Associations between brain gene expression perturbations implicated by COVID-19 and psychiatric disorders.

BACKGROUND: Currently, there is increasing evidence from clinic, epidemiology, as well as neuroimaging, demonstrating neuropsychiatric abnormalities in COVID-19, however, whether there were associations between brain changes caused by COVID-19 and genetic susceptibility of psychiatric disorders was still unknown. METHODS: In this study, we performed a meta-analysis to investigate these associations by combing single-cell RNA sequencing datasets of brain tissues of COVID-19 and genome-wide association study summary statistics of psychiatric disorders. RESULTS: The analysis demonstrated that among ten psychiatric disorders, gene expression perturbations implicated by COVID-19 in excitatory neurons of choroid plexus were significantly associated with schizophrenia. CONCLUSIONS: Our analysis might provide insights for the underlying mechanism of the psychiatric consequence of COVID-19.

Preparation of Micro-Nano-Structured FePO4·2H2O for LiFePO4 Cathode Materials by the Turbulent Flow Cycle Method.

The micro-nano-structured FePO4·2H2O was prepared from mixed solution of FeSO4 oxidized in diluted H3PO4 with H2O2 and NaOH solution in the turbulent flow cycle state at 90 °C. The resulting products were characterized by thermogravimetric analysis (TGA), scanning electron microscopy (SEM), and transmission electron microscopy (TEM). Constant current charge/discharge tests were adopted to investigate the electrochemical performance and the rate capability (from 0.1C to 5C) of the carbon-coated LiFePO4 composite materials prepared from the micro-nano-structured FePO4. The carbon-coated LiFePO4 composite materials deliver a high specific discharge capacity of 153.7 mAh·g-1, exhibit excellent cycle performance with 98.6% of the capacity retained after 30 cycles. This study demonstrates that the turbulent flow cycle method may be an economical and effective method for industrial production of fine and uniform micro-nano-structured FePO4·2H2O particles for LiFePO4 cathode materials for Li-ion batteries.

Anti-inflammatory effect of IGF-1 is mediated by IGF-1R cross talk with GPER in MPTP/MPP+-induced astrocyte activation.

Insulin-like growth factor-1 (IGF-1) is a potent neuroprotective polypeptide that exerts neuroprotective effects via the IGF-1 receptor (IGF-1R). Our previous study reported that G protein-coupled estrogen receptor (GPER) was involved in the anti-apoptotic effect of IGF-1. The present study was designed to investigate the anti-inflammatory effect of IGF-1 in association with astrocyte activation and the molecular details of the interaction between IGF-1R and GPER. We showed that IGF-1 could improve 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced motor deficits and attenuate the upregulation of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) both in vivo and in vitro. The IGF-1R antagonist JB-1 and the GPER antagonist G15 could antagonize the anti-inflammatory effect of IGF-1. Silencing GPER abrogated the inhibitory effect of IGF-1 on 1-methyl-4-phenylpyridinium (MPP+)-induced upregulation of COX-2 and iNOS in primary astrocytes. Moreover, the MPP + -induced inflammatory response was related to the activation of mitogen-activated protein kinases (MAPKs) and NF-κB signaling pathways. The inhibitory effects of IGF-1 on the phosphorylation of p38, JNK and IκB could be blocked by JB-1. G15 antagonized the inhibitory effects of IGF-1 on p-JNK and p-IκB, but not p-p38. Furthermore, IGF-1 treatment alone increased the expression of GPER, which was blocked by JB-1, the phosphatidylinositol 3-kinase (PI3-K) antagonist LY294002 and the MEK antagonist PD98059 in primary astrocytes. Overall, we show for the first time that GPER may contribute to the anti-inflammatory effect of IGF-1 against MPTP/MPP + -induced astrocyte activation. IGF-1 could regulate the expression of GPER via the IGF-1R/PI3-K/MAPK signaling pathway in primary astrocytes.

IGF-1 inhibits MPTP/MPP+-induced autophagy on dopaminergic neurons through the IGF-1R/PI3K-Akt-mTOR pathway and GPER.

Autophagy dysfunctions are involved in the pathogenesis of Parkinson's disease (PD). In the present study, we aimed to evaluate the involvement of G protein-coupled estrogen receptor (GPER) in the inhibitory effect of insulin-like growth factor-1 (IGF-1) against excessive autophagy in PD animal and cellular models. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment significantly induced mouse movement disorder and decreased the protein level of tyrosine hydroxylase (TH) in the substantia nigra (SN) and dopamine (DA) content in striatum. Along with the dopamine neuron injury, we observed significant upregulations of microtubule-associated light chain-3 II (LC3-II) and α-synuclein as well as a downregulation of P62 in MPTP-treated mice. These changes could be restored by IGF-1 pretreatment. Cotreatment with IGF-1R antagonist JB-1 or GPER antagonist G15 could block the neuroprotective effects of IGF-1. 1-Methy-4-phenylpyridinium (MPP+) treatment could also excessively activate autophagy along with the reduction of cell viability in SH-SY5Y cells. IGF-1 could inhibit the neurotoxicity through promoting the phosphorylation of Akt and mammalian target of rapamycin (mTOR), which could also be antagonized by JB-1 or G15. These data suggest that IGF-1 inhibits MPTP/MPP+-induced autophagy on dopaminergic neurons through the IGF-1R/PI3K-Akt-mTOR pathway and GPER.

Ginsenoside Rg1 Exerts Anti-inflammatory Effects via G Protein-Coupled Estrogen Receptor in Lipopolysaccharide-Induced Microglia Activation.

Neuroinflammation plays a pivotal role in the pathogenesis of Parkinson's disease. Ginsenoside Rg1, the most active ingredient of ginseng, has been reported to exert neuroprotective effects via estrogen and glucocorticoid receptors. The present study evaluated the involvement of the G protein-coupled estrogen receptor (GPER) in the anti-inflammatory effects of ginsenoside Rg1 against lipopolysaccharide (LPS)-induced microglia activation in the BV2 microglial cell line and ventral mesencephalic primary microglial culture. The pharmacological blockade and lentivirus-mediated small interfering RNA (siRNA) knockdown of GPER were used to study the underlying mechanism. Rg1 attenuated LPS-induced upregulation of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) mRNA and protein levels. The GPER antagonist G15 blocked the inhibitory effects of Rg1 and the GPER-specific agonist G1 on LPS-induced microglia activation. Rg1 mimicked the effects of G1 by inhibiting the LPS-induced activation of nuclear transcription factor-kappa B (NF-κB) and mitogen activated protein kinase signaling pathways, which was also blocked by G15. Moreover, lentivirus-mediated siRNA knockdown of GPER inhibited the anti-inflammatory effects of Rg1. Taken together, our results indicate that GPER is involved in the anti-inflammatory effects of Rg1 against LPS-induced microglia activation. These findings provide a new biological target of Rg1 for the treatment of neuroinflammatory disorders.

G protein-coupled estrogen receptor is involved in the neuroprotective effect of IGF-1 against MPTP/MPP+-induced dopaminergic neuronal injury.

Insulin-like growth factor-1 (IGF-1), an endogenous peptide, exerts important role in brain development, neurogenesis and neuroprotection. There are accumulating evidence for the interaction of IGF-1 and 17ß-estradiol systems. IGF-1/IGF-1 receptor (IGF-1R) signaling has been reported to regulate G-protein estrogen receptor (GPER) expression in cancer cells. Whether GPER is involved in the neuroprotective effect of IGF-1 against MPTP/MPP+-induced dopaminergic neuronal injury remains unclear. We showed that IGF-1 could improve MPTP-induced motor deficits and ameliorate the decreased contents of DA and its metabolites in striatum as well as the loss of TH-IR neurons in the substantia nigra (SN). IGF-1 pretreatment also reversed the changes of Bcl-2 and Bax protein expressions in SN in MPTP mice. These effects were abolished by IGF-1 receptor (IGF-1R) antagonist JB-1 or GPER antagonist G15 except the inhibitory effect of G15 on Bax protein expression. Moreover, IGF-1 pretreatment enhanced cell survival against MPP+-induced neurotoxicity in SH-SY5Y cells. IGF-1 exerted anti-apoptotic effects by restoring MPP+-induced changes of Bcl-2 and Bax protein expressions as well as mitochondria membrane potential. Co-treatment with JB-1 or G15 could block these effects. Furthermore, IGF-1 regulated the protein expression of GPER through activation of phosphatidylinositol 3-kinase (PI3-K) and mitogen-activated protein kinase (MAPK) signaling pathways. Overall, we show for the first time that GPER may contribute to the neuroprotective effects of IGF-1 against MPTP/MPP+-induced dopaminergic neuronal injury.

(AEDPH3)·(BtaH): a novel supramolecular plaster with formaldehyde adsorption and formaldehyde/ultraviolet ray-induced luminescence switching performance.

A novel supramolecular plaster, (AEDPH(3))·(BtaH) (1), is synthesised and characterized. The supramolecular plaster is easy to synthesise and process, and displays good mechanical properties. It can adsorb and eliminate formaldehyde (HCHO) with high efficiency and exhibits very interesting HCHO/ultraviolet ray-induced luminescence switching.

[Synthesis and spectral properties of tailed sercine tetraphenylporphyrin cobalt complex].

A new tailed sercine tetraphenylporphinatozinc, 5-(p-butoxyphenyl-10,15,20-trichlorophenyl)porphine and cobalt complex (Co[Ser-TPP]) was synthesized and characterized by elementary analysis, UV, IR, 1HNMR and Raman spectra. The electronic absorption spectra of axial coordination reactions of Co[Ser-TPP] with pyridine, 4-methylpyridine, 4-aminopyridine, 4,4-bipyridine, imidazole, 1-methylimidazole and 2-methylimidazole were inverstigated. The results showed that the changes of electronic absorption spectra of Co[Ser-TPP] could be attributed to the axial coordination reactions of Co[Ser-TPP] with pyridine and imidazole series.

[Rheological phase synthesis and characterization of lanthanum salicylate and luminescence properties of Tb3+ -doped lanthanum salicylate].

Lanthanum salicylate and Tb3+ -doped lanthanum salicylate were synthesized with the rheological phase reaction method. Elemental analysis, IR, TG, DTA and powder X-ray diffraction were investigated to determine the composition, crystal structure and coordination manner between the COO- and ion La3+ of lanthanum salicylate. The emission and excitation spectra of Tb3+ -doped lanthanum salicylate were also discussed. Powder X-ray diffraction suggests that the compound has a layered monoclinic structure, and the lattice parameters are a = 21.6010 A, b = 13.8015 A , c = 3.8103 A, beta = 97.11 degrees, V = 1127.2 A3, Z = 2, rhocal = 1.621 g x cm(-3) and rhoexp = 1.653 g x cm(-3). The Tb3+ -doped lanthanum salicylate exhibits very strong green luminescence of Tb3+ under the excitation of UV light. And the transition from 5D4 to 7F5 is the strongest one.