An alpha-herpesvirus employs host HEXIM1 to promote viral transcription.

Although it is widely accepted that herpesviruses utilize host RNA polymerase II (RNAPII) to transcribe viral genes, the mechanism of utilization varies significantly among herpesviruses. With the exception of herpes simplex virus 1 (HSV-1) in alpha-herpesviruses, the mechanism by which RNAPII transcribes viral genes in the remaining alpha-herpesviruses has not been reported. In this study, we investigated the transcriptional mechanism of an avian alpha-herpesvirus, Anatid herpesvirus 1 (AnHV-1).

A conformationally-locked p-hydroxybenzylidene imidazolinone derivative for detecting Aβ aggregation.

Alzheimer's disease (AD) is a common type of neurodegenerative disease, which can only be symptomatically relieved but does not yet have a cure. Among the different Aβ species, amyloid-β (Aβ) aggregates are proposed to be more neurotoxic than that of Aβ, and oligomeric Aβ is thought to play a harmful role in the pathophysiology of AD. Therefore, the detection of Aβ aggregation is very meaningful in the AD field.

Alloprevotella Can be Considered as a Potential Oral Biomarker in Intestinal Metaphase of Gastric Patients.

Gastric cancer is a malignant tumor with high incidence and death rate. Every year, Approximately 950,000 new cases of gastric cancer occur globally with nearly 700000 deaths,so gastric precancerous lesions(GPL) was crucial and important.At present, the effective diagnostic methods for gastric precancerous lesions are generally gastroscope and pathological changes of gastric mucosal, but those methods were invasive and would bring some pains to patients and not suitable for frequent and large-scale screening of gastric cancer or GPL.

Oxytocinergic neurons, but not oxytocin, are crucial for male penile erection.

The cumulative evidence suggests that oxytocin is involved in the male sexual behaviors. However, no significant sexual impairments were observed in oxytocin gene knock-out (KO) mice, suggesting that oxytocin is not necessary for sexual behavior in male mice. To better understand the role of oxytocin in male erection, two types of oxytocin gene KO mice were created.

Differential expression profile and in-silico functional analysis of long noncoding RNA and mRNA in duck embryo fibroblasts infected with duck plague virus.

Background: Duck plague virus (DPV), belonging to herpesviruses, is a linear double-stranded DNA virus. There are many reports about the outbreak of the duck plague in a variety of countries, which caused huge economic losses. Recently, increasing reports revealed that multiple long non-coding RNAs (lncRNAs) can possess great potential in the regulation of host antiviral immune response.

Dual-Emission GFP Chromophore-Based Derivative for Imaging and Discriminating Aβ Oligomers and Aggregates.

β-Amyloid deposition is one of the main pathological features of Alzheimer's disease (AD). The development of fluorescent probes targeting specific β-amyloid species has recently become an attractive strategy to achieve the early diagnosis of AD. In this work, a dual-channel fluorescent protein chromophore derivative was rationally designed and synthesized for the detection and discrimination of Aβ aggregates and oligomers.

Dual-functional AIE fluorescent probes for imaging β-amyloid plaques and lipid droplets.

Alzheimer's disease (AD) is a chronic neurodegenerative disease. Better imaging and early diagnosis of biomarkers of AD is extremely important for therapeutic interventions. The amyloid cascade hypothesis and its revised version identify insoluble β-amyloid deposition as a good diagnostic biomarker for AD.

Novel D-π-A type near-infrared fluorescent probes for the detection of Aβ aggregates.

Aberrant accumulation of Amyloid-β (Aβ) peptide is closely related to Alzheimer's disease. Thus, it is important to develop featured probes for the specific detection of Aβ species. Herein, we designed and synthesized a novel near-infrared fluorescent probe SDPY based on the D-π-A architecture for the detection of Aβ aggregates.

A novel near-infrared fluorescent probe for detection of early-stage Aβ protofibrils in Alzheimer's disease.

Detection of Aβ protofibrils at the early stage of Alzheimer's disease was realized by a novel near-infrared probe (DCM-AN) based on dicyanomethylene-4H-pyran. This probe exhibits high affinity towards Aβ protofibrils in vitro and in brain sections of transgenic mouse models for Alzheimer's disease.

NIR fluorescent probes with good water-solubility for detection of amyloid beta aggregates in Alzheimer's disease.

Two quinoline-malononitrile-based NIR fluorescent probes with good water-solubility have been developed for detecting and imaging of Aβ aggregates in Alzheimer's disease. In vitro studies demonstrated that both probes exhibited high affinity to Aβ aggregates with an increase of fluorescence intensity due to the intramolecular charge transfer effect. Moreover, the probes could particularly image Aβ plaques in brain sections of triple transgenic AD mice.

Fluoro-substituted cyanine for reliable labelling of amyloid-β oligomers and neuroprotection against amyloid-β induced toxicity.

Alzheimer's disease (AD) is the most prevalent but still incurable neurodegenerative form of dementia. Early diagnosis and intervention are crucial for delaying the onset and progression of the disease. We herein report a novel fluoro-substituted cyanine, F-SLOH, which exhibits good Aβ oligomer selectivity with a high binding affinity, attributed to the synergistic effect of strong π-π stacking and intermolecular CH···O and CH···F interactions.

A spiropyran-based fluorescent probe for the specific detection of β-amyloid peptide oligomers in Alzheimer's disease.

We report a new spiropyran-based fluorescent probe that exhibits high affinity and specificity towards Aβ oligomers both in vitro and in vivo. This probe can penetrate the blood brain barrier and specifically target Aβ oligomers in the brains of transgenic mice in models for Alzheimer's disease.

G-protein-coupled receptors regulate autophagy by ZBTB16-mediated ubiquitination and proteasomal degradation of Atg14L.

Autophagy is an important intracellular catabolic mechanism involved in the removal of misfolded proteins. Atg14L, the mammalian ortholog of Atg14 in yeast and a critical regulator of autophagy, mediates the production PtdIns3P to initiate the formation of autophagosomes. However, it is not clear how Atg14L is regulated.

The transcription factor c-Myc suppresses MiR-23b and MiR-27b transcription during fetal distress and increases the sensitivity of neurons to hypoxia-induced apoptosis.

Previous studies reported that the expression of miR-23b-27b cluster was downregulated in embryonic brain cortices during hypoxia-induced neuronal apoptosis. However, the mechanism underlying this downregulation is not completely understood. Here, we report that the transcription factor c-Myc plays an important role in regulating the expression of miR-23b-27b cluster during hypoxia.

Diarylethene based fluorescent switchable probes for the detection of amyloid-β pathology in Alzheimer's disease.

Two fluorescent switchable diarylethene derivatives which exhibit high affinity for amyloid-β aggregates with the increase of fluorescence intensity were reported. Moreover, the probes show excellent photochromic and anti-photobleaching properties both in vitro and in vivo.

Cocaine withdrawal reduces group I mGluR-mediated long-term potentiation via decreased GABAergic transmission in the amygdala.

Cocaine relapse can occur when cocaine-associated environmental cues induce craving. Conditioned place preference (CPP) is a behavioral paradigm modeling the association between cocaine exposure and environmental cues. The amygdala is involved in cocaine cue associations with the basolateral amygdala (BLA) and central amygdala (CeA) acting differentially in cue-induced relapse.

Deletion of tau attenuates heat shock-induced injury in cultured cortical neurons.

The microtubule-associated protein tau has been implicated in beta-amyloid- and glutamate-induced neurotoxicity. However, the potential role of tau in response to other insults to neurons remains unclear. In this study, we examined whether deletion of tau would change cell injury induced by heat shock in primary cultures of cortical neurons.

Thiamine deficiency increases β-secretase activity and accumulation of β-amyloid peptides.

Thiamine pyrophosphate (TPP) and the activities of thiamine-dependent enzymes are reduced in Alzheimer's disease (AD) patients. In this study, we analyzed the relationship between thiamine deficiency (TD) and amyloid precursor protein (APP) processing in both cellular and animal models of TD. In SH-SY5Y neuroblastoma cells overexpressing APP, TD promoted maturation of β-site APP cleaving enzyme 1 (BACE1) and increased β-secretase activity which resulted in elevated levels of β-amyloid (Aβ) as well as β-secretase cleaved C-terminal fragment (β-CTF).

Senescence accelerated mouse strain is sensitive to neurodegeneration induced by mild impairment of oxidative metabolism.

Neuronal loss and impairment of oxidative metabolism are frequently observed in aging associated neurodegenerative diseases. Thiamine deficiency (TD) induces the region selective neuronal loss in the brain, which has been used to model neurodegeneration, accompanied by mild impairment of oxidative metabolism. C57BL/6 mice were commonly used animals for TD experiments; however, the individual variations among C57BL/6 mice in response to TD limited the consistence of brain pathology.

Role of caspase-3 in tau truncation at D421 is restricted in transgenic mouse models for tauopathies.

Truncated tau is widely detected in Alzheimer's disease brain, and caspase-3 has been considered as a major executioner for tau truncation at aspartate421 (D421), according to its capability of cleaving recombinant tau in vitro. Here we investigated the relationship between D421 truncated tau and caspase-3 in two transgenic mouse models for tauopathies. In adult transgenic mice, activated caspase-3 could not be detected in neurons containing truncated tau, with the exception of a few glia-like cells or neurons in postnatal mice.

Truncated tau at D421 is associated with neurodegeneration and tangle formation in the brain of Alzheimer transgenic models.

In addition to tau hyperphosphorylation, tau truncation is also detected in Alzheimer's disease (AD) patients. In the brain of AD transgenic mouse models, the pathological details of truncated tau are not well characterized. In this study, we analyzed spatial relationships among tau truncation, tau phosphorylation and neurodegeneration or tangle formation in a tau(P301L) single transgenic mouse model and a triple transgenic mouse model that produces both amyloid plaques, and neurofibrillary tangles.

Improving the specificity of immunological detection in aged human brain tissue samples.

Immunological analyses of aged human brain tissues are widely used in characterizing the physiology or pathophysiology of brain aging or neurological diseases such as Alzheimer's disease. The primary antibodies used in immunological detection mainly originate from rabbit and mouse species. In the present study, we showed an unexpected cross-immunoreactivity between anti-rabbit immunoglobulin G and diffuse lipofuscin-associated protein(s) in aged human brain tissues.

Subclinical concentration of sevoflurane potentiates neuronal apoptosis in the developing C57BL/6 mouse brain.

The effect of general anesthetics on the developing brain is receiving growing attention. Nonetheless, there remains a paucity of evidence regarding the effect of sevoflurane, a widely used anesthetic in pediatric anesthesia. This study was designed to investigate the effect of sevoflurane on nerve cell apoptosis in the developing brain.

Pin1 has opposite effects on wild-type and P301L tau stability and tauopathy.

Tau pathology is a hallmark of many neurodegenerative diseases including Alzheimer disease (AD) and frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17). Genetic tau mutations can cause FTDP-17, and mice overexpressing tau mutants such as P301L tau are used as AD models. However, since no tau mutations are found in AD, it remains unclear how appropriate tau mutant mice are as an AD model.