A monocarboxylic acid induction strategy to prepare tough and thermo-reversible poly(vinyl alcohol) physical gels with high transparency.

To date, poly(vinyl alcohol) (PVA) gels attract tremendous attention because of their potential applications in a wide variety of fields. Here, a novel monocarboxylic acid induction strategy was developed to fabricate tough and thermo-reversible PVA physical gels by introducing monocarboxylic acids into the PVA/dimethyl sulfoxide (DMSO) system. The obtained PVA gels exhibited appropriate crystalline architectures, leading to superior mechanical properties and high transparency. Furthermore, the role of monocarboxylic acids in the formation of PVA physical gels and the effects of alkyl chain length, concentration, and the induction time of monocarboxylic acids on the properties of PVA physical gels were also investigated.

Thermal- and pH-responsive triple-shape memory hydrogel based on a single reversible switch.

Here we provide a novel method for fabricating a pH- and thermal-responsive triple-shape memory hydrogel based on a single reversible switch phase. A high-density quadruple hydrogen-bonding ureido-pyrimidinone (UPy) system was introduced into the hydrogel network, which can occur to varied degrees of dissociation under different pH and temperature conditions. Different degrees of dissociation and reassociation can be viewed as different subsets of memory elements to freeze and unfreeze the temporary shapes. Although this class of hydrogels contains only a single transition phase, they feature a large dissociative differential in response to varied external stimuli to provide multiple windows for programming different temporary shapes.

[A multi-behavior recognition method for macaques based on improved SlowFast network].

Macaque is a common animal model in drug safety assessment. Its behavior reflects its health condition before and after drug administration, which can effectively reveal the side effects of drugs. At present, researchers usually rely on artificial methods to observe the behavior of macaque, which cannot achieve uninterrupted 24-hour monitoring. Therefore, it is urgent to develop a system to realize 24-hour observation and recognition of macaque behavior. In order to solve this problem, this paper constructs a video dataset containing nine kinds of macaque behaviors (MBVD-9), and proposes a network called Transformer-augmented SlowFast for macaque behavior recognition (TAS-MBR) based on this dataset. Specifically, the TAS-MBR network converts the red, green and blue (RGB) color mode frame input by its fast branches into residual frames on the basis of SlowFast network and introduces the Transformer module after the convolution operation to obtain sports information more effectively. The results show that the average classification accuracy of TAS-MBR network for macaque behavior is 94.53%, which is significantly improved compared with the original SlowFast network, proving the effectiveness and superiority of the proposed method in macaque behavior recognition. This work provides a new idea for the continuous observation and recognition of the behavior of macaque, and lays the technical foundation for the calculation of monkey behaviors before and after medication in drug safety evaluation.

[Intelligence-aided diagnosis of Parkinson's disease with rapid eye movement sleep behavior disorder based on few-channel electroencephalogram and time-frequency deep network].

Aiming at the limitations of clinical diagnosis of Parkinson's disease (PD) with rapid eye movement sleep behavior disorder (RBD), in order to improve the accuracy of diagnosis, an intelligent-aided diagnosis method based on few-channel electroencephalogram (EEG) and time-frequency deep network is proposed for PD with RBD. Firstly, in order to improve the speed of the operation and robustness of the algorithm, the 6-channel scalp EEG of each subject were segmented with the same time-window. Secondly, the model of time-frequency deep network was constructed and trained with time-window EEG data to obtain the segmentation-based classification result. Finally, the output of time-frequency deep network was postprocessed to obtain the subject-based diagnosis result. Polysomnography (PSG) of 60 patients, including 30 idiopathic PD and 30 PD with RBD, were collected by Nanjing Brain Hospital Affiliated to Nanjing Medical University and the doctor's detection results of PSG were taken as the gold standard in our study. The accuracy of the segmentation-based classification was 0.902 4 in the validation set. The accuracy of the subject-based classification was 0.933 3 in the test set. Compared with the RBD screening questionnaire (RBDSQ), the novel approach has clinical application value.

DNA repair enzyme OGG1 promotes alveolar progenitor cell renewal and relieves PM2.5-induced lung injury and fibrosis.

Fine particulate matter (PM2.5) airborne pollution increases the risk of chronic respiratory diseases, such as idiopathic pulmonary fibrosis (IPF), which is characterized by non-specific inflammation of the interstitial lung and extensive deposition of collagen fibers. Type 2 alveolar epithelial cells (AEC2s) are alveolar stem cells in the adult lung that contribute to the lung repair process through complex signaling. Our previous studies demonstrated that OGG1, a kind of DNA repair enzyme, have a critical role in protecting cells from oxidative damage and apoptosis induced by PM2.5, but the contribution of OGG1 in proliferation and self-renewal of AEC2s is not known. Here, we constructed OGG1-/-mice to test the effect and mechanism of OGG1 on PM2.5-induced pulmonary fibrosis and injury in vivo. We detected proliferation and self-renewal of OGG1 overexpression or OGG1 knockout AEC2s after PM2.5 injury by flow cytometry and clone formation. We observed that knockout of OGG1 aggravated pulmonary fibrosis, oxidative stress, and AEC2 cell death in PM2.5-injured mice. In addition, OGG1 is required for the proliferation and renewal of AEC2s after PM2.5 injury. Overexpression of OGG1 promotes the proliferation and self-renewal of AEC2s by inhibiting PM2.5-mediated oxidative stress and NF-κB signaling hyperactivation in vitro. Furthermore, NF-κB inhibitors promoted proliferation and self-renewal of OGG1-deficient AEC2s cells after PM2.5 injury, and attenuated PM2.5-induced pulmonary fibrosis and injury in mice. These data establish OGG1 as a regulator of NF-κB signal that serves to regulate AEC2 cell proliferation and self-renewal, and suggest a mechanism that inhibition of the NF-κB signaling pathway may represent a potential therapeutic strategy for IPF patients with low-expression of OGG1.

Association of vascular endothelial growth factor polymorphisms with clinical outcome of renal cell carcinoma patients.

We investigated the association of three single nucleotide polymorphisms (SNPs) in VEGF gene with the prognosis of renal cell carcinoma (RCC) and its association with clinical characteristics of RCC, such as tumor stages, metastasis, and tumor size. Polymerase chain reaction (PCR) restriction fragment length polymorphism analysis was used to genotype specimens for three polymorphisms (-2578C/A, -1154G/A, and -634G/C) in the VEGF gene. Hazard ratios (HRs) and their confidence intervals (CIs) were used to analyze the association of three SNPs in the VEGF gene with survival time using a multivariate Cox proportional hazards model. Frequencies of VEGF-2578AA genotype and A allele were significantly higher in patients with III-IV tumor stage or larger tumor size when compared with CC genotype. Moreover, frequencies of VEGF-634CC genotype and C allele were significantly higher in patients with tumor size >4 cm when compared with -634GG genotype. By Cox proportional hazards model, patients carrying VEGF-2578AA genotype and A allele significantly increased the risk of death from RCC, with the adjusted HRs (95 % CI) of 2.23 (1.15-4.36) and 1.55 (1.11-2.17), respectively. Our study suggests that VEGF-2578C/A and VEGF-634G/C polymorphisms may have effects on the prognosis of RCC. This finding might help in clarifying the mechanisms of RCC development and progression.

BIRC6 Modulates the Protein Stability of Axin to Regulate the Growth, Stemness, and Resistance of Renal Cancer Cells via the ß-Catenin Pathway.

The mechanism underlying the development of renal cell carcinoma (RCC) remains unclear, and effective prevention and therapeutic measures are lacking. BIRC6, a protein inhibitor of apoptosis, has attracted great interest. Our data indicated that overexpression of BIRC6 elevated cell growth, colony formation, migration, and invasion of cultured RCC cells, while siRNA knockdown of BIRC6 suppressed these processes. Additionally, BIRC6 was highly expressed in RCC clinical samples along with a downregulated level of Axin. Immunoprecipitation assays found that BIRC6 interacted with Axin and the two proteins colocalized within the cytoplasm of RCC cells. Overexpression of BIRC6 promoted the ubiquitination modification of Axin, while genetic knockdown of BIRC6 suppressed it. Furthermore, overexpression of BIRC6 significantly promoted the turnover of Axin, suggesting BIRC6's inhibitory effect on Axin protein stability. BIRC6 was also upregulated in cancer stem-like cells of RCC and increased the drug resistance of RCC cells against sunitinib. Western blotting assays showed that the overexpression of BIRC6 upregulated CXCR4 protein expression and activated the ß-catenin pathway. Two cell lines were then constructed with BIRC6 overexpressed by lentiviruses. Pharmacological administration of a Wnt/ß-catenin inhibitor, XAV-939, or genetic knockdown of ß-catenin inhibited cell growth, tumor sphere formation, colony formation, migration, and invasion of BIRC6-overexpressed cells. In vivo administration of XAV-939 markedly suppressed the tumorigenesis of BIRC6-overexpressed RCC cells in nude mice. In conclusion, we propose that BIRC6 activates the ß-catenin signaling pathway via mediating the ubiquitination and degradation of Axin, promoting the growth, stemness, and drug resistance of RCC cells. This project aims to elucidate the role of BIRC6 as a potential therapeutic target and provide new insights into the clinical treatment of RCC.

Prognostic significance of immune evasion-related genes in clear cell renal cell carcinoma immunotherapy.

Clear cell renal cell carcinoma (ccRCC) represents a prevalent malignancy of the urinary system. Despite the integration of immune checkpoint inhibitors (ICIs) into the treatment paradigm for advanced RCC, resistance to immunotherapy has emerged as a pivotal determinant impacting the clinical outlook of ccRCC. Accumulating evidence underscores the pivotal role of immune evasion-related genes and pathways in enabling tumor escape from host immune surveillance, consequently influencing patients' responsiveness to immunotherapy. Nonetheless, the clinical relevance of immune evasion-related genes in ccRCC patients undergoing immunotherapy remains inadequately understood. In this study, we aggregated RNA sequencing and clinical data from ccRCC patients across three cohorts: the Cancer Genome Atlas (TCGA), CheckMate cohorts, and the JAVELIN Renal 101 trial. Leveraging a curated immune evasion-related gene set from Lawson et al., we employed the LASSO algorithm and Cox regression analysis to identify eight genes (LPAR6, RGS5, NFYC, PCDH17, CENPW, CNOT8, FOXO3, SNRPB) significantly associated with immune therapy prognosis (HR, 3.57; 95 % CI, 2.38-5.35; P<0.001). A predictive algorithm developed utilizing these genes exhibited notable accuracy in forecasting patients' progression-free survival in the training set (AUC, 0.835). Furthermore, stratification of patients by risk score revealed discernible differences in immunotherapy response and tumor microenvironment. In summary, we present a prognostic model intricately linked with immune status and treatment response. For ccRCC patients undergoing immunotherapy, this approach holds promise in aiding clinical decision-making by providing more precise and tailored treatment recommendations.

Influence of Psychological Nursing Intervention on Psychological State, Treatment Compliance, and Immune Function of Postoperative Patients with Rectal Cancer.

In order to explore the clinical effect of psychological nursing intervention on postoperative chemotherapy for rectal cancer, 120 cases of rectal cancer patients were selected as the research subjects. The control group received conventional nursing treatment after operation, and the research group received comprehensive psychological nursing intervention on this basis. The self-rating anxiety scale (SAS) scores, self-rating depression scale (SDS) scores, hope level scores, nursing satisfaction, mental state changes, treatment compliance, and immune function of two groups were analyzed and compared. There was no significant difference between the two groups of patients in the preoperative SAS, SDS, and hope level scale scores. After the intervention, postoperative SAS and SDS scores and CD8+ value of the research group were significantly lower than those of the control group. In contrast, the postoperative hope level score, treatment compliance, and postoperative CD4+/CD8+ of the research group were significantly higher, and the nursing satisfaction was better than that of the control group. The application of psychological nursing intervention in postoperative chemotherapy for patients with rectal cancer can effectively relieve anxiety and depression of patients, promote patients to establish a healthy and coordinated mental state, improve treatment compliance, improve immune function, and promote disease recovery.

Suppression of ANT2 by miR-137 Inhibits Prostate Tumorigenesis.

Prostate cancer (PCa) is a serious disease that affects men's health. To date, no effective and long-lasting treatment option for this condition is available in clinical practice. ANT2 is highly expressed in a variety of hormone-related cancers, but its relationship and regulatory mechanism with PCa are unclear. In this study, we found that ANT2 expression was significantly upregulated in PCa tissues relative to control samples. Genetic knockdown of ANT2 effectively inhibited, while overexpression promoted, proliferation, migration, and invasion of PCa cells. In addition, miR-137 expression was reduced in prostate cancer tissues relative to control tissues. We identified a regulatory site for miR-137 in the 3'-UTR of ANT2 mRNA; luciferase reporter assays indicated that ANT2 is a direct target gene for miR-137. Transfecting cells with miR-137 mimics and/or an ANT2-encoding plasmid revealed that ANT2 promotes proliferation, migration, and invasion of PCa, whereas co-expression of miR-137 mimics inhibited these behaviors. These observations suggest that miR-137 mimics inhibit development of PCa by antagonizing expression of ANT2. Furthermore, tumorigenic assays in nude mice showed that miR-137 inhibitors abolished the inhibitory effect of ANT2 knockdown on PCa tumor growth. Collectively, our findings suggest that ANT2, a target gene of miR-137, is intimately involved in development of PCa, providing new evidence for the mechanism underlying pathogenesis of PCa as well as new options for targeted therapy.

[Effect of small interfering RNA-mediated BIRC6 silencing on apoptosis and autophagy of renal cancer 786-O cells].

OBJECTIVE: To study the expression of BIRC6 in renal cancer tissues and investigate the effect of BIRC6 silencing on apoptosis and autophagy of 786-O cells. METHODS: Twenty surgical specimens of renal cancer tissues and adjacent renal tissues were collected from Meizhou People's Hospital between February, 2016 and December, 2018 for detection of BIRC6 protein expression using immunohistochemistry. Renal cancer 786-O cells were transfected with a control small interfering RNA (siRNA) or BIRC6 siRNA via lipofectamine 2000, and the changes in cell proliferation and apoptosis following 5-FU treatment were assessed using CCK8 assay and flow cytometry; the expressions of autophagy-related proteins Beclin and LC3A/B were detected by Western blotting. RESULTS: The expression of BIRC6 protein was significantly higher in renal cancer tissues than in the adjacent renal tissues. Western blotting showed that siRNA-mediated silencing of BIRC6 significantly lowered the expression of BIRC6 in 786-O cells. In the cells with BIRC6 silencing, treatment with 12.5, 25, 50, 100 and 200 µg/mL 5-FU resulted in significantly higher proliferation inhibition rates than in the cells transfected with the control siRNA (P < 0.01). BIRC6 silencing also significantly increased the apoptosis rate of 786-O cells following 5-FU treatment (P < 0.01). The results of Western blotting showed that BIRC6 silencing significantly lowered the protein expressions of Beclin and LC3A/B in 786-O cells. CONCLUSIONS: Interference of BIRC6 mediated by siRNA can inhibit autophagy and promote 5-FU-induced apoptosis to enhance the sensitivity of 786-O cells to 5-FU.

BRDT is a novel regulator of eIF4EBP1 in renal cell carcinoma.

Among all types of kidney diseases, renal cell carcinoma (RCC) has the highest mortality, recurrence and metastasis rates, which results in high numbers of tumor­associated mortalities in China. Identifying a novel therapeutic target has attracted increasing attention. Bromodomain and extraterminal domain (BET) proteins have the ability to read the epigenome, leading to regulation of gene transcription. As an important member of the BET family, bromodomain testis­specific protein (BRDT) has been well studied; however, the mechanism underlying BRDT in the regulation of RCC has not been fully investigated. Eukaryotic translation initiation factor 4E­binding protein 1 (eIF4EBP1) is a binding partner of eIF4E that is involved in affecting the progression of various cancer types via regulating gene transcription. To identify novel regulators of eIF4EBP1, an immunoprecipitation assay and mass spectrometry analysis was performed in RCC cells. It was revealed that eIF4EBP1 interacted with BRDT, a novel interacting protein. In addition, the present study further demonstrated that BRDT inhibitors PLX51107 and INCB054329 blocked the progression of RCC cells, along with suppressing eIF4EBP1 and c­myc expression. Small interfering (si) RNAs were used to knock down BRDT expression, which suppressed RCC cell proliferation and eIF4EBP1 protein expression. In addition, overexpression of eIF4EBP1 partially abolished the inhibited growth function of PLX51107 but knocking down eIF4EBP1 improved the inhibitory effects of PLX51107. Furthermore, treatment with PLX51107 or knockdown of BRDT expression decreased c­myc expression at both the mRNA and protein levels, and attenuated its promoter activity, as determined by luciferase reporter assays. PLX51107 also significantly altered the interaction between the c­myc promoter with eIF4EBP1 and significantly attenuated the increase of RCC tumors, accompanied by decreased c­myc mRNA and protein levels in vivo. Taken together, these data suggested that blocking of BRDT by PLX51107, INCB054329 or BRDT knockdown suppressed the growth of RCC via decreasing eIF4EBP1, thereby leading to decreased c­myc transcription levels. Considering the regulatory function of BET proteins in gene transcription, the present study suggested that there is a novel mechanism underlying eIF4EBP1 regulation by BRDT, and subsequently decreased c­myc in RCC, and further identified a new approach by regulating eIF4EBP1 or c­myc for enhancing BRDT­targeting RCC therapy.

Force ripple compensation in a PMLSM position servo system using periodic adaptive learning control.

Force ripple deteriorates the performance of permanent magnet linear synchronous motor (PMLSM) servo systems. Using a model reference adaptive control and periodic adaptive learning control (MRAC-PALC) algorithm, this paper presents a novel compensation method to eliminate the influence of force ripple on the system performance of a position servo system under repetitive motion tasks. The key idea of the proposed method is to utilize the periodic characteristics of both force ripple and system motion. The controller consists of four components: a PD component, a feedforward component, a velocity feedback component and an MRAC-PALC compensator. The first three components are designed in a conventional way. The compensator is divided into two parts: in the 0th-iteration, an MRAC algorithm is employed to obtain the initial information, and in the ith-iteration (i≥ 1), a PALC algorithm is used to learn from the information obtained in the previous period and update the controller parameters for estimating force ripple. Moreover, a theoretical stability analysis is given via Lyapunov stability theorem, and some comparative results are provided through simulations and experiments.

Eupatilin Inhibits Renal Cancer Growth by Downregulating MicroRNA-21 through the Activation of YAP1.

Renal cell carcinoma (RCC) is the second most common human urinary tumor. Eupatilin is the main active ingredient of the traditional Chinese medicine Artemisia asiatica. The effect of Eupatilin on RCC and the underlying mechanism remain unknown. Here, we investigated the anticancer effects and mechanisms of Eupatilin in RCC in vivo and in vitro, laying an experimental foundation for the clinical application of Eupatilin in the treatment of RCC. The results showed that Eupatilin significantly inhibited 786-O cell viability and migration and promoted apoptosis. Eupatilin inhibited the expression of miR-21 in 786-O cells, and overexpression of miR-21 suppressed the effect of Eupatilin on viability, apoptosis, and migration in 786-O cells. Eupatilin inhibited the growth of renal tumors in nude mice by downregulating miR-21. YAP1, which was identified as a target of miR-21, showed significantly lower expression in RCC tissues than in healthy tissues. miR-21 significantly inhibited YAP1 protein expression in 786-O cells and tumor tissues isolated from nude mice, and YAP1 attenuated the effect of miR-21 on the viability, apoptosis, and migration of 786-O cells. In conclusion, Eupatilin inhibited the expression of miR-21, which mediated the proapoptotic and antimigratory effects of Eupatilin by suppressing YAP1 in renal cancer cells. These results suggested that Eupatilin could be a potent agent for the treatment of RCC.

IGHG1 Regulates Prostate Cancer Growth via the MEK/ERK/c-Myc Pathway.

Increasing evidence indicates that immunoglobulins are important for the regulation of various cancers including prostate cancer (PCa). However, the underlying mechanisms of IgG regulated PCa development remain to be further explored. Here, we demonstrated that IgG1 heavy chain (IGHG1) was increased in tissues from PCa patients. Inhibition of IGHG1 by antibody blocking or genetic knockdown suppressed cell growth and induced cell cycle arrest and ultimate apoptosis. Expression levels of c-Myc were positively correlated with the levels of IGHG1. Furthermore, MEK/ERK/c-Myc pathway lied downstream of IGHG1 in cultured prostate cancer cells. Inhibition of IGHG1 restrained the tumor growth in nude mice and inactivated MEK/ERK/c-Myc pathway both in vitro and in vivo. These findings suggest that IGHG1 play a crucial role during the development of prostate cancer and inhibition of IGHG1 may be a potential therapy in the treatment of PCa.

Reduced hepcidin level features osteoporosis.

Osteoporosis (OP) is a common serious skeletal disorder marked by increased risk of bone fracture due to fragility. OP has been taken to be a disease linked with abnormal calcium metabolism that alone is obviously insufficient to explain the development of OP. Iron overload has been associated with the development of OP and increasing studies have suggested the association. However, direct evidence for this has not been clinically established. To this end, using the Roche biochemical autoanalyzer, we detected the concentration of iron, soluble transferrin receptor 2 (TFR2), and hepcidin, a key peptide regulating iron homeostasis, in the sera from patients with OP. It was shown that the iron and TFR2 concentration was markedly higher than that of healthy control; whereas the concentration of hepcidin was markedly lower than that in control. In addition, to pilot explore the underlying mechanism by which hepcidin was downregulated, we present that hepcidin can directly interact with TFR2 using immunoprecipitation. The present study first established the direct biochemical evidence for the involvement of hepcidin in the pathogenesis of OP, indicating that the upregulation of hepcidin could be used as a novel alternative therapeutic strategy in the management of OP.

URG11 Regulates Prostate Cancer Cell Proliferation, Migration, and Invasion.

Upregulated gene 11 (URG11), a new gene upregulated by hepatitis B virus X protein, is involved in the development and progression of several tumors, including liver, stomach, lung, and colon cancers. However, the role of URG11 in prostate cancer remains yet to be elucidated. By determined expression in human prostate cancer tissues, URG11 was found significantly upregulated and positively correlated with the severity of prostate cancer, compared with that in benign prostatic hyperplasia tissues. Further, the mRNA and protein levels of URG11 were significantly upregulated in human prostate cancer cell lines (DU145, PC3, and LNCaP), compared with human prostate epithelial cell line (RWPE-1). Moreover, by the application of siRNA against URG11, the proliferation, migration, and invasion of prostate cancer cells were markedly inhibited. Genetic knockdown of URG11 also induced cell cycle arrest at G1/S phase, induced apoptosis, and decreased the expression level of ß-catenin in prostate cancer cells. Overexpression of URG11 promoted the expression of ß-catenin, the growth, the migration, and invasion ability of prostate cancer cells. Taken together, this study reveals that URG11 is critical for the proliferation, migration, and invasion in prostate cancer cells, providing the evidence of URG11 to be a novel potential therapeutic target of prostate cancer.

QoS Differential Scheduling in Cognitive-Radio-Based Smart Grid Networks: An Adaptive Dynamic Programming Approach.

As the next-generation power grid, smart grid will be integrated with a variety of novel communication technologies to support the explosive data traffic and the diverse requirements of quality of service (QoS). Cognitive radio (CR), which has the favorable ability to improve the spectrum utilization, provides an efficient and reliable solution for smart grid communications networks. In this paper, we study the QoS differential scheduling problem in the CR-based smart grid communications networks. The scheduler is responsible for managing the spectrum resources and arranging the data transmissions of smart grid users (SGUs). To guarantee the differential QoS, the SGUs are assigned to have different priorities according to their roles and their current situations in the smart grid. Based on the QoS-aware priority policy, the scheduler adjusts the channels allocation to minimize the transmission delay of SGUs. The entire transmission scheduling problem is formulated as a semi-Markov decision process and solved by the methodology of adaptive dynamic programming. A heuristic dynamic programming (HDP) architecture is established for the scheduling problem. By the online network training, the HDP can learn from the activities of primary users and SGUs, and adjust the scheduling decision to achieve the purpose of transmission delay minimization. Simulation results illustrate that the proposed priority policy ensures the low transmission delay of high priority SGUs. In addition, the emergency data transmission delay is also reduced to a significantly low level, guaranteeing the differential QoS in smart grid.

Fair Energy Scheduling for Vehicle-to-Grid Networks Using Adaptive Dynamic Programming.

Research on the smart grid is being given enormous supports worldwide due to its great significance in solving environmental and energy crises. Electric vehicles (EVs), which are powered by clean energy, are adopted increasingly year by year. It is predictable that the huge charge load caused by high EV penetration will have a considerable impact on the reliability of the smart grid. Therefore, fair energy scheduling for EV charge and discharge is proposed in this paper. By using the vehicle-to-grid technology, the scheduler controls the electricity loads of EVs considering fairness in the residential distribution network. We propose contribution-based fairness, in which EVs with high contributions have high priorities to obtain charge energy. The contribution value is defined by both the charge/discharge energy and the timing of the action. EVs can achieve higher contribution values when discharging during the load peak hours. However, charging during this time will decrease the contribution values seriously. We formulate the fair energy scheduling problem as an infinite-horizon Markov decision process. The methodology of adaptive dynamic programming is employed to maximize the long-term fairness by processing online network training. The numerical results illustrate that the proposed EV energy scheduling is able to mitigate and flatten the peak load in the distribution network. Furthermore, contribution-based fairness achieves a fast recovery of EV batteries that have deeply discharged and guarantee fairness in the full charge time of all EVs.

Inhibition of prostate cancer growth by solanine requires the suppression of cell cycle proteins and the activation of ROS/P38 signaling pathway.

Solanine, a naturally steroidal glycoalkaloid in nightshade (Solanum nigrum Linn.), can inhibit proliferation and induce apoptosis of tumor cells. However, the mechanism of solanine-suppressing prostate cancer cell growth remains to be elucidated. This study investigates the inhibition mechanism of solanine on cancer development in vivo and in cultured human prostate cancer cell DU145 in vitro. Results show that solanine injection significantly suppresses the tumor cell growth in xenograft athymic nude mice. Solanine regulates the protein levels of cell cycle proteins, including Cyclin D1, Cyclin E1, CDK2, CDK4, CDK6, and P21 in vivo and in vitro. Also, in cultured DU145 cell, solanine significantly inhibits cell growth. Moreover, the administration of NAC, an active oxygen scavenger, markedly reduces solanine-induced cell death. Blockade of P38 MAPK kinase cannot suppress reactive oxygen species (ROS), but can suppress solanine-induced cell apoptosis. Also, inhibition of ROS by NAC inactivates P38 pathway. Taken together, the data suggest that inhibition of prostate cancer growth by solanine may be through blocking the expression of cell cycle proteins and inducing apoptosis via ROS and activation of P38 pathway. These findings indicate an attractive therapeutic potential of solanine for suppression of prostate cancer.