Temporal Logic Disturbance Rejection Control of Nonlinear Systems Using Control Barrier Functions.

The high level of autonomy within autonomous systems demands new control strategies to achieve more complex objectives while ensuring both safety and robustness, rather than relying solely on a given reference. To this end, this article addresses the problem of temporal logic disturbance rejection control (TLDRC) for a class of nonlinear systems subject to disturbances. Signal temporal logic (STL) specifications are introduced for the representation of complex tasks.

Ribosome-associated pathological TDP-43 alters the expression of multiple mRNAs in the monkey brain.

Cytoplasmic accumulation of TDP-43 is a pathological hallmark of amyotrophic lateral sclerosis (ALS) and other neurodegenerative diseases. While current studies have primarily focused on gene regulation mediated by full-length nuclear TDP-43, the potential effects of cytoplasmic TDP-43 fragments remain less explored. Our previous findings demonstrated that primate-specific cleavage of TDP-43 contributes to its cytoplasmic localization, prompting further investigation into its pathological effects.

Long-Distance Passive Sensing Tag Design Based on Multi-Source Energy Harvesting and Reflection Amplification.

Wireless sensor networks often rely on battery power, which incurs high costs, considerable volume, and a limited lifespan. Additionally, the communication range of existing passive sensor tags remains short, which challenges their suitability for evolving Internet of Things (IoT) applications. This paper, therefore, presents a long-distance passive RFID sensing tag that integrates multi-source energy harvesting and reflection amplification.

Application of antisense oligonucleotide drugs in amyotrophic lateral sclerosis and Huntington's disease.

Amyotrophic lateral sclerosis (ALS) and Huntington's disease (HD) are diverse in clinical presentation and are caused by complex and multiple factors, including genetic mutations and environmental factors. Numerous therapeutic approaches have been developed based on the genetic causes and potential mechanisms of ALS and HD. Currently, available treatments for various neurodegenerative diseases can alleviate symptoms but do not provide a definitive cure.

RNA-Targeting CRISPR/CasRx system relieves disease symptoms in Huntington's disease models.

Background: HD is a devastating neurodegenerative disorder caused by the expansion of CAG repeats in the HTT. Silencing the expression of mutated proteins is a therapeutic direction to rescue HD patients, and recent advances in gene editing technology such as CRISPR/CasRx have opened up new avenues for therapeutic intervention.

Methods: The CRISPR/CasRx system was employed to target human HTT exon 1, resulting in an efficient knockdown of HTT mRNA.

Non-smooth fixed-time state feedback stabilization of uncertain switched systems with output constraints.

In this paper, non-smooth fixed-time state feedback stabilization of output-constrained uncertain switched systems has been investigated. First, to deal with the output constraints implicitly, a tangent-type barrier Lyapunov function (T-BLF), which degenerates into a quadratic function as the output constraints tend to infinity, is constructed deliberately. Then, the fixed-time state feedback control scheme for the output-constrained uncertain switched systems is established with remoulding the technique called adding a power integrator (AAPI).

Combining fire needle plus cupping with famciclovir and gabapentin in the treatment of acute herpes zoster: a revised intervention approach.

This study aimed to investigate the efficacy and safety of fire needle plus cupping (FC) combined with oral famciclovir and gabapentin for the treatment of acute-phase herpes zoster (AHZ). This study was conducted as a superiority, randomized controlled trial in which 84 patients with AHZ who met the diagnostic criteria were selected and randomly assigned to three groups on a 1:1 basis. Group A: received oral famciclovir with gabapentin treatment (FG); Group B: received fire needle plus cupping (FC) with FG.

Satellite-Based Monitoring of Methane Emissions from China's Rice Hub.

Rice cultivation is one of the major anthropogenic methane sources in China and globally. However, accurately quantifying regional rice methane emissions is often challenging due to highly heterogeneous emission fluxes and limited measurement data. This study attempts to address this issue by quantifying regional methane emissions from rice cultivation with a high-resolution inversion of satellite methane observations from the Tropospheric Monitoring Instrument (TROPOMI).

Organotropic Engineering of Luminescent Gold Nanoclusters for In Vivo Imaging of Lung Orthotopic Tumors.

Gold nanoclusters (AuNCs) are emerging as promising functional probes for bioapplications. However, because of rapid renal clearance, it is a challenge to tailor their biofate and improve their disease-targeting ability in vivo. Herein, we report an efficient strategy to tailor their organotropic actions by rationally designing AuNC assemblies.

Increased expression of mesencephalic astrocyte-derived neurotrophic factor (MANF) contributes to synapse loss in Alzheimer's disease.

Background: The activation of endoplasmic reticulum (ER) stress is an early pathological hallmark of Alzheimer's disease (AD) brain, but how ER stress contributes to the onset and development of AD remains poorly characterized. Mesencephalic astrocyte-derived neurotrophic factor (MANF) is a non-canonical neurotrophic factor and an ER stress inducible protein. Previous studies reported that MANF is increased in the brains of both pre-symptomatic and symptomatic AD patients, but the consequence of the early rise in MANF protein is unknown.

Tumor Suppressor Inhibits the Progression of Cervical Cancer by Regulating the PTEN/Akt/mTOR Pathway.

Objective: Cervical cancer (CC) ranks among the most prevalent malignant tumors affecting the female reproductive system. Nonetheless, various shortcomings exist within current treatment approaches for CC. Therefore, the quest for new intervention targets holds significant importance.

Pathogenic TDP-43 accelerates the generation of toxic exon1 HTT in Huntington's disease knock-in mice.

Huntington's disease (HD) is caused by a CAG repeat expansion in exon1 of the HTT gene that encodes a polyglutamine tract in huntingtin protein. The formation of HTT exon1 fragments with an expanded polyglutamine repeat has been implicated as a key step in the pathogenesis of HD. It was reported that the CAG repeat length-dependent aberrant splicing of exon1 HTT results in a short polyadenylated mRNA that is translated into an exon1 HTT protein.

Suppressing UBE2N ameliorates Alzheimer's disease pathology through the clearance of amyloid beta.

Introduction: Aging is one of the risk factors for the early onset of Alzheimer's disease (AD). We previously discovered that the age-dependent increase in Ubiquitin Conjugating Enzyme E2 N (UBE2N) plays a role in the accumulation of misfolded proteins through K63 ubiquitination, which has been linked to AD pathogenesis. However, the impact of UBE2N on amyloid pathology and clearance has remained unknown.

Differential distribution of PINK1 and Parkin in the primate brain implies distinct roles.

JOURNAL/nrgr/04.03/01300535-202504000-00028/figure1/v/2024-07-06T104127Z/r/image-tiff The vast majority of in vitro studies have demonstrated that PINK1 phosphorylates Parkin to work together in mitophagy to protect against neuronal degeneration. However, it remains largely unclear how PINK1 and Parkin are expressed in mammalian brains.

Reduced mesencephalic astrocyte-derived neurotrophic factor expression by mutant androgen receptor contributes to neurodegeneration in a model of spinal and bulbar muscular atrophy pathology.

JOURNAL/nrgr/04.03/01300535-202509000-00027/figure1/v/2024-11-05T132919Z/r/image-tiff Spinal and bulbar muscular atrophy is a neurodegenerative disease caused by extended CAG trinucleotide repeats in the androgen receptor gene, which encodes a ligand-dependent transcription factor. The mutant androgen receptor protein, characterized by polyglutamine expansion, is prone to misfolding and forms aggregates in both the nucleus and cytoplasm in the brain in spinal and bulbar muscular atrophy patients.

Deciphering a reliable synergistic bispecific strategy of rescuing antibodies for SARS-CoV-2 escape variants, including BA.2.86, EG.5.1, and JN.1.

The game between therapeutic monoclonal antibodies (mAbs) and continuously emerging severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants has favored the virus, as most therapeutic mAbs have been evaded. Addressing this challenge, we systematically explored a reproducible bispecific antibody (bsAb)-dependent synergistic effect in this study. It could effectively restore the neutralizing activity of the bsAb when any of its single mAbs is escaped by variants.

Coxsackievirus A10 impairs nail regeneration and induces onychomadesis by mimicking DKK1 to attenuate Wnt signaling.

Coxsackievirus A10 (CV-A10) infection, a prominent cause of childhood hand-foot-and-mouth disease (HFMD), frequently manifests with the intriguing phenomenon of onychomadesis, characterized by nail shedding. However, the underlying mechanism is elusive. Here, we found that CV-A10 infection in mice could suppress Wnt/β-catenin signaling by restraining LDL receptor-related protein 6 (LRP6) phosphorylation and β-catenin accumulation and lead to onychomadesis.

Bispecific antibodies targeting two glycoproteins on SFTSV exhibit synergistic neutralization and protection in a mouse model.

Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease with a high fatality rate of up to 30% caused by SFTS virus (SFTSV). However, no specific vaccine or antiviral therapy has been approved for clinical use. To develop an effective treatment, we isolated a panel of human monoclonal antibodies (mAbs).

TRIM37 is a primate-specific E3 ligase for Huntingtin and accounts for the striatal degeneration in Huntington's disease.

Huntington's disease (HD) is an autosomal dominant neurodegenerative disease characterized by preferential neuronal loss in the striatum. The mechanism underlying striatal selective neurodegeneration remains unclear, making it difficult to develop effective treatments for HD. In the brains of nonhuman primates, we examined the expression of Huntingtin (), the gene responsible for HD.