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Germination can improve the level of the free amino acid, and further improve the nutritious value of the foxtail millet. However, the effect of germination temperature and time on them is still unclear. The free amino acid of the germinated foxtail millet has been analyzed at different germination temperatures (20, 25, 30, 35, and 40 ℃) and time (0, 6, 12, 18, 24, and 30 h). Results reveal that 21 components of free amino acids increased. The lower temperature or higher temperature is not suitable for the accumulation of the free amino acid. The free amino acids increase to the maximum at the germination temperature of 30 ℃ for 30 h. The total free amino acids and total essential free amino acids can reach (810.7±69.0) and (367.8± 30.2) mg/100g, respectively. Among the amino acids, the contents of alanine and threonine increase to the highest level. The alanine has increased to (120.0±12.0) and (115.0±14.0) mg/100g at the temperature of 30 and 35 ℃, respectively. The threonine has increased to (106.0±1.0) mg/100g at the temperature of 35 ℃. The γ-aminobutyric acid reaches the maximum level at the germination temperature of 35 ℃ and reaches (60.1±1.8) mg/100g. In conclusion, the germination can promote the increase of the free amino acid and adjust the nutrition of the foxtail millet, and the germinated foxtail millet is a potential source for functional food.

Neurological diseases in the central nervous system are mostly characterized by the failure of endogenous repair to restore tissue damage and salvage lost function. Currently, studies have shown that neural stem cell transplantation provides a good therapeutic effect on neurological diseases. For this reason, neural stem cell transplantation has been explored as a cell replacement therapy. Although transplanted cells can replace cells lost during or post central nervous system injury, many studies have shown that this mechanism is insufficient as most of these newly formed cells fail to integrate and eventually die. Although it was initially thought that neural stem cell could only replace lost cells, recent experiments have shown that transplanted neural stem cell can also play bystander roles such as neuroprotection and immune regulation, promote tissue repair by preventing tissue damage, interfere with pathogenic processes, or by rescuing endogenous nerve cells. However, compelling evidence has raised concerns about this bystander effect, which can be caused by several biologically active molecules (collectively known as the secretome) produced by neural stem cells. These results also raise the possibility of the neural stem cell secretome as a potential candidate for neural stem cell transplantation therapies based on the bystander effect. A better understanding of the molecules and mechanisms of this effect is of critical importance for neural stem cell-based therapies. This review aims to discuss the function and application of neural stem cell secretome in the treatment of neurodegenerative disorders.

Objective To observe the effects and mechanisms of Apelin-13 on expression of pyroptosis related proteins in aorta of diabetic mice. Methods C57/BL mice of eight weeks old were used as control group;kkAy mice of eight weeks old were used as type 2 diabetic models;osmotic pumps were used to treat kkAy mice with apelin-13 at a rate of 30 μg/(kg·d),and L-NAME(eNOS inhibitor) was injected intraperitoneally at a dose of 10 mg/(kg·d) to kkAy mice. Blood was collected for detection of Hb1Ac. The aortae were harvested and fixed. Morphological changes were observed with HE staining. Expression of eNOS,NLRP3,caspase-1 and gasdermin D were measured with immunohistochemical staining. Results Compared to the control group, the level of eNOS in the aorta of diabetic mice was significantly higher than that in control mice (P＜0.05),the levels of NLRP3,caspase-1 and gasdermin D were also higher than that in control mice. After apelin-13 treatment,the expressions of eNOS,NLRP3,caspase-1 and gasdermin D were further increased (P＜0.05). After L-NAME and apelin-13 treatment, the expressions of eNOS, NLRP3,caspase-1 and gasdermin D were reduced as compared to apelin-13 treatment alone(P＜0.05). Conclusions Apelin-13 may promote the expression of pyroptosis related protein in aortic cells by increasing eNOS/NO pathway,which would induce structural and functional damage in diabetic arteries.

Based on two-band isotropic Ginzburg-Landau theory, we study the temperature dependence of upper critical field and London penetration depth for non-centrosymmetric superconductor LaNi[C.sub.2]. All the theoretical calculations fit the experimental data very well, especially the upward curvature of upper critical field near the critical temperature. Our results thus indicate that the two-gap scenario is better to account for the superconductivity of LaNi[C.sub.2], and the Cooper pairs of this superconductor are in the conventional s-wave state. Key words: non-centrosymmetric superconductor, Ginzburg-Landau theory, upper critical field, London penetration depth. Sur la base de la theorie isotrope a deux bandes de Ginzberg-Landau, nous etudions la dependance en temperature du champ critique superieur et de la profondeur de la penetration de Landau pour le supraconducteur non centro-symetrique LaNi[C.sub.2]. Tous les calculs theoriques sont en tres bon accord avec les valeurs experimentales, specialement la courbure superieure du champ critique superieur pres de la temperature critique. Nos resultats indiquent ainsi que le scenario a deux bandes est le meilleur pour decrire la supraconductivite de LaNi[C.sub.2] et que la paire de Cooper est dans l'etat conventionnel de l'onde s. [Traduit par la Redaction] Mots-cles: supraconducteur non centro-symetrique, theorie de Ginzberg-Landau, champ critique superieur, profondeur de la penetration de London, scenario a deux bandes., 1. Introduction In the past 10 years, non-centrosymmetric superconductors have gained huge interest since the discovery of superconductivity in heavy-fermion material Ce[Pt.sub.3]Si [1]. For the superconductors with unbroken inversion symmetry, [...]

As an internal driving force to promote economic growth, residents’ consumption also has an important impact on energy consumption. Based on the difference of consumption structure between urban and rural residents, this paper introduces the income gap variable of urban and rural residents, analyzes the impact of urban and rural residents’ consumption on energy consumption, and provides reference for the implementation of energy conservation and emission reduction policies. On this basis, the author believes that the government should take flexible measures to control energy consumption according to the differences between urban and rural areas, make accurate efforts, and steadily promote the implementation of energy conservation and emission reduction.

Based on two-band isotropic Ginzburg-Landau theory, we study the temperature dependence of upper critical field and London penetration depth for non-centrosymmetric superconductor LaNiC2. All the theoretical calculations fit the experimental data very well, especially the upward curvature of upper critical field near the critical temperature. Our results thus indicate that the two-gap scenario is better to account for the superconductivity of LaNiC2, and the Cooper pairs of this superconductor are in the conventional s-wave state. [ABSTRACT FROM AUTHOR]

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Autophagy plays a pivotal role in diverse biological processes, including the maintenance and differentiation of neural stem cells (NSCs). Interestingly, while complete deletion of Fip200 severely impairs NSC maintenance and differentiation, inhibiting canonical autophagy via deletion of core genes, such as Atg5 , Atg16l1 , and Atg7 , or blockade of canonical interactions between FIP200 and ATG13 (designated as FIP200-4A mutant or FIP200 KI) does not produce comparable detrimental effects. This highlights the likely critical involvement of the non-canonical functions of FIP200, the mechanisms of which have remained elusive. Here, utilizing genetic mouse models, we demonstrated that FIP200 mediates non-canonical autophagic degradation of p62/sequestome1, primarily via TAX1BP1 in NSCs. Conditional deletion of Tax1bp1 in fip200 hGFAP conditional knock-in (cKI) mice led to NSC deficiency, resembling the fip200 hGFAP conditional knockout (cKO) mouse phenotype. Notably, reintroducing wild-type TAX1BP1 not only restored the maintenance of NSCs derived from tax1bp1 -knockout fip200 hGFAP cKI mice but also led to a marked reduction in p62 aggregate accumulation. Conversely, a TAX1BP1 mutant incapable of binding to FIP200 or NBR1/p62 failed to achieve this restoration. Furthermore, conditional deletion of Tax1bp1 in fip200 hGFAP cKO mice exacerbated NSC deficiency and p62 aggregate accumulation compared to fip200 hGFAP cKO mice. Collectively, these findings illustrate the essential role of the FIP200-TAX1BP1 axis in mediating the non-canonical autophagic degradation of p62 aggregates towards NSC maintenance and function, presenting novel therapeutic targets for neurodegenerative diseases.

This study aimed to explore whether the combined application of desflurane and dexmedetomidine (Dex) reduces the occurrence of postoperative neurocognitive disorders (PND) in patients. We selected patients in our hospital who underwent surgery under general anesthesia, and divided them into two groups: Dex and desflurane (Dex + Des) and desflurane (Des) groups. The data of patients were collected and the Mini-Mental State Examination (MMSE) score was used to assess cognitive status. The blood cell counts were determined preoperatively and on postoperative days 1, 3, and 6, and the percentage of neutrophils and lymphocytes were also recorded. The statistical methods used were the independent-samples t -test and the χ 2 test. Pearson's correlation was used to analyze the correlation between PND and inflammation. The incidence of PND in the Dex + Des group was lower than that in the Des group. The postoperative MMSE scores in the Dex + Des group were higher than those in the Des group ( p  = 0.032). The percentage of neutrophils in the Dex + Des group was significantly lower than that in the Des group on the first and third days after surgery ( p  = 0.007; p  = 0.028). The MMSE scores on the first day after surgery were negatively correlated with the multiple changes in white blood counts and the percentage of neutrophils ( r  = -0.3038 and -0.3330). Dex combined with Des reduced the incidence of PND and reduced the postoperative inflammatory cell counts., Competing Interests: The authors declare no conflict of interest., (© 2022 The Authors. Ibrain published by Affiliated Hospital of Zunyi Medical University and Wiley‐VCH GmbH.)

Osteoporosis, diabetes, and hypertension are common concurrent chronic disorders. This study aimed to explore the respective effects of angiotensin II (ANG II) and angiotensin(1-7) [ANG(1-7)], active peptides in the renin-angiotensin system, on osteoblasts and osteoclasts under high-glucose level, as well as to investigate the osteo-preservative effects of ANG II type 1 receptor (AT1R) blocker and ANG(1-7) in diabetic spontaneously hypertensive rats (SHR). ANG II and ANG(1-7), respectively, decreased and increased the formation of calcified nodules and alkaline phosphatase activity in MC3T3-E1 cells under high-glucose level, and respectively stimulated and inhibited the number of matured osteoclasts and pit resorptive area in RANKL-induced bone marrow macrophages. Olmesartan and Mas receptor antagonist A779 could abolish those effects. ANG II and ANG(1-7), respectively, downregulated and upregulated the expressions of osteogenesis factors in MC3T3-E1 cells. ANG II promoted the expressions of cathepsin K and MMP9 in RAW 264.7 cells, whereas ANG(1-7) repressed these osteoclastogenesis factors. ANG II rapidly increased the phosphorylation of Akt and p38 in RAW 264.7 cells, whereas ANG(1-7) markedly reduced the phosphorylation of p38 and ERK under high-glucose condition. After treatments of diabetic SHR with valsartan and ANG(1-7), a significant increase in trabecular bone area, bone mineral density, and mechanical strength was only found in the ANG(1-7)-treated group. Treatment with ANG(1-7) significantly suppressed the increase in renin expression and ANG II content in the bone of SHR. Taken together, ANG II/AT1R and ANG(1-7)/Mas distinctly regulated the differentiation and functions of osteoblasts and osteoclasts upon exposure to high-glucose condition. ANG(1-7) could protect SHR from diabetes-induced osteoporosis.

With the technological advances in cancer diagnosis and treatment, the survival rates for patients with cancer are prolonged. The issue of figuring out how to improve the life quality of patients with cancer has become increasingly prominent. Pain, especially bone pain, is the most common symptom in malignancy patients, which seriously affects the life quality of patients with cancer. The research of cancer pain has a breakthrough due to the development of the animal models of cancer pain in recent years, such as the animal models of mouse femur, humerus, calcaneus, and rat tibia. The establishment of several kinds of animal models related to cancer pain provides a new platform in vivo to investigate the molecular mechanisms of cancer pain. In this review, we focus on the advances of cancer pain from bone metastasis, the mechanisms involved in cancer pain, and the drug treatment of cancer pain in the animal models.