Are the magnetic fields of millisecond pulsars ~ 10^8 G?

It is generally assumed that the magnetic fields of millisecond pulsars (MSPs) are $\sim 10^{8}$G. We argue that this may not be true and the fields may be appreciably greater. We present six evidences for this: (1) The $\sim 10^{8}$ 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 $\sim 10^{8}$ 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 $\sim 10^{8}$ G fields of MSPs are wrong; (6) When magnetic fields are measured directly with cyclotron lines in X-ray binaries, fields $\gg 10^{8}$ 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.Comment: 16 pages, accept for publication in Astrophysics and Space Scienc

Low temperature electronic properties of Sr_2RuO_4 II: Superconductivity

The body centered tetragonal structure of Sr_2RuO_4 gives rise to umklapp scattering enhanced inter-plane pair correlations in the d_{yz} and d_{zx} orbitals. Based on symmetry arguments, Hund's rule coupling, and a bosonized description of the in-plane electron correlations the superconducting order parameter is found to be a orbital-singlet spin-triplet with two spatial components. The spatial anisotropy is 7%. The different components of the order parameter give rise to two-dimensional gapless fluctuations. The phase transition is of third order. The temperature dependence of the pair density, specific heat, NQR, Knight shift, and susceptibility are in agreement with experimental results.Comment: 20 pages REVTEX, 3 figure

Applications of electrified dust and dust devil electrodynamics to Martian atmospheric electricity

Atmospheric transport and suspension of dust frequently brings electrification, which may be substantial. Electric fields of 10 kVm-1 to 100 kVm-1 have been observed at the surface beneath suspended dust in the terrestrial atmosphere, and some electrification has been observed to persist in dust at levels to 5 km, as well as in volcanic plumes. The interaction between individual particles which causes the electrification is incompletely understood, and multiple processes are thought to be acting. A variation in particle charge with particle size, and the effect of gravitational separation explains to, some extent, the charge structures observed in terrestrial dust storms. More extensive flow-based modelling demonstrates that bulk electric fields in excess of 10 kV m-1 can be obtained rapidly (in less than 10 s) from rotating dust systems (dust devils) and that terrestrial breakdown fields can be obtained. Modelled profiles of electrical conductivity in the Martian atmosphere suggest the possibility of dust electrification, and dust devils have been suggested as a mechanism of charge separation able to maintain current flow between one region of the atmosphere and another, through a global circuit. Fundamental new understanding of Martian atmospheric electricity will result from the ExoMars mission, which carries the DREAMS (Dust characterization, Risk Assessment, and Environment Analyser on the Martian Surface)-MicroARES (Atmospheric Radiation and Electricity Sensor) instrumentation to Mars in 2016 for the first in situ measurements

Multicenter Studies Of Oral Ziprazidone For The Treatment Of Patients With Schizophrenia And Schizoaffective Disorder [estudos Multicêntricos Da Ziprasidona Oral No Tratamento De Pacientes Com Esquizofrenia Ou Transtorno Esquizoafetivo]

Background: The oral ziprasidone efficacy, safety, and tolerability on Brazilian patients with schizophrenic and schizoaffective disorder were evaluated through two sequential clinical trials. Methods: Prospective open studies. At the first 6-week trial patients received 80 to 160 mg/day of ziprasidone, and were evaluated using the Positive and Negative Symptom Scale (PANSS), Clinical Global Impression-Severity Scale (CGI-S), Intensity Care Questionnaire (ICQ) e Patient Preference Scale (PPS). Safety and tolerability were evaluated by clinical, EKG, and laboratorial analysis, Extrapyramidal Symptom Rating Scale (ESRS), and Barnes Akathisia Scale (BAS). Responsive patients were included on one up to 12-month second trial. Results: 162 patients were analyzed regarding drug efficacy, and 164 regarding tolerability at first clinical trial. From baseline to endpoint treatment decreased PANSS scores from 94.3 to 76.2 (P<.0001). Either scores on CGI-S and ICQ showed significantly reduction. Ziprasidone had the patient's preference (64.8%) compared to the last medication used through the PPS application. Neither, extrapyramidal symptoms or EKG alterations were found. From 106 included patients at the second trial, 86 were analyzed regarding efficacy. The median of treatment duration was 5.6 months, and the mean of PANSS was kept during the evaluation. The adverse events profiles from both studies were similar. Conclusion: Oral ziprasidone is an effective and safe drug for chronic treatment of patients with schizophrenic and schizoaffective disorder. © Copyright Moreira Jr. Editora.644170176Kane, J., Honigfeld, G., Singer, J., Meltzer, H., Clozapine for the treatment-resistant schizophrenic. A double-blind comparison with chlorpromazine (1988) Arch Gen Psychiatry, 45, pp. 789-796Freedman, R., Schizophrenia (2003) N Engl J Med, 349, pp. 1738-1749Meltzer, H.Y., Clinical studies on the mechanism of action of clozapine: The dopamine-serotonin hypothesis of schizophrenia (1989) Psychopharmacology (Berl), 99, pp. S18-S27Kane, J.M., Oral ziprasidone in the treatment of schizophrenia: A review of short-term trials (2003) J Clin Psychiatry, 64 (SUPPL. 19), pp. 19-25Gunasekara, N.S., Spencer, C.M., Keating, G.M., Ziprasidone: A review of its use in schizophrenia and schizoaffective disorder (2002) Drugs, 62 (8), pp. 1217-1251Glassman, A.H., Bigger Jr., J.T., Antipsychotic drugs: Prolonged QTc interval, torsade de pointes, and sudden death (2001) Am J Psychiatry, 158, pp. 1774-1782Diagnostic and Statistical Manual of Mental Disorders, 4th ed.: DSM-IV. Washington, D.C.: American Psychiatric Association, 1994Chaves, A.C., Shirakawa, I., Escala das síndromes negativa e positiva - PANSS e seu uso no Brasil (1998) Rev Psiq Clín, 25 (6), pp. 337-343Clinical Global Impression Severity Scale (1976) ECDEU Assessment Manual of Psychopharmacology, , National Institute of Mental Health, Guy W Ed, Washington, DC: U. S. Government Printing OfficeChouinard, G., Margolese, H.C., Manual for the Extrapyramidal Symptom Rating Scale (ESRS) (2005) Schizophr Res, 76 (2-3), pp. 247-265Barnes, T.R., A rating scale for drug-induced akathisia (1989) B J Psychiatry, 154, pp. 672-676Awad, A.G., Hogan, T.P., Subjective response to neuroleptic drugs and the quality of life: Implication for treatment outcome (1994) Acta psychiatr Scand, p. 89. , spplm 380 27-32Arato, M., O'Connor, R., Meltzer, H.Y., A 1-year, double-blind, placebo-controlled trial of ziprasidone 40, 80 and 160 mg/day in chronic schizophrenia: The Ziprasidone Extended Use in Schizophrenia (ZEUS) study (2002) Int Clin Psychopharmacol, 17, pp. 207-215Hirsch, S.R., Kissling, W., Bauml, J., Power, A., O'Connor, R., A 28-week comparison of ziprasidone and haloperidol in outpatients with stable schizophrenia (2002) J Clin Psychiatry, 63, pp. 516-523Weiden, P.J., Simpson, G.M., Potkin, S.G., O'Sullivan, R.L., Effectiveness of switching to ziprasidone for stable but symptomatic outpatients with schizophrenia (2003) J Clin Psychiatry, 64, pp. 580-588Harvey, P.D., Meltzer, H., Simpson, G.M., Potkin, S.G., Loebel, A., Siu, C., Romano, S.J., Improvement in cognitive function following a switch to ziprasidone from conventional antipsychotics, olanzapine, or risperidone in outpatients with schizophrenia (2004) Schizophr Res, 66, pp. 101-113Weiden, P.J., Daniel, D.G., Simpson, G.M., Romano, S.J., Improvement in indices of health status in outpatients with schizophrenia switched to ziprasidone (2003) J Clin Psychopharmacol, 23, pp. 595-600Lieberman, J.A., Stroup, T.S., McEvoy, J.P., Swartz, M.S., Rosenheck, R.A., Perkins, D.O., Effectiveness of antipsychotic drugs in patients with chronic schizophrenia (2005) N Engl J Med, 353, pp. 1209-1223Kingsbury, S.J., Fayek, M., Trufasiu, D., Zada, J., Simpson, G.M., The apparent effects of ziprasidone on plasma lipids and glucose (2001) J Clin Psychiatry, 62, pp. 347-349Cohen, S., Fitzgerald, B., Okos, A., Khan, S., Khan, A., Weight, lipids, glucose, and behavioral measures with ziprasidone treatment in a population with mental retardation (2003) J Clin Psychiatry, 64, pp. 60-6

Derived vascular endothelial cells induced by mucoepidermoid carcinoma cells: 3-dimensional collagen matrix model*

Mucoepidermoid carcinoma undergoes uniquely vigorous angiogenic and neovascularization processes, possibly due to proliferation of vascular endothelial cells (ECs) induced by mucoepidermoid carcinoma cells (MCCs) in their three-dimensional (3D) microenvironment. To date, no studies have dealt with tumor cells and vascular ECs from the same origin of mucoepidermoid carcinoma using the in vitro 3D microenvironment model. In this context, the current research aims to observe neovascularization with mucoepidermoid carcinoma microvascular ECs (MCMECs) conditioned by the microenvironment in the 3D collagen matrix model. We observed the growth of MCMECs purified by immunomagnetic beads and induced by MCCs, and characteristics of tubule-like structures (TLSs) formed by induced MCMECs or non-induced MCMECs. The assessment parameters involved the growth curve, the length, the outer and inner diameters, and the wall thickness of the TLSs, and the cell cycle. Results showed that MCCs induced formation of the TLSs in the 3D collagen matrix model. A statistically significant difference was noted regarding the count of TLSs between the control group and the induction group on the 4th day of culture (t=5.00, P=0.001). The outer and inner diameters (t 1=5.549, P 1=0.000; t 2=10.663, P 2=0.000) and lengths (t=18.035, P=0.000) of the TLSs in the induction group were statistically significant larger than those in the control group. The TLSs were formed at the earlier time in the induction group compared with the control group. It is concluded that MCCs promote growth and migration of MCMECs, and formation of the TLSs. The 3D collagen matrix model with MCMECs induced by MCCs in the current research may be a favorable choice for research on pro-angiogenic factors in progression of mucoepidermoid carcinoma

Recessive <em>NUP54</em> variants underlie early-onset dystonia with striatal lesions.

Infantile striatonigral degeneration is caused by a homozygous variant of the nuclear-pore complex (NPC) gene NUP62, involved in nucleo-cytoplasmic trafficking. By querying sequencing-datasets of patients with dystonia and/or Leigh(-like) syndromes, we identified three unrelated individuals with biallelic variants in NUP54. All variants clustered in the C-terminal protein region that interacts with NUP62. Associated phenotypes were similar to those of NUP62-related disease, including early-onset dystonia with dysphagia, choreoathetosis, and T2-hyperintense lesions in striatum. In-silico and protein-biochemical studies gave further evidence for the argument that the variants were pathogenic. We expand the spectrum of NPC component-associated dystonic conditions with localized basal-ganglia abnormalities