Are the magnetic fields of millisecond pulsars similar to 10(8) G?

It is generally assumed that the magnetic fields of millisecond pulsars (MSPs) are similar to 10(8) G. We argue that this may not be true and the fields may be appreciably greater. We present six evidences for this: (1) The similar to 10(8)G field estimate is based on magnetic dipole emission losses which is shown to be questionable; (2) The MSPs in low mass X-ray binaries (LMXBs) are claimed to have < 10(11) G on the basis of a Rayleygh-Taylor instability accretion argument. We show that the accretion argument is questionable and the upper limit 10(11) G may be much higher; (3) Low magnetic field neutron stars have difficulty being produced in LMXBs; (4) MSPs may still be accreting indicating a much higher magnetic field; (5) The data that predict similar to 10(8) G for MSPs also predict ages on the order of, and greater than, ten billion years, which is much greater than normal pulsars. If the predicted ages are wrong, most likely the predicted similar to 10(8) G fields of MSPs are wrong; (6) When magnetic fields are measured directly with cyclotron lines in X-ray binaries, fields a parts per thousand << 10(8) G are indicated. Other scenarios should be investigated. One such scenario is the following. Over 85% of MSPs are confirmed members of a binary. It is possible that all MSPs are in large separation binaries having magnetic fields > 10(8) G with their magnetic dipole emission being balanced by low level accretion from their companions.

Exercise-stimulated GLUT4 Expression is Similar in Normotensive and Hypertensive Rats

The effects of exercise training on systolic blood pressure (BP), insulin sensitivity, and plasma membrane GLUT4 protein content in spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats were compared. 16 SHR and 16 WKY male rats, aged 6 months, were randomized into sedentary and trained (tread-mill running, 5 days/week, 60 min/day for 10 weeks) groups (n = 8/group). At baseline, SHR had lower insulin sensitivity than WKY rats, however, there were no differences between WKY and SHR GLUT4 expression. The 10-week training reduced BP by similar to 19% in SHR, improved insulin sensitivity by similar to 24% in SHR, but not in WKY, and increased GLUT4 expression in both animal models. Compared to the sedentary group, there was an increase of GLUT4 in WKY rats by similar to 25% in the heart, by similar to 23% in the gastrocnemius, and by similar to 15% in the fat tissue. Trained SHR presented an increase in GLUT4 of similar to 21%, similar to 20%, and similar to 14%, in the same tissues, respectively. There were no differences between SHR and WKY rats in post-training GLUT4 expression. We conclude that training determined BP and insulin resistance reduction in SHR, and increased GLUT4 expression in both normotensive and hypertensive rats. However, considering the similar rise in GLUT4-induced training in SHR and WKY, it is possible that GLUT4 levels in plasma membrane fraction do not have a pivotal role in the exercise-induced improvement of insulin sensitivity in SHR.

CD4(+) CD25(+) Foxp3(+) Regulatory T Cells, Dendritic Cells, and Circulating Cytokines in Uncomplicated Malaria: Do Different Parasite Species Elicit Similar Host Responses?

Clearing blood-stage malaria parasites without inducing major host pathology requires a finely tuned balance between pro- and anti-inflammatory responses. The interplay between regulatory T (Treg) cells and dendritic cells (DCs) is one of the key determinants of this balance. Although experimental models have revealed various patterns of Treg cell expansion, DC maturation, and cytokine production according to the infecting malaria parasite species, no studies have compared all of these parameters in human infections with Plasmodium falciparum and P. vivax in the same setting of endemicity. Here we show that during uncomplicated acute malaria, both species induced a significant expansion of CD4(+) CD25(+) Foxp3(+) Treg cells expressing the key immunomodulatory molecule CTLA-4 and a significant increase in the proportion of DCs that were plasmacytoid (CD123(+)), with a decrease in the myeloid/plasmacytoid DC ratio. These changes were proportional to parasite loads but correlated neither with the intensity of clinical symptoms nor with circulating cytokine levels. One-third of P. vivax-infected patients, but no P. falciparum-infected subjects, showed impaired maturation of circulating DCs, with low surface expression of CD86. Although vivax malaria patients overall had a less inflammatory cytokine response, with a higher interleukin-10 (IL-10)/tumor necrosis factor alpha (TNF-alpha) ratio, this finding did not translate to milder clinical manifestations than those of falciparum malaria patients. We discuss the potential implications of these findings for species-specific pathogenesis and longlasting protective immunity to malaria.

Nil graded self-similar algebras

In [19], [24] we introduced a family of self-similar nil Lie algebras L over fields of prime characteristic p > 0 whose properties resemble those of Grigorchuk and Gupta-Sidki groups. The Lie algebra L is generated by two derivations v(1) = partial derivative(1) + t(0)(p-1) (partial derivative(2) + t(1)(p-1) (partial derivative(3) + t(2)(p-1) (partial derivative(4) + t(3)(p-1) (partial derivative(5) + t(4)(p-1) (partial derivative(6) + ...))))), v(2) = partial derivative(2) + t(1)(p-1) (partial derivative(3) + t(2)(p-1) (partial derivative(4) + t(3)(p-1) (partial derivative(5) + t(4)(p-1) (partial derivative(6) + ...)))) of the truncated polynomial ring K[t(i), i is an element of N vertical bar t(j)(p) =0, i is an element of N] in countably many variables. The associative algebra A generated by v(1), v(2) is equipped with a natural Z circle plus Z-gradation. In this paper we show that for p, which is not representable as p = m(2) + m + 1, m is an element of Z, the algebra A is graded nil and can be represented as a sum of two locally nilpotent subalgebras. L. Bartholdi [3] andYa. S. Krylyuk [15] proved that for p = m(2) + m + 1 the algebra A is not graded nil. However, we show that the second family of self-similar Lie algebras introduced in [24] and their associative hulls are always Z(p)-graded, graded nil, and are sums of two locally nilpotent subalgebras.