The 18th Knesset: Obama, Netanyahu, and the Future of the U.S.-Israel Relationship

The University Archives has determined that this item is of continuing value to OSU's history.Elliott Abrams is senior fellow for Middle Eastern studies at the Council on Foreign Relations in Washington, D.C. He served as deputy assistant to the president and deputy national security adviser in the administration of President George W. Bush, where he supervised U.S. policy in the Middle East for the White House. Abrams joined the Bush administration in June 2001 as special assistant to the president and senior director of the National Security Council (NSC) for democracy, human rights, and international organizations. From December 2002 to February 2005, he served as special assistant to the president and senior director of the National Security Council for Near East and North African affairs. He served as deputy assistant to the president and deputy national security adviser for global democracy strategy from February 2005 to January 2009, and in that capacity supervised both the Near East and North African affairs, and the democracy, human rights, and international organizations directorates of the NSC. Abrams was president of the Ethics and Public Policy Center in Washington, D.C., from 1996 until joining the White House staff. He was a member of the United States Commission on International Religious Freedom from 1999 to 2001, and chairman of the commission in the latter year. Abrams is currently a member of the U.S. Holocaust Memorial Council, which directs the activities of the U.S. Holocaust Memorial Museum. Abrams was educated at Harvard College (BA, 1969), the London School of Economics (MSc, 1970) and Harvard Law School (JD, 1973). He is the author of three books, Undue Process (1993), Security and Sacrifice (1995), and Faith or Fear: How Jews Can Survive in a Christian America (1997); and the editor of three more, Close Calls: Intervention, Terrorism, Missile Defense and "Just War” Today; Honor Among Nations: Intangible Interests and Foreign Policy; and The Influence of Faith: Religion and American Foreign Policy.Ohio State University. Mershon Center for International Security StudiesHillel CenterEvent webpage, event photo

Acetylation of C-terminal lysines modulates protein turnover and stability of Connexin-32

Background The gap junction protein, Connexin32 (Cx32), is expressed in various tissues including liver, exocrine pancreas, gastrointestinal epithelium, and the glia of the central and peripheral nervous system. Gap junction-mediated cell-cell communication and channel-independent processes of Cx32 contribute to the regulation of physiological and cellular activities such as glial differentiation, survival, and proliferation; maintenance of the hepatic epithelium; and axonal myelination. Mutations in Cx32 cause X-linked Charcot–Marie–Tooth disease (CMT1X), an inherited peripheral neuropathy. Several CMT1X causing mutations are found in the cytoplasmic domains of Cx32, a region implicated in the regulation of gap junction assembly, turnover and function. Here we investigate the roles of acetylation and ubiquitination in the C-terminus on Cx32 protein function. Cx32 protein turnover, ubiquitination, and response to deacetylase inhibitors were determined for wild-type and C-terminus lysine mutants using transiently transfected Neuro2A (N2a) cells. Results We report here that Cx32 is acetylated in transfected N2a cells and that inhibition of the histone deacetylase, HDAC6, results in an accumulation of Cx32. We identified five lysine acetylation targets in the C-terminus. Mutational analysis demonstrates that these lysines are involved in the regulation of Cx32 ubiquitination and turnover. While these lysines are not required for functional Cx32 mediated cell-cell communication, BrdU incorporation studies demonstrate that their relative acetylation state plays a channel-independent role in Cx32-mediated control of cell proliferation. Conclusion Taken together these results highlight the role of post translational modifications and lysines in the C-terminal tail of Cx32 in the fine-tuning of Cx32 protein stability and channel-independent functions

Charged Majoron Emission in Neutrinoless Double Beta Decay

We examine in detail the predictions of the charged majoron model, introduced recently by Burgess and Cline, for 0+ --> 0+ double beta decay transitions. The relevant nuclear matrix elements are evaluated, within the quasiparticle random phase approximation, for 76Ge, 82Se, 100Mo, 128Te and 150Nd nuclei. The calculated transition rates turn out to be much smaller than the experimental upper limits on possible majoron emission, except in a small region of the model's parameter space.Comment: 9 pages, 1 encapsulated postscript figure, uses epsf.tex; reference [15] has been correcte

Double Beta Decay in pn-QRPA Model with Isospin and SU(4) Symmetry Constraints

The transition matrix elements for the $0^{+}\to 0^{+}$ double beta decays are calculated for $^{48}Ca$, $^{76}Ge$, $^{82}Se$, $^{100}Mo$, $^{128}Te$ and $^{130}Te$ nuclei, using a ${\delta}$-interaction. As a guide, to fix the particle-particle interaction strengths, we exploit the fact that the missing symmetries of the mean field approximation are restored in the random phase approximation by the residual interaction. Thus, the T=1, S=0 and T=0, S=1 coupling strengths have been estimated by invoking the partial restoration of the isospin and Wigner SU(4) symmetries, respectively. When this recipe is strictly applied, the calculation is consistent with the experimental limit for the $2\nu$ lifetime of $^{48}Ca$ and it also correctly reproduces the $2\nu$ lifetime of $^{82}Se$. In this way, however, the two-neutrino matrix elements for the remaining nuclei are either underestimated (for $^{76}Ge$ and $^{100}Mo$) or overestimated (for $^{128}Te$ and $^{130}Te$) approximately by a factor of 3. With a comparatively small variation ($<10$) of the spin-triplet parameter, near the value suggested by the SU(4) symmetry, it is possible to reproduce the measured $T_{1/2}^{2\nu}$ in all the cases. The upper limit for the effective neutrino mass, as obtained from the theoretical estimates of $0\nu$ matrix elements, is $\cong 1$ eV. The dependence of the nuclear matrix elements on the size of the configuration space has been also analyzed.Comment: 25 pages (LaTex) and 3 figures upon request, to be published in Nucl. Phys.

Downregulation of IRF8 in Alveolar Macrophages by G-CSF Promotes Metastatic Tumor Progression

Tissue-resident macrophages (TRMs) are abundant immune cells within pre-metastatic sites, yet their functional contributions to metastasis remain incompletely understood. Here, we show that alveolar macrophages (AMs), the main TRMs of the lung, are susceptible to downregulation of the immune stimulatory transcription factor IRF8, impairing anti-metastatic activity in models of metastatic breast cancer. G-CSF is a key tumor-associated factor (TAF) that acts upon AMs to reduce IRF8 levels and facilitate metastasis. Translational relevance of IRF8 downregulation was observed among macrophage precursors in breast cancer and

Brain size and brain/intracranial volume ratio in major mental illness

<p>Abstract</p> <p>Background</p> <p>This paper summarizes the findings of a long term study addressing the question of how several brain volume measure are related to three major mental illnesses in a Colorado subject group. It reports results obtained from a large N, collected and analyzed by the same laboratory over a multiyear period, with visually guided MRI segmentation being the primary initial analytic tool.</p> <p>Methods</p> <p>Intracerebral volume (ICV), total brain volume (TBV), ventricular volume (VV), ventricular/brain ratio (VBR), and TBV/ICV ratios were calculated from a total of 224 subject MRIs collected over a period of 13 years. Subject groups included controls (C, N = 89), and patients with schizophrenia (SZ, N = 58), bipolar disorder (BD, N = 51), and schizoaffective disorder (SAD, N = 26).</p> <p>Results</p> <p>ICV, TBV, and VV measures compared favorably with values obtained by other research groups, but in this study did not differ significantly between groups. TBV/ICV ratios were significantly decreased, and VBR increased, in the SZ and BD groups compared to the C group. The SAD group did not differ from C on any measure.</p> <p>Conclusions</p> <p>In this study TBV/ICV and VBR ratios separated SZ and BD patients from controls. Of interest however, SAD patients did not differ from controls on these measures. The findings suggest that the gross measure of TBV may not reliably differ in the major mental illnesses to a degree useful in diagnosis, likely due to the intrinsic variability of the measures in question; the differences in VBR appear more robust across studies. Differences in some of these findings compared to earlier reports from several laboratories finding significant differences between groups in VV and TBV may relate to phenomenological drift, differences in analytic techniques, and possibly the "file drawer problem".</p

Long-Term Arrhythmic Follow-Up and Risk Stratification of Patients With Desmoplakin-Associated Arrhythmogenic Right Ventricular Cardiomyopathy

Background: Patients with likely pathogenic/pathogenic desmoplakin (DSP) variants are poorly characterized. Some of them meet diagnostic criteria for arrhythmogenic right ventricular cardiomyopathy (ARVC), but it is unclear how risk stratification strategies for ARVC perform in this setting. / Objectives: The purpose of this study was to characterize arrhythmic outcomes and to test the performance of the recently validated ARVC risk calculator in patients with DSP likely pathogenic/pathogenic variants fulfilling definite 2010 ARVC Task Force Criteria (DSP-TFC+)./ Methods: DSP-TFC+ patients were enrolled from 20 institutions across 3 continents. Ventricular arrhythmias (VA), defined as a composite of sustained ventricular tachycardia (VT), appropriate implantable cardioverter defibrillator therapies, and ventricular fibrillation/sudden cardiac death events in follow-up, were reported as the primary outcome. We tested the performance of the ARVC risk calculator for VA prediction, reporting c-statistics. / Results: Among 252 DSP-TFC+ patients (age 39.6 ± 16.9 years, 35.3% male), 94 (37.3%) experienced VA over 44.5 [IQR: 19.6-78.3] months. Patients with left ventricle involvement (n = 194) were at higher VA risk (log-rank P = 0.0239). History of nonsustained VT (aHR 2.097; P = 0.004) showed the strongest association with VA occurrence during the first 5-year follow-up. Neither age (P = 0.723) nor male sex (P = 0.200) was associated with VAs at follow-up. In 204 patients without VA at diagnosis, incident VA rate was high (32.8%; 7.37%/y). The ARVC risk calculator performed poorly overall (c-statistic 0.604 [0.594-0.614]) and very poorly in patients with left ventricular disease (c-statistic 0.558 [0.556-0.560]). / Conclusions: DSP-TFC+ patients are at substantial risk for VAs. The ARVC risk calculator performs poorly in DSP-TFC+ patients suggesting need for a gene-specific risk algorithm. Meanwhile, DSP-TFC+ patients with nonsustained VT should be considered as high-risk