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Background Drought stress limits significantly the crop productivity. However, plants have evolved various strategies to cope with the drought conditions by adopting complex molecular, biochemical, and physiological mechanisms. Members of the nuclear factor Y (NF-Y) transcription factor (TF) family constitute one of the largest TF classes and are involved in plant responses to abiotic stresses. Results TaNF-YB2 , a NY-YB subfamily gene in T. aestivum , was characterized in this study focusing on its role in mediating plant adaptation to drought stress. Yeast two-hybrid (Y-2 H), biomolecular fluoresence complementation (BiFC), and Co-immunoprecipitation (Co-IP) assays indicated that TaNF-YB2 interacts with the NF-YA member TaNF-YA7 and NF-YC family member TaNF-YC7, which constitutes a heterotrimer TaNF-YB2/TaNF-YA7/TaNF-YC7. The TaNF-YB2 transcripts are induced in roots and aerial tissues upon drought signaling; GUS histochemical staining analysis demonstrated the roles of cis -regulatory elements ABRE and MYB situated in TaNF-YB2 promoter to contribute to target gene response to drought. Transgene analysis on TaNF-YB2 confirmed its functions in regulating drought adaptation via modulating stomata movement, osmolyte biosynthesis, and reactive oxygen species (ROS) homeostasis. TaNF-YB2 possessed the abilities in transcriptionally activating TaP5CS2 , the P5CS family gene involving proline biosynthesis and TaSOD1 , TaCAT5 , and TaPOD5 , the genes encoding antioxidant enzymes. Positive correlations were found between yield and the TaNF-YB2 transcripts in a core panel constituting 45 wheat cultivars under drought condition, in which two types of major haplotypes including TaNF-YB2-Hap1 and -Hap2 were included, with the former conferring more TaNF-YB2 transcripts and stronger plant drought tolerance. Conclusions TaNF-YB2 is transcriptional response to drought stress. It is an essential regulator in mediating plant drought adaptation by modulating the physiological processes associated with stomatal movement, osmolyte biosynthesis, and reactive oxygen species (ROS) homeostasis, depending on its role in transcriptionally regulating stress response genes. Our research deepens the understanding of plant drought stress underlying NF-Y TF family and provides gene resource in efforts for molecular breeding the drought-tolerant cultivars in T. aestivum .

Aim： To investigate the potential of propofol in suppressing ventricular arrhythmias and to examine whether mitochondrial ATP-sensitive potassium channels are involved. Methods： Male Sprague-Dawley rats were pretreated with intravenous infusion of propofol （Prop）, a selective mitochondrial KATP channel inhibitor 5-hydroxydecanoate （5-HD）, propofol plus 5-HD （Prop＋5-HD）, a potent mitochondrial KATP channel opener diazoxide （DZ） or NS, respectively. The dosage of each drug was 10 mg/kg. The animals then underwent a 30 min-ligation of the left anterior descending artery. The severity of arrhythmias, the incidence of ventricular fibrillation （VF）, and the time of the first run of ventricular arrhythmias were documented using an arrhythmia scoring system. Mitochondrial membrane potential （h△ψm） was measured in freshly isolated rat cardiomyocytes with a fluorescence microscope. Results： The arrhythmia scores in the Prop and DZ group were 2.6（0-5） and 2.4（0-5）, respectively, which were significantly lower than that in the control group [4.9（2-8）]. VF was not observed in both Prop and DZ groups. The first run of ventricular arrhythmias was significantly postponed in the Prop group （10.5＋2.2 vs 7.3＋1.9 min）. Bracketing of propofol with 5-HD eliminated the anti-arrhythmic effect of propofol. In isolated rat cardiomyocytes, propofol （50 μmol/L） significantly decreased △ψm, but when propofol was co-admin- istered with 5-HD, the effect on △ψm was reversed. Conclusion： Propofol preconditioning suppresses ischemia-induced ventricular arrhythmias in the rat heart, which are proposed to be caused by opening of mitochondrial KATe channels.

The licensed adjuvanted recombinant glycoprotein E (gE) subunit vaccine (HZ/su) is highly effective against herpes zoster (HZ). This randomised, active-controlled, non-inferiority trial (ChiCTR2300079076) compared the immunogenicity and safety of a novel gE-Fc fusion protein vaccine candidate (LZ901) with HZ/su in 300 healthy adults aged ≥50 years without prior HZ vaccination in Wuxi, China. Participants received either two doses of LZ901 (30-day interval; n = 151) or HZ/su (60-day interval; n = 149). The primary outcomes was the proportion of participants with simultaneous positive responses to two or more cytokines (IFN-γ, IL-2, TNF-α, or CD40L) 30 days after the second dose (referred to as gE-specific CD4 2+ /CD8 2+ T-cell responses). LZ901 demonstrated non-inferiority to HZ/su (margin > −10%) for both CD4 + and CD8 + T-cell responses. Significantly higher response rates were observed with LZ901 for CD4 2  + T-cell responses (83.0% [117/141] vs 58.1% [79/136]; p < 0.0001) and CD8 2  + T-cell responses (46.8% [66/141] vs 8.8% [12/136]; p < 0.0001). Adverse reactions were markedly lower with LZ901 (41.1% [62/151] vs 87.9% [131/149]; p < 0.0001), including grade 3 events (0.7% [1/151] vs 6.0% [9/149]). LZ901 induced superior cellular immunogenicity and exhibited a better safety profile than HZ/su in adults ≥50 years, supporting its potential as a promising HZ prevention candidate vaccine. In this clinical trial, the authors demonstrate that recombinant gE-Fc Fusion Protein Vaccine LZ901 for herpes zoster induces superior cellular immunogenicity and exhibits a better safety profile than HZ/su in adults ≥50 years, supporting its potential as vaccine candidate.

Purpose This study aims to identify the neuropsychological tests commonly used for assessment in each neurocognitive domain, and quantify the post-operative changes in neurocognitive function in the immediate post-operation and follow-up. Methods With the use of the PubMed, a comprehensive search of the English literature was performed following PRISMA (Preferred Reporting Items for Systematic reviews and Meta-Analyses) guidelines. There were 1021 publications identified for screening. Standardized mean differences (SMD) in neuropsychological task performance were calculated both for immediate post-operation (up to 1 week) and follow-up (up to 6 months). Results Out of 12 studies which met the inclusion criteria, 11 studies were analyzed in this meta-analysis, with a total of 313 patients (age range 18–82, 50% males) with intracranial gliomas (45% high-grade, 55% low-grade). Complex attention, language and executive function were the most frequently tested neurocognitive domains. Surgery had a positive impact in the domains of complex attention, language, learning and memory tasks in the immediate post-operative period and sustained improvement at follow-up. In contrast, surgery was found to negatively impact performance for executive function in the immediate post-operative period with sustained decline in performance in the long term. Conclusions This meta-analysis suggests that surgery for glioma confers a benefit for the domains of complex attention, language, learning and memory, while negatively affecting executive function, in the periods immediately after surgery and at 6 months follow-up. In addition, awake surgery seemed to confer a beneficial effect on neurocognitive functions. Future research should attempt to standardize a battery of neuropsychological tests for patients undergoing surgical resection for glioma, perhaps with a particular focus on executive function.

This paper proposes a design methodology for the regulation mechanism of compression system of a variable cycle engine. Taking the simultaneous work mode of all valves in operation into account, the movement of mode selector vales might be reduced to that of a slider-crank linkage. By analyzing the two extreme working conditions of the slider-crank linkage, we obtain the excellent mechanism in geometry. Replacing all sliders with one integrated floating ring in structure, the mode selector valves can be driven by one source of hydraulic system. This fulfills the design of the regulation mechanism in movement. However, to meet the sealing requirement of a circular space, the regular octagon is used to approximate the circle of duct. Eight sectors of the truncated cone profile are attached with the sides of the moving octagon and the fixed octagon through eight curved plates (links) correspondingly. To satisfy the limited space of an engine, we designed a double parabolic strengthening structure to minimize the internal stress resulting from the offset of cylinder. Both theoretical analysis and finite element method simulation validate the strengthening structure in improving the working condition of the hydraulic cylinder. This design methodology from geometry to internal stress analysis might be generalized to the design of other mechanical systems.

Atherosclerotic plaque vulnerability and rupture increase the risk of acute coronary syndromes. Advanced lesion macrophage apoptosis plays important role in the rupture of atherosclerotic plaque, and endoplasmic reticulum stress (ERS) has been proved to be a key mechanism of macrophage apoptosis. Intermedin (IMD) is a regulator of ERS. Here, we investigated whether IMD enhances atherosclerotic plaque stability by inhibiting ERS-CHOP-mediated apoptosis and subsequent inflammasome in macrophages. We studied the effects of IMD on features of plaque vulnerability in hyperlipemia apolipoprotein E-deficient (ApoE −/− ) mice. Six-week IMD 1-53 infusion significantly reduced atherosclerotic lesion size. Of note, IMD 1-53 lowered lesion macrophage content and necrotic core size and increased fibrous cap thickness and vascular smooth muscle cells (VSMCs) content thus reducing overall plaque vulnerability. Immunohistochemical analysis indicated that IMD 1-53 administration prevented ERS activation in aortic lesions of ApoE −/− mice, which was further confirmed in oxidized low-density lipoproteins (ox-LDL) induced macrophages. Similar to IMD, taurine (Tau), a non-selective ERS inhibitor significantly reduced atherosclerotic lesion size and plaque vulnerability. Moreover, C/EBP-homologous protein (CHOP), a pro-apoptosis transcription factor involved in ERS, was significantly increased in advanced lesion macrophages, and deficiency of CHOP stabilized atherosclerotic plaques in AopE −/− mice. IMD 1-53 decreased CHOP level and apoptosis in vivo and in macrophages treated with ox-LDL. In addition, IMD 1-53 infusion ameliorated NLRP3 inflammasome and subsequent proinflammatory cytokines in vivo and in vitro. IMD may attenuate the progression of atherosclerotic lesions and plaque vulnerability by inhibiting ERS-CHOP-mediated macrophage apoptosis, and subsequent NLRP3 triggered inflammation. The inhibitory effect of IMD on ERS-induced macrophages apoptosis was probably mediated by blocking CHOP activation.

Vascular calcification (VC) is a common pathophysiological process of chronic kidney disease (CKD). Sirtuin 3 (Sirt3), a major NAD+-dependent protein deacetylase predominantly in mitochondria, is involved in the pathogenesis of VC. We previously reported that intermedin (IMD) could protect against VC. In this study, we investigated whether IMD attenuates VC by Sirt3-mediated inhibition of mitochondrial oxidative stress. A rat VC with CKD model was induced by the 5/6 nephrectomy plus vitamin D3. Vascular smooth muscle cell (VSMC) calcification was induced by CaCl2 and β-glycerophosphate. IMD1-53 treatment attenuated VC in vitro and in vivo, rescued the depressed mitochondrial membrane potential (MMP) level and decreased mitochondrial ROS levels in calcified VSMCs. IMD1-53 treatment recovered the reduced protein level of Sirt3 in calcified rat aortas and VSMCs. Inhibition of VSMC calcification by IMD1-53 disappeared when the cells were Sirt3 absent or pretreated with the Sirt3 inhibitor 3-TYP. Furthermore, 3-TYP pretreatment blocked IMD1-53-mediated restoration of the MMP level and inhibition of mitochondrial oxidative stress in calcified VSMCs. The attenuation of VSMC calcification by IMD1-53 through upregulation of Sirt3 might be achieved through activation of the IMD receptor and post-receptor signaling pathway AMPK, as indicated by pretreatment with an IMD receptor antagonist or AMPK inhibitor blocking the inhibition of VSMC calcification and upregulation of Sirt3 by IMD1-53. AMPK inhibitor treatment reversed the effects of IMD1-53 on restoring the MMP level and inhibiting mitochondrial oxidative stress in calcified VSMCs. In conclusion, IMD attenuates VC by improving mitochondrial function and inhibiting mitochondrial oxidative stress through upregulating Sirt3.

Background and aims: The senescent phenotype transition of vascular smooth muscle cells (VSMCs) is a crucial risk factor for the occurrence and development of vascular diseases. Intermedin (IMD) has various protective effects on cardiovascular diseases. In this study, we aimed to explore the role and the related mechanism of IMD in the senescent phenotype transition of VSMCs of aorta in mice. Methods: The senescent phenotype transition of VSMCs was induced by angiotensin II (Ang II) administered by mini-osmotic pumps in Adm2fl/fl and Adm2fl/flTagCre mice. Mouse VSMCs from aorta were used in in vitro experiments. Results: The aortic mRNA level of IMD, namely Adm2, was significantly decreased in Ang II-treated mice. Senescence-associated β-galactosidase activity and protein expressions of p16 and p21 were increased in the aortas of Adm2fl/flTagCre mice, which were further elevated in Ang II-treated Adm2fl/flTagCre mice. In addition, Adm2 deficiency in VSMCs further increased the protein expressions of DNA damage markers including 53BP1 and γH2AX in aortas of Adm2fl/flTagCre mice, and Ang II treatment increased their levels in aortas of Adm2fl/flTagCre mice or in VSMCs. However, Ang II-induced increases in senescence-associated proteins and DNA damage markers could be mitigated by the administration of IMD in vitro. Mechanistically, IMD increased intracellular NAD+ by activating nicotinamide phosphoribosyl transferase (NAMPT), followed by enhancing poly (ADP-ribose) polymerase-1 (PARP1) activity. Inhibitors of PARP1 or NAMPT effectively blocked the beneficial role of IMD in the DNA damage of VSMCs. Conclusions: IMD alleviates DNA damage partially by activating NAMPT/PARP1, thereby inhibiting the senescent phenotype transition of VSMCs of aorta, which might shed new light on the prevention of vascular aging.

Mild stroke is a known risk factor for dementia. The relationship between cerebral white matter (WM) integrity and cognitive impairment (CI) in mild stroke patients with basal ganglia region infarcts is unknown. Total of 33 stroke patients and 19 age-matched controls underwent diffusion tensor imaging scans and a formal neuropsychological test battery. CI was defined as having a performance score 1.5 SD below the established norm. We compared the differences in Z-scores and Fraction Anisotropy (FA) values among controls, stroke with no CI (NCI) and stroke with CI groups. Multiple linear regressions were performed between FA values in affected regions and neuropsychological tests in stroke patients. The majority of stroke patients were in their 50s (56.90 ± 9.23 years). CI patients exhibited a significantly decreased Z score in visual delayed memory and remarkably decreased FA values in the right external capsule and right fornix (FWE-corrected) compared with NCI patients and controls. In stroke patients, the FA value in the right fornix was positively correlated with delayed visual memory. Mild stroke with basal ganglia region infarcts may be related to widespread abnormality of WM integrity. The lower WM integrity in the right fornix may be a marker of impaired delayed visual memory.

The oil–oil and oil–source rock correlations, also termed as geochemical correlations, play an essential role in the construction of petroleum systems, guidance of petroleum exploration, and definition of reservoir compartments. In this study, the problems arising from oil–oil and oil– source rock correlations were investigated using chemometric methods on oil and source rock samples from the WZ12 oil field in the Weixinan sag in the Beibuwan Basin. Crude oil from the WZ12 oil field can be classified into two genetic families: group A and B, using multidimensional scaling and principal component analysis. Similarly, source rocks of the Liushagang Formation, including its first, second, and third members, can be classified into group I and II, corresponding to group B and A crude oils, respectively. The principle geochemical parameters in the geochemical correlation for the characterisation and classification of crude oils and source rocks were 4MSI, C27Dia/C27S, and C24 Tet/C26 TT. This study provides insights into the selection of appropriate geochemical parameters for oil–oil and oil–source rock correlations, which can also be applied to other sedimentary basins.