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ABSTRACTObjectivesTo compare the long‐term efficacy and safety of transjugular intrahepatic portosystemic shunt (TIPS) combined with concurrent antegrade embolization in treating portal hypertension with oesophagogastric variceal bleeding in patients with and without large spontaneous portosystemic shunts (L‐SPSSs).Materials and MethodsWe retrospectively analysed data from patients with portal hypertension who underwent TIPS from November 2015 to April 2022. The patients were screened according to the inclusion criteria and were divided into L‐SPSSs group (L‐S group) and Non L‐SPSSs group (Non L‐S group). The primary outcome was the 2‐year liver transplantation‐free survival (TFS) rate. Secondary outcomes contained the incidence of overt hepatic encephalopathy (OHE), ectopic embolization and the 2‐year rebleeding rate.ResultsA total of 259 patients were enrolled (64 patients in L‐S group and 195 patients in Non L‐S group). The average age was 57.2 years, and the success rate of procedure was 100%. Baseline data showed no significant differences between two groups. There was a statistically significant difference in the 2‐year liver transplantation‐free rate between two groups (L‐S vs. Non L‐S, 84.38% vs. 71.28%; p = 0.045). OHE occurred in 19 (29.69%) patients with L‐SPSSs and 104 (53.33%) patients without L‐SPSSs, with a statistically significant difference (p = 0.001). And no statistically significant difference was found in ectopic embolism incidence rate and the 2‐year rebleeding rate between two groups. Multivariate Cox regression analysis identified male gender, portal vein thrombosis and preoperative high blood ammonia levels as independent risk factors for long‐term survival.ConclusionCompared to Non L‐S group, the patients in L‐S group achieve longer liver transplantation‐free survival and lower incidence rate of OHE without increasing the risk of 2‐year rebleeding and ectopic embolization.- Book : ()
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Abstract
Spin qubits in silicon are strong contenders for the realization of a practical quantum computer, having demonstrated single- and two-qubit gates with fidelities above the fault-tolerant threshold, and entanglement of three qubits. However, maintaining high-fidelity operations while increasing the qubit count remains challenging and therefore only two-qubit algorithms have been executed. Here we utilize a four-qubit silicon processor with all control fidelities above the fault-tolerant threshold and demonstrate a three-qubit Grover’s search algorithm with a ~95% probability of finding the marked state. Our processor is made of three phosphorus atoms precision-patterned into isotopically pure silicon, which localise one electron. The long coherence times of the qubits enable single-qubit fidelities above 99.9% for all qubits. Moreover, the efficient single-pulse multi-qubit operations enabled by the electron–nuclear hyperfine interaction facilitate controlled-Z gates between all pairs of nuclear spins with fidelities above 99% when using the electron as an ancilla. These control fidelities, combined with high-fidelity non-demolition readout of all nuclear spins, allow the creation of a three-qubit Greenberger–Horne–Zeilinger state with 96.2% fidelity. Looking ahead, coupling neighbouring nuclear spin registers, as the one shown here, via electron–electron exchange may enable larger, fault-tolerant quantum processors.- Book : ()
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2025
Abstract
In recent years, the roles of mitochondrial RNA and its associated human diseases have been reported to increase significantly. Treatments based on mtRNA metabolic processes and nuclear gene mutations are thus discussed. The mitochondrial oxidative phosphorylation process is affected by mtRNA metabolism, including mtRNA production, maturation, stabilization, and degradation, which leads to a variety of inherited human mitochondrial diseases. Moreover, mitochondrial diseases are caused by mitochondrial messenger RNA, mitochondrial transfer RNA, and mitochondrial ribosomal RNA gene mutations. This review presents the molecular mechanisms of human mtRNA metabolism and pathological mutations in mtRNA metabolism-related nuclear-encoded/nonencoded genes and mitochondrial DNA mutations to highlight the importance of mitochondrial RNA-related diseases and treatments.
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