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ABSTRACT Background and Objectives Guillain–Barré syndrome (GBS), an acute inflammatory disorder of the peripheral nervous system, is characterized by muscle weakness and paralysis. Prompt identification of patients at a high risk of poor outcomes is crucial for timely intervention. In this study, we combined clinical data with nerve conduction study and electromyography data to identify the predictors of GBS outcomes. Methods We retrospectively analyzed the data of patients with GBS who had received treatment at Chang Gung Memorial Hospital, Taiwan, between 1998 and 2022. Comprehensive clinical and electrophysiological data were collected. Statistical analyses were performed to identify the predictors of poor outcomes. The patients were stratified into two groups by their scores on the GBS Disability Scale: good (score ≤ 2) and poor (score > 2) outcome groups. Results The study finally included 24 GBS patients (mean age: 53.0 ± 20.9 years; female‐to‐male ratio: 2.3; good outcome group: 13; poor outcome group: 11). Compared with the good outcome group, the poor outcome group was old (43.0 ± 20.4 vs. 64.0 ± 15.7, p = 0.011), had a short time‐to‐treatment period (12.9 ± 7.8 vs. 6.5 ± 5.4 days, p = 0.033), exhibited more prevalent mechanical ventilation use (0 vs. 36.4%, p = 0.017), and had a prolonged hospitalization duration (14.7 ± 10.2 vs. 53.1 ± 20.0 days, p < 0.001). Poor outcomes were associated with low compound muscle action potential (CMAP), slow motor nerve conduction velocity (MNCV), abnormal F‐wave latency, and more conduction block and temporal dispersion. In the subgroup of acute inflammatory demyelinating polyradiculoneuropathy (AIDP), there were 19 patients, out of which 10 had good outcomes, while nine had poor outcomes. The clinical features that differentiate between good and poor outcomes in the AIDP subgroup were similar to those observed in all GBS patients. Notably, the motor conduction features, including distal and proximal CMAP and MNCV of the median and tibial nerves (all p < 0.05), were particularly important electrodiagnostic features of outcome discrimination in the AIDP subgroup. Discussion Combining clinical data with nerve conduction study and electromyography data can assist in predicting outcomes of both GBS patients and the AIDP subgroup. Poor outcomes are associated with older age, a more abrupt onset pattern, low CMAP, and slow nerve conduction, and abnormal tibial F responses can predict poor outcomes. Early identification of high‐risk patients facilitates tailored interventions. This highlights the importance of combining clinical and electrophysiological data in GBS management.

The role of microRNA (miRNA) in influenza A virus (IAV) host species specificity is not well understood as yet. Here, we show that a host miRNA, miR-1290, is induced through the extracellular signal-regulated kinase (ERK) pathway upon IAV infection and is associated with increased viral titers in human cells and ferret animal models. miR-1290 was observed to target and reduce expression of the host vimentin gene. Vimentin binds with the PB2 subunit of influenza A virus ribonucleoprotein (vRNP), and knockdown of vimentin expression significantly increased vRNP nuclear retention and viral polymerase activity. Interestingly, miR-1290 was not detected in either chicken cells or mouse animal models, and the 3′ UTR of the chicken vimentin gene contains no binding site for miR-1290. These findings point to a host species-specific mechanism by which IAV upregulates miR-1290 to disrupt vimentin expression and retain vRNP in the nucleus, thereby enhancing viral polymerase activity and viral replication. Keywords: influenza A virus, miR-1290, vimentin, viral ribonucleoprotein, vRNP, miRNA, virus, host species-specificity, ferret

We present a quantum algorithm for the dynamical simulation of time-dependent Hamiltonians. Our method involves expanding the interaction-picture Hamiltonian as a sum of generalized permutations, which leads to an integral-free Dyson series of the time-evolution operator. Under this representation, we perform a quantum simulation for the time-evolution operator by means of the linear combination of unitaries technique. We optimize the time steps of the evolution based on the Hamiltonian’s dynamical characteristics, leading to a gate count that scales with an L^{1}-norm-like scaling with respect only to the norm of the interaction Hamiltonian, rather than that of the total Hamiltonian. We demonstrate that the cost of the algorithm is independent of the Hamiltonian’s frequencies, implying its advantage for systems with highly oscillating components, and for time-decaying systems the cost does not scale with the total evolution time asymptotically. In addition, our algorithm retains the near optimal log⁡(1/ϵ)/loglog⁡(1/ϵ) scaling with simulation error ϵ.

Performing measurements for high-weight operators has been a practical problem in quantum computation, especially for quantum codes in the stabilizer formalism. The conventional procedure of measuring a high-weight operator requires multiple pairwise unitary operations, which can be slow and prone to errors. We provide an alternative method to passively detect the value of a high-weight operator using only two-local interactions and single-qubit continuous measurements. This approach involves joint interactions between the system and continuously monitored ancillary qubits. The measurement outcomes from the monitor qubits reveal information about the value of the operator. This information can be retrieved by using a numerical estimator or by evaluating the time average of the signals. The interaction Hamiltonian can be effectively built using only two-local operators, based on techniques from perturbation theory. We apply this indirect detection scheme to the four-qubit Bacon-Shor code, where the two stabilizers are indirectly monitored using four ancillary qubits. Due to the fact that the four-qubit Bacon-Shor code is an error-detecting code and that the quantum Zeno effect can suppress errors, we also study the error suppression under the indirect measurement process. In this example, we show that various types of non-Markovian errors can be suppressed.

ABSTRACT Avian influenza A viruses generally do not replicate efficiently in human cells, but substitution of glutamic acid (Glu, E) for lysine (Lys, K) at residue 627 of avian influenza virus polymerase basic protein 2 (PB2) can serve to overcome host restriction and facilitate human infectivity. Although PB2 residue 627 is regarded as a species-specific signature of influenza A viruses, host restriction factors associated with PB2627E have yet to be fully investigated. We conducted immunoprecipitation, followed by differential proteomic analysis, to identify proteins associating with PB2627K (human signature) and PB2627E (avian signature) of influenza A/WSN/1933(H1N1) virus, and the results indicated that Tu elongation factor, mitochondrial (TUFM), had a higher binding affinity for PB2627E than PB2627K in transfected human cells. Stronger binding of TUFM to avian-signature PB2590G/591Q and PB2627E in the 2009 swine-origin pandemic H1N1 and 2013 avian-origin H7N9 influenza A viruses was similarly observed. Viruses carrying avian-signature PB2627E demonstrated increased replication in TUFM-deficient cells, but viral replication decreased in cells overexpressing TUFM. Interestingly, the presence of TUFM specifically inhibited the replication of PB2627E viruses, but not PB2627K viruses. In addition, enhanced levels of interaction between TUFM and PB2627E were noted in the mitochondrial fraction of infected cells. Furthermore, TUFM-dependent autophagy was reduced in TUFM-deficient cells infected with PB2627E virus; however, autophagy remained consistent in PB2627K virus-infected cells. The results suggest that TUFM acts as a host restriction factor that impedes avian-signature influenza A virus replication in human cells in a manner that correlates with autophagy. IMPORTANCE An understanding of the mechanisms that influenza A viruses utilize to shift host tropism and the identification of host restriction factors that can limit infection are both critical to the prevention and control of emerging viruses that cross species barriers to target new hosts. Using a proteomic approach, we revealed a novel role for TUFM as a host restriction factor that exerts an inhibitory effect on avian-signature PB2627E influenza virus propagation in human cells. We further found that increased TUFM-dependent autophagy correlates with the inhibitory effect on avian-signature influenza virus replication and may serve as a key intrinsic mechanism to restrict avian influenza virus infection in humans. These findings provide new insight regarding the TUFM mitochondrial protein and may have important implications for the development of novel antiviral strategies.

Tardive dyskinesia (TD) is a severe adverse effect induced by prolonged treatment with antipsychotics. The development of TD is usually associated with advanced age, female sex, prior extrapyramidal adverse effects, and a longer duration or an intermittent course of antipsychotic treatment. Older age, however, is the most robust risk factor for TD. Tardive diaphragmatic flutter is an uncommon form of TD and may lead to great distress in the patient's life. No effective treatment advice for tardive diaphragmatic flutter has been suggested. We herein report the case of a 65-year-old male with bipolar disorder who suffered from tardive diaphragmatic flutter associated with the long-term usage of risperidone. The diaphragmatic flutter remitted for 2 years under the monotherapy with aripiprazole. Potential mechanisms, such as the dopamine stabilization in aripiprazole, are discussed.