A brain-to-spinal sensorimotor loop for repetitive self-grooming.

Self-grooming is a complex behavior with important biological functions and pathological relevance. How the brain coordinates with the spinal cord to generate the repetitive movements of self-grooming remains largely unknown. Here, we report that in the caudal part of the spinal trigeminal nucleus (Sp5C), neurons that express Cerebellin-2 (Cbln2) form a neural circuit to the cervical spinal cord to maintain repetitive orofacial self-grooming.

SETD5 modulates homeostasis of hematopoietic stem cells by mediating RNA Polymerase II pausing in cooperation with HCF-1.

SETD5 mutations were identified as the genetic causes of neurodevelopmental disorders. While the whole-body knockout of Setd5 in mice leads to embryonic lethality, the role of SETD5 in adult stem cell remains unexplored. Here, a critical role of Setd5 in hematopoietic stem cells (HSCs) is identified.

Corrigendum: MiR-29a Knockout Aggravates Neurological Damage by Pre-polarizing M1 Microglia in Experimental Rat Models of Acute Stroke.

[This corrects the article DOI: 10.3389/fgene.2021.

Inclusion of cGAMP within virus-like particle vaccines enhances their immunogenicity.

Cyclic GMP-AMP (cGAMP) is an immunostimulatory molecule produced by cGAS that activates STING. cGAMP is an adjuvant when administered alongside antigens. cGAMP is also incorporated into enveloped virus particles during budding.

Dl-3-n-Butylphthalide Alleviates Behavioral and Cognitive Symptoms Via Modulating Mitochondrial Dynamics in the A53T-α-Synuclein Mouse Model of Parkinson's Disease.

Background: Aggregation and neurotoxicity of the presynaptic protein α-synuclein and the progressive loss of nigral dopaminergic neurons are believed to be the key hallmarks of Parkinson's disease (PD). A53T mutant α-synuclein causes early onset PD and more severe manifestations. A growing body of evidence shows that misfolding or deposition of α-synuclein is linked to the maintenance of mitochondrial dynamics, which has been proven to play an important role in the pathogenesis of PD.

EphA4 is highly expressed in the atria of heart and its deletion leads to atrial hypertrophy and electrocardiographic abnormalities in rats.

Aims: EphA4 is a member of the Eph receptor family, and expressed mainly in central nervous system (CNS), which is involved in CNS development and multiple diseases. Due to the variability in EphA4 expression, we wondered if EphA4 is expressed in other tissues, and what role does EphA4 play?

Materials And Methods: We generated an EphA4 knockout (KO) rat line with red fluorescent marker protein encoded by the mCherry cassette inserted downstream of the EphA4 promoter as a reporter. Using this system, we observed high expression of EphA4 in the heart atria and in the brain.

SARS-CoV-2 infection aggravates chronic comorbidities of cardiovascular diseases and diabetes in mice.

Background: Cardiovascular diseases (CVDs) and diabetes mellitus (DM) are top two chronic comorbidities that increase the severity and mortality of COVID-19. However, how SARS-CoV-2 alters the progression of chronic diseases remain unclear.

Methods: We used adenovirus to deliver h-ACE2 to lung to enable SARS-CoV-2 infection in mice.

Multifunctional Transferrin Encapsulated GdF Nanoparticles for Sentinel Lymph Node and Tumor Imaging.

The transferrin encapsulated GdF nanoparticles have been fabricated via biomineralization method. The obtained GdF@Tf NPs show an attractive T2MRI and CT enhancement effect. Furthermore, PET and NIR imaging capacity are integrated into nanoparticles through conjugating with radionuclide Cu and fluorescent dye Cy7.

Clinical application of combined detection of SARS-CoV-2-specific antibody and nucleic acid.

Background: The global outbreak of human severe acute respiratory syndrome coronavirus (SARS-CoV)-2 infection represents an urgent need for readily available, accurate and rapid diagnostic tests. Nucleic acid testing of respiratory tract specimens for SARS-CoV-2 is the current gold standard for diagnosis of coronavirus disease 2019 (COVID-19). However, the diagnostic accuracy of reverse transcription polymerase chain reaction (RT-PCR) tests for detecting SARS-CoV-2 nucleic acid may be lower than optimal.

Knock in of a hexanucleotide repeat expansion in the gene induces ALS in rats.

Background: The GGGGCC (G4C2) repeat expansion in the human open reading frame 72 on chromosome 9, , is the most common cause of amyotrophic lateral sclerosis (ALS). Studies in transgenic mouse models have linked the pathogenic mechanism of G4C2 repeat expansion to RNA foci or the accumulation of unnatural dipeptide repeats in neurons. However, only one of the existing transgenic mouse lines developed typical ALS.

Ablation of C9orf72 together with excitotoxicity induces ALS in rats.

Pathogenesis of familial amyotrophic lateral sclerosis (ALS) linked to expansion of the chromosome 9 open reading frame 72 (C9orf72) hexanucleotide repeat that impairs C9orf72 expression. Loss of function of the C9orf72 protein is one of the three main proposed C9orf72-related ALS mechanisms. However, C9orf72 loss of function, by itself, is insufficient to cause severe phenotypes in mice.

Density-induced social stress alters oxytocin and vasopressin activities in the brain of a small rodent species.

It is known that social stress could alter oxytocin (OT) and arginine-vasopressin (AVP) expression in specific regions of brains which regulate the aggressive behavior of small rodents, but the effects of density-induced social stress are still unknown. Brandt's voles (Lasiopodomys brandtii) are small herbivores in the grassland of China, but the underlying neurological mechanism of population regulation is still unknown. We tested the effects of housing density of Brandt's voles on OT/AVP system with physical contact (allowing aggression) and without physical contact (not allowing aggression) under laboratory conditions.

Galectin-7 overexpression destroys airway epithelial barrier in transgenic mice.

When the integrity of airway epithelium is destroyed, the ordered airway barrier no longer exists and increases sensitivity to viral infections and allergens, leading to the occurrence of airway inflammation such as asthma. Here, we found that galectin-7 transgenic(+) mice exhibited abnormal airway structures as embryos and after birth. These abnormalities included absent or substantially reduced pseudostratified columnar ciliated epithelium and increased monolayer cells with irregular arrangement and widening of intercellular spaces.

Overexpression of human-derived induced intergenerational inheritance of DNA methylation and gene expression variations in rat brain and testis.

In mammals, DNA methylation patterns are established by various types of DNA methyltransferases and can be stably passed on during cell division, thus creating a paradigm for epigenetic regulation that can mediate long-lasting changes in gene expression even when the initial triggering signal has disappeared. Although functional deficiency of , one of the methyltransferases, leads to abnormal DNA methylation patterns that result in developmental deficits in mammals, the impacts of its overexpression on tissue gene expression and DNA methylation patterns remain unclear. Here, our previously established transgenic rat model and mRNA sequencing and bisulphite sequencing PCR were used to analyse the impact of overexpression on tissue transcriptome and methylome, and whether the impact could be inherited intergenerationally was subsequently investigated.

Regulation of social behaviors by p-Stat3 via oxytocin and its receptor in the nucleus accumbens of male Brandt's voles (Lasiopodomys brandtii).

Social behavior plays a significant role in the formation of social structure and population regulation in both animals and humans. Oxytocin (OXT) and its receptor (OXTR) are well known for regulating social behaviors, but their upstream regulating factors are rarely investigated. We hypothesized that the phosphorylation of the signal transducer and activator of transcription 3 (p-Stat3) may regulate social and aggressive behaviors via the OXT system in the nucleus accumbens (NAc).

PINK1 Deficiency Ameliorates Cisplatin-Induced Acute Kidney Injury in Rats.

Mitophagy plays a key role in cleaning damaged and depolarized mitochondria to maintain cellular homeostasis and viability. Although it was originally found in neurodegenerative diseases, mitophagy is reported to play an important role in acute kidney injury. PINK1 and Parkin are key molecules in mitophagy pathway.

Interferon-inducible cytoplasmic lncLrrc55-AS promotes antiviral innate responses by strengthening IRF3 phosphorylation.

Type I interferon (IFN-I) production is efficiently induced to ensure a potent innate immune response to viral infection. How this response can be enhanced, however, remains to be explored. Here, we identify a new cytoplasmic long non-coding RNA (lncRNA), lncLrrc55-AS, that drives a positive feedback loop to promote interferon regulatory factor 3 (IRF3) signaling and IFN-I production.

IMM-H004 therapy for permanent focal ischemic cerebral injury via CKLF1/CCR4-mediated NLRP3 inflammasome activation.

Chemokine-like factor 1 (CKLF1) is a potential target for ischemic stroke therapy. The NOD-like receptor protein 3 (NLRP3) inflammasome has been postulated to mediate inflammatory responses during ischemic/reperfusion (I/R) injury. The compound IMM-H004 is a novel coumarin derivative that can improve cerebral I/R injury.

The first genetically gene-edited babies: It's "irresponsible and too early".

A scientist, Jiankui He of Southern University of Science and Technology of China, recently claimed at the Second International Summit on Human Genome Editing in Hong Kong on 29 November that he has created the world's first genetically altered babies using CRISPR. This announcement sparked controversy and criticism. The newly developed CRISPR/Cas9 technique has been applied to genetic modification of many kinds of animals.

CKLF1 Aggravates Focal Cerebral Ischemia Injury at Early Stage Partly by Modulating Microglia/Macrophage Toward M1 Polarization Through CCR4.

CKLF1 is a chemokine with increased expression in ischemic brain, and targeting CKLF1 has shown therapeutic effects in cerebral ischemia model. Microglia/macrophage polarization is a mechanism involved in poststroke injury expansion. Considering the quick and obvious response of CKLF1 and expeditious evolution of stroke lesions, we focused on the effects of CKLF1 on microglial/macrophage polarization at early stage of ischemic stroke (IS).

Improving Drug Delivery of Micellar Paclitaxel against Non-Small Cell Lung Cancer by Coloading Itraconazole as a Micelle Stabilizer and a Tumor Vascular Manipulator.

Although polymeric micelles of paclitaxel (PTX) significantly reduce excipient-induced toxicity compared with Taxol, they exhibit few clinical advantages in tumor inhibition and overall survival. To improve, itraconazole (ITA), an antifungal drug with potent anti-angiogenesis activity, is co-encapsulated together with PTX within the PEG-PLA micelles. The strong intermolecular interactions between the payloads inhibit drug crystallization and prevent drugs from binding with external proteins, render super-stable micelles upon dilution and exposure to biological environment, and enter the tumor cells through endocytosis.

Correction to: White paper: statement on conflicts of interest.

The original version of this article unfortunately contained a mistake.

White paper: statement on conflicts of interest.

Introduction: Conflicts of interest are a normal part of human social intercourse. They become problematic when there is a power differential between participants in the setting of relationships requiring a high degree of trust, as in healthcare. In this white paper we consider how these conflicts may be detected and mitigated.