Pairwise Tomlinson-Harashima precoding for multiple-lane IM-DD transmissions.

As for the photonic interconnection based on the multiple-lane intensity modulation direct detection (IM-DD) transmission, both intra-channel inter-symbol-interference (ISI) originating from bandwidth constraint, and inter-channel performance discrepancy emerging from inter-channel component differences are the major bottleneck for the throughput enhancement. Here, we propose a pairwise Tomlinson-Harshima precoding (P-THP) scheme, in order to simultaneously deal with both intra-channel ISI and inter-channel performance discrepancy. The effective function of the proposed P-THP scheme is experimentally evaluated by transmitting 4-channel 81-GBaud PAM4 signals over 2 km standard single-mode fiber (SSMF). Compared with the conventional scheme with only applying THP on individual wavelength channel, the required optical received power (ROP) under the back-to-back (B2B) transmission can be reduced by 0.75∼1 dB with the help of proposed P-THP in different experimental component configurations, at the 7% hard decision forward error correction (HD-FEC) threshold of BER = 3.8 × 10-3. After the 2 km SSMF transmission, only the use of proposed P-THP can guarantee to reach the designated HD-FEC threshold, leading to a net rate of >600 Gbit/s.

On the multipath interference mitigation for high-speed IM-DD transmissions with Nyquist subcarrier modulation.

The performance of high-speed intensity modulation direct detection (IM-DD) transmissions is severely degraded due to the occurrence of multipath interference (MPI), especially when a higher-order modulation format is utilized. Here, we propose and demonstrate, for the first time to the best of our knowledge, that a Nyquist subcarrier modulation (Nyquist-SCM) format inherently exhibits resistance to the MPI. We experimentally evaluate the MPI tolerance by transmitting 56 Gbit/s PAM-4 signals and Nyquist-SCM 16QAM signals over the 2 km standard single-mode fiber (SSMF) when the C-band semiconductor laser with a linewidth of 1.7 MHz is utilized. In comparison with the PAM-4 format, the Nyquist-SCM 16QAM format can lead to an enhanced MPI tolerance of 4 dB at the KP4-FEC threshold of BER = 2 × 10-4. In addition, even with the help of MPI mitigation for the PAM-4 signals based on two newly reported methods, the utilization of Nyquist-SCM 16QAM signal can still guarantee an improved MPI tolerance of 1 dB.

Minimally invasive transurethral holmium laser surgery for the management of an IUD with bladder migration.

CASE: Intrauterine device (IUD) is used worldwide as an effective contraceptive method, but the migration of IUD is a serious complication. We report the case of IUD migration leading to bladder calculus formation and a minimally invasive transurethral surgical approach was performed for treatment. Holmium laser was used to break up the bladder calculus and cut through the bladder mucosa where the IUD was attached, finally the IUD was removed through the urethra. This minimally invasive procedure is a safe and effective treatment for IUD migration, and similar cases have not been reported in the literature. CONCLUSION: That the secondary bladder calculus were smashed by intense pulse mode of holmium laser, and the bladder tissue around the attached IUD was opened by cutting mode of holmium laser, and finally the IUD was completely removed from urethra, this surgical method is safe and effective, and there is no case report on IUD removal of transurethral cystoscope in the literature.

Effects of xenon anesthesia on postoperative neurocognitive disorders: a systematic review and meta-analysis.

The latest clinical trials have reported conflicting outcomes regarding the effectiveness of xenon anesthesia in preventing postoperative neurocognitive dysfunction; thus, this study assessed the existing evidence. We searched the PubMed, Embase, Cochrane Library, and Web of Science databases from inception to April 9, 2023, for randomized controlled trials of xenon anesthesia in postoperative patients. We included English-language randomized controlled studies of adult patients undergoing surgery with xenon anesthesia that compared its effects to those of other anesthetics. Duplicate studies, pediatric studies, and ongoing clinical trials were excluded. Nine studies with 754 participants were identified. A forest plot revealed that the incidence of postoperative neurocognitive dysfunction did not differ between the xenon anesthesia and control groups (P = 0.43). Additionally, xenon anesthesia significantly shortened the emergence time for time to opening eyes (P < 0.001), time to extubation (P < 0.001), time to react on demand (P = 0.01), and time to time and spatial orientation (P = 0.04). However, the Aldrete score significantly increased with xenon anesthesia (P = 0.005). Postoperative complications did not differ between the anesthesia groups. Egger's test for bias showed no small-study effect, and a trim-and-fill analysis showed no apparent publication bias. In conclusion, xenon anesthesia probably did not affect the occurrence of postoperative neurocognitive dysfunction. However, xenon anesthesia may effectively shorten the emergence time of certain parameters without adverse effects.

A Soybean Sucrose Non-Fermenting Protein Kinase 1 Gene, GmSNF1, Positively Regulates Plant Response to Salt and Salt-Alkali Stress in Transgenic Plants.

Soybean is one of the most widely grown oilseed crops worldwide. Several unfavorable factors, including salt and salt-alkali stress caused by soil salinization, affect soybean yield and quality. Therefore, exploring the molecular basis of salt tolerance in plants and developing genetic resources for genetic breeding is important. Sucrose non-fermentable protein kinase 1 (SnRK1) belongs to a class of Ser/Thr protein kinases that are evolutionarily highly conserved direct homologs of yeast SNF1 and animal AMPKs and are involved in various abiotic stresses in plants. The GmPKS4 gene was experimentally shown to be involved with salinity tolerance. First, using the yeast two-hybrid technique and bimolecular fluorescence complementation (BiFC) technique, the GmSNF1 protein was shown to interact with the GmPKS4 protein. Second, the GmSNF1 gene responded positively to salt and salt-alkali stress according to qRT-PCR analysis, and the GmSNF1 protein was localized in the nucleus and cytoplasm using subcellular localization assay. The GmSNF1 gene was then heterologously expressed in yeast, and the GmSNF1 gene was tentatively identified as having salt and salt-alkali tolerance function. Finally, the salt-alkali tolerance function of the GmSNF1 gene was demonstrated by transgenic Arabidopsis thaliana, soybean hairy root complex plants overexpressing GmSNF1 and GmSNF1 gene-silenced soybean using VIGS. These results indicated that GmSNF1 might be useful in genetic engineering to improve plant salt and salt-alkali tolerance.

Dopamine 1 receptors inhibit apoptosis via activating CSE/H2 S pathway in high glucose-induced vascular endothelial cells.

High glucose (HG)-induced dysfunction of vascular endothelial cells plays a crucial role in the development of diabetic vascular complications. Inhibition of cystathionine γ-synthase/hydrogen sulfide (CSE/H2 S) pathway is one of the causes of vascular endothelial cell injury induced by HG. Dopamine D1 receptors (DR1) are widely expressed and regulate important physiological functions in the vascular system. However, the effect of DR1 inhibition on HG-induced vascular endothelial apoptosis by regulating the CSE/H2 S pathway is unclear. Therefore, we aimed to determine if DR1 can regulate the CSE/H2 S pathway and regulate the effect of DR1 on HG-induced apoptosis in human umbilical vein endothelial cells. In this study, we found that HG treatment significantly decreased the expression of DR1 and CSE and the endogenous content of H2 S; DR1 agonist SKF 38393 reversed these effects, while sodium hydrosulfide (NaHS) only increased CSE expression and the endogenous H2 S production and had no effect on DR1 expression. Meanwhile, HG significantly increased the intracellular calcium concentration ([Ca2+ ]i ), and SKF 38393 further increased HG-induced [Ca2+ ]i . In addition, HG increased the lactate dehydrogenase activity, malondialdehyde and reactive oxygen species contents, apoptotic rate, the expression of cleaved caspase-3, caspase-9, and cytochrome c, and the activity of phosphorylated-inhibitor of nuclear factor-kappaBα (NF-κBα) (p-IκBα) and phosphorylated-NF-κB (p-NF-κB), and reduced cell viability, superoxide dismutase activity, and Bcl-2 expressions. SKF 38393 and NaHS markedly reversed the effect of HG. The effect of SKF 38393 was similar to N-acetyl- l-cysteine (an inhibitor of oxidative stress) or pyrrolidinedithiocarbamate ammonium (an NF-kB inhibitor). Taken together, DR1 upregulates the CSE/H2 S pathway by increasing the [Ca2+ ]i , which inhibits HG-induced apoptosis via downregulating NF-κB/IκBα pathway in vascular endothelial cells.

Wogonoside attenuates liver fibrosis by triggering hepatic stellate cell ferroptosis through SOCS1/P53/SLC7A11 pathway.

Wogonoside (WG) is a flavonoid chemical component extracted from Scutellaria baicalensis, which exerts therapeutic effects on liver diseases. Ferroptosis, a novel form of programmed cell death, regulates diverse physiological/pathological processes. In this study, we attempted to investigate a novel mechanism by which WG mitigates liver fibrosis by inducing ferroptosis in hepatic stellate cells (HSCs). A CCl4 -induced mouse liver fibrosis model and a rat HSC line were employed for in vivo and in vitro experiments, both treated with WG. Firstly, the levels of the fibrotic markers α-smooth muscle actin (α-SMA) and α1(I)collagen (COL1α1) were effectively decreased by WG in CCl4 -induced mice and HSC-T6 cells. Additionally, mitochondrial condensation and mitochondrial ridge breakage were observed in WG-treated HSC-T6 cells. Furthermore, ferroptotic events including depletion of SLC7A11, GPX4 and GSH, and accumulation of iron, ROS and MDA were discovered in WG-treated HSC-T6 cells. Intriguingly, these ferroptotic events did not appear in hepatocytes or macrophages. WG-elicited HSC ferroptosis and ECM reduction were dramatically abrogated by ferrostatin-1 (Fer-1), a ferroptosis inhibitor. Importantly, our results confirm that SOCS1/P53/SLC7A11 is a signaling pathway which promotes WG attenuation of liver fibrosis. On the contrary, WG mitigated liver fibrosis and inducted HSC-T6 cell ferroptosis were hindered by SOCS1 siRNA and pifithrin-α (PFT-α). These findings demonstrate that SOCS1/P53/SLC7A11-mediated HSC ferroptosis is associated with WG alleviating liver fibrosis, which provides a new clue for the treatment of liver fibrosis.

Atorvastatin Exerts Protective Effect on Cardiopulmonary Bypass Induced Renal Injury in Rats via PPAR-γ.

BACKGROUND: To investigate the protective effect and possible mechanism of atorvastatin pretreatment on renal function after cardiopulmonary bypass (CPB) in rats. METHODS: Twenty-four adult male Sprague-Dawley (SD) rats randomly were divided into three groups: Sham operation group, CPB group, and administration group (N = 8 in each group). The caudal artery and right jugular vein were used to establish the CPB circuit for the CPB and administration groups. Drugs were administered by oral gavage one week before the operation. All rats were executed for succeeding experiments 72h after the operation. Plasma levels of creatinine (Cre) and IL-8 at different time points and levels of TNF-α and MPO in renal tissue were detected by ELISA. Renal pathological changes were observed by HE staining. PPAR-γ expression was determined by immunohistochemistry and western blot. RESULTS: All rats survived the whole process without incident. Renal function of rats undergoing CPB was impaired to varying degrees based on the plasma Cre concentration, and atorvastatin pretreatment alleviated this effect. The concentrations of six inflammatory cytokines (IL-1ß, IL-6,IL-8, IFN-γ,TNF-α, and MPO) were significantly elevated after CPB procedure, while atorvastatin pretreatment ameliorated the inflammatory condition caused by CPB. Further analysis showed that in both HK-2 cells and renal tissues, atorvastatin promoted the expression of PPAR-γ. CONCLUSION: Atorvastatin pretreatment exerted protective effect on CPB-associated kidney injury and inflammation in rats. The activation of PPAR-γ may contribute to the protective effect of Atorvastatin.

Smart Sensing Multifunctionalities Based on Barium Strontium Titanate Thin Films.

Sensors that have low power consumption, high scalability and the ability of rapidly detecting multitudinous external stimulus are of great value in cyber-physical interactive applications. Herein, we reported the fabrication of ferroelectric barium strontium titanate ((Ba70Sr30)TiO3, BST) thin films on silicon substrates by magnetron sputtering. The as-grown BST films have a pure perovskite structure and exhibit excellent ferroelectric characteristics, such as a remnant polarization of 2.4 µC/cm2, a ferro-to-paraelectric (tetragonal-to-cubic) phase transition temperature of 31.2 °C, and a broad optical bandgap of 3.58 eV. Capacitor-based sensors made from the BST films have shown an outstanding average sensitivity of 0.10 mV·Pa-1 in the 10-80 kPa regime and work extremely steadily over 1000 cycles. More importantly, utilizing the Pockels effect, optical manipulation in BST can be also realized by a smaller bias and its electro-optic coefficient reff is estimated to be 83.5 pmV-1, which is 2.6 times larger than in the current standard material (LiNbO3) for electro-optical devices. Our work established BST thin film as a powerful design paradigm toward on-chip integrations with diverse electronics into sensors via CMOS-comparable technique.

Transplantation of mesenchymal stem cells for spinal cord injury: a systematic review and network meta-analysis.

Spinal cord injury (SCI) is a severe traumatic disease of the central nervous system, with a global prevalence of 236-4187 per million people. This meta-analysis aimed to evaluate the safety and efficacy of mesenchymal stem cells (MSCs) in treating patients with SCI as well as the optimal source and transplantation method of MSCs. PubMed, OVID, Cochrane, Web of Science, and China Biomedical Database were searched up until April 01, 2021. The study was conducted for five endpoints: American Spinal Injury Association (ASIA) motor and sensory score, ASIA grade improvement, Barthel Index (BI), and adverse reactions. Standard meta-analysis and network meta-analysis were performed using Stata 14.0. Eighteen studies with a total of 949 patients, were included in the meta-analysis. Standard meta-analysis showed that MSCs significantly improved ASIA motor score (P < 0.001), sensory score (P < 0.001), ASIA grade (P < 0.001), and BI (P < 0.001) compared to rehabilitation. In addition, in the network meta-analysis, autologous MSCs significantly improved the ASIA motor [MD = 8.01, 95% CI (4.27, 11.76)], sensory score [MD = 17.98, 95% CI (10.04, 25.91)], and BI [MD = 7.69, 95% CI (2.10, 13.29)] compared to rehabilitation. Similarly, compared to rehabilitation, intrathecal injection (IT) of MSCs significantly improved the ASIA motor [MD = 7.97, 95% CI (4.40, 11.53)] and sensory score [MD = 19.60, 95% CI (9.74, 29.46)]. Compared to rehabilitation, however, only the IL of MSCs was associated with more adverse reactions [OR = 17.82, 95% CI (2.48, 128.22)]. According to the results of SUCRA, both autologous MSCs and IT transplantation approaches most improved the neurological function in SCI patients. Cell transplantation using MSCs is effective in patients with SCI and IT of autologous MSCs may be more beneficial.

Nickel-Catalyzed Cross-Coupling of Aryl 2-Pyridyl Ethers with Organozinc Reagents: Removal of the Directing Group via Cleavage of the Carbon-Oxygen Bonds.

Reaction of aryl 2-pyridyl ethers with arylzinc reagents under catalysis of NiCl2(PCy3)2 affords aryl-aryl cross-coupling products via selective cleavage of CAr-OPy bonds. The reaction features a wide substrate range and good compatibility of functional groups. ß-H-free alkylzinc reagents are also applicable as the nucleophiles in the transformation, whereas ß-H-containing alkylzinc reagents lead to a mixture of cross-coupling and hydrogenation products.

Spermine Protects Cardiomyocytes from High Glucose-Induced Energy Disturbance by Targeting the CaSR-gp78-Ubiquitin Proteasome System.

PURPOSE: To determine the mediation of spermine on energy metabolism disorder and diabetic cardiomyopathy (DCM) development as well as the underlying mechanisms. METHODS: An in vitro model of DCM was established by incubating primary cultured neonatal rat cardiomyocytes with high glucose (HG). Spermine content was assessed by RP-HPLC. The protein levels were detected by western blot. Mitochondrial functions were analyzed using the respiratory chain complex assay kit and immunofluorescence staining. RESULTS: The endogenous content of spermine was decreased in the HG group, and the protein levels of ornithine decarboxylase, respiratory chain complex (I-V), mitochondrial fusion-related protein (Mfn1, Mfn2), Cx43, N-cadherin, CaSR, and ß-catenin (in cytomembrane) were also down-regulated by HG. In contrast, the protein levels of spermine-N1-acetyltransferase, gp78, Fis1, Drp1, and ß-catenin were up-regulated by HG. Meanwhile, we observed that HG increased ubiquitination levels of Mfn1, Mfn2, and Cx43, decreased membrane potential (ΔΨm), and the opening of mitochondrial permeability transport pore (mPTP) followed by intracellular ATP leakage. The supplement of spermine or siRNA-mediated knockdown of gp78 significantly alleviated the detrimental effects of HG, while downregulation of CaSR aggravated the development of DCM. We further confirmed that the lower level of spermine by HG activates the gp78-ubiquitin-proteasome pathway via downregulation of CaSR protein level, which in turn damages mitochondrial gap junction intercellular communication and leads to reduced ATP level. CONCLUSION: The protective role of spermine on energy metabolism disorder is based on higher CaSR protein level and lower gp78 activation, pointing to the possibility that spermine can be a target for the prevention and treatment of DCM.

Dopamine 1 receptor activation protects mouse diabetic podocytes injury via regulating the PKA/NOX-5/p38 MAPK axis.

Diabetic nephropathy (DN) is a major microvascular complication of diabetes that can lead to end-stage renal disease. Podocytes constitute the last barrier of glomerular filtration, whose damage are the direct cause of proteinuria. Dopamine receptors are involved in the regulation of diabetes-induced glomerular hyperfiltration, and only dopamine 1 receptor (D1R) can be amplified in cultured mouse podocytes. However, the exact effect of D1R on diabetic podocytes remains unclear. This study aims to investigate the protective role of D1R activation on diabetic podocytes injury in vivo and vitro as well as its potential mechanism. We observed D1R protective effect respectively in streptozotocin (STZ)-induced type 1 diabetes (T1D) mice as well as mouse podocytes (MPC5) cultured in high glucose (HG, 40 mM) medium. It showed that D1R and podocyte-associated proteins (Podocin, CD2AP and Nephrin) expression were significantly decreased both in the T1D mice (fed for 8 and 12 weeks) and HG-cultured MPC5 cells, while the NOX-5 expression increased. In T1D mice, the levels of 24-h urine protein, serum creatinine and urinary 8-OHdG were increased in a time-dependent manner, at the same time, hematoxylin-eosin (HE) staining and electron microscope observed the kidney lesion and podocytes injury. In vitro, HG induced podocytes oxidative stress and apoptosis, which could be inhibited by SKF38393 (a D1R agonist) and N-acetyl-l-cysteine (NAC, a reactive oxygen species scavenger). Furthermore, there was a decreasing Podocin expression and a significant increasing NOX-5 expression in podocytes transfected with D1R-small interfering RNA (siRNA). More importantly, the expression of phospho-CREB (the PKA downstream transcription factor) was decreased and phospho-p38 MAPK was increased in HG-induced podocytes, which can respectively be activated or blocked by SKF38393, 8-Bromo-CAMP (a PKA activator), NAC, and SB20380 (a p38 MAPK inhibitor). In conclusion, D1R activation can protect diabetic podocytes from apoptosis and oxidative damage, in part through the PKA/NOX-5/p38 MAPK pathway.

Dopamine receptor D2 inhibition alleviates diabetic hepatic stellate cells fibrosis by regulating the TGF-ß1/Smads and NFκB pathways.

Diabetic hepatic fibrosis (DHF) is a progressive liver disease and a chronic complication of diabetes mellitus. The main cause of DHF is the activation of quiescent hepatic stellate cells (HSCs) by high glucose stimulation. Dopamine receptor D2 (DRD2)-mediated dopamine signalling can be involved in the regulation of diabetic liver disease, but the exact role of DRD2 in DHF is still poorly understood. This study aimed to investigate the protective effect of DRD2 inhibition on diabetic liver fibrosis and the potential mechanism. We established both streptozotocin (STZ)-induced type 1 diabetes (T1D, fed for 20 weeks) rat model and high glucose (HG, 40 mmol/L)-stimulated HSCs model. The results from both the rats with STZ and the HSCs treated with HG showed increased expression of DRD2, NOX-5, inflammation-related proteins (IL-6 and TNFα) and fibrosis-related proteins (TGF-ß1, CO-Ⅰ/Ⅲ/ IV, MMP-2/9 and fibronectin). In vivo, the serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and total antioxidant capacity (T-AOC) levels were significantly increased, and hematoxylin-eosin (HE) staining, Masson staining, and electron microscopy revealed liver lesions and hepatocyte injury. In addition, HG-treated HSCs exhibited altered oxidative stress - related indexes, including superoxide dismutase (SOD), malondialdehyde (MDA) and reactive oxygen species (ROS), changed and abnormally proliferated in vitro. TGF-ß1, the phosphorylated Smad2, nuclear NFκB-p65, phosphorylated NFκB-p65 and phosphorylated IκBα were also increased. Interestingly, haloperidol (DRD2 inhibitor) and n-acetyl-L-cysteine (NAC, an active oxygen scavenger) reduced the above-mentioned changes. In conclusion, DRD2 inhibition can reduce diabetic HSCs oxidative damage and fibrotic proliferation partly via the TGF-ß1/Smads and NFκB pathways.

TRPM7 modulates macrophage polarization by STAT1/STAT6 pathways in RAW264.7 cells.

Macrophages, diversity and plasticity immune cells, participate in immune response and maintain homeostasis through M1/M2 phenotype transformation. Transient receptor potential melastatin 7 (TRPM7) is a widely expressed divalent cation channel with protein serine/threonine kinase activity, which has recently been found to affect macrophage proliferation and function. This study aimed to identify the role of TRPM7 in macrophage polarization. Our results suggested that TRPM7 was highly expressed in M1-type macrophages rather than M2-type macrophages. Interestingly, we detected that M1-type macrophages decreased while M2-type macrophages enhanced through blockade of TRPM7, which manifest as decreased TNF-α, iNOS and elevated Arg-1, CD206. Furthermore, blockade of TRPM7 could inhibit STAT1 phosphorylation and promote STAT6 phosphorylation. In conclusion, TRPM7 could regulate macrophage polarization via STAT1/STAT6 pathways. Taken together, it is suggested that TRPM7 might serve as a molecular regulator in macrophage polarization and is a potential therapeutic target for inflammatory diseases.

Exogenous spermine attenuates myocardial fibrosis in diabetic cardiomyopathy by inhibiting endoplasmic reticulum stress and the canonical Wnt signaling pathway.

Myocardial fibrosis is one of the main pathological manifestations of diabetic cardiomyopathy (DCM). Spermine (SPM), a product of polyamine metabolism, plays an important role in many cardiac diseases including hypertrophy, ischemia, and infarction, but its role in diabetic myocardial fibrosis has not been clarified. This study aimed to investigate the role of polyamine metabolism, specifically SPM, in diabetic myocardial fibrosis and to explore the related mechanisms. We used intraperitoneal injection of streptozotocin (STZ, 60 mg/kg) in Wistar rats and high glucose (HG, 40 mM) stimulated cardiac fibroblasts (CFs) to established a type 1 diabetes (T1D) model in vivo and in vitro, which were pretreated with exogenous SPM (5 mg/kg per day and 5 µM). The results showed that hyperglycemia induced the expression of the key polyamine synthesis enzyme ornithine decarboxylase (ODC) decreased and the key catabolic enzyme spermidine/spermine N1 -acetyltransferase (SSAT) increased compared with those in the control group. The body weight, blood insulin level, and cardiac ejection function were decreased, while blood glucose, heart weight, the ratio of heart weight to body weight, myocardial interstitial collagen deposition, and endoplasmic reticulum stress (ERS)-related protein (glucose-regulated protein-78, glucose-regulated protein-94, activating transcription factor-4, and C/EBP homology protein) expression in the T1D group were all significantly increased. HG also caused an increased expression of Wnt3, ß-catenin (in cytoplasm and nucleus), while Axin2 and phosphorylated ß-catenin decreased. Exogenous SPM improved the above changes caused by polyamine metabolic disorders. In conclusion, polyamine metabolism disorder occurs in the myocardial tissue of diabetic rats, causing myocardial fibrosis and ERS. Exogenous SPM plays a myocardial protective role via inhibiting of ERS and the canonical Wnt/ß-catenin signaling pathway.

The items in the Chinese version of the Montreal cognitive assessment basic discriminate among different severities of Alzheimer's disease.

BACKGROUND: To determine whether items of the Chinese version of the Montreal Cognitive Assessment Basic (MoCA-BC) could discriminate among cognitively normal controls (NC), and those with mild cognitive impairment (MCI), mild Alzheimer's disease (AD), and moderate-severe (AD), as well as their sensitivity and specificity. METHODS: MCI (n = 456), mild AD (n = 502) and moderate-severe AD (n = 102) patients were recruited from the memory clinic, Huashan Hospital, Shanghai, China. NC (n = 329) were recruited from health checkup outpatients. Five MoCA-BC item scores were collected in interviews. RESULTS: The MoCA-BC orientation test had high sensitivity and specificity for discrimination among MCI, mild AD and moderate-severe AD. The delayed recall memory test had high sensitivity and specificity for MCI screening. The verbal fluency test was efficient for detecting MCI and differentiating AD severity. CONCLUSIONS: Various items of the MoCA-BC can identify MCI patients early and identify the severity of dementia.

Wogonoside Inhibits Prostate Cancer Cell Growth and Metastasis via Regulating Wnt/ß-Catenin Pathway and Epithelial-Mesenchymal Transition.

BACKGROUND: Wogonoside, an effective component of Scutellaria baicalensis extract, has recently become a hot topic for its newly discovered anticancer efficacy, but the underlying pharmacological mechanism is still unclear. In this study, we tested the inhibitory effects of wogonoside in human prostate cancer PC3 cells in vitro and vivo. METHODS: The effects of wogonoside on cell viability, cycle progression, invasion, migration, and apoptosis were assessed in vitro. The levels of proteins in related signaling pathways were detected by western blotting assay. Finally, nude mouse tumorigenicity assay was conducted to detect the anticancer effect of wogonoside in vivo. RESULTS: Wogonoside inhibited cell viability, invasive and migratory ability in a time- and dose-dependent manner. Flow cytometry indicated that wogonoside could induce cell apoptosis and S phase cell-cycle arrest. Mechanically, wogonoside suppressed the Wnt/ß-catenin signaling pathway, and the level of p-glycogen synthase kinase-3ß (GSK-3ß; Ser9) was inhibited by wogonoside. The epithelial-mesenchymal transition (EMT) process was also reversed in PC3 cell line after wogonoside treatment. In vivo experiments showed that wogonoside inhibited tumor growth in xenograft mouse models. CONCLUSION: These findings revealed that wogonoside could suppress Wnt/ß-catenin pathway and reversing the EMT process in PC3 cells. GSK-3ß acts as a tumor suppressor in prostate cancer. Wogonoside may serve as an effective agent for treating prostate cancer.

Overexpression of GmCAMTA12 Enhanced Drought Tolerance in Arabidopsis and Soybean.

Fifteen transcription factors in the CAMTA (calmodulin binding transcription activator) family of soybean were reported to differentially regulate in multiple stresses; however, their functional analyses had not yet been attempted. To characterize their role in stresses, we first comprehensively analyzed the GmCAMTA family in silico and thereafter determined their expression pattern under drought. The bioinformatics analysis revealed multiple stress-related cis-regulatory elements including ABRE, SARE, G-box and W-box, 10 unique miRNA (microRNA) targets in GmCAMTA transcripts and 48 proteins in GmCAMTAs' interaction network. We then cloned the 2769 bp CDS (coding sequence) of GmCAMTA12 in an expression vector and overexpressed in soybean and Arabidopsis through Agrobacterium-mediated transformation. The T3 (Transgenic generation 3) stably transformed homozygous lines of Arabidopsis exhibited enhanced tolerance to drought in soil as well as on MS (Murashige and Skoog) media containing mannitol. In their drought assay, the average survival rate of transgenic Arabidopsis lines OE5 and OE12 (Overexpression Line 5 and Line 12) was 83.66% and 87.87%, respectively, which was ~30% higher than that of wild type. In addition, the germination and root length assays as well as physiological indexes such as proline and malondialdehyde contents, catalase activity and leakage of electrolytes affirmed the better performance of OE lines. Similarly, GmCAMTA12 overexpression in soybean promoted drought-efficient hairy roots in OE chimeric plants as compare to that of VC (Vector control). In parallel, the improved growth performance of OE in Hoagland-PEG (polyethylene glycol) and on MS-mannitol was revealed by their phenotypic, physiological and molecular measures. Furthermore, with the overexpression of GmCAMTA12, the downstream genes including AtAnnexin5, AtCaMHSP, At2G433110 and AtWRKY14 were upregulated in Arabidopsis. Likewise, in soybean hairy roots, GmELO, GmNAB and GmPLA1-IId were significantly upregulated as a result of GmCAMTA12 overexpression and majority of these upregulated genes in both plants possess CAMTA binding CGCG/CGTG motif in their promoters. Taken together, we report that GmCAMTA12 plays substantial role in tolerance of soybean against drought stress and could prove to be a novel candidate for engineering soybean and other plants against drought stress. Some research gaps were also identified for future studies to extend our comprehension of Ca-CaM-CAMTA-mediated stress regulatory mechanisms.

Comprehensive Genomic Analysis and Expression Profiling of Diacylglycerol Kinase (DGK) Gene Family in Soybean (Glycine max) under Abiotic Stresses.

Diacylglycerol kinase (DGK) is an enzyme that plays a pivotal role in abiotic and biotic stress responses in plants by transforming the diacylglycerol into phosphatidic acid. However, there is no report on the characterization of soybean DGK genes in spite of the availability of the soybean genome sequence. In this study, we performed genome-wide analysis and expression profiling of the DGK gene family in the soybean genome. We identified 12 DGK genes (namely GmDGK1-12) which all contained conserved catalytic domains with protein lengths and molecular weights ranging from 436 to 727 amino acids (aa) and 48.62 to 80.93 kDa, respectively. Phylogenetic analyses grouped GmDGK genes into three clusters-cluster I, cluster II, and cluster III-which had three, four, and five genes, respectively. The qRT-PCR analysis revealed significant GmDGK gene expression levels in both leaves and roots coping with polyethylene glycol (PEG), salt, alkali, and salt/alkali treatments. This work provides the first characterization of the DGK gene family in soybean and suggests their importance in soybean response to abiotic stress. These results can serve as a guide for future studies on the understanding and functional characterization of this gene family.