Genomic characterization and pathogenicity of a novel fowl adenovirus serotype 11 isolated from chickens with inclusion body hepatitis in China.

Fowl adenovirus serotype 11 (FAdV-11) is one of the primary causative agents of inclusion body hepatitis (IBH), which causes substantial economic losses in the world poultry industry. In this study, we characterized the genome of the fowl adenovirus serotype 11 (FAdV-11) isolate FJSW/2021. The full genome of FJSW/2021 was 44, 154 base pairs (bp) in length and had a similar organization to that of previously reported FAdV-11 isolates. Notably, compared with those of other reported FAdV-11 strains, the preterminal protein (pTP) of FAdV-11 FJSW/2021 has six amino acid (aa) insertions (S-L-R-I-I-C) between 470 and 475 and one aa mutation of L476F; moreover, the tandem repeat (TR) regions of TR1 and TR2 were 33 bp (1 repeat) and 1,080 bp (8 repeats) shorter than those of the Canadian nonpathogenic isolate ON NP2, respectively. The pathogenicity of FJSW/2021 was studied in 10-day-old specific pathogen-free chicken embryos following allantoic cavity inoculation and in 1-day-old, 1-wk-old and 2-wk-old SPF chickens following intramuscular inoculation with 107 TCID50 of the virus. The results showed that FJSW/2021 can induce typical severe IBH in chicks less than 2 wk old. These findings highlighted the genetic differences between the pathogenic and non-pathogenic FAdV-11 isolates. The data will provide guidance for identifying the virulence factors of FAdV-11 strains. The animal challenge model developed in our study will allow precise evaluation of the efficacy of potential FAdV-11 vaccine candidates.

Cerebellum and hippocampus abnormalities in patients with insomnia comorbid depression: a study on cerebral blood perfusion and functional connectivity.

Chronic insomnia disorder and major depressive disorder are highly-occurred mental diseases with extensive social harm. The comorbidity of these two diseases is commonly seen in clinical practice, but the mechanism remains unclear. To observe the characteristics of cerebral blood perfusion and functional connectivity in patients, so as to explore the potential pathogenesis and biological imaging markers, thereby improving the understanding of their comorbidity mechanism. 44 patients with chronic insomnia disorder comorbid major depressive disorder and 43 healthy controls were recruited in this study. The severity of insomnia and depression were assessed by questionnaire. The cerebral blood perfusion and functional connectivity values of participants were obtained to, analyze their correlation with questionnaire scores. The cerebral blood flow in cerebellum, vermis, right hippocampus, left parahippocampal gyrus of patients were reduced, which was negatively related to the severity of insomnia or depression. The connectivities of left cerebellum-right putamen and right hippocampus-left inferior frontal gyrus were increased, showing positive correlations with the severity of insomnia and depression. Decreased connectivities of left cerebellum-left fusiform gyrus, left cerebellum-left occipital lobe, right hippocampus-right paracentral lobule, right hippocampus-right precentral gyrus were partially associated with insomnia or depression. The connectivity of right hippocampus-left inferior frontal gyrus may mediate between insomnia and depression. Insomnia and depression can cause changes in cerebral blood flow and brain function. Changes in the cerebellar and hippocampal regions are the result of insomnia and depression. They reflect abnormalities in sleep and emotion regulation. That may be involved in the pathogenesis of comorbidity.

Aberrant structural and functional alterations in postpartum depression: a combined voxel-based morphometry and resting-state functional connectivity study.

Objectives: Postpartum depression (PPD) is a severe postpartum psychiatric disorder with unclear pathogenesis. Previous neuroimaging studies have reported structural or functional alterations in areas associated with emotion regulation, cognitive disorder, and parenting behaviors of PPD. The primary goal of this investigation was to explore the presence of brain structural alterations and relevant functional changes in PPD patients. Methods: A total of 28 patients and 30 matched healthy postnatal women (HPW) underwent both three-dimensional T1-weighted magnetic resonance imaging (MRI) and resting-state functional MRI. Structural analysis was performed by voxel-based morphometry (VBM), followed by resting-state functional analysis using a seed-based whole-brain functional connectivity (FC) approach with abnormal gray matter volume (GMV) regions as seed. Results: Compared with HPW, the PPD patients showed increased GMV in the left dorsolateral prefrontal cortex (DLPFC.L), the right precentral gyrus (PrCG.R), and the orbitofrontal cortex (OFC). In the PPD group, the DLPFC.L showed increased FC with the right anterior cingulate and paracingulate gyri (ACG.R) and the right middle frontal gyrus (MFG.R); the FC between the PrCG.R and the right median cingulate and paracingulate gyri (DCG.R) exhibited enhanced; the OFC showed increased FC with MFG.R and the left inferior occipital gyrus (IOG.L). In PPD, GMV of DLPFC.L was positively correlated with EDPS scores (r = 0.409 p = 0.031), and FC of PrCG.R-DCG.R was positively correlated with EDPS scores (r = 0.483 p = 0.020). Conclusion: Structural and functional damage of the DLPFC.L and OFC is associated with cognitive disorders and parenting behaviors in PPD, while structural abnormalities of the DLPFC.L and PrCG.R are involved in impaired executive function. The increased GMV of DLPFC.L may be a unique structural pathological mechanism of PPD related to the inability of PPD patients to withstand long-term parenting stress. These findings have important implications for understanding neural mechanisms in PPD.