Research on Dynamic Measurement Method of Flow Rate in Tea Processing.

Tea flow rate is a key indicator in tea production and processing. Due to the small real-time flow of tea leaves on the production line, the noise caused by the transmission system is greater than or close to the real signal of tea leaves. This issue may affect the dynamic measurement accuracy of tea flow. Therefore, a variational mode decomposition combined with a wavelet threshold (VMD-WT) denoising method is proposed to improve the accuracy of tea flow measurement. The denoising method of the tea flow signal based on VMD-WT is established, and the results are compared with WT, VMD, empirical mode decomposition (EMD), and empirical mode decomposition combined with wavelet threshold (EMD-WT). In addition, the dynamic measurement of different tea flow in tea processing is carried out. The result shows that the main noise of tea flow measurement comes from mechanical vibration. The VMD-WT method can effectively remove the noise in the tea dynamic weighing signal, and the denoising performance is better than WT, VMD, EMD, and EMD-WT methods. The average cumulative measurement accuracy of the tea flow signal based on the VMD-WT algorithm is 0.88%, which is 55% higher than that before denoising. This study provides an effective method for dynamic and accurate measurement of tea flow and offers technical support for digital control of the tea processing.

Effect of sitagliptin on tubulointerstitial Wnt/ß-catenin signalling in diabetic nephropathy.

AIM: To investigate the effect of sitagliptin on Wnt/ß-catenin signalling in the tubulointerstitium of diabetic nephropathy. METHODS: Forty male Wistar rats were divided into normal control (NC), diabetic model (DM), low and high-dose sitagliptin intervention groups (ST1 and ST2, respectively). Changes in the biochemical parameters and tubulointerstitial fibrosis index were observed. The levels of protein and gene expression of different indicators were detected via immunohistochemistry and real-time polymerase chain reaction. NRK-52E cells were divided into the normal control group, mannitol control group, high glucose group (HG), high glucose plus sitagliptin intervention group (HG + ST) and high glucose plus Wnt/ß-catenin inhibitor group (HG + XAV939). The relevant indicators were examined by Western blot or enzyme-linked immunosorbent assay. RESULTS: Compared with the NC group, the blood glucose, glycosylated haemoglobin, 24 h urinary albumin, creatinine clearance and tubulointerstitial fibrosis index were significantly increased in the DM group. These parameters were decreased in the ST1 and ST2 groups compared to the DM group. Compared with the NC group, the levels of Wnt4, ß-catenin, dipeptidyl peptidase-4 and α-smooth muscle actin were higher and E-cadherin was lower in the DM group. Sitagliptin treatment reversed these changes. In the high glucose-stimulated NRK-52E cells, sitagliptin and XAV939 inhibited the elevated expression of Wnt4, ß-catenin, dipeptidyl peptidase-4, α-smooth muscle actin, transforming growth factor-ß and fibronectin and restored E-cadherin activity. CONCLUSION: Sitagliptin may inhibit the tubulointerstitial Wnt/ß-catenin signalling pathway in diabetic nephropathy and provide renal protection by alleviatinge renal tubulointerstitial transdifferentiation and fibrosis.

Influence of Dipeptidyl Peptidase-IV Inhibitor Sitagliptin on Extracellular Signal-Regulated Kinases 1/2 Signaling in Rats with Diabetic Nephropathy.

The protective effects of sitagliptin on the kidneys of rats with diabetic nephropathy (DN) and its influence on extracellular signal-regulated kinases 1/2 (ERK1/2) signaling were investigated. Male Wistar rats (n = 40) were randomly assigned to normal control, DN, low-dose sitagliptin intervention (ST1), or high-dose sitagliptin intervention (ST2) groups. Animals were euthanized after a 16-week treatment, and blood glucose (BG), glycosylated hemoglobin (HbA1c), urinary albumin excretion rate (AER), serum creatinine (Scr), creatinine clearance rate (Ccr), active glucagon-like peptide-1 (GLP-1) levels, kidney hypertrophy index, and renal pathohistology were determined. Immunohistochemical methods and real-time polymerase chain reaction (PCR) were used to detect protein and mRNA expression of podocalyxin, ERK1/2, GLP-1 receptor (GLP-1R) and transforming growth factor-ß (TGF-ß). After 16 weeks, BG, AER, Scr, HbA1c and the kidney hypertrophy index were all significantly decreased (p < 0.05) in ST1 and ST2 groups, while Ccr and active GLP-1 levels were increased (p < 0.05), with changes more pronounced in ST2 (p < 0.05). Glomerular pathological lesions were also improved following sitagliptin treatment, especially in ST2. Immunohistochemical and real-time PCR revealed that protein and mRNA expression levels of podocalyxin and GLP-1R were increased significantly in ST1 and ST2, while expression of ERK1/2 and TGF-ß was decreased (p < 0.05). Sitagliptin therefore delayed DN progression, possibly via the inhibition of ERK1/2 signaling and promotion of the interaction between GLP-1 and the GLP-1R.

Midkine promotes kidney injury in diabetic kidney disease by increasing neutrophil extracellular traps formation.

Background: We sought to investigate the role of midkine (MK) on neutrophil extracellular trap formation (NETosis) and diabetic kidney disease (DKD) progression. Methods: The expression of MK and NETosis in the renal tissue of DKD patients was examined by immunohistochemistry and immunofluorescence, respectively. Neutrophils extracted from mouse bone marrow by gradient centrifugation were treated with MK for this in-vitro study. A mouse diabetes model was induced by a high-fat diet combined with an intraperitoneal injection of streptozocin (STZ). Antisense oligodeoxynucleotide (ODN) for MK inhibition was administered via tail vein injection. Results: We found that the expression of MK was increased in the kidney tissue of DKD patients. Additionally, a greater number of neutrophils were primed toward NETosis in the kidney tissue of DKD patients, which was manifested by the increased expression of NETosis biomarkers citrullinated histone H3 (H3Cit) and myeloperoxidase (MPO). In vitro, MK treatment concentration-dependently increased neutrophil proliferation (cell counting kit-8). Further, western blot and enzyme-linked immunosorbent assays showed that MK (100 ng/mL) significantly promoted NETosis and the expression of inflammatory factors interleukin (IL)-1 and IL-6 secretion in high-glucose treated neutrophils. In the mouse diabetes model, MK promoted the pathological damage and fibrosis of kidney tissue, as demonstrated by the reversion of the pathological damage and fibrosis by the MK antisense ODN [diabetes mellitus (DM) + MK - ODN] treatment. Additionally, the inhibition of MK reduced the formation of NETs. Conclusions: MK promotes DKD progression by increasing NETosis.

Enhancement of Room-Temperature Photoluminescence and Valley Polarization of Monolayer and Bilayer WS2 via Chiral Plasmonic Coupling.

Transition-metal dichalcogenides with intrinsic spin-valley degree of freedom have enabled great potentials for valleytronic and optoelectronic applications. However, the degree of valley polarization is usually low under nonresonant excitation at room temperature due to the phonon-assisted intervalley scattering. Here, achiral and chiral Au arrays are designed to enhance the optical response and valley polarization in monolayer and bilayer WS2. A considerable band edge emission with 7 times increment is realized under the resonant coupling with Au dimer-prism arrays. Valley polarization enhancement is quantitatively predicted by the inherent mechanisms from elevated electromagnetic field intensity and radiation efficiency and further realized in polarized photoluminescence. A tunable valley polarization up to 30.0% is achieved in bilayer WS2 under a nonresonant excitation at room temperature. All of these results provide a promising route toward the development of room-temperature valley-dependent optoelectronic devices.

Deeply Exploring Anisotropic Evolution toward Large-Scale Growth of Monolayer ReS2.

Among large numbers of transition metal dichalcogenides (TMDCs), monolayer rhenium disulfide (ReS2) is of particular interest due to its unique structural anisotropy, which opens up unprecedented opportunities in dichroic atomical electronics. Understanding the domain structure and controlling the anisotropic evolution of ReS2 during the growth is considered critical for increasing the domain size toward a large-scale growth of monolayer ReS2. Herein, by employing angle-resolved Raman spectroscopy, we reveal that the hexagonal ReS2 domain is constructed by six well-defined subdomains with each b-axis parallel to the diagonal of the hexagon. By further combining the first-principles calculations and the transmission electron microscopy (TEM) characterization, a dislocation-involved anisotropic evolution is proposed to explain the formation of the domain structures and understand the limitation of the domain size. Based on these findings, growth rates of different crystal planes are well controlled to enlarge the domain size, and moreover, single-crystal domains with a triangle shape are obtained. With the improved domain size, large-scale uniform, strictly monolayer ReS2 films are grown further. Scalable field-effect transistor (FET) arrays are constructed, which show good electrical performances comparable or even superior to that of the single domains reported at room temperature. This work not only sheds light on comprehending the novel growth mechanism of ReS2 but also offers a robust and controllable strategy for the synthesis of large-area and high-quality two-dimensional materials with low structural symmetry.

Effect of activin A on tubulointerstitial fibrosis in diabetic nephropathy.

AIM: The effect of activin A on tubulointerstitial fibrosis in diabetic nephropathy (DN) using streptozotocin (STZ)-induced diabetic rats and high glucose-cultured HK-2 cells was investigated. METHODS: Male Wistar rats were randomized into a normal control group (NC) and diabetes mellitus group (DM). Diabetes was induced by i.p. injection of STZ. Six rats were respectively killed 4, 8, 12 and 16 weeks after model establishment in each group. The changes of kidney weight/bodyweight (KW/BW), urine albumin excretion rate (AER) and creatinine clearance rate (Ccr) were determined. The morphology of tubulointerstitium was observed by light microscopy. Further biochemical analysis was provided using immunohistochemistry and real-time polymerase chain reaction. The different parameters in high glucose-cultured HK-2 cells were monitored by western blotting or enzyme-linked immunosorbent assay (ELISA) and the intervention of rh-follistatin on them was investigated. RESULTS: Compared with the NC group, there was marked enlargement in the levels of KW/BW, AER, Ccr and interstitial fibrosis index, and the production of P-Smad2/3 and fibronectin in the DM group from 8 to 16 weeks. Activin betaA, mainly located in tubular epithelial cells, was significantly higher in the DM group than that in the NC group throughout the study periods. Follistatin was abundant in the NC group, but was diminished gradually in the DM group. High glucose may facilitate the synthesis of activin betaA, transforming growth factor (TGF)-beta, P-Smad2/3 and fibronectin in HK-2 cells while rh-follistatin inhibited them except TGF-beta. CONCLUSION: Activin A is involved in tubulointerstitial fibrosis in DN by inducing the production of fibronectin through Smad signal pathway.

Irbesartan ameliorates diabetic nephropathy by reducing the expression of connective tissue growth factor and alpha-smooth-muscle actin in the tubulointerstitium of diabetic rats.

The effect of irbesartan on the expression of connective tissue growth factor (CTGF) and alpha-smooth-muscle actin (alpha-SMA) in the renal tubulointerstitium of diabetic rats was investigated in our study. Diabetes was induced in male Wistar rats by intraperitoneal administration of streptozotocin (STZ), 60 mg.kg(-1) body weight. The rats were then randomized to a diabetic group (DM) and an irbesartan therapy group (DM + Irb). The normal group (non-DM) rats were administered only citrate buffer. At the end of the 16th week, blood glucose, kidney weight/body weight, urine albumin (UAlb) and creatinine clearance rate were determined. The renal histopathology was observed by light microscopy. Further biochemical analysis of CTGF and alpha-SMA was provided using real-time reverse transcription PCR, immunostaining and Western blotting techniques. Compared with the non-DM group, blood glucose, kidney weight/body weight, UAlb, creatinine clearance and interstitial fibrotic lesions were increased in the DM group (p < 0.01). Treatment with irbesartan improved these parameters except blood glucose. Compared with the non-DM group, expressions of CTGF and alpha-SMA in the renal tubulointerstitium were highly upregulated in the DM group (p < 0.01). Administration of irbesartan prevented the high expressions of CTGF and alpha-SMA in renal tissue of diabetic rats. These results indicated that irbesartan can protect the kidney of STZ-diabetic rats by reducing the expression of CTGF and alpha-SMA in the renal tubulointerstitium.