Whole-genome sequencing of Paracoccus species isolated from the healthy human eye and description of Paracoccus shanxieyensis sp. nov.

Currently, the genus Paracoccus comprises 76 recognized species. Members of Paracoccus are mostly isolated from environmental, animal, and plant sources. This report describes and proposes a novel species of Paracoccus isolated from clinical specimens of the human ocular surface. We isolated two aerobic, Gram-stain-negative, non-spore-forming, coccoid or short rod-shaped, and non-motile strains (designated DK398T and DK608) from conjunctival sac swabs of two healthy volunteers. The results showed that the strains grew best under the conditions of 28°C, pH 7.0, and 1.0 % (w/v) NaCl. Sequence analysis based on the 16S rRNA gene showed that strains DK398T and DK608 were members of Paracoccus, most similar to Paracoccus laeviglucosivorans 43PT (98.54 and 98.62 %), Paracoccus litorisediminis GHD-05T (98.34 and 98.41 %), and Paracoccus limmosus NB88T (98.21 and 98.29 %). Phenotypic analysis showed that DK398T and DK608 were positive for catalase and oxidase, negative for producing N-acetyl-ß-glucosaminic acid, arginine dihydrolase, and ß-glucuronidase but positive for leucine arylamidase. The predominant isoprenoid quinone was Q-10, and the major polar lipids included phosphatidylethanolamine, diphosphatidylglycerol, phosphatidylglycerol, phosphatidylcholine, and an unidentified glycolipid. The major fatty acids (>10%) were summed feature 8 (C18 : 1 ω7c and/or C18 : 1 ω6c) and C16 : 0. The meso-diaminopimelic acid was found in the cell wall peptidoglycan of DK398T. The major cell wall sugars were ribose and galactose. Based on the results of phylogenetic analyses, low (<83.22 %) average nucleotide identity, digital DNA-DNA hybridization (<26.0%), chemotaxonomic analysis, and physiological properties, strain DK398T represents a novel species of the genus Paracoccus, for which the name Paracoccus shanxieyensis sp. nov. is proposed. The type strain is DK398T (=CGMCC 1.17227T=JCM 33719T).

S-adenosylmethionine reduces the inhibitory effect of Aß on BDNF expression through decreasing methylation level of BDNF exon â £ in rats.

The structure of brain-derived neurotrophic factor (BDNF) gene is complex, which is composed of eight non-coding exons and one coding exon, each of them has its own unique promoter. Multiple BDNF transcripts have distinct functional properties and epigenetic modulation of BDNF gene transcription is implicated in the neurological disorders. In the present study, rat models with amyloid-ß (Aß) intrahippocampal injection and PC12 cells were used to explore the role of DNA methylation in the promoters of BDNF exon Ⅳ and exon Ⅵ in BDNF suppression caused by Aß. We found that Aß inhibited BDNF expression accompanying with hypermethylation in BDNF exon Ⅳ promoter, meanwhile, S-adenosylmethionine (SAM), primary methyl donor, reversed the low BDNF expression through demethylation in BDNF exon Ⅳ promoter. No methylation change was observed in BDNF exon Ⅵ promoter. The alteration of DNA methylation caused by Aß or SAM was mediated by DNA methyltransferase 3A (DNMT3A). These data suggest that methylation change in BDNF exon Ⅳ is involved in the regulation of BDNF expression by Aß or SAM, and further support the view of specific epigenetic modifications of a certain BDNF gene transcript.

Overview of the Complex Figure Test and Its Clinical Application in Neuropsychiatric Disorders, Including Copying and Recall.

The Rey-Osterrieth Complex Figure (ROCF) test is a commonly used neuropsychological assessment tool. It is widely used to assess the visuo-constructional ability and visual memory of neuropsychiatric disorders, including copying and recall tests. By drawing the complex figure, the functional decline of a patient in multiple cognitive dimensions can be assessed, including attention and concentration, fine-motor coordination, visuospatial perception, non-verbal memory, planning and organization, and spatial orientation. This review first describes the different versions and scoring methods of ROCF. It then reviews the application of ROCF in the assessment of visuo-constructional ability in patients with dementia, other brain diseases, and psychiatric disorders. Finally, based on the scoring method of the digital system, future research hopes to develop a new digital ROCF scoring method combined with machine learning algorithms to standardize clinical practice and explore the characteristic neuropsychological structure information of different disorders.

S-Adenosylmethionine Attenuates Oxidative Stress and Neuroinflammation Induced by Amyloid-ß Through Modulation of Glutathione Metabolism.

Oxidative stress and neuroinflammation are mainly involved in the pathogenic mechanisms of Alzheimer's disease (AD). Amyloid-ß (Aß), the main component of senile plaques, is a kind of strong inducer of oxidative stress. Glutathione is an endogenous antioxidant protecting cells from oxidative injury. S-adenosylmethionine (SAM) produced in the methionine cycle is the primary methyl donor and the precursor of glutathione. In this study, the Aß intrahippocampal injection rat model and cultured SH-SY5Y cells were used to explore the neuroprotective effect of SAM. We found that SAM could protect cells against Aß-induced cellular injury by inhibition of oxidative stress and neuroinflammation. SAM administration could increase the endogenous antioxidant glutathione and potentiate the antioxidant enzymes activities. SAM might act as an antioxidant and be a potential candidate therapy for AD patients.

MicroRNA-181c Ameliorates Cognitive Impairment Induced by Chronic Cerebral Hypoperfusion in Rats.

Chronic cerebral hypoperfusion (CCH) characterized by global cerebral ischemia is an important risk factor contributing to the development of dementia. MicroRNAs (miRNAs) play important roles in the cellular adaptation to long-term ischemia/hypoxia by turning off or on the expression of target genes. MiR-181c is widely expressed in the nervous system, and tripartite motif 2 (TRIM2) is one of its target genes. In this work, we had identified that progressive spatial memory deficiency was induced in the bilateral common carotid artery occlusion (2-VO) rat models. Meanwhile, inhibition of miR-181c expression and upregulation of TRIM2 in the hippocampus of 2-VO rats were found accompanying with reduction in the dendritic branching and dendrite spine density of the hippocampal neurons. Viral vector-mediated miR-181c delivery might improve the cognitive deficiency via TRIM2 on neurofilament light (NF-L) ubiquitination resulting in remodeling of the hippocampal neurons as well as increase in N-methyl-D-aspartate receptor 1 (NR1) subunit cell surface expression. Meanwhile, miR-181c might rescue the cellular activity from ischemia/hypoxia. These results indicated a novel miRNA-mediated mechanism involving miR-181c and TRIM2 in the cognitive impairment induced by CCH and provided a rationale for the development of miRNA-based strategies for prevention of dementia.