Interview of Jeff Schwartz by Bill Shkurti

Aptheker, Herbert: Marxist historian, political activist (pp. 7, 9, 13-17, 20, 22) -- Brauner, Charles: Professor, College of Education (p. 6) -- Bricker, John: U.S. Senator, member of the OSU Board of Trustees (pp. 10,17) -- Darling, Stan: President, Undergraduate Student Government (pp. 7, 26) -- Fawcett, Novice: President, OSU (pp. 6-7, 10, 17-18, 20) -- Knepley, Dennis: Co-founder of the Free Speech Front (pp.6-7) -- Lenzo, Bob: Co-founder of the Free Speech Front (pp.6-7) -- Loop, Alan: Chairman of the Board of Trustees (pp. 21-22) -- Ochs, Phil: OSU alumnus, folk singer (pp. 9-10) -- Rhodes, James: Governor of Ohio (pp. 20-21) -- Schwartz, Niki: Politically active OSU student and Jeff Schwartz’ brother (pp. 2-3, 5-6, 26) -- Shocknessy, James: Member of the OSU Board of Trustees (pp. 21).Interview conducted at The Ohio State University Archives, Columbus, Ohio.The interview discusses OSU alumnus Jeff Schwartz's work on campus with the free-speech movement in the mid-1960s, particularly 1965. As an undergraduate, he became involved with the OSU student group, the Free Speech Front (FSF), because of his earlier involvement in the civil rights movement in Louisiana. He was a participant and important contributor to the Free Speech Front's goal of eradicating the University's restriction on campus speakers, known as the Speakers Rule. One strategy was for Schwartz and others in the FSF to participate in two sit-ins in the Administration Building to influence University officials to change the rule. A later strategy was to invite noted Marxist historian Herbert Aptheker to campus to not speak, but instead have students read his work as he stood by. Several months after that event in 1965, the OSU Board of Trustees effectively abolished the rule. Schwartz also discusses how his involvement in the free-speech movement influenced his later career as a lawyer and organizational-effectiveness coach and consultant

Skeletal remains from punic carthage do not support systematic sacrifice of infants

Two types of cemeteries occur at Punic Carthage and other Carthaginian settlements: one centrally situated housing the remains of older children through adults, and another at the periphery of the settlement (the "Tophet") yielding small urns containing the cremated skeletal remains of very young animals and humans, sometimes comingled. Although the absence of the youngest humans at the primary cemeteries is unusual and worthy of discussion, debate has focused on the significance of Tophets, especially at Carthage, as burial grounds for the young. One interpretation, based on two supposed eye-witness reports of large-scale Carthaginian infant sacrifice [Kleitarchos (3rd c. BCE) and Diodorus Siculus (1st c. BCE)], a particular translation of inscriptions on some burial monuments, and the argument that if the animals had been sacrificed so too were the humans, is that Tophets represent burial grounds reserved for sacrificial victims. An alternative hypothesis acknowledges that while the Carthaginians may have occasionally sacrificed humans, as did their contemporaries, the extreme youth of Tophet individuals suggests these cemeteries were not only for the sacrificed, but also for the very young, however they died. Here we present the first rigorous analysis of the largest sample of cremated human skeletal remains (348 burial urns, N = 540 individuals) from the Carthaginian Tophet based on tooth formation, enamel histology, cranial and postcranial metrics, and the potential effects of heat-induced bone shrinkage. Most of the sample fell within the period prenatal to 5-to-6 postnatal months, with a significant presence of prenates. Rather than indicating sacrifice as the agent of death, this age distribution is consistent with modern-day data on perinatal mortality, which at Carthage would also have been exacerbated by numerous diseases common in other major cities, such as Rome and Pompeii. Our diverse approaches to analyzing the cremated human remains from Carthage strongly support the conclusion that Tophets were cemeteries for those who died shortly before or after birth, regardless of the cause. © 2010 Schwartz et al

Immune-Mediated Inflammation May Contribute to the Pathogenesis of Cardiovascular Disease in Mucopolysaccharidosis Type I.

BackgroundCardiovascular disease, a progressive manifestation of α-L-iduronidase deficiency or mucopolysaccharidosis type I, continues in patients both untreated and treated with hematopoietic stem cell transplantation or intravenous enzyme replacement. Few studies have examined the effects of α-L-iduronidase deficiency and subsequent glycosaminoglycan storage upon arterial gene expression to understand the pathogenesis of cardiovascular disease.MethodsGene expression in carotid artery, ascending, and descending aortas from four non-tolerized, non-enzyme treated 19 month-old mucopolysaccharidosis type I dogs was compared with expression in corresponding vascular segments from three normal, age-matched dogs. Data were analyzed using R and whole genome network correlation analysis, a bias-free method of categorizing expression level and significance into discrete modules. Genes were further categorized based on module-trait relationships. Expression of clusterin, a protein implicated in other etiologies of cardiovascular disease, was assessed in canine and murine mucopolysaccharidosis type I aortas via Western blot and in situ immunohistochemistry.ResultsGene families with more than two-fold, significant increased expression involved lysosomal function, proteasome function, and immune regulation. Significantly downregulated genes were related to cellular adhesion, cytoskeletal elements, and calcium regulation. Clusterin gene overexpression (9-fold) and protein overexpression (1.3 to 1.62-fold) was confirmed and located specifically in arterial plaques of mucopolysaccharidosis-affected dogs and mice.ConclusionsOverexpression of lysosomal and proteasomal-related genes are expected responses to cellular stress induced by lysosomal storage in mucopolysaccharidosis type I. Upregulation of immunity-related genes implicates the potential involvement of glycosaminoglycan-induced inflammation in the pathogenesis of mucopolysaccharidosis-related arterial disease, for which clusterin represents a potential biomarker

Age-Gender Influence on the Rate-Corrected QT Interval and the QT-Heart Rate Relation in Families With Genotypically Characterized Long QT Syndrome

AbstractObjectives. We sought to analyze age-gender differences in the rate-corrected QT (QTc) interval in the presence of a QT-prolonging gene.Background. Compared with men, women exhibit a longer QTc interval and an increased propensity toward torsade de pointes. In normal subjects, the QTc gender difference reflects QTc interval shortening in men during adolescence.Methods. QTc intervals were analyzed according to age (<16 or ≥16 years) and gender in 460 genotyped blood relatives from families with long QT syndrome linked to chromosome 11p (KVLQT1; n = 199), 7q (HERG; n = 208) or 3p (SCN5A; n = 53).Results. The mean QTc interval in genotype-negative blood relatives (n = 240) was shortest in men, but similar among women, boys and girls. For genotype-positive blood relatives, men exhibited the shortest mean QTc interval in chromosome 7q- and 11p-linked blood relatives (n = 194), but not in the smaller 3p-linked group (n = 26). Among pooled 7q- and 11p-linked blood relatives, multiple regression analysis identified both genotype (p < 0.001) and age-gender group (men vs. women/children; p < 0.001) as significant predictors of the QTc interval; and heart rate (p < 0.001), genotype (p < 0.001) and age-gender group (p = 0.01) as significant predictors of the absolute QT interval. A shorter mean QT interval in men was most evident for heart rates <60 beats/min.Conclusions. In familial long QT syndrome linked to either chromosome 7q or 11p, men exhibit shorter mean QTc values than both women and children, for both genotype-positive and -negative blood relatives. Thus, adult gender differences in propensity toward torsade de pointes may reflect the relatively greater presence in men of a factor that blunts QT prolongation responses, especially at slow heart rates.(J Am Coll Cardiol 1997;29:93–9)

Efficacy and safety of tafamidis doses in the Tafamidis in Transthyretin Cardiomyopathy Clinical Trial (ATTR-ACT) and long-term extension study.

Aims Tafamidis is an effective treatment for transthyretin amyloid cardiomyopathy (ATTR-CM) in the Tafamidis in Transthyretin Cardiomyopathy Clinical Trial (ATTR-ACT). While ATTR-ACT was not designed for a dose-specific assessment, further analysis from ATTR-ACT and its long-term extension study (LTE) can guide determination of the optimal dose. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Methods and results In ATTR-ACT, patients were randomized (2:1:2) to tafamidis 80 mg, 20mg, or placebo for 30months. Patients completing ATTR-ACT could enrol in the LTE (with placebo-treated patients randomized to tafamidis 80 or 20 mg; 2:1) and all patients were subsequently switched to high-dose tafamidis. All-cause mortality was assessed in ATTR-ACT combined with the LTE (median follow-up 51 months). In ATTR-ACT, the combination of all-cause mortality and cardiovascular-related hospitalizations over 30 months was significantly reduced with tafamidis 80mg (P = 0.0030) and 20mg (P = 0.0048) vs. placebo. All-cause mortality vs. placebo was reduced with tafamidis 80mg [Cox hazards model (95% confidence interval (CI): 0.690 (0.487–0.979), P = 0.0378] and 20mg [0.715 (0.450–1.137), P = 0.1564]. The mean (standard error) change in N-terminal pro-B-type natriuretic peptide from baseline to Month 30 was −1170.51 (587.31) (P = 0.0468) with tafamidis 80 vs. 20 mg. In ATTR-ACT combined with the LTE there was a significantly greater survival benefit with tafamidis 80 vs. 20 mg [0.700 (0.501–0.979), P = 0.0374]. Incidence of adverse events in both tafamidis doses were comparable to placebo. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Conclusion Tafamidis, both 80 and 20mg, effectively reduced mortality and cardiovascular-related hospitalizations in patients with ATTR-CM. The longer-term survival data and the lack of dose-related safety concerns support tafamidis 80mg as the optimal dose. Clinical Trial Registration: ClinicalTrials.gov NCT01994889; NCT02791230post-print369 K

Ubiquitous outflows in DEEP2 spectra of star-forming galaxies at z=1.4

Galactic winds are a prime suspect for the metal enrichment of the intergalactic medium and may have a strong influence on the chemical evolution of galaxies and the nature of QSO absorption line systems. We use a sample of 1406 galaxy spectra at z~1.4 from the DEEP2 redshift survey to show that blueshifted Mg II 2796, 2803 A absorption is ubiquitous in starforming galaxies at this epoch. This is the first detection of frequent outflowing galactic winds at z~1. The presence and depth of absorption are independent of AGN spectral signatures or galaxy morphology; major mergers are not a prerequisite for driving a galactic wind from massive galaxies. Outflows are found in coadded spectra of galaxies spanning a range of 30x in stellar mass and 10x in star formation rate (SFR), calibrated from K-band and from MIPS IR fluxes. The outflows have column densities of order N_H ~ 10^20 cm^-2 and characteristic velocities of ~ 300-500 km/sec, with absorption seen out to 1000 km/sec in the most massive, highest SFR galaxies. The velocities suggest that the outflowing gas can escape into the IGM and that massive galaxies can produce cosmologically and chemically significant outflows. Both the Mg II equivalent width and the outflow velocity are larger for galaxies of higher stellar mass and SFR, with V_wind ~ SFR^0.3, similar to the scaling in low redshift IR-luminous galaxies. The high frequency of outflows in the star-forming galaxy population at z~1 indicates that galactic winds occur in the progenitors of massive spirals as well as those of ellipticals. The increase of outflow velocity with mass and SFR constrains theoretical models of galaxy evolution that include feedback from galactic winds, and may favor momentum-driven models for the wind physics.Comment: Accepted by ApJ. 25 pages, 17 figures. Revised to add discussions of intervening absorbers and AGN-driven outflows; conclusions unchange

The Persistence of Cool Galactic Winds in High Stellar Mass Galaxies Between z~1.4 and ~1

We present an analysis of the MgII 2796, 2803 and FeII 2586, 2600 absorption line profiles in coadded spectra of 468 galaxies at 0.7 < z < 1.5. The galaxy sample, drawn from the Team Keck Treasury Redshift Survey of the GOODS-N field, has a range in stellar mass (M_*) comparable to that of the sample at z~1.4 analyzed in a similar manner by Weiner et al. (2009; W09), but extends to lower redshifts and has specific star formation rates which are lower by ~0.6 dex. We identify outflows of cool gas from the Doppler shift of the MgII absorption lines and find that the equivalent width (EW) of absorption due to outflowing gas increases on average with M_* and star formation rate (SFR). We attribute the large EWs measured in spectra of the more massive, higher-SFR galaxies to optically thick absorbing clouds having large velocity widths. The outflows have hydrogen column densities N(H) > 10^19.3 cm^-2, and extend to velocities of ~500 km/s. While galaxies with SFR > 10 Msun/yr host strong outflows in both this and the W09 sample, we do not detect outflows in lower-SFR (i.e., log M_*/Msun < 10.5) galaxies at lower redshifts. Using a simple galaxy evolution model which assumes exponentially declining SFRs, we infer that strong outflows persist in galaxies with log M_*/Msun > 10.5 as they age between z=1.4 and z~1, presumably because of their high absolute SFRs. Finally, using high resolution HST/ACS imaging in tandem with our spectral analysis, we find evidence for a weak trend (at 1 sigma significance) of increasing outflow absorption strength with increasing galaxy SFR surface density.Comment: Submitted to ApJ. 25 pages, 19 figures, Figure 2 reduced in resolution. Uses emulateapj forma

Genotype-Phenotype Correlation in the Long-QT Syndrome

Background —The congenital long-QT syndrome (LQTS) is caused by mutations on several genes, all of which encode cardiac ion channels. The progressive understanding of the electrophysiological consequences of these mutations opens unforeseen possibilities for genotype-phenotype correlation studies. Preliminary observations suggested that the conditions ("triggers") associated with cardiac events may in large part be gene specific. Methods and Results —We identified 670 LQTS patients of known genotype (LQT1, n=371; LQT2, n=234; LQT3, n=65) who had symptoms (syncope, cardiac arrest, sudden death) and examined whether 3 specific triggers (exercise, emotion, and sleep/rest without arousal) differed according to genotype. LQT1 patients experienced the majority of their events (62%) during exercise, and only 3% occurred during rest/sleep. These percentages were almost reversed among LQT2 and LQT3 patients, who were less likely to have events during exercise (13%) and more likely to have events during rest/sleep (29% and 39%). Lethal and nonlethal events followed the same pattern. Corrected QT interval did not differ among LQT1, LQT2, and LQT3 patients (498, 497, and 506 ms, respectively). The percent of patients who were free of recurrence with β-blocker therapy was higher and the death rate was lower among LQT1 patients (81% and 4%, respectively) than among LQT2 (59% and 4%, respectively) and LQT3 (50% and 17%, respectively) patients. Conclusions —Life-threatening arrhythmias in LQTS patients tend to occur under specific circumstances in a gene-specific manner. These data allow new insights into the mechanisms that relate the electrophysiological consequences of mutations on specific genes to clinical manifestations and offer the possibility of complementing traditional therapy with gene-specific approaches

Learning-based Calibration of Flux Crosstalk in Transmon Qubit Arrays

Superconducting quantum processors comprising flux-tunable data and coupler qubits are a promising platform for quantum computation. However, magnetic flux crosstalk between the flux-control lines and the constituent qubits impedes precision control of qubit frequencies, presenting a challenge to scaling this platform. In order to implement high-fidelity digital and analog quantum operations, one must characterize the flux crosstalk and compensate for it. In this work, we introduce a learning-based calibration protocol and demonstrate its experimental performance by calibrating an array of 16 flux-tunable transmon qubits. To demonstrate the extensibility of our protocol, we simulate the crosstalk matrix learning procedure for larger arrays of transmon qubits. We observe an empirically linear scaling with system size, while maintaining a median qubit frequency error below $300$ kHz