519 research outputs found

    Can Quantum de Sitter Space Have Finite Entropy?

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    If one tries to view de Sitter as a true (as opposed to a meta-stable) vacuum, there is a tension between the finiteness of its entropy and the infinite-dimensionality of its Hilbert space. We invetsigate the viability of one proposal to reconcile this tension using qq-deformation. After defining a differential geometry on the quantum de Sitter space, we try to constrain the value of the deformation parameter by imposing the condition that in the undeformed limit, we want the real form of the (inherently complex) quantum group to reduce to the usual SO(4,1) of de Sitter. We find that this forces qq to be a real number. Since it is known that quantum groups have finite-dimensional representations only for q=q= root of unity, this suggests that standard qq-deformations cannot give rise to finite dimensional Hilbert spaces, ruling out finite entropy for q-deformed de Sitter.Comment: 10 pages, v2: references added, v3: minor corrections, abstract and title made more in-line with the result, v4: published versio

    DNA damage response at telomeres boosts the transcription of SARS-CoV-2 receptor ACE2 during aging

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    The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes the coronavirus disease 2019 (COVID-19), known to be more common in the elderly, who also show more severe symptoms and are at higher risk of hospitalization and death. Here, we show that the expression of the angiotensin converting enzyme 2 (ACE2), the SARS-CoV-2 cell receptor, increases during aging in mouse and human lungs. ACE2 expression increases upon telomere shortening or dysfunction in both cultured mammalian cells and in vivo in mice. This increase is controlled at the transcriptional level, and Ace2 promoter activity is DNA damage response (DDR)-dependent. Both pharmacological global DDR inhibition of ATM kinase activity and selective telomeric DDR inhibition by the use of antisense oligonucleotides prevent Ace2 upregulation following telomere damage in cultured cells and in mice. We propose that during aging telomere dysfunction due to telomeric shortening or damage triggers DDR activation and this causes the upregulation of ACE2, the SARS-CoV-2 cell receptor, thus contributing to make the elderly more susceptible to the infection

    Quantum Deconstruction of a 5D SYM and its Moduli Space

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    We deconstruct the fifth dimension of the 5D SYM theory with SU(M) gauge symmetry and Chern-Simons level k=M and show how the 5D moduli space follows from the non-perturbative analysis of the 4D quiver theory. The 5D coupling h=1/(g_5)^2 of the un-broken SU(M) is allowed to take any non-negative values, but it cannot be continued to h<0 and there are no transitions to other phases of the theory. The alternative UV completions of the same 5D SYM -- via M theory on the C^3/Z_2M orbifold or via the dual five-brane web in type IIB string theory -- have identical moduli spaces: h >= 0 only, and no flop transitions. We claim these are intrinsic properties of the SU(M) SYM theory with k=M.Comment: 46 Page

    Non-Critical String Duals of N=1 Quiver Theories

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    We construct N=1 non-critical strings in four dimensions dual to strongly coupled N=1 quiver gauge theories in the Coulomb phase, generalizing the string duals of Argyres-Douglas points in N=2 gauge theories. They are the first examples of superstrings vacua with an exact worldsheet description dual to chiral N=1 theories. We identify the dual of the non-critical superstring using a brane setup describing the field theory in the classical limit. We analyze the spectrum of chiral operators in the strongly coupled regime and show how worldsheet instanton effects give non-perturbative information about the gauge theory. We also consider aspects of D-branes relevant for the holographic duality.Comment: JHEP style; 40 pages, 3 figures; v2: minor corrections, refs added, version to appear in JHE

    Inflammatory Markers and Outcomes in Cardiovascular Disease

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    In a commentary on two new research studies in PLoS Medicine, Leonard Kritharides discusses the role of inflammatory markers in predicting cardiovascular outcomes and patients' responses to treatment

    Pathological complete response induced by first-line chemotherapy with single agent docetaxel in a patient with advanced non small cell lung cancer

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    <p>Abstract</p> <p>Background</p> <p>Defining the optimal treatment for patients with inoperable non small cell lung cancer (NSCLC), presenting with metastatic mediastinal lymph nodes, is challenging. Nevertheless, preoperative chemotherapy or radiotherapy might offer a chance for these patients for radical surgical resection and, possibly, complete recovery.</p> <p>Case Presentation</p> <p>A 62-year old man with IIIA-N2 inoperable NSCLC was treated with first-line single agent docetaxel. A platinum-based treatment, though considered more active, was ruled out because of renal impairment. The patient tolerated the treatment very well and, although his initial response was not impressive, after 14 cycles he obtained a complete clinical response, which was confirmed pathologically after he underwent surgical lobectomy.</p> <p>Conclusion</p> <p>In non-operable NSCLC patients not eligible for a platinum-based treatment, single-agent docetaxel can provide complete pathologic responses. Failure to obtain a response after the first few cycles should not automatically discourage to continue treatment.</p

    Observation of the TeV gamma-ray source MGRO J1908+06 with ARGO-YBJ

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    The extended gamma ray source MGRO J1908+06, discovered by the Milagro air shower detector in 2007, has been observed for about 4 years by the ARGO-YBJ experiment at TeV energies, with a statistical significance of 6.2 standard deviations. The peak of the signal is found at a position consistent with the pulsar PSR J1907+0602. Parametrizing the source shape with a two-dimensional Gauss function we estimate an extension \sigma = 0.49 \pm 0.22 degrees, consistent with a previous measurement by the Cherenkov Array H.E.S.S.. The observed energy spectrum is dN/dE = 6.1 \pm 1.4 \times 10^-13 (E/4 TeV)^{-2.54 \pm 0.36} photons cm^-2 s^-1 TeV^-1, in the energy range 1-20 TeV. The measured gamma ray flux is consistent with the results of the Milagro detector, but is 2-3 times larger than the flux previously derived by H.E.S.S. at energies of a few TeV. The continuity of the Milagro and ARGO-YBJ observations and the stable excess rate observed by ARGO-YBJ along 4 years of data taking support the identification of MGRO J1908+06 as the steady powerful TeV pulsar wind nebula of PSR J1907+0602, with an integrated luminosity above 1 TeV about 1.8 times the Crab Nebula luminosity.Comment: 6 pages, accepted for pubblication by ApJ. Replaced to correct the author lis

    C-reactive protein in the very early phase of acute ischemic stroke: association with poor outcome and death

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    Acute ischemic stroke may trigger an inflammatory response that leads to increased levels of C-reactive protein (CRP). High levels of CRP may be associated with poor outcome because they reflect either an inflammatory reaction or tissue damage. We evaluated the prognostic value of CRP within 12 h of onset of ischemic stroke. Levels of CRP were routinely obtained within 12 h of symptom onset in 561 patients with ischemic stroke. CRP values were dichotomized as <7 or ≥7 mg/L. The full range of CRP values was used to detect a possible level-risk relationship. We studied the relation between CRP values and poor outcome (modified Rankin Scale score >2) or death at 3 months. A multiple logistic regression model was applied to adjust for age, sex, NIHSS score, current cigarette smoking, diabetes mellitus, hypertension, statin use, and stroke subtype. After adjustment for potential confounders, patients with CRP levels ≥7 mg/L had a significantly increased risk of poor outcome (adjusted OR 1.6, 95% CI 1.1–2.4) or death (adjusted OR 1.7, 95% CI 1.0–2.9) at 3 months. In addition, the risk of poor outcome or death at 3 months increased with higher levels of CRP. CRP within 12 h of ischemic stroke is an independent prognostic factor of poor outcome at 3 months

    Influence of Maternal Dysmetabolic Conditions During Pregnancy on Cardiovascular Disease

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    Pathogenic factors associated with maternal hypercholesterolemia, obesity, and diabetic conditions during pregnancy influence fetal development and predispose offspring to cardiovascular disease. Animal models have established cause–effect relationships consistent with epidemiological findings in humans and have demonstrated, in principle, that interventions before or during pregnancy can reduce or prevent pathogenic in utero programming. However, little is known about the mechanisms by which maternal dysmetabolic conditions enhance disease susceptibility in offspring. Identification of these mechanisms is rendered more difficult by the fact that programming effects in offspring may be latent and may require conventional risk factors and inherited genetic co-factors to become clinically manifest. Given the increasing prevalence of maternal risk factors, which is expected to lead to a wave of cardiovascular disease in the coming decades, and the length of prospective studies on developmental programming in humans, greater-than-usual emphasis on experimental models and translational studies is necessary
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