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Aihua Chen

Publications and source records attributed to Aihua Chen.

6 recordsLinked to original sources
PubMed2026

Conflict-dependent gain control in area VIP during visual-vestibular self-motion processing.

Visual and vestibular signals are continuously integrated to estimate self-motion, yet these sensory cues are often inconsistent under natural conditions. How cortical circuits regulate multisensory interactions under cue conflict while preserving stable heading representations remains poorly understood. Here, we recorded neurons in male macaque ventral intraparietal area (VIP) during passive movement stimulation while systematically varying visual-vestibular heading offsets. VIP neurons exhibited strong conflict-sensitive gain modulation: congruent cues enhanced neuronal responses, whereas increasing cue offsets progressively suppressed response gain. This effect was observed not only in multisensory neurons but also in neurons classified as predominantly visual or vestibular, indicating widespread cross-modal interactions across the population. In contrast, preferred-heading shifts remain modest, suggesting that cue conflict primarily modulated response gain rather than altering heading tuning. Despite substantial suppression at the single-neuron level under large cue offsets, population Fisher information was largely preserved, indicating robust heading discriminability. Further analyses revealed flexible sensory weighting in VIP, with visual and vestibular contributions shifting as cue conflict increased. Finally, a feedforward-gated normalization model substantially improved the characterization of VIP responses by allowing cue conflict to dynamically regulate the effective normalization pool, thereby capturing both multisensory enhancement at small visual-vestibular heading offset and suppression under large cue conflict. Together, these findings show that VIP exhibits conflict-dependent regulation of multisensory gain, preserving robust self-motion representations under sensory conflict.Significance statement Visual and vestibular cues are often misaligned in natural environments, creating a challenge for accurate self-motion perception. We demonstrate that neurons in the macaque ventral intraparietal area (VIP) dynamically adjust multisensory gain according to the degree of visual-vestibular conflict. As the visual-vestibular heading offset increases, neuronal responses are progressively enhanced or suppressed, while population coding of heading direction remains largely preserved. A conflict-sensitive normalization model accounts for these response dynamics and outperforms traditional multisensory integration models, suggesting that VIP implements adaptive gain-control computations to regulate interactions between visual and vestibular signals. These results identify a cortical mechanism that links sensory conflict detection to robust perceptual coding, advancing our understanding of multisensory processing in the brain.

Journal Article↗
PubMed2005

Formation process of silver-polypyrrole coaxial nanocables synthesized by redox reaction between AgNO3 and pyrrole in the presence of poly(vinylpyrrolidone).

We have recently demonstrated a one-step process to fabricate silver-polypyrrole (PPy) coaxial nanocables (Chen, A.; Wang, H.; Li, X. Chem. Commun. 2005, 14, 1863). The formation process of silver-PPy coaxial nanocables is discussed in this article. It was found from the results of TEM and SEM images that large numbers of silver atoms were formed when AgNO3 was added to a pyrrole solution. Then silver atoms transform to silver-PPy nanosheets with regular morphology, which will connect together to be more stable. Silver-PPy nanocables will be able to grow at the expense of the silver-PPy nanosheets. Poly(vinylpyrrolidone) (PVP) plays crucial roles in this process: as a capping agent to form silver nanowires, and as a dispersant of pyrrole monomers, which can influence the site at which pyrrole monomer exists. On the basis of experimental analysis, the possible mechanism was proposed. Because of the effect of PVP, silver ions and pyrrole monomers are apt to be adsorbed at the [111] and [100] facets of silver nanosheets, respectively. Obvious polymerization will take place on the boundary of the [111] and [100] facets. The PPy layer stays stable on the [100] facets. Meanwhile, newly formed silver atoms and silver nanosheets will further ripen and grow on the [111] facets. In a word, the morphology of final products and the formation process are determined by the reaction site between AgNO3 and the pyrrole monomer, which is influenced by PVP.

Journal Article↗
PubMed2005

Cellular fate of truncated slow skeletal muscle troponin T produced by Glu180 nonsense mutation in amish nemaline myopathy.

A nonsense mutation at codon Glu180 in exon 11 of slow skeletal muscle troponin T (TnT) gene (TNNT1) causes an autosomal-recessive inherited nemaline myopathy. We previously reported the absence of intact or prematurely terminated slow TnT polypeptide in Amish nemaline myopathy (ANM) patient muscle. The present study further investigates the expression and fate of mutant slow TnT in muscle cells. Intact slow TnT mRNA was readily detected in patient muscle, indicating unaffected transcription and RNA splicing. Sequence of the cloned cDNAs revealed the single nucleotide mutation in two alternatively spliced isoforms of slow TnT mRNA. Mutant TNNT1 cDNA is translationally active in Escherichia coli and non-muscle eukaryotic cells, producing the expected truncated slow TnT protein. The mutant mRNA was expressed at significant levels in differentiated C2C12 myotubes, but unlike intact exogenous TnT, truncated slow TnT protein was not detected. Transfective expression in undifferentiated myoblasts produced slow TnT mRNA but not a detectable amount of truncated or intact slow TnT proteins, indicating a muscle cell-specific proteolysis of TnT when it is not integrated into myofilaments. The slow TnT-(1-179) fragment has substantially lower affinity for binding to tropomyosin, in keeping with the loss of one of two tropomyosin-binding sites. Our findings suggest that inefficient incorporation into myofilament is responsible for the instability of mutant slow TnT in ANM muscle. Rapid degradation of the truncated slow TnT protein, rather than instability of the nonsense mRNA, provides the protective mechanism against the potential dominant negative effect of the mutant TnT fragment.

Alternative Splicing↗
PubMed2005

[The effects of pronuciferine on NO and NOS production in cultured human umbilical vein endothelium cells].

OBJECTIVE: To investigate the effects of Pronuciferine on nitric oxide (NO), total nitric oxide synthase (tNOS) and inducible nitric oxide synthase (iNOS) production in cultured Human Umbilical Vein Endothelium Cells (HUVECs). METHODS: Pronuciferine was extracted from plumula nelumbinis. The experiments were performed in HUVECs in vitro. Cell-morphology was observed by light microscope. Cells viability was assessed by MTT assay. NO, tNOS and iNOS were measured by Colorimetry. RESULTS: Cell- morphology and viability weren't affected by Pronuciferine. Pronuciferine significantly increased the level of NO and the activity of tNOS, but had no effect on the activity of iNOS. CONCLUSION: Pronuciferine increases the level of NO by the enhancement of the activity of tNOS. It may have the protection on endothelial function.

Alkaloids↗
PubMed2002

[The relationship of aldosterone synthase gene polymorphism with hypertension and left ventricular hypertrophy].

OBJECTIVE: To investigate the relationship of gene polymorphism of angiotension converting enzyme (ACE), aldosterone synthase (CYP11B2) with essential hypertension (EH) and left ventricular hypertrophy (LVH) in hypertensive patients. METHODS: (1) Left ventricular mass and geometry were assessed with ECG and echocardiography in 136 hypertensive patients. (2) The insertion/deletion polymorphism of ACE gene and the -344C/T polymorphism of CYP11B2 gene were monitored by polymerase chain reaction (PCR). RESULTS: (1) ACE and CYP11B2 gene showed significant difference in genotype or allele frequency distribution in the group with LVH as compared with the group without (P < 0.05). (2) There was a significant difference in CT + II combined genotype frequency distribution in the group with LVH as compared with the group without (P < 0.05). CONCLUSIONS: (1) No relationship between the polymorphism of CYP11B2 gene and ACE gene with essential hyptension could be found. (2) A significant relationship between the polymorphism of ACE and CYP11B2 gene with LVH in EH could be found. I allele of ACE gene and C allele of CYP11B2 gene may be independent risk factors for LVH in hypertensive patients. (3) There is a synergistic effect between the polymorphism of ACE gene and CYP11B2 gene to result in LVH in EH.

Cytochrome P-450 CYP11B2↗