BPS States in Omega Background and Integrability

We reconsider string and domain wall central charges in N=2 supersymmetric gauge theories in four dimensions in presence of the Omega background in the Nekrasov-Shatashvili (NS) limit. Existence of these charges entails presence of the corresponding topological defects in the theory - vortices and domain walls. In spirit of the 4d/2d duality we discuss the worldsheet low energy effective theory living on the BPS vortex in N=2 Supersymmetric Quantum Chromodynamics (SQCD). We discuss some aspects of the brane realization of the dualities between various quantum integrable models. A chain of such dualities enables us to check the AGT correspondence in the NS limit.Comment: 48 pages, 10 figures, minor changes, references added, typos correcte

Long-term Effectiveness and Tolerability of Topiramate in Children with Epilepsy under the Age of 2 Years: 4-Year Follow-up

This is a long-term, open label, observational study aimed to broaden our clinical experiences in managing infants and toddlers with epilepsy. The long-term retention rate and side effects of topiramate (TPM) in them were evaluated and compared with carbamazepine (CBZ). A total of 146 children were involved in the study (TPM=41, CBZ=105). The retention rates at 24 , 36, and 48 months were 46.3%, 34.1%, 26.8% for TPM and 36.2%, 23.8%, 13.3% for CBZ, respectively. At 6 months after starting antiepileptic drugs (AED), the seizure freedom or clinical efficacy (seizure reduction rate more than 50 percent) were 73.2% for TPM and 62.9% for CBZ. The major side effects led to discontinuation included psychomotor slowing, poor oral intake from TPM and sleepiness and skin rash from CBZ. TPM was discontinued due to side effects in one case (2.4%) and lack of efficacy in five cases (12.2%), whereas CBZ was discontinued due to lack of efficacy (22.9%) and side effects (6.7%). As compared with CBZ, TPM showed the same long-term retention rate in children under the age of 2 yr, and no serious side effects. It is therefore concluded that TPM can be considered as a major AED for treating children with epilepsy under the age of 2 yr

Measurement of local optomechanical properties of a direct bandgap 2D semiconductor

Strain engineering is a powerful tool for tuning physical properties of 2D materials, including monolayer transition metal dichalcogenides (TMDs)—direct bandgap semiconductors with strong excitonic response. Deformation of TMD monolayers allows inducing modulation of exciton potential and, ultimately, creating single-photon emitters at desired positions. The performance of such systems is critically dependent on the exciton energy profile and maximum possible exciton energy shift that can be achieved under local impact until the monolayer rupture. Here, we study the evolution of two-dimensional exciton energy profile induced in a MoSe2 monolayer under incremental local indentation until the rupture. We controllably stress the flake with an atomic force microscope tip and perform in situ spatiospectral mapping of the excitonic photoluminescence in the vicinity of the indentation point. In order to accurately fit the experimental data, we combine numerical simulations with a simple model of strain-induced modification of the local excitonic response and carefully account for the optical resolution of the setup. This allows us to extract deformation, strain, and exciton energy profiles obtained at each indentation depth. The maximum exciton energy shift induced by local deformation achieved at 300 nm indentation reaches the value of 36.5 meV and corresponds to 1.15% strain of the monolayer. Our approach is a powerful tool for in situ characterization of local optomechanical properties of 2D direct bandgap semiconductors with strong excitonic response

Nicotine Promotes Tumor Growth and Metastasis in Mouse Models of Lung Cancer

Nicotine is the major addictive component of tobacco smoke. Although nicotine is generally thought to have limited ability to initiate cancer, it can induce cell proliferation and angiogenesis in a variety of systems. These properties might enable nicotine to facilitate the growth of tumors already initiated. Here we show that nicotine significantly promotes the progression and metastasis of tumors in mouse models of lung cancer. This effect was observed when nicotine was administered through intraperitoneal injections, or through over-the-counter transdermal patches.In the present study, Line1 mouse adenocarcinoma cells were implanted subcutaneously into syngenic BALB/c mice. Nicotine administration either by intraperitoneal (i.p.) injection or transdermal patches caused a remarkable increase in the size of implanted Line1 tumors. Once the tumors were surgically removed, nicotine treated mice had a markedly higher tumor recurrence (59.7%) as compared to the vehicle treated mice (19.5%). Nicotine also increased metastasis of dorsally implanted Line1 tumors to the lungs by 9 folds. These studies on transplanted tumors were extended to a mouse model where the tumors were induced by the tobacco carcinogen, NNK. Lung tumors were initiated in A/J mice by i.p. injection of NNK; administration of 1 mg/kg nicotine three times a week led to an increase in the size and the number of tumors formed in the lungs. In addition, nicotine significantly reduced the expression of epithelial markers, E-Cadherin and beta-Catenin as well as the tight junction protein ZO-1; these tumors also showed an increased expression of the alpha(7) nAChR subunit. We believe that exposure to nicotine either by tobacco smoke or nicotine supplements might facilitate increased tumor growth and metastasis.Our earlier results indicated that nicotine could induce invasion and epithelial-mesenchymal transition (EMT) in cultured lung, breast and pancreatic cancer cells. This study demonstrates for the first time that administration of nicotine either by i.p. injection or through over-the-counter dermal patches can promote tumor growth and metastasis in immunocompetent mice. These results suggest that while nicotine has only limited capacity to initiate tumor formation, it can facilitate the progression and metastasis of tumors pre-initiated by tobacco carcinogens

An overlooked connection: serotonergic mediation of estrogen-related physiology and pathology

BACKGROUND: In humans, serotonin has typically been investigated as a neurotransmitter. However, serotonin also functions as a hormone across animal phyla, including those lacking an organized central nervous system. This hormonal action allows serotonin to have physiological consequences in systems outside the central nervous system. Fluctuations in estrogen levels over the lifespan and during ovarian cycles cause predictable changes in serotonin systems in female mammals. DISCUSSION: We hypothesize that some of the physiological effects attributed to estrogen may be a consequence of estrogen-related changes in serotonin efficacy and receptor distribution. Here, we integrate data from endocrinology, molecular biology, neuroscience, and epidemiology to propose that serotonin may mediate the effects of estrogen. In the central nervous system, estrogen influences pain transmission, headache, dizziness, nausea, and depression, all of which are known to be a consequence of serotonergic signaling. Outside of the central nervous system, estrogen produces changes in bone density, vascular function, and immune cell self-recognition and activation that are consistent with serotonin's effects. For breast cancer risk, our hypothesis predicts heretofore unexplained observations of the opposing effects of obesity pre- and post-menopause and the increase following treatment with hormone replacement therapy using medroxyprogesterone. SUMMARY: Serotonergic mediation of estrogen has important clinical implications and warrants further evaluation

Reactive oxygen species-mediated regulation of the Na+- H+exchanger 1 gene expression connects intracellular redox status with cells' sensitivity to death triggers

Cell Death and Differentiation134628-64