14 research outputs found
Evolution of opinions on social networks in the presence of competing committed groups
Public opinion is often affected by the presence of committed groups of
individuals dedicated to competing points of view. Using a model of pairwise
social influence, we study how the presence of such groups within social
networks affects the outcome and the speed of evolution of the overall opinion
on the network. Earlier work indicated that a single committed group within a
dense social network can cause the entire network to quickly adopt the group's
opinion (in times scaling logarithmically with the network size), so long as
the committed group constitutes more than about 10% of the population (with the
findings being qualitatively similar for sparse networks as well). Here we
study the more general case of opinion evolution when two groups committed to
distinct, competing opinions and , and constituting fractions and
of the total population respectively, are present in the network. We show
for stylized social networks (including Erd\H{o}s-R\'enyi random graphs and
Barab\'asi-Albert scale-free networks) that the phase diagram of this system in
parameter space consists of two regions, one where two stable
steady-states coexist, and the remaining where only a single stable
steady-state exists. These two regions are separated by two fold-bifurcation
(spinodal) lines which meet tangentially and terminate at a cusp (critical
point). We provide further insights to the phase diagram and to the nature of
the underlying phase transitions by investigating the model on infinite
(mean-field limit), finite complete graphs and finite sparse networks. For the
latter case, we also derive the scaling exponent associated with the
exponential growth of switching times as a function of the distance from the
critical point.Comment: 23 pages: 15 pages + 7 figures (main text), 8 pages + 1 figure + 1
table (supplementary info
Human Iron−Sulfur Cluster Assembly, Cellular Iron Homeostasis, and Disease†
ABSTRACT: Iron-sulfur (Fe-S) proteins contain prosthetic groups consisting of two or more iron atoms bridged by sulfur ligands, which facilitate multiple functions, including redox activity, enzymatic function, and maintenance of structural integrity. More than 20 proteins are involved in the biosynthesis of iron-sulfur clusters in eukaryotes. Defective Fe-S cluster synthesis not only affects activities of many iron-sulfur enzymes, such as aconitase and succinate dehydrogenase, but also alters the regulation of cellular iron homeostasis, causing both mitochondrial iron overload and cytosolic iron deficiency. In this work, we review human Fe-S cluster biogenesis and human diseases that are caused by defective Fe-S cluster biogenesis. Fe-S cluster biogenesis takes place essentially in every tissue of humans, and products of human disease genes, including frataxin, GLRX5, ISCU, and ABCB7, have important roles in the process. However, the human diseases, Friedreich ataxia, glutaredoxin 5-deficient sideroblastic anemia, ISCU myopathy, and ABCB7 sideroblastic anemia/ataxia syndrome, affect specific tissues, while sparing others. Here we discuss the phenotypes caused by mutations in these different disease genes, and we compare the underlying pathophysiology and discuss the possible explanations for tissue-specific pathology in these diseases caused by defective Fe-S cluster biogenesis. HUMAN CELLULAR IRON HOMEOSTASI
A methodology for creating a statistically derived shape grammar composed of non-obvious shape chunks
A new recombinant MnSOD prevents the cyclosporine A-induced renal impairment
Background. Cyclosporine A (CsA) is one of the most frequently used anticalcineurinic drugs for preventing graft rejection and autoimmune disease. Its use is hampered by nephrotoxic effects, namely an impairment of the glomerular filtration rate (GFR) and hypertension. Evidence suggests that reactive oxygen species (ROS) play a causal role in the nephrotoxicity. The present study aims to investigate in vivo the effects of a new recombinant mitochondrial manganese-containing superoxide dismutase (rMnSOD), a strong antioxidant, on the CsA-induced nephotoxicity. Methods. Rats were treated with CsA (25 mg/kg/day) alone or in combination with rMnSOD (10 μg/kg/day) for 7 days. At the end of the treatment, GFR was estimated by inulin clearance (mL/min/100 g b.w.) and the mean arterial pressure (MAP) was recorded through a catheter inserted in the carotid artery. Superoxide concentration within the cells of the abdominal aorta was quantified from the oxidation of dihydroethidium (DHE). In kidney tissues, ROS levels were measured by the 2′7′ dichloroflurescin diacetate assay. Renal morphology was examined at the histochemistry level. Results. CsA-treated rats showed a severe decrease in GFR (0.34 ± 0.17 versus 0.94 ± 0.10 in control, P < 0.001) which was prevented by rMnSOD co-administration (0.77 ± 0.10). CsAinjected animals presented with higher blood pressure which was unaffected by rMnSOD. ROS levels both in the aorta and in renal tissue were significantly increased by CsA treatment, and normalized by the co-administration with rMnSOD. This effect was, partly, paralleled by the recovery from CsA-induced morphological lesions. Conclusions. Administration of rMnSOD prevents CsA-mediated impairment of the GFR along with morphological alteration. This effect could be related to the inhibition of ROS. © The Author 2012
The Evolution and Devolution of Speed Limit Law and the Effect on Fatality Rates
The three most recent decades provide an outstanding opportunity to study the changing federalist landscape concerning the regulation of speed on the nation's highways. Speed limits were the province of the states until the 1970s when, in an effort to save energy, the central government nationalized the maximum speed at 55 miles per hour. The national standard remained until the 1980s, when a partial devolution transferred some power to set speed limits back to the individual states. At that time, states could increase the maximum speed to 65 miles per hour on (at fewest) four-lane, controlled access highways in low population density areas. Some states elected to loosen the limits within their borders, while others did not, citing concerns of highway safety as paramount. The 1990s saw the complete devolution of speed limit control to the states, when Congress returned to the states unlimited control. States reacted differently in both of the two latter phases, providing a fruitful landscape for comparative analysis of the effects of the devolution of speed limit control. Copyright 2005 by The Policy Studies Organization.
Biophysical Characterization of the Iron in Mitochondria from Atm1p-Depleted Saccharomyces cerevisiae
Direct evidence that the N-terminal extensions of the TAP complex act as autonomous interaction scaffolds for the assembly of the MHC I peptide-loading complex.
The loading of antigenic peptides onto major histocompatibility complex class I (MHC I) molecules is an essential step in the adaptive immune response against virally or malignantly transformed cells. The ER-resident peptide-loading complex (PLC) consists of the transporter associated with antigen processing (TAP1 and TAP2), assembled with the auxiliary factors tapasin and MHC I. Here, we demonstrated that the N-terminal extension of each TAP subunit represents an autonomous domain, named TMD(0), which is correctly targeted to and inserted into the ER membrane. In the absence of coreTAP, each TMD(0) recruits tapasin in a 1:1 stoichiometry. Although the TMD(0)s lack known ER retention/retrieval signals, they are localized to the ER membrane even in tapasin-deficient cells. We conclude that the TMD(0)s of TAP form autonomous interaction hubs linking antigen translocation into the ER with peptide loading onto MHC I, hence ensuring a major function in the integrity of the antigen-processing machinery