Biomarkers of Oxidative Stress and Endogenous Antioxidants for Patients with Chronic Subjective Dizziness

As a neurotologic disorder of persistent non-vertiginous dizziness, chronic subjective dizziness (CSD) arises unsteadily by psychological and physiological imbalance. The CSD is hypersensitivity reaction due to exposure to complex motions visual stimuli. However, the pathophysiological features and mechanism of the CSD still remains unclearly. The present study was purposed to establish possible endogenous contributors of the CSD using serum samples from patients with the CSD. A total 199 participants were gathered and divided into two groups; healthy (n = 152, male for 61, and female for 91) and CSD (n = 47, male for 5, female for 42), respectively. Oxidative stress parameters such as, hydrogen peroxide and reactive substances were significantly elevated (p < 0.01 or p < 0.001), whereas endogenous antioxidant components including total glutathione contents, and activities of catalase and superoxide dismutase were significantly deteriorated in the CSD group (p < 0.01 or p < 0.001) as comparing to the healthy group, respectively. Serum levels of tumor necrosis factor -α and interferon-γ were significantly increased in the CSD participants (p < 0.001). Additionally, emotional stress related hormones including cortisol, adrenaline, and serotonin were abnormally observed in the serum levels of the CSD group (p < 0.01 or p < 0.001). Our results confirmed that oxidative stress and antioxidants are a critical contributor of pathophysiology of the CSD, and that is first explored to establish features of redox system in the CSD subjects compared to a healthy population

Little SUSY hierarchy in mixed modulus-anomaly mediation

Motivated by the KKLT string compactification involving a supersymmetry-breaking uplifting potential, we examine 4D effective supergravity with a generic form of uplifting potential, focusing on the possibility that the resulting mixed modulus-anomaly mediated soft terms realize the little hierarchy between the Higgs boson masses $m_H$ and the sparticle masses $m_{SUSY}$. It is noted that for some type of uplifting potential, the anomaly-mediated contribution to $m_H^2$ at $M_{GUT}$ can cancel the subsequent renormalization group evolution of $m_H^2$ down to TeV scale, thereby the model can naturally realize the little hierarchy $m_H^2\sim m_{SUSY}^2/8\pi^2$ which is desirable for the lightest Higgs boson mass to satisfy the experimental bound. In such models, the other Higgs mass parameters $\mu$ and $B$ can have the desirable size $\mu \sim B \sim m_H$ without severe fine-tuning of parameters, although the gravitino is much heavier than the Higgs boson. Those models for the little hierarchy avoid naturally the dangerous SUSY flavor and CP violations, and predict nearly degenerate low energy gaugino masses, pure Higgsino LSP, and also a specific relation between the stop and gaugino masses.Comment: revtex4, 16 page

A Novel Addressing Scheme for PMIPv6 Based Global IP-WSNs

IP based Wireless Sensor Networks (IP-WSNs) are being used in healthcare, home automation, industrial control and agricultural monitoring. In most of these applications global addressing of individual IP-WSN nodes and layer-three routing for mobility enabled IP-WSN with special attention to reliability, energy efficiency and end to end delay minimization are a few of the major issues to be addressed. Most of the routing protocols in WSN are based on layer-two approaches. For reliability and end to end communication enhancement the necessity of layer-three routing for IP-WSNs is generating significant attention among the research community, but due to the hurdle of maintaining routing state and other communication overhead, it was not possible to introduce a layer-three routing protocol for IP-WSNs. To address this issue we propose in this paper a global addressing scheme and layer-three based hierarchical routing protocol. The proposed addressing and routing approach focuses on all the above mentioned issues. Simulation results show that the proposed addressing and routing approach significantly enhances the reliability, energy efficiency and end to end delay minimization. We also present architecture, message formats and different routing scenarios in this paper

Tricuspid regurgitation: a hidden risk factor for atrial fibrillation related stroke?

Background and purposeTricuspid regurgitation (TR) is a common but overlooked valvular disease, and its association with the etiologic subtypes of ischemic stroke is unclear. We explored the relationship between TR and atrial fibrillation (AF) in patients with acute ischemic stroke.MethodsThis retrospective analysis of ongoing stroke registry assessed 6,886 consecutive acute ischemic stroke patients who underwent transthoracic echocardiography during their in-hospital care. Multivariable logistic regression models adjusted for age, sex, stroke characteristics, and echocardiographic indices were used to investigate the association between TR and total AF, and newly diagnosed AF during hospitalization and a 1-year follow-up period, respectively.ResultsTR was present in 877 (12.7%) patients (mild, 9.9%; moderate, 2.4%; severe, 0.5%). AF was identified in 24.1% (medical history, 11.1%; first detected in the emergency room, 6.6%; newly diagnosed after admission, 6.4%). TR was associated with AF [adjusted odds ratio (aOR) 4.87 (95% confidence interval (CI), 2.63–9.03)], compared with no/trivial TR. The association between TR and AF was consistent regardless of severity (aOR [95% CI], 4.57 [2.63–7.94] for mild and 7.05 [2.57–19.31] for moderate-to-severe TR) or subtype of TR (5.44 [2.91–10.14] for isolated and 3.81 [2.00–7.28] for non-isolated TR). Among the AF-naïve patients at admission, TR was associated with newly diagnosed AF during hospitalization and a 1-year follow-up period (aOR [95% CI], 2.68 [1.81–3.97]).ConclusionsTR is associated with AF in acute ischemic stroke patients regardless of severity and subtypes of TR. TR is also associated with newly diagnosed AF after stroke

Satellite Data-Based Phenological Evaluation of the Nationwide Reforestation of South Korea

Through the past 60 years, forests, now of various age classes, have been established in the southern part of the Korean Peninsula through nationwide efforts to reestablish forests since the Korean War (1950-53), during which more than 65% of the nation&apos;s forest was destroyed. Careful evaluation of long-term changes in vegetation growth after reforestation is one of the essential steps to ensuring sustainable forest management. This study investigated nationwide variations in vegetation phenology using satellite-based growing season estimates for 1982-2008. The start of the growing season calculated from the normalized difference vegetation index (NDVI) agrees reasonably with the ground-observed first flowering date both temporally (correlation coefficient, r = 0.54) and spatially (r = 0.64) at the 95% confidence level. Over the entire 27-year period, South Korea, on average, experienced a lengthening of the growing season of 4.5 days decade(-1), perhaps due to recent global warming. The lengthening of the growing season is attributed mostly to delays in the end of the growing season. The retrieved nationwide growing season data were used to compare the spatial variations in forest biomass carbon density with the time-averaged growing season length for 61 forests. Relatively higher forest biomass carbon density was observed over the regions having a longer growing season, especially for the regions dominated by young (&lt;30 year) forests. These results imply that a lengthening of the growing season related to the ongoing global warming may have positive impacts on carbon sequestration, an important aspect of large-scale forest management for sustainable development.open2

Roles of Arrest-Defective Protein 1225 and Hypoxia-Inducible Factor 1α in Tumor Growth and Metastasis

Background Vascular endothelial growth factor A (VEGFA), a critical mediator of tumor angiogenesis, is a well-characterized target of hypoxia-inducible factor 1 (HIF-1). Murine arrest-defective protein 1A (mARD1A225) acetylates HIF-1??, triggering its degradation, and thus may play a role in decreased expression of VEGFA.Methods We generated ApcMin/+/mARD1A225 transgenic mice and quantified growth of intestinal polyps. Human gastric MKN74 and murine melanoma B16F10 cells overexpressing mARD1A225 were injected into mice, and tumor growth and metastasis were measured. VEGFA expression and microvessel density in tumors were assessed using immunohistochemistry. To evaluate the role of mARD1A 225 acetylation of Lys532 in HIF-1??, we injected B16F10-mARD1A225 cell lines stably expressing mutant HIF-1??/K532R into mice and measured metastasis. All statistical tests were two-sided, and P values less than. 05 were considered statistically significant.Results ApcMin/+/mARD1A225 transgenic mice (n = 25) had statistically significantly fewer intestinal polyps than Apc Min/+ mice (n = 21) (number of intestinal polyps per mouse: Apc Min/+ mice vs ApcMin/+/mARD1A225 transgenic mice, mean = 83.4 vs 38.0 polyps, difference = 45.4 polyps, 95% confidence interval [CI] = 41.8 to 48.6; P &lt;. 001). The growth and metastases of transplanted tumors were also statistically significantly reduced in mice injected with mARD1A225-overexpressing cells than in mice injected with control cells (P &lt;. 01). Moreover, overexpression of mARD1A 225 decreased VEGFA expression and microvessel density in tumor xenografts (P &lt;. 04) and ApcMin/+ intestinal polyps (P =. 001). Mutation of lysine 532 of HIF-1?? in B16F10-mARD1A225 cells prevented HIF-1?? degradation and inhibited the antimetastatic effect of mARD1A225 (P &lt;. 001).Conclusion mARD1A225 may be a novel upstream target that blocks VEGFA expression and tumor-related angiogenesis

A multi-targeted approach to suppress tumor-promoting inflammation

Cancers harbor significant genetic heterogeneity and patterns of relapse following many therapies are due to evolved resistance to treatment. While efforts have been made to combine targeted therapies, significant levels of toxicity have stymied efforts to effectively treat cancer with multi-drug combinations using currently approved therapeutics. We discuss the relationship between tumor-promoting inflammation and cancer as part of a larger effort to develop a broad-spectrum therapeutic approach aimed at a wide range of targets to address this heterogeneity. Specifically, macrophage migration inhibitory factor, cyclooxygenase-2, transcription factor nuclear factor-κB, tumor necrosis factor alpha, inducible nitric oxide synthase, protein kinase B, and CXC chemokines are reviewed as important antiinflammatory targets while curcumin, resveratrol, epigallocatechin gallate, genistein, lycopene, and anthocyanins are reviewed as low-cost, low toxicity means by which these targets might all be reached simultaneously. Future translational work will need to assess the resulting synergies of rationally designed antiinflammatory mixtures (employing low-toxicity constituents), and then combine this with similar approaches targeting the most important pathways across the range of cancer hallmark phenotypes

Epigenetic inactivation of the NORE1 gene correlates with malignant progression of colorectal tumors

<p>Abstract</p> <p>Background</p> <p>NORE1 (RASSF5) is a newly described member of the RASSF family with Ras effector function. <it>NORE1 </it>expression is frequently inactivated by aberrant promoter hypermethylation in many human cancers, suggesting that NORE1 might be a putative tumor suppressor. However, expression and mutation status of <it>NORE1 </it>and its implication in colorectal tumorigenesis has not been evaluated.</p> <p>Methods</p> <p>Expression, mutation, and methylation status of <it>NORE1A </it>and <it>NORE1B </it>in 10 cancer cell lines and 80 primary tumors were characterized by quantitative PCR, SSCP, and bisulfite DNA sequencing analyses. Effect of NORE1A and NORE1B expression on tumor cell growth was evaluated using cell number counting, flow cytometry, and colony formation assays.</p> <p>Results</p> <p>Expression of <it>NORE1A </it>and <it>NORE1B </it>transcript was easily detectable in all normal colonic epithelial tissues, but substantially decreased in 7 (70%) and 4 (40%) of 10 cancer cell lines and 31 (38.8%) and 25 (31.3%) of 80 primary carcinoma tissues, respectively. Moreover, 46 (57.6%) and 38 (47.5%) of 80 matched tissue sets exhibited tumor-specific reduction of <it>NORE1A </it>and <it>NORE1B</it>, respectively. Abnormal reduction of <it>NORE1 </it>was more commonly observed in advanced stage and high grade tumors compared to early and low grade tumors. While somatic mutations of the gene were not identified, its expression was re-activated in all low expressor cells after treatment with the demethylating agent 5-aza-dC. Bisulfite DNA sequencing analysis of 31 CpG sites within the promoter region demonstrated that abnormal reduction of <it>NORE1A </it>is tightly associated with promoter CpG sites hypermethylation. Moreover, transient expression and siRNA-mediated knockdown assays revealed that both NORE1A and NORE1B decrease cellular growth and colony forming ability of tumor cells and enhance tumor cell response to apoptotic stress.</p> <p><b>Conclusion</b></p> <p>Our data indicate that epigenetic inactivation of <it>NORE1 </it>due to aberrant promoter hypermethylation is a frequent event in colorectal tumorigenesis and might be implicated in the malignant progression of colorectal tumors.</p

Search for New Physics with Jets and Missing Transverse Momentum in pp collisions at sqrt(s) = 7 TeV

A search for new physics is presented based on an event signature of at least three jets accompanied by large missing transverse momentum, using a data sample corresponding to an integrated luminosity of 36 inverse picobarns collected in proton--proton collisions at sqrt(s)=7 TeV with the CMS detector at the LHC. No excess of events is observed above the expected standard model backgrounds, which are all estimated from the data. Exclusion limits are presented for the constrained minimal supersymmetric extension of the standard model. Cross section limits are also presented using simplified models with new particles decaying to an undetected particle and one or two jets