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Following on our initial discovery of S-CN-DABOs as non-nucleoside reverse transcriptase inhibitors (NNRTIs), a series of novel S-N

Effects of three compound growth regulators formulated with hypersensitivity protein, spermidine, salicylic acid and DA-6 (diethyl aminoethanol hexanoate) were tested on Xinjiang Jun Jujube. The doses of compound growth regulators were named as A (Hypersensitivity protein + spermidine + salicylic acid at the rate of 30 mg/L, 0.1 mmol/L and 0.25 mmol/L, respectively), B (Hypersensitive protein + spermidine + DA-6 at the rate of 30 mg/L, 0.1 mmol/L and 30 mg/L, respectively) and C (Spermidine + salicylic acid + DA-6 at the rate of 0.1 mmol/L, 0.25 mmol/L and 30 mg/L, respectively) versus a control group CK (contained only water). Fruit anatomical structures were compared after spraying. The results indicated that after spraying, the thickness of the upper and lower epidermal cells and the stratum corneum were increased. However, the upper epidermal stratum corneum became significantly thicker than the lower epidermis. Spraying with A improved the thickness of upper and lower epidermal cells, stratum corneum, the central vein and mesophyll. The cumulative effects of all these changes in leaf and fruit anatomical structures provided the resistance of the experimental fruit plant to stress. While the B and C regulators had inhibitory effects. So, the results obtained after spraying A category were beneficial to improve the stress resistance of the fruits. The length and cell area of pericarp and sarcocarp cells in the treatment groups were not changed significantly. But the length, number of sarcocarp cells and number of gaps were lower than those in the CK. This study can provide new measures for improving plant resistance in jujube production.

BACKGROUND Ovarian cancer (OC) is one of the most malignant gynecological cancers. Platelets play a profound role in cancer growth and metastasis. Platelet distribution width (PDW) is an indicator of platelet activation and is altered in malignancies. However, the prognostic value of PDW in OC remains unclear. This present study aimed to investigate the predictive significance of PDW in OC. METHODS 221 OC patients, between January 2013 and December 2013, were included in this study. The correlations between PDW and clinicopathological features were analyzed. Kaplan-Meier method and Cox regression were used to evaluate the prognostic impact of PDW. RESULTS Of the 221 patients, increased PDW levels were observed in 163 (73.6%) patients. Kaplan-Meier analysis revealed that higher PDW levels were associated with poor progression-free survival and overall survival (both p< 0.001). Cox-regression analysis confirmed the independent predictive value of PDW on overall survival (HR = 2.820, 95% CI = 1.776-4.476, p< 0.001). CONCLUSION Higher PDW levels predict poor prognosis in patients with OC. Elevated PDW may be a novel target for therapy.

Excessive exposure to light at night (LAN) has become a serious public health concern. However, little is known about the impact of indoor LAN exposure on blood pressure, particularly among young adults. We aimed to investigate the effects of bedroom individual-level LAN exposure in real-world environment on blood pressure and hypertension among vulnerable young adults, and to evaluate the possible buffering effect of physical activity. In this cross-sectional study, a total of 400 healthy young adults aged 16-22 years were included. Bedroom LAN exposure was recorded at 1-min intervals for two consecutive nights using a TES-1339 R illuminance meter. Blood pressure was measured three times (8-11 a.m. in the physical examination day) in the seated position using an Omron HEM-7121 digital sphygmomanometer. A wrist-worn triaxial accelerometer (ActiGraph GT3X-BT) was used to assess physical activity for seven consecutive days. Each 1 lx increase of bedroom LAN intensity was associated with 0.55 mmHg-increase in SBP (95% CI: 0.15, 0.95), 0.30 mmHg-increase in DBP (95% CI: 0.06, 0.54), and 0.38 mmHg-increase in MAP (95% CI: 0.12, 0.65). Higher levels of LAN exposure were associated with increased risk of hypertension (LAN ≥ 3lx vs. LAN3lx: OR = 3.30, 95%CI = 1.19-9.19; LAN ≥ 5lx vs. LAN5lx: OR = 3.87, 95%CI = 1.37-10.98). However, these detrimental effects of bedroom LAN exposure on blood pressure and hypertension were not observed among young adults with high MVPA (≥2 h/day) level. MVPA can alleviate negative effects of bedroom LAN exposure on blood pressure and hypertension. Maintaining bedroom settings darkness at night may be an important strategy for reducing the risk of hypertension. Furthermore, for individuals living with high levels of indoor LAN exposure, regular physical activity may be a good option for preventing cardiovascular disease and hypertension.

We report two-dimensional correlation spectroscopy (2D-COS) analyses of the Raman spectra of NiO nanoparticles over a temperature range from 100 to 300 K. 2D-Raman correlation spectra suggest strong correlation of the phonon spectral intensity variation with the magnetic ordering in NiO nanoparticles. It is revealed that the antiferromagnetic ordering affects the TO phonon anisotropy in NiO nanoparticles. We elucidate the complex spectral features of two-magnon (2 M) bands by performing appropriate 2D-COS model simulations. Significant spin-phonon coupling in NiO nanoparticles is supported by our results. High energy magnon-magnon interaction tails are also found to be involved in the spin-phonon coupling. 2D-COS analyses provide rich information regarding the nature of the phonon and magnon excitations of NiO nanoparticles.

NAC(NAM/ATAF/CUC) protein plays an important role in plant growth and development, secondary cell wall formation and stress response. In this study, based on the sequencing data of Angelica dahurica, the NAC family was systematically analyzed using bioinformatics methods and its expression pattern was analyzed. Studies showed that 75 candidate genes had been selected from the NAC transcription factor family of A. dahurica, with the protein size of 148-641, all of which were unstable hydrophilic proteins. Most NAC proteins were localized in the nucleus, and had complete NAC domain. Phylogenetic analysis of NAC family proteins of A.dahurica and Arabidopsis thaliana showed that among the 17 subfamilies, NAC members were unevenly distributed in each subfamily, indicating that the evolution of species is developing in multiple directions. Among them, ANAC063 subfamily contained no NAC sequence of A. dahurica, which might be due to the functional evolution of the species. Analysis of protein transmembrane structure and signal peptide showed that NAC transcription factor could carry out transmembrane transportation, but its signal peptide function had not been found. Expression analysis showed that most transcription factors responded to abiotic stress and hormones to varying degrees, and the effects of hormones were obvious, especially ABA and IAA. In different organs of A. dahurica, most members of the NAC family had higher expression in root phloem, followed by root xylem. This study lays a foundation for further research on the function of A. dahurica NAC transcription factor and for solving the biological problems of A. dahurica.

Aims. Acute kidney injury (AKI) can lead to chronic kidney disease (CKD), and macrophages play a key role in this process. The aim of this study was to discover the role of IκB kinase α (IKKα) in macrophages in the process of AKI-to-CKD transition. Main Methods. We crossed lyz2-Cre mice with IKKα-floxed mice to generate mice with IKKα ablation in macrophages (Mac IKKα-/-). A mouse renal ischemia/reperfusion injury (IRI) model was induced by clamping the renal artery for 45 minutes. Treated mice were evaluated for blood biochemistry, tissue histopathology, and fibrosis markers. Macrophages were isolated from the peritoneal cavity for coculturing with tubular epithelial cells (TECs) and flow cytometry analysis. Key Findings. We found that fibrosis and kidney function loss after IRI were significantly alleviated in Mac IKKα-/- mice compared with wild-type (WT) mice. The expression of fibrosis markers and the infiltration of M2 macrophages were decreased in the kidneys of Mac IKKα-/- mice after IRI. The in vitro experiment showed that the IRI TECs cocultured with IKKα-/- macrophages (KO MΦs) downregulated the fibrosis markers accompanied by a downregulation of Wnt/β-catenin signaling. Significance. These data support the hypothesis that IKKα is involved in mediating macrophage polarization and increasing the expression of fibrosis-promoting inflammatory factors in macrophages. Therefore, knockdown of IKKα in macrophages may be a potential method that can be used to alleviate the AKI-to-CKD transition after IRI.

BACKGROUND: Platelets play a key role in tumor progression and metastasis. C-type lectin-like receptor 2 (CLEC-2) is the receptor expressed on platelets and the marker of platelet activation. OBJECTIVE: This study aims to determine whether soluble CLEC-2 levels differ between patients with benign colorectal polyps and those with colorectal cancer (CRC). METHODS: We measured plasma soluble CLEC-2 by enzyme-linked immunosorbent assay in 150 patients with colorectal polyps, 150 CRC patients without metastasis, 150 CRC liver metastasis, and 150 control subjects. RESULTS: The CRC patients had higher soluble CLEC-2 levels than patients with colorectal polyps (p< 0.001). Moreover, CRC patients with liver metastases displayed higher CLEC-2 levels than those in CRC patients without metastases (p< 0.001). In the CRC patients, CLEC-2 levels were correlated with lymph node metastasis and advanced stage. In the patients with polyps, there was a significant difference in CLEC-2 levels among patients with hyperplastic polyp, sessile serrated adenoma, and traditional serrated adenoma (p< 0.001). The ROC curve analysis revealed CLEC-2 had an optimal sensitivity of 77.3% and specificity of 94.6% for the screening of CRC, and sensitivity of 71.0% and specificity of 76.7% for the differential diagnosis of colorectal polyps and CRC. CONCLUSIONS: CRC patients have higher CLEC-2 levels than patients with colorectal polyps and healthy controls. Moreover, there is a significant difference in CLEC-2 levels among polyp subtypes. Further research is warranted.

Background The microsatellite instability (MSI) in colorectal cancer (CRC) has a more favorable clinical outcome and is characterized by highly upregulated expression of various immunological checkpoints than microsatellite stable (MSS) tumors. Apoptosis inhibitor of macrophage (AIM) is a circulating protein and circulates throughout the body to remove cellular debris. The aim of this study was to evaluate the association between MSI status and AIM levels in CRC patients. Methods In this study, we evaluated the levels of AIM by Enzyme Linked Immuno-Sorbent Assay (ELISA) in serum of 430 CRC patients. All patients’ clinical and laboratory characteristics at initial diagnosis were collected. The relationship between AIM levels and MSI status was examined. Results 64 patients (14.9%) were identified as having MSI-H (high-frequency MSI) and 366 casess (85.1%) having MSS. Patients with an MSI-H phenotype had lower AIM levels compared with MSS patients. Moreover, AIM levels were correlated with histological type and MSI status. Logistic regression analysis revealed that decreased AIM levels were independently associated with MSI-H phenotype after adjusting confounding factors. Conclusion Reduced AIM levels are associated with MSI-H subtyping of CRC. Further research on the involvement of AIM in MSI-H CRC is needed.

Background: Postoperative sepsis in cancer patients becomes a major problem at present, but the efficiently prognostic biomarkers are limited. The present study was sought to evaluate the prognostic relevance of absolute lymphocyte counts (ALCs) in cancer patients with postoperative sepsis, which might help patients to get early treatment and improve their prognosis.Methods: Retrospective study was conducted under 368 cancer patients with postoperative sepsis who were admitted in ICU of two Chinese tertiary care hospitals from January 1, 2016 to December 31, 2017. ALCs were daily collected during the first week after being enrolled in the study. The primary outcomes of the study included 28-day and 90-day mortalities, while the secondary outcomes were hospital and ICU length of stay.Results: The absolute lymphocyte counts on day 3 were reduced in the survivors comparing with those in non-survivors. Statistically, the significantly decreased 28-day and 90-day survival rates were detected in the patients with severe and moderate lymphopenia, compared to those with no lymphopenia. These present results were consistently found and evidently confirmed in the two different hospitals.Conclusions: In accordance with the day-4 lymphopenia prediction of sepsis diagnosis, this present study revealed that lymphopenia on the day 3 after the diagnosis of sepsis was able to predict the early mortality in postoperative cancer patients. Earlier monitoring and management of lymphopenia may be needed for cancer patients with postoperative sepsis.

// Chang-Cheng Zhou 1,* , Wen-Tao Yao 1,* , Yu-Zheng Ge 1 , Lu-Wei Xu 1 , Ran Wu 1 , Xiao-Fei Gao 2 , Kai-Wei Song 1 , Xiao-Min Jiang 2 , Min Wang 1 , Wen-Juan Huang 3 , Yun-Peng Zhu 1 , Liang-Peng Li 4 , Liu-Hua Zhou 1 , Zhong-Le Xu 1,5 , Sheng-Li Zhang 1 , Jia-Geng Zhu 1 , Wen-Cheng Li 1 and Rui-Peng Jia 1 1 Department of Urology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China 2 Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China 3 Department of Nephrology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China 4 Department of Cardiothoracic Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, China 5 Department of Radiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China * These authors have contributed equally to this work Correspondence to: Rui-Peng Jia, email: // Yu-Zheng Ge, email: // Keywords : remote ischemic conditioning, contrast-induced acute kidney injury, randomized controlled trial, meta-analysis, trial sequential analysis Received : December 21, 2016 Accepted : May 12, 2017 Published : May 23, 2017 Abstract Objective: We conducted this meta-analysis to examine the effect of remote ischemic conditioning (RIC) on contrast-induced acute kidney injury (CI-AKI) in patients undergoing intravascular contrast administrationon. Methods: Pubmed, Embase, and Cochrane Library were comprehensively searched to identify all eligible studies by 15th March, 2017. Risk ratio (RR) and weighted mean difference with the corresponding 95% confidence intervals (CI) were used to examine the treatment effect. The heterogeneity and statistical significance were assessed with Q-test and Z-test, respectively. Results: A total of 16 RCTs including 2175 patients were eventually analyzed. Compared with the control group, RIC could significantly decrease the incidence of CI-AKI (RR=0.58; 95% CI: 0.46, 0.74; P < 0.001), which was further confirmed by the trial sequential analysis. Subgroup analyses showed that remote ischemic preconditioning (RIPrC) and remote ischemic postconditioning (RIPoC) were both obviously effective, and perioperative hydration might enhance the efficiency of RIC. RIC also significantly reduced the major adverse cardiovascular events within six months. Conclusion: RIC, whether RIPrC or RIPoC, could effectively exert renoprotective role in intravascular contrast administration and reduce the incidence of relevant adverse events.

Multiple sclerosis (MS) is a complex neurodegenerative disease affecting the central nervous system (CNS). The onset of MS has been typically observed in individuals aged from 20 to 40-years, with the female to male ratio of 1:2. MS appears as abrupt onset of focal sensory disturbances that is accompanied by unilateral painless damage of vision, double vision, limb weakness, unsteadiness of gait, and bowel or bladder symptoms. Whereas the exact etiology of the disease is unknown, observational research has suggested genetic and environment influences through an underlined pathophysiology widely believed to be autoimmune in nature. Indeed, plaque of demyelination inside of the CNS with relative conservation of axons remains the clinical symptoms of MS. However, considerable advances in understanding the pathology have contributed to an early diagnosis, particularly the exact neuroanatomical setting of plaques. Accordingly, magnetic resonance imaging has been considered as the primarily adjunctive modality for the constant detection of abnormal white matter. In addition, the analysis of cerebrospinal fluid contents has also been of interest for the diagnosis to discriminate other affections such infection or vasculitis. These resulted in a broad variety of therapies that considerably control the activity and change the course and prognosis of the disease. In the present review, we evaluate the current state of knowledge on MS with emphasis on the pathology itself, the diagnosis and common therapeutical approaches accurately used.

Neuropathy is associated with side effects of frontline chemotherapeutics, which is a prominent therapy utilized in prevalent cancers. Peripheral neuropathy negatively impacts quality of life in cancer patients and survivors. It also affects the dose plan of the treatment, thereby limiting the efficacy of the treatment. We searched the electronic database PubMed for pre-clinically and clinically controlled trials reporting neuropathy of adverse effects, a result of chemotherapy in cancer patients. It was observed clearly that many reports provide clinical evidence to rapidly growing neuropathy cases of cancer patients. Furthermore, the reports clearly showed enhanced cold pain, sensorimotor deficits, sensory innervation of the skin and sensorimotor deficits in the patients with cancer who underwent treatment mainly with the chemotherapeutic approach. The present review highlighted the current view of peripheral neuropathy during chemotherapeutic approaches.

Central nervous system-based cancers have a much higher mortality rate with the 2016 estimates at 6.4 for incidence and 4.3 for deaths per 100,000 individuals. Grade IV astrocytomas, known as glioblastomas are highly aggressive and show a high proliferation index, diffused infiltration, angiogenesis, microvascular proliferation and pleomorphic vessels, resistance to apoptosis, and pseudopalisading necrosis. Extensive hypoxic regions in glioblastomas contribute to the highly malignant phenotype of these tumors. Hypoxic regions of glioblastoma exacerbate the prognosis and clinical outcomes of the patients as hypoxic tumor cells are resistant to chemo- and radiation therapy and are also protected by the malfunctional vasculature that developed due to hypoxia. Predominantly, hypoxia-inducible factor-1α, vascular endothelial growth factor (VEGF)/VEGF receptor, transforming growth factor-β, epidermal growth factor receptor and PI3 kinase/Akt signaling systems are involved in tumor progression and growth. Glioblastomas are predominantly glycolytic and hypoxia-induced factors are useful in the metabolic reprogramming of these tumors. Abnormal vessel formation is crucial in generating pseudopalisading necrosis regions that protect cancer stem cells residing in that region from therapeutic agents and this facilitates the cancer stem cell niche to expand and contribute to cell proliferation and tumor growth. Therapeutic approaches that target hypoxia-induced factors, such as use of the monoclonal antibody against VEGF, bevacizumab, have been useful only in stabilizing the disease but failed to increase overall survival. Hypoxia-activated TH-302, a nitroimidazole prodrug of cytotoxin bromo-isophosphoramide mustard, appears to be more attractive due to its better beneficial effects in glioblastoma patients. A better understanding of the hypoxia-mediated protection of glioblastoma cells is required for developing more effective therapeutics.

Alzheimer's diseases (AD) is the most common type of dementia and a neurodegenerative disease that occurs when the nerve cells in the brain die. The cause and treatment of AD remain unknown. However, AD is a disease that affects the brain, an organ that controls behavior. Accordingly, anything that can interact with the brain may affect this organ positively or negatively, thereby protecting or encouraging AD. In this regard, modern life encompasses microwaves for all issues including industrial, communications, medical and domestic tenders, and among all applications, the cell phone wave, which directly exposes the brain, continues to be the most used. Evidence suggests that microwaves may produce various biological effects on the central nervous system (CNS) and many arguments relay the possibility that microwaves may be involved in the pathophysiology of CNS disease, including AD. By contrast, previous studies have reported some beneficial cognitive effects and that microwaves may protect against cognitive impairment in AD. However, although many of the beneficial effects of microwaves are derived from animal models, but can easily be extrapolated to humans, whether microwaves cause AD is an important issue that is to be addressed in the current review.

Pain and anxiety are the most common neurological responses to many harmful or noxious stimuli and their management clinically is often challenging. Many of the frequently used morphine-based drugs, non-steroid anti-inflammatory drugs and acetaminophen, while efficient for treating pain, lead to patients suffering from several unwanted side effects. Melatonin, produced from the pineal body is a hormone of darkness, is involved in the control of circadian rhythms, and exerts a number of pharmacological effects. Melatonin mediates its actions through MT1/MT2 melatonin receptors on the cell membrane and also through RZR/ROR nuclear orphan receptors. Chronic pain syndromes are often associated with the desynchronization of circadian and biological rhythms, which also cause disturbances in the sleep-wake cycle. Melatonin-mediated analgesic effects seem to involve β-endorphins, GABA receptor, opioid receptors and the nitric oxide-arginine pathway. The effectiveness of melatonin as an analgesic and anxiolytic agent has been demonstrated in various animal models of pain and this led to the use of melatonin clinically in different pathological conditions and also in patients undergoing surgery. Melatonin was found to be effective in many of these cases as an anxiolytic and analgesic agent, indicating its clinical application.

Depression and pain co-exist in almost 80% of patients and are associated with impaired health-related quality of life, often contributing to high mortality. However, the majority of patients who suffer from the comorbid depression and pain are not responsive to pharmacological treatments that address either pain or depression, making this comorbidity disorder a heavy burden on patients and society. In ancient times, this depression-pain comorbidity was treated using extracts of the Cannabis sativa plant, known now as marijuana and the mode of action of Δ9-tetrahydrocannabinol, the active cannabinoid ingredient of marijuana, has only recently become known, with the identification of cannabinoid receptor type 1 (CB1) and CB2. Subsequent investigations led to the identification of endocannabinoids, anandamide and 2-arachidonoylglycerol, which exert cannabinomimetic effects through the CB1 and CB2 receptors, which are located on presynaptic membranes in the central nervous system and in peripheral tissues, respectively. These endocannabinoids are produced from membrane lipids and are lipohilic molecules that are synthesized on demand and are eliminated rapidly after their usage by hydrolyzing enzymes. Clinical studies revealed altered endocannabinoid signaling in patients with chronic pain. Considerable evidence suggested the involvement of the endocannabinoid system in eliciting potent effects on neurotransmission, neuroendocrine, and inflammatory processes, which are known to be deranged in depression and chronic pain. Several synthetic cannabinomimetic drugs are being developed to treat pain and depression. However, the precise mode of action of endocannabinoids on different targets in the body and whether their effects on pain and depression follow the same or different pathways, remains to be determined.

Alzheimer's disease (AD) is a neurodegenerative disease characterized by dense deposition of amyloid-β (Aβ) protein in the brain, failure of the memory and dementia. At present, there is no cure for AD and current treatments only provide a temporary reduction of symptoms. Thus, there is a need for effective preventive/curative strategic approaches. Accordingly, epidemiological studies have reported a reduction in the prevalence of AD in individuals ingesting low amounts of alcohol, while a moderate consumption of ethanol may protect against Aβ. These data are conflicting with other observations that assigned detrimental effects of heavy alcohol use on brain function, which are apparently similar to those observed in AD. These discrepancies questioned whether or not alcohol is a protective agent against the development of AD, whether the probable protective effects are influenced by the quantity and/or frequency of drinking. These issues are addressed in this review with the aim to suggest the real risk of alcohol for developing or preventing AD.

Alzheimer's disease (AD) is the most common cause of disability in individuals aged >65 years worldwide. AD is characterized by the abnormal deposition of amyloid β (Aβ) peptide, and intracellular accumulation of neurofibrillary tangles of hyperphosphorylated τ protein and dementia. The neurotoxic oligomer Aβ peptide, which is the neuropathological diagnostic criterion of the disease, together with τ protein, are mediators of the neurodegeneration that is among the main causative factors. However, these phenomena are mainly initiated and enhanced by oxidative stress, a process referring to an imbalance between antioxidants and oxidants in favour of oxidants. This imbalance can occur as a result of increased free radicals or a decrease in antioxidant defense, free radicals being a species that contains one or more unpaired electrons in its outer shell. The major source of potent free radicals is the reduction of molecular oxygen in water, that initially yields the superoxide radical, which produces hydrogen peroxide by the addition of an electron. The reduction of hydrogen peroxide produces highly reactive hydroxyl radicals, termed reactive oxygen species (ROS) that can react with lipids, proteins, nucleic acids, and other molecules and may also alter their structures and functions. Thus, tissues and organs, particularly the brain, a vulnerable organ, are affected by ROS due to its composition. The brain is largely composed of easily oxidizable lipids while featuring a high oxygen consumption rate. The current review examined the role of oxidative stress in AD.

The benefits of physical exercise on the brain and general wellness are well recognised, but not particularly well known to the general public. Understanding the importance of integrating active behavior for overall health is crucial at any age and particularly for the elderly who are at risk of developing Alzheimer's disease (AD), a disease mainly affecting individuals aged >65 years. AD is a neurodegenerative disease characterized by extracellular senile plaques of amyloid-β, intracellular neurofibrillary tangles of the protein tau, brain atrophy and dementia. The beneficial effects of physical exercise have been observed on the maintenance of brain size and efficiency for the prevention of AD risks, such as obesity, hypertension and stroke. These effects are extended to individuals with, or at risk of dementia and other age-related neurodegenerative disorders. Accordingly, although extensive studies are required to fully understand the mechanisms by which physical exercise procures beneficial effects, data suggest the relevance of integrating physical exercise in the prevention and/or cure of AD, disease whose incidence is predicted to increase in the future. Such an increase, may pose medical, social and economical challenges for populations and the health care system worldwide. In the present review we assess the positive aspects of physical exercise with regard to prevention and cure of AD.

Neurodegeneration is a phenomenon that occurs in the central nervous system through the hallmarks associating the loss of neuronal structure and function. Neurodegeneration is observed after viral insult and mostly in various so-called 'neurodegenerative diseases', generally observed in the elderly, such as Alzheimer's disease, multiple sclerosis, Parkinson's disease and amyotrophic lateral sclerosis that negatively affect mental and physical functioning. Causative agents of neurodegeneration have yet to be identified. However, recent data have identified the inflammatory process as being closely linked with multiple neurodegenerative pathways, which are associated with depression, a consequence of neurodegenerative disease. Accordingly, pro‑inflammatory cytokines are important in the pathophysiology of depression and dementia. These data suggest that the role of neuroinflammation in neurodegeneration must be fully elucidated, since pro‑inflammatory agents, which are the causative effects of neuroinflammation, occur widely, particularly in the elderly in whom inflammatory mechanisms are linked to the pathogenesis of functional and mental impairments. In this review, we investigated the role played by the inflammatory process in neurodegenerative diseases.

As the incomparable advantages, permanent magnetic synchronous motor (PMSM) has been used widely in servo system, numerical control machine. The paper introduces an EKF (extended Kalman filter)-based sensorless vector control system of permanent magnet synchronous motor. The rotorfield-oriented control strategy based on id=0 is selected. After expounding the principle of EKF and recursion algorithm, it derives the Kalman state equation in PMSM rest coordinate, makes a discretization processing, and constructs vector control system based on EKF estimator. The simulation model of vector control system of PMSM with MATLAB/Simulink is built and on this basis, it observes the position and speed of the motor rotor by the use of the EKF estimator. Simulation results demonstrate the EKF estimator can accurate estimates of the PMSM rotor position and speed.

Glioblastomas (GBM) are the tumors originating from the star shaped supportive cells in brain known as astrocytes. These tumors are highly cancerous as they have the ability to proliferate very quickly. New therapeutic strategies are being developed worldwide to fight against deadly GBM, which has median survival time of just 14 months. Proteasome inhibition is an upcoming strategy for GBM. Proteasome inhibition has shown promising results in cancers such as myeloma. However, in the recent past this form of therapy has also shown positive results in brain tumors in the form of elevated apoptosis. We searched the electronic database PubMed for pre-clinical as well as clinical controlled trials reporting importance of proteasome inhibitors during GBM. It was observed clearly that this approach is evolving and has been observed to be promising therapeutic avenue against GBM. Thus, the present review aims to enlighten the present views on use of proteasome inhibition strategy in the case of GBM.

Background: Renal ischemia-reperfusion (IR) injury is a frequent cause of acute kidney injury, which results in high morbidity and mortality. Inflammation is an important factor that is involved in kidney repair after renal IR injury. IL-10 is a potent anti-inflammatory cytokine that inhibits inflammatory pathways, but the role of IL-10 in repairing renal IR injury is not known. Here, we investigated the role of IL-10 in kidney repair after renal IR injury. Methods: We used an IL-10-/- mouse model and examined the serologic and histomorphology of kidney after IR injury. We also measured ki67, TNF-α, IL-6, and macrophages with immunohistochemistry or Western blotting. Results: There was a greater increase in serum creatinine in IL-10-/- mice than in wild-type (WT) mice. And compared with WT mice, IL-10-/- mice had increased histologic renal injury and decreased proliferation. Moreover, the expression of TNF-α, IL-6 and macrophages was clearly increased in IL-10-/- mice compared with the WT mice. Conclusion: These data reveal an important role for IL-10 in the improvement of renal IR injury, acting through suppression of inflammatory mediators, and that IL-10 would be a crucial target for the treatment of IR injury.

With the social development and technological progress, automatic detecting and recording system of cars for violation of traffic signal, as an important part of intelligent transportation systems, is entering the stage of full implementation. For the dependence on external systems, inconvenience of construction and maintenance, and poor flexibility of the traditional automatic detecting and recording system based on magnetic induction coil, the introduction of video-based detecting and recording system of cars for violation of traffic signal is present. In the video detection, the detection of illegal vehicles is completed by virtual coil detection algorithm based on regional changes. This system is simple, requiring only the camera installed in intersection to capture video, and junctions control terminal. At the same time, its process is easy to implement, and has a huge cost-effective.

This paper describes robot soccer, it studies the organizational model of the soccer robot, and centralized decision-making system is analyzed. With the deep research of the three-layered hierarchical decision-making model on the basis of decision-making, management and executive, the paper achieves the basic control of the robot.

In this paper, a real-time monitoring system of all-weather fatigue driving which is based on DSP (TMS320DM643) is introduced. The method of regional area combining the skin color model, can quickly locate the drivers face. The paper also presents the judgment of eye state, the fetch of fatigue parameters (PERCLOS, ECT and EBF), and the general method for the determination of fatigue degree. The system has very strong using value, and practical significance.

A double mutant with streaked leaf and abnormal floret was found and temporarily named streaked leaf and floral organ number mutant (st-fon). For this mutant, besides white streak appeared on culm, leaves and panicles, the number of floral organs increased and florets cracked. The extreme phenotype was that several small florets grew from one floret or branch rachis in small florets extended and developed into panicles. By using transmission electron microscope to observe the ultrastructure of white histocytes of leaves at the seedling stage, the white tissues which showed abnormal plastids, lamellas and thylakoids could not develop into normal chloroplast, and the development of chloroplast was blocked at the early growth stage of plastid. Scanning electron microscope and paraffin section were also used to observe the development of floral organs, and the results indicated that the development of floral meristem was out of order and unlimited, whereas in the twisty leaves, vascular bundle sheath cells grew excessively, or some bubbly cells increased. Genetic analyses carried out by means of cross and backcross with four normal-leaf-color materials revealed that the mutant is of cytoplasm inheritance.

采用溶剂热法和热分解法分别制备纳/微米的β-NaYF 4 :20%Yb 3+ ,2%Er 3+ 晶体. 根据两种不同粒径颗粒的TG-DTA测试分析, 对其进行不同温度的热处理。通过XRD、SEM、FT-IR以及PL等手段研究不同热处理温度对两种粒径的颗粒的尺寸、形貌以及上转换发光性能的影响. 研究结果表明, 随着热处理温度的升高, 纳/微米颗粒的发光性能主要呈现出先升高后下降的趋势。与未作热处理样品对比发现, 适当的热处理(580℃)可以提高纳米颗粒的发光强度, 却不利于改善微米颗粒发光性能。分析认为, 结晶质量的提高、缺陷浓度的降低以及有机配体的去除, 导致了纳/微米颗粒的发光性能的逐步提高。而过高处理温度(>580℃)引起的相转变(β→α)和表面Na 2 CO 3 的生成又大大降低了稀土离子的发光效率。热处理过程中颗粒之间的不同团聚程度是造成纳/微米颗粒发光性能差异变化的主要原因。

Recent genetic discoveries have dramatically changed our understanding of two major neurodegenerative conditions. Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are common, devastating diseases of the brain. For decades, ALS and FTD were classified as movement and cognitive disorders, respectively, due to their distinct clinical phenotypes. The recent identification of chromosome 9 open reading frame 72 (C9orf72) as the major gene causative of familial forms of ALS and FTD uncovered a new reality of a continuous FTD/ALS spectrum. The finding that up to 50% of all patients present some degree of ALS and FTD phenotypes supports this ALS/FTD continuum. Now >100 genes are known to contribute to ALS/FTD, with a few major contributors that are reviewed below. The low penetrance of C9orf72 mutations, its contribution to sporadic cases, and its combination with other genes support an oligogenic model where two or more genes contribute to disease risk, onset, progression and phenotype: from 'pure' ALS or FTD to combined ALS/FTD. These advances in the genetics of ALS/FTD will soon lead to a better mechanistic understanding of the pathobiology of the disease, which should result in the development of effective therapies in the near future.