Partial Wave Analyses of the pp data alone and of the np data alone

We present results of the Nijmegen partial-wave analyses of all NN scattering data below Tlab = 500 MeV. We have been able to extract for the first time the important np phase shifts for both I = 0 and I = 1 from the np scattering data alone. This allows us to study the charge independence breaking between the pp and np I = 1 phases. In our analyses we obtain for the pp data chi^2_{min}/Ndf = 1.13 and for the np data chi^2_{min}/Ndf = 1.12.Comment: Report THEF-NYM 94.04, 4 pages LaTeX, one PostScript figure appended. Contribution to the 14th Few-Body Conference, May 26 - 31, Williamsburg, V

How the Devil Ray Got Its Horns: The Evolution and Development of Cephalic Lobes in Myliobatid Stingrays (Batoidea: Myliobatidae)

Manta rays and their relatives of the family Myliobatidae have pectoral fins that have been modified for underwater flight, as well as a pair of fleshy projections at the anterior of the body called cephalic lobes, which are specialized for feeding. As a unique trait with a dedicated function, cephalic lobes offer an excellent opportunity to elucidate the processes by which diverse body plans and features evolve. To shed light on the morphological development and genetic underpinnings of cephalic lobes, we examined paired fin development in cownose rays, which represent the sister taxon to manta rays in the genus Mobula. We find that cephalic lobes develop as anterior pectoral fin domains and lack independent posterior patterning by 5\u27 HoxD genes and Shh, indicating that cephalic lobes are not independent appendages but rather are modified pectoral fin domains. In addition, by leveraging interspecies comparative transcriptomics and domain-specific RNA-sequencing, we identify shared expression of anterior patterning genes, including Alx1, Alx4, Pax9, Hoxa13, Hoxa2, and Hoxd4, in the pectoral fins of cownose ray (Rhinoptera bonasus) and little skate (Leucoraja erinacea), providing evidence supporting homology between the cephalic lobes of myliobatids and the anterior pectoral fins of skates. We also suggest candidate genes that may be involved in development of myliobatid-specific features, including Omd, which is likely associated with development of thick anterior pectoral fin radials of myliobatids, and Dkk1, which may inhibit tissue outgrowth at the posterior boundary of the developing cephalic lobes. Finally, we observe that cephalic lobes share a surprising number of developmental similarities with another paired fin modification: the claspers of male cartilaginous fishes, including enrichment of Hand2, Hoxa13, and androgen receptor. These results suggest that cephalic lobes may have evolved by co-opting developmental pathways that specify novel domains in paired fins. Taken together, these data on morphological development and comparative gene expression patterns illustrate how distinct body plans and seemingly novel features can arise via subtle changes to existing developmental pathways

Comment on piNN Coupling from High Precision np Charge Exchange at 162 MeV

In this updated and expanded version of our delayed Comment we show that the np backward cross section, as presented by the Uppsala group, is seriously flawed (more than 25 sd.). The main reason is the incorrect normalization of the data. We show also that their extrapolation method, used to determine the charged piNN coupling constant, is a factor of about 10 less accurate than claimed by Ericson et al. The large extrapolation error makes the determination of the coupling constant by the Uppsala group totally uninteresting.Comment: 5 pages, latex2e with a4wide.sty. This is an updated and extended version of the Comment published in Phys. Rev. Letters 81, 5253 (1998

Expanding the clinical spectrum of 3-phosphoglycerate dehydrogenase deficiency

3-Phosphoglycerate dehydrogenase (3-PGDH) deficiency is considered to be a rare cause of congenital microcephaly, infantile onset of intractable seizures and severe psychomotor retardation. Here, we report for the first time a very mild form of genetically confirmed 3-PGDH deficiency in two siblings with juvenile onset of absence seizures and mild developmental delay. Amino acid analysis showed serine values in CSF and plasma identical to what is observed in the severe infantile form. Both patients responded favourably to relatively low dosages of serine supplementation with cessation of seizures, normalisation of their EEG abnormalities and improvement of well-being and behaviour. These cases illustrate that 3-PGDH deficiency can present with mild symptoms and should be considered as a treatable disorder in the differential diagnosis of mild developmental delay and seizures. Synopsis: we present a novel mild phenotype in patients with 3-PGDH deficiency

Fiscal redistribution around elections when democracy is not "the only game in town"

This paper seeks to examine the implications of policy intervention around elections on income inequality and fiscal redistribution. We first develop a simplified theoretical framework that allows us to examine election-cycle fiscal redistribution programs in the presence of a revolutionary threat from some groups of agents, i.e., when democracy is not “the only game in town”. According to our theoretical analysis, when democracy is not “the only game in town”, incumbents implement redistributive policies not only as a means of improving their reelection prospects, but also in order to signal that “democracy works”, thereby preventing a reversion to an autocratic status quo ante at a time of the current regime’s extreme vulnerability. Subsequently, focusing on 65 developed and developing countries over the 1975–2010 period, we report robust empirical evidence of pre-electoral budgetary manipulation in new democracies. Consistent with our theory, this finding is driven by political instability that induces incumbents to redistribute income—through tax and spending policies—in a relatively broader coalition of voters with the aim of consolidating the vulnerable newly established democratic regime

The gene product Murr1 restricts HIV-1 replication in resting CD4(+) lymphocytes

Although human immunodeficiency virus-1 (HIV-1) infects quiescent and proliferating CD4(+) lymphocytes, the virus replicates poorly in resting T cells(1-6). Factors that block viral replication in these cells might help to prolong the asymptomatic phase of HIV infection(7); however, the molecular mechanisms that control this process are not fully understood. Here we show that Murr1, a gene product known previously for its involvement in copper regulation(8,9), inhibits HIV-1 growth in unstimulated CD4(+) T cells. This inhibition was mediated in part through its ability to inhibit basal and cytokine-stimulated nuclear factor (NF)-kappaB activity. Knockdown of Murr1 increased NF-kappaB activity and decreased IkappaB-alpha concentrations by facilitating phospho-IkappaB-alpha degradation by the proteasome. Murr1 was detected in CD4(+) T cells, and RNA-mediated interference of Murr1 in primary resting CD4(+) lymphocytes increased HIV-1 replication. Through its effects on the proteasome, Murr1 acts as a genetic restriction factor that inhibits HIV-1 replication in lymphocytes, which could contribute to the regulation of asymptomatic HIV infection and the progression of AIDS.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/62709/1/nature02171.pd