The telomere-to-telomere gap-free reference genome of wild blueberry (Vaccinium duclouxii) provides its high soluble sugar and anthocyanin accumulation.

Vaccinium duclouxii, endemic to southwestern China, is a berry-producing shrub or small tree belonging to the Ericaceae family, with high nutritive, medicinal, and ornamental value, abundant germplasm resources, and good edible properties. In addition, V. duclouxii exhibits strong tolerance to adverse environmental conditions, making it a promising candidate for research and offering wide-ranging possibilities for utilization. However, the lack of V. duclouxii genome sequence has hampered its development and utilization. Here, a high-quality telomere-to-telomere genome sequence of V. duclouxii was de novo assembled and annotated. All of 12 chromosomes were assembled into gap-free single contigs, providing the highest integrity and quality assembly reported so far for blueberry. The V. duclouxii genome is 573.67 Mb, which encodes 41 953 protein-coding genes. Combining transcriptomics and metabolomics analyses, we have uncovered the molecular mechanisms involved in sugar and acid accumulation and anthocyanin biosynthesis in V. duclouxii. This provides essential molecular information for further research on the quality of V. duclouxii. Moreover, the high-quality telomere-to-telomere assembly of the V. duclouxii genome will provide insights into the genomic evolution of Vaccinium and support advancements in blueberry genetics and molecular breeding.

Neurotropin alleviates cognitive impairment by inhibiting TLR4/MyD88/NF-κB inflammation signaling pathway in mice with vascular dementia.

Vascular dementia (VD) is the second most common cause of dementia after Alzheimer's disease. Neuroinflammation contributes to pathogenesis of VD. Neurotropin (NTP) is an analgesic that has been shown to suppress inflammation and neural repair. But its effects on VD are still unclear. Therefore, this study aimed to investigate the therapeutic effects and potential mechanisms of NTP in the VD model mice established by bilateral common carotid artery stenosis method. In VD mice, we found that NTP treatment increased cerebral blood flow by Laser speckle imaging, reduced neuron loss by Nissl, HE and immunochemistry staining, attenuated white matter damage by magnetic resonance imaging and ultrastructural damage by transmission electron microscope, improved cognitive functions by new object recognition test and three-chamber test, Y maze test and Morris water maze test, inhibited significantly glial activation by immunofluorescence methods, reduced the expression of TLR4, down-regulated expression of MyD88 and phosphorylation of NF-κB P65, decreased the levels of pro-inflammatory cytokines IL-1ß, IL-6 and TNFα. Further, we showed that administration of a TLR4 inhibitor TAK242 had a similar effect to NTP, while the TLR4 agonist CRX-527 attenuated the effect of NTP in the VD mice. Collectively, our study suggested that NTP alleviates cognitive impairment by inhibiting TLR4/MyD88/NF-κB inflammation signaling pathway in the VD mice. Thus, NTP may be a promising therapeutic approach and a potential TLR4 inhibitor for VD.

High-Frequency Repetitive Magnetic Stimulation at the Sacrum Alleviates Chronic Constipation in Parkinson's Patients.

Objective: This study was to investigate the therapeutic effect of high-frequency repetitive magnetic stimulation (HF-rMS) at the sacrum for chronic constipation in Parkinson's patients (PD). Materials and Methods: Eventually 48 PD patients were enrolled from July 2019 to October 2020, and randomly divided into the HF-rMS group (the intervention group, n = 24) and the sham HF-rMS group (the control group, n = 24). The intervention group received HF-rMS at the sacrum, whereas the control group received ineffective magnetic stimulation. We performed clinical evaluation before and after HF-rMS treatment, including constipation score scale (KESS questionnaire), Unified Parkinson's Disease Rating Scale (UPDRS-III exercise examination), Hoehn-Yahr (H-Y) stage of motor function; simple mental status scale (MMSE), anxiety/depression table (HAD-A/HAD-D), the activity of daily living (ADL), and quality of life scale for patients with constipation (PAC-QOL) to evaluate symptoms and satisfaction of PD patients with chronic constipation. Results: There was no significant difference in the clinical characteristics between the two groups. As compared to the control group, the HF-rMS group displayed a larger change (pre and posttreatment) in the KESS scores of PD patients with chronic constipation, suggesting a significant improvement. Moreover, HF-rMS significantly promoted the mood, activity of daily living, and quality of life of PD patients when comparing the alteration of HAD-A/HAD-D scores, ADL scores, and PAC-QOL scores between the two groups. Finally, there was no significant difference in the change of the UPDRS III score and the MMSE score between the two groups. Conclusion: HF-rMS at the sacrum can improve chronic constipation in PD patients.

Inflammatory mechanisms of Ginkgo Biloba extract in improving memory functions through lncRNA-COX2/NF-κB pathway in mice with status epilepticus.

PURPOSE: This study was to explore whether Ginkgo biloba extract (GBE) improve memory impairment by alleviating neuroinflammation signaling in mice with status epilepticus. METHODS: The status epilepticus (SE) mice model was established by pilocarpine and treated with 100 mg / kg of GBE for 14 days. Spontaneous alternation of Y-maze and new object recognition were used to explore memory impairment. To examine glial cell activation, we performed immunohistochemistry and immunofluorescence staining. The activation of NF-κB signaling and the expression level of lncRNA-COX2 were detected by Western blot and qRT-PCR, respectively. Adeno-associated virus lncRNA-COX2 was injected into mice for overexpression of lncRNA-COX2. RESULTS: After GBE treatment, the spontaneous alternation rate and the recognition coefficient in SE mice were both increased. Moreover, activation of glial cells, NF-κB signaling and lncRNA-COX2 were significantly decreased in SE mice. In the GBE-treated SE mice with lncRNA-COX2 overexpression, NF-κB signaling was up-regulated again; the reduced level of inflammation factors was reversed; the GBE-rescued spontaneous alternation rate of Y-maze was eliminated. CONCLUSION: Our results suggested that GBE reduces the hippocampal inflammation by down-regulating lncRNA-COX2 / NF-κB signaling in the SE mice, leading to the decrease of neuronal damage and the improvement of memory functions.