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Inspired by Xiao’s work on Hankel measures for Hardy and Bergman spaces [‘Pseudo-Carleson measures for weighted Bergman spaces’. Michigan Math. J.47 (2000), 447–452], we introduce Hankel measures for Fock space $F^p_\alpha $ . Given $p\ge 1$ , we obtain several equivalent descriptions for such measures on $F^p_\alpha $ .

In this paper, the initial value problem is discussed for the local fractional Caudrey-Dodd-Gibbon-Kaeada equation. The fractional complex transform and the new iterative method are used to solve the problem, and the approximate analytical solutions are obtained.

In this paper, given $$f \in BMO$$, for all possible $$0< p< q

Given f in the Fock space Fα∞ , for all possible 1≤p,q

The genetic predisposition to chronic kidney disease (CKD) has been widely evaluated especially using the genome-wide association studies, which highlighted some novel genetic susceptibility variants in many genes, and estimated glomerular filtration rate to diagnose and stage CKD. Of these variants, rs7805747 in PRKAG2 was identified to be significantly associated with both serum creatinine and CKD with genome wide significance level. Until now, the potential mechanism by which rs7805747 affects CKD risk is still unclear. Here, we performed a functional analysis of rs7805747 variant using multiple bioinformatics software and databases. Using RegulomeDB and HaploReg (version 4.1), rs7805747 was predicated to locate in enhancer histone marks (Liver, Duodenum Mucosa, Fetal Intestine Large, Fetal Intestine Small, and Right Ventricle tissues). Using GWAS analysis in PhenoScanner, we showed that rs7805747 is not only associated with CKD, but also is significantly associated with other diseases or phenotypes. Using metabolite analysis in PhenoScanner, rs7805747 is identified to be significantly associated with not only the serum creatinine, but also with other 16 metabolites. Using eQTL analysis in PhenoScanner, rs7805747 is identified to be significantly associated with gene expression in multiple human tissues and multiple genes including PRKAG2. The gene expression analysis of PRKAG2 using 53 tissues from GTEx RNA-Seq of 8555 samples (570 donors) in GTEx showed that PRKAG2 had the highest median expression in Heart-Atrial Appendage. Using the gene expression profiles in human CKD, we further identified different expression of PRKAG2 gene in CKD cases compared with control samples. In summary, our findings provide new insight into the underlying susceptibility of PRKAG2 gene to CKD.

Diabetic nephropathy (DN) is the leading cause of end-stage renal disease, partly because of the lack of effective treatments for DN. Curcumin has been shown to exert strong antifibrotic effects in DN, but the underlying mechanisms are not well characterized. In this study, we sought to determine the effects of curcumin on diabetic renal disease in db/db mice and characterize the underlying mechanism of action. We administered curcumin to db/db mice for 16 weeks. In comparison to mock-treated db/db mice, curcumin-treated mice showed diminished renal hypertrophy, reduced mesangial matrix expansion, and a lower level of albuminuria. Furthermore, the upregulated protein and mRNA expressions of collagen IV and fibronectin in the renal cortices of the db/db mice were inhibited by curcumin treatment. Additionally, curcumin treatment was associated with significant reductions in mature interleukin-1β, cleaved caspase-1, and NLRP3 protein levels in the renal cortices of db/db mice as well as in HK-2 cells exposed to high glucose concentration. In summary, curcumin, a potent antifibrotic agent, is a promising treatment for DN, and its renoprotective effects appear to be mediated by the inhibition of NLRP3 inflammasome activity.

For 3-d laser scanning point clouds of an expressway tunnel, a method of automatically extracting complete contours of cross-sections from them is proposed. By taking advantage of abundant normal vectors embedded in point clouds, this method can accurately compute the central axis of the tunnel and build a reference cylinder surface coaxial with the tunnel. To rebuild the surface model for tunnels, a cylindrical projection is used to map all point clouds into a 2-d space firstly, and an improved 2-d Delaunay algorithm which can deal with the border-less circumferential angles is subsequently employed to construct the triangulated mesh from projection points in this two-dimensional space. Following the one-to-one mapping from the original point cloud to the projection point set, a corresponding 3-d triangulated mesh of the original point cloud is finally constructed in accordance with the 2-d triangulation result. By intersecting 3-d triangular mesh of tunnel with cross sections perpendicular to the tangential direction of axis, a series of contours are generated at the specified locations. For the curved tunnel, this method can adjust the direction of sections finely to make them always suitable for the constant change of tunnel direction. At the end of this paper, the experimental result demonstrate the effectiveness and high efficiency of this method by the use of the point clouds acquired from a real highway tunnel.

Postoperative cognitive dysfunction (POCD), commonly observed in elderly patients, is characterized by impaired concentration, memory and learning following surgery, and may persist for a long duration or progress into serious central nervous system diseases. It has been demonstrated neuroinflammation caused by surgery is involved in the development of POCD. However, the detailed molecular mechanism remains to be fully elucidated. The present study aimed to reveal the role of tumor necrosis factor (TNF)-α in the development of POCD in aged rats. Laparotomy was performed to mimic human abdominal surgery in the aged rats. Following surgery, the memory and learning functions were impaired, with significant upregulation of pro-inflammatory cytokines, including TNF-α, interleukin (IL)-1β, IL-4 and IL-6 in the hippocampal tissues. However, intracisternal administration of the TNF-α receptor antagonist, R-7050, during surgery attenuated these defects in cognitive function and inhibited the production of the pro-inflammatory cytokines in the hippocampal tissues. Furthermore, intracisternal administration of R-7050 inhibited the activation of the downstream nuclear factor-κB and mitogen-activated protein kinase signaling pathway in the hippocampal tissues. Therefore, the results of the present study suggested a key role of the TNF-α-mediated signaling pathway in the development of POCD.

We determined the physiological importance of endogenous estrogen in the regulation of angiotensinogen synthesis in the liver. The plasma levels of angiotensinogen and hepatic levels of angiotensinogen mRNA were studied in the rat in comparison to those of T-kininogen, a plasma protein whose synthesis in the liver is primarily estrogen-dependent. Plasma levels of T-kininogen and hepatic levels of T-kininogen mRNA were 3- and 2-fold higher in adult females, respectively, than in adult males, whereas there were no sex differences in levels of either plasma angiotensinogen or hepatic angiotensinogen mRNA. Ovariectomy in female rats abolished the sex differences in the levels of plasma T-kininogen and hepatic T-kininogen mRNA, but it did not affect those of plasma angiotensinogen and hepatic angiotensinogen mRNA. These results suggest that, in contrast to T-kininogen, angiotensinogen synthesis in the liver is unlikely to be controlled by endogenous levels of estrogen.

To determine the source of angiotensinogen excreted in urine, urine angiotensinogen was measured in male and female rats during growth. Angiotensinogen in 24-hr urine, measured by direct radioimmunoassay with antibody against rat angiotensinogen, increased fourfold in males between the ages of 5 and 7 weeks, whereas no significant changes were observed in females or castrated males. Plasma levels of angiotensinogen, in contrast, showed no significant differences between these groups at any age. Castration of adult males caused a significant reduction of urinary angiotensinogen after 4 weeks. Consecutive s.c. administration of 17α-methyltestosterone for 3 weeks in castrated males resulted in a threefold increase in the urinary excretion of angiotensinogen, as well as a twofold increase in the renal expression of angiotensinogen messenger RNA (mRNA). Renal levels of angiotensinogen mRNA in intact adult males were about threefold higher than those in females and castrated males, whereas there were no significant differences in hepatic angiotensinogen mRNA between these animals. These results suggest that the sexual differences in the urinary excretion of angiotensinogen are primarily due to the androgen-dependent dimorphic expression of angiotensinogen mRNA in the kidney; thus, levels of angiotensinogen in urine might reflect intrarenal production.