards advanced gate oxide stacks in electronic devices beyond conventional HfO2-based high-dielectric-constant materials.

In this work, the ferroelectric characteristic of a 5 nm Hf0.5Zr0.5O2 (HZO) metal-ferroelectric-insulator-semiconductor (MFIS) device is enhanced through strained complementary metal oxide semiconductor (CMOS)-compatible TiN electrode engineering. Strained TiN top-layer electrodes with different nitrogen (N) concentrations are deposited by adjusting the sputtering process conditions. The TiN electrode with 18% N exhibits a compressive characteristic, which induces tensile stress in a 5 nm HZO film. A device with 18% N in TiN shows a higher remanent polarization (2Pr) and larger capacitance value than the compared sample, indicating that the strained TiN is promising for enhancing the ferroelectricity of sub-5 nm HZO devices.

Broodiness, a maternal behavior, is accompanied by the atresia of follicles and the serious degradation of poultry reproductive performance. The comparison of follicles between brooding and laying hens is usually an ideal model for exploring the regulation mechanism of follicle atresia. In this study, we selected three brooding hens and three laying hens to collect their follicles for whole transcriptome sequencing. The results demonstrated different expression patterns between the follicles of brooding hens and laying hens. In the top 10 differentially expressed genes with the highest expression, MMP10 was relatively low expressed in the follicles of brooding hens, but other nine genes were relatively highly expressed, including LRR1, RACK1, SPECC1L, ABHD2, COL6A3, RPS17, ATRN, BIRC6, PGAM1 and SPECC1L. While miR-21-3p, miR-146a-5p, miR-142-5p and miR-1b-3p were highly expressed in the follicles of brooding hen, miR-106-5p, miR-451, miR-183, miR-7, miR-2188-5p and miR-182-5p were lowly expressed in brooding hen. In addition, we identified 124 lncRNAs specifically expressed in the follicles of brooding hens and 147 lncRNAs specifically expressed in the follicles of laying hens. Our results may provide a theoretical basis for further exploration of the molecular mechanism of broodiness in broilers. [ABSTRACT FROM AUTHOR]

Granulosa cell (GC) apoptosis is the main trigger of follicular atresia. MicroRNAs (miRNAs) are 18–22 nt RNAs whose function is primarily determined by their extended seed region and are considered to be involved in the biological functions of follicular development, including follicular atresia, folliculogenesis, and oogenesis. MiR-138-5p is known to act on chicken GCs. In this study, we found that miR-138-5p was enriched in reproductive organs, such as the uterus and ovaries. To examine whether miR-138-5p could regulate the biological process of GCs, miR-138-5p was examined by transfection of cells with a mimic or inhibitor of miR-138-5p. Expression levels of caspase-3 and caspase-9 mRNA and protein were markedly increased or decreased after transfection of the mimic or inhibitor, respectively. Furthermore, following miR-138-5p inhibition, SIRT1, one of the target genes of miR-138-5p, was found to increase the mRNA, which is correlated with the increased levels of BCL2 expression, an anti-apoptotic gene in the chicken GCs. These results suggest that miR-138-5p promotes apoptosis in chicken GCs by targeting SIRT1. [ABSTRACT FROM AUTHOR]