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Operation speed and coherence time are two core measures for the viability of a qubit. Strong spin-orbit interaction (SOI) and relatively weak hyperfine interaction make holes in germanium (Ge) intriguing candidates for spin qubits with rapid, all-electrical coherent control. Here we report ultrafast single-spin manipulation in a hole-based double quantum dot in a germanium hut wire (GHW). Mediated by the strong SOI, a Rabi frequency exceeding 540 MHz is observed at a magnetic field of 100 mT, setting a record for ultrafast spin qubit control in semiconductor systems. We demonstrate that the strong SOI of heavy holes (HHs) in our GHW, characterized by a very short spin-orbit length of 1.5 nm, enables the rapid gate operations we accomplish. Our results demonstrate the potential of ultrafast coherent control of hole spin qubits to meet the requirement of DiVincenzo’s criteria for a scalable quantum information processor. Hole-spin qubits in germanium are promising candidates for rapid, all-electrical qubit control. Here the authors report Rabi oscillations with the record frequency of 540 MHz in a hole-based double quantum dot in a germanium hut wire, which is attributed to strong spin-orbit interaction of heavy holes.

This study aimed to investigate the efficacy of preoperative aspartate aminotransferase-to-platelet-ratio index (APRI) score to predict the risk of posthepatectomy liver failure (PHLF) in patients with hepatocellular carcinoma (HCC) after liver resection, and to compare the discriminatory performance of the APRI with the Child-Pugh score, model for end-stage liver disease (MELD) score, and albumin-bilirubin (ALBI) score. A total of 1,044 consecutive patients with HCC who underwent liver resection were enrolled and studied. Univariate and multivariate analyses were performed to investigate risk factors associated with PHLF. Predictive discrimination of Child-Pugh, MELD, ALBI, and APRI scores for predicting PHLF were assessed according to area under the ROC curve. The cutoff value of the APRI score for predicting PHLF was determined by ROC analysis. APRI scores were stratified by dichotomy to analyze correlations with incidence and grade of PHLF. PHLF occurred in 213 (20.4%) patients. Univariate and multivariate analyses revealed that Child-Pugh, MELD, ALBI, and APRI scores were significantly associated with PHLF. Area under the ROC analysis revealed that the APRI score for predicting PHLF was significantly more accurate than Child-Pugh, MELD, or ALBI scores. With an optimal cutoff value of 0.55, the sensitivity and specificity of the APRI score for predicting PHLF were 72.2% and 68.0%, respectively, and the incidence and grade of PHLF in patients with high risk (APRI score >0.55) was significantly higher than in the low-risk cohort (APRI score <0.55). The APRI score predicted PHLF in patients with HCC undergoing liver resection more accurately than Child-Pugh, MELD, or ALBI scores.

Utilizing colloidal probe, lateral force microscopy and simultaneous confocal microscopy, combined with finite element analysis, we investigate how a microparticle starts moving laterally on a soft, adhesive surface. We find that the surface can form a self-contacting crease at the leading front, which results from a buildup of compressive stress. Experimentally, creases are observed on substrates that exhibit either high or low adhesion when measured in the normal direction, motivating the use of simulations to consider the role of adhesion energy and interfacial strength. Our simulations illustrate that the interfacial strength plays a dominating role in the nucleation of a crease. After the crease forms, it progresses through the contact zone in a Schallamach wave-like fashion. Interestingly, our results suggest that this Schallamach wave-like motion is facilitated by free slip at the adhesive, self-contacting interface within the crease. Soft friction remains elusive due to the complication at microscales where the elastic forces are comparable to capillarity and adhesion. Glover et al. show that a moving microparticle can induce a cease at the leading front of the underlying soft surface as a result of a build-up of compressive stress.

Powerful optical tools have revolutionized science and technology. The prevalent fluorescence detection offers superb sensitivity down to single molecules but lacks sufficient chemical information1–3. In contrast, Raman-based vibrational spectroscopy provides exquisite chemical specificity about molecular structure, dynamics and coupling, but is notoriously insensitive3–5. Here, we report a hybrid technique of stimulated Raman excited fluorescence (SREF) that integrates superb detection sensitivity and fine chemical specificity. Through stimulated Raman pumping to an intermediate vibrational eigenstate, followed by an upconversion to an electronic fluorescent state, SREF encodes vibrational resonance into the excitation spectrum of fluorescence emission. By harnessing the narrow vibrational linewidth, we demonstrated multiplexed SREF imaging in cells, breaking the ‘colour barrier’ of fluorescence. By leveraging the superb sensitivity of SREF, we achieved all-far-field single-molecule Raman spectroscopy and imaging without plasmonic enhancement, a long-sought-after goal in photonics. Thus, through merging Raman and fluorescence spectroscopy, SREF would be a valuable tool for chemistry and biology.A hybrid technique of stimulated Raman excited fluorescence that integrates superb detection sensitivity and fine chemical specificity is demonstrated, offering all-far-field single-molecule Raman spectroscopy and imaging without plasmonic enhancement.

The Phase 3 RATIONALE-312 trial (NCT04005716) showed that tislelizumab plus chemotherapy led to a noteworthy enhancement resulted in a significant improvement in overall survival among patients diagnosed with extensive-stage small-cell lung cancer (ES-SCLC) compared to chemotherapy alone. The treatment also had an acceptable level of safety. Nevertheless, the debate over the efficacy of implementing several treatment plans in competition continues due to the significant expenses involved. Therefore, we aimed to evaluate the potential efficacy and cost of tislelizumab treatment as a first-line treatment for the ES-SCLC patient population in China. The study assessed primary health outcomes by measuring life years (LYs), quality-adjusted life years (QALYs), and incremental cost-effectiveness ratios (ICERs). This was done using a Markov model considering three health states with a 15-year horizon. To assess its model resilience, we conducted one-way sensitivity analyses with probability. In addition, subgroup analyses of some pre-specified patients was performed. Compared to chemotherapy alone, tislelizumab plus chemotherapy resulted in an additional 0.34 ($8,028) QALYs, leading to an ICER of $23,553 per QALY for the overall patient population. The ICER was lower than the assumed willingness-to-pay threshold of $35,367 per QALY. Approximately 60% of simulations suggested that tislelizumab in combination with chemotherapy was cost-effective, while 40% suggested that chemotherapy alone was cost-effective. The subsequent sensitivity analyses revealed that the health utility value associated with the disease progression parameter had the greatest influence on ICER. Tislelizumab plus chemotherapy was a preferable treatment option for regimens for patients with ES-SCLC in China. This finding is important in guiding the Chinese healthcare system.

MicroRNAs (miRNAs) exert critical effects in spinal cord injury (SCI). The miR‐33‐5p level is found to be lower in rats with SCI compared with that in control (untreated) and sham‐operated (laminectomy but no contusion) rats. Therefore, we investigated the biological functions of miR‐33‐5p and related mechanisms in SCI pathogenesis and development. An in vivo SCI model and a lipopolysaccharide (LPS)‐induced cell model of SCI were established. A downregulated level of miR‐33‐5p in experimental SCI and in LPS‐treated PC12 cells was revealed by reverse transcriptase‐quantitative polymerase chain reaction (RT‐qPCR). MiR‐33‐5p upregulation alleviated the leakage of the blood–spinal cord barrier (BSCB) induced by SCI and improved the neurological functions of SCI rats, as evidenced by the Basso, Beattie, and Bresnahan (BBB) scores and Evans blue staining. The regulatory relationship between miR‐33‐5p and Rps6kb1 was verified by luciferase reporter assays, which demonstrated that miR‐33‐5p bound to the Rps6kb1 3′UTR. Moreover, as MTT assays and flow cytometry showed, the suppressive effects of miR‐33‐5p upregulation on cell apoptosis were attenuated by Rps6kb1 upregulation. In conclusion, miR‐33‐5p ameliorates SCI in rats and inhibits the LPS‐induced apoptosis of PC12 cells.

Bacterial wilt caused by Ralstonia solanacearum is a devastating disease affecting hundreds of plant species, yet the host factors remain poorly characterized. The leucine-rich repeat receptor-like kinase gene AhRLK1, characterized as CLAVATA1, was found to be up-regulated in peanut upon inoculation with R. solanacearum. The AhRLK1 protein was localized in the plasma membrane and cell wall. qPCR results showed AhRLK1 was induced in a susceptible variety but little changed in a resistant cultivar after inoculated with R. solanacearum. Hormones such as salicylic acid, abscisic acid, methyl jasmonate, and ethephon induced AhRLK1 expression. In contrast, AhRLK1 expression was down-regulated under cold and drought treatments. Transient overexpression of AhRLK1 led to a hypersensitive response (HR) in Nicotiana benthamiana. Furthermore, AhRLK1 overexpression in tobacco significantly increased the resistance to R. solanacearum. Besides, the transcripts of most representative defense responsive genes in HR and hormone signal pathways were significantly increased in the transgenic lines. EDS1 and PAD4 in the R gene signaling pathway were also up-regulated, but NDR1 was down-regulated. Accordingly, AhRLK1 may increase the defense response to R. solanacearum via HR and hormone defense signaling, in particular through the EDS1 pathway of R gene signaling. These results provide a new understanding of the CLAVATA1 function and will contribute to genetic enhancement of peanut.

Achieving high-fidelity and robust qubit manipulations is a crucial requirement for realizing fault-tolerant quantum computation. Here, we demonstrate a single-hole spin qubit in a germanium quantum dot and characterize its control fidelity using gate set tomography. The maximum control fidelities reach 97.48%, 99.81%, 99.88% for the I , X /2 and Y /2 gate, respectively. These results reveal that off-resonance noise during consecutive I gates in gate set tomography sequences severely limits qubit performance. Therefore, we introduce geometric quantum computation to realize noise-resilient qubit manipulation. The geometric gate control fidelities remain above 99% across a wide range of Rabi frequencies. The maximum fidelity surpasses 99.9%. Furthermore, the fidelities of geometric X /2 and Y /2 ( I ) gates exceed 99% even when detuning the microwave frequency by  ± 2.5 MHz (± 1.2 MHz), highlighting the noise-resilient feature. These results demonstrate that geometric quantum computation is a potential method for achieving high-fidelity qubit manipulation reproducibly in semiconductor quantum computation. Geometric quantum gates—engineered evolution paths for qubit control—promise noise resilience but have shown limited fidelity in prior implementations in semiconductor quantum computation. Here the authors demonstrate high-fidelity single-qubit gates in a single-hole quantum dot in Ge, outperforming conventional dynamical gates.

Given the conceptual differences between different types of job insecurity, it is important to distinguish qualitative job insecurity from quantitative job insecurity when examining their motivational consequences. Building on the approach and avoidance framework, we expect that quantitative job insecurity influences avoid-performance goal orientation (avoidance form of motivation) via psychological safety, whereas qualitative job insecurity influences learning goal orientation (approach form of motivation) via psychological meaningfulness. We also examine the moderating role of organizational justice in such effects. Using two-wave data collected from 281 employees in China, we found that quantitative job insecurity had a positive indirect effect on employee avoid-performance goal orientation via decreased psychological safety, whereas qualitative job insecurity had a negative indirect effect on employee learning goal orientation via decreased psychological meaningfulness. In addition, organizational justice buffered the direct effect of quantitative job insecurity on employee psychological safety and the subsequent indirect effect on employee avoid-performance goal orientation. However, organizational justice did not moderate the influence of qualitative job insecurity on employee outcomes. Our findings provide new insights into the motivational implications of job insecurity.

microRNAs (miRNAs) have been reported to regulate angiogenesis by down-regulating the expression of pro-angiogenic or anti-angiogenic factors. The aims of this study were to investigate whether miR-26a inhibited angiogenesis by down-regulating vascular endothelial growth factor A (VEGFA) and its clinical relevance in hepatocellular carcinoma (HCC). The expression of miR-26a was modified in HepG2 and HCCLM3 cell lines respectively, and a panel of angiogenic factors was measured by real-time PCR in the cells. A luciferase reporter assay was used to validate the target gene of miR-26a. Specific inhibitors of signal transduction pathway and siRNA approaches were used to explore the regulatory mechanism of miR-26a. Migration and tube forming assays were conducted to show the changes of angiogenesis induced by miR-26a and its target genes. Finally animal studies were used to further validate those findings. Ectopic expression of miR-26a exhibited decreased levels of VEGFA in HepG2 cells. Migration and tube forming of human umbilical vein endothelial cells (HUVECs) were decreased in the conditioned medium from ectopic expression of miR-26a in HepG2 cells compared to control HepG2 cells. The pro-angiogenic effects of the conditioned medium of HepG2 cells on HUVECs were specifically decreased by LY294002, YC-1, and bevacizumab. Integrated analysis disclosed PIK3C2α as a downstream target gene of miR-26a. Ectopic expression of miR-26a suppressed ectopic and orthotopic tumor growth and vascularity in nude mice. The results in HCCLM3 were consistent with those in HepG2. miR-26a expression was inversely correlated with VEGFA expression in HCC patients. miR-26a modulated angiogenesis of HCC through the PIK3C2α/Akt/HIF-1α/VEGFA pathway. The expression of VEGFA was inversely correlated with miR-26a expression in HCC tumors.