Earth's ambipolar electrostatic field and its role in ion escape to space.

Cold plasma of ionospheric origin has recently been found to be a much larger contributor to the magnetosphere of Earth than expected1-3. Numerous competing mechanisms have been postulated to drive ion escape to space, including heating and acceleration by wave-particle interactions4 and a global electrostatic field between the ionosphere and space (called the ambipolar or polarization field)5,6. Observations of heated O+ ions in the magnetosphere are consistent with resonant wave-particle interactions7. By contrast, observations of cold supersonic H+ flowing out of the polar ionosphere8,9 (called the polar wind) suggest the presence of an electrostatic field. Here we report the existence of a +0.55 ± 0.09 V electric potential drop between 250 km and 768 km from a planetary electrostatic field (E∥⊕ = 1.09 ± 0.17 µV m-1) generated exclusively by the outward pressure of ionospheric electrons. We experimentally demonstrate that the ambipolar field of Earth controls the structure of the polar ionosphere, boosting the scale height by 271%. We infer that this increases the supply of cold O+ ions to the magnetosphere by more than 3,800%, in which other mechanisms such as wave-particle interactions can heat and further accelerate them to escape velocity. The electrostatic field of Earth is strong enough by itself to drive the polar wind9,10 and is probably the origin of the cold H+ ion population1 that dominates much of the magnetosphere2,3.

The genetic basis of asymptomatic codon 8 frame-shift (HBB:c25_26delAA) ß(0) -thalassaemia homozygotes.

Two 21-year old dizygotic twin men of Iraqi descent were homozygous for HBB codon 8, deletion of two nucleotides (-AA) frame-shift ß(0) -thalassaemia mutation (FSC8; HBB:c25_26delAA). Both were clinically well, had splenomegaly, and were never transfused. They had mild microcytic anaemia (Hb 120-130 g/l) and 98% of their haemoglobin was fetal haemoglobin (HbF). Both were carriers of Hph α-thalassaemia mutation. On the three major HbF quantitative trait loci (QTL), the twins were homozygous for G>A HBG2 Xmn1 site at single nucleotide polymorphism (SNP) rs7482144, homozygous for 3-bp deletion HBS1L-MYB intergenic polymorphism (HMIP) at rs66650371, and heterozygous for the A>C BCL11A intron 2 polymorphism at rs766432. These findings were compared with those found in 22 other FSC8 homozygote patients: four presented with thalassaemia intermedia phenotype, and 18 were transfusion dependent. The inheritance of homozygosity for HMIP 3-bp deletion at rs66650371 and heterozygosity for Hph α-thalassaemia mutation was found in the twins and not found in any of the other 22 patients. Further studies are needed to uncover likely additional genetic variants that could contribute to the exceptionally high HbF levels and mild phenotype in these twins.

Identification of the first mutation in a BRE motif of the ß-globin gene and its inheritance with two other α-globin gene mutations in a Lebanese family.

A 7-year old boy presented with a history of recurrent respiratory infections and hypochromic microcytic anemia. Iron profiles were normal thereby prompting genetic analysis of α- and ß-globin mutations. The first mutation in a BRE motif of the ß-globin gene in the proband, sibling and the mother was identified. The proband and his sibling also inherited common α-globin mutations from the father and mother. In all cases, no serious thalassemia disease was detected.

Hemoglobin Kenya composed of alpha- and ((A)gammabeta)-fusion-globin chains, associated with hereditary persistence of fetal hemoglobin.

Hb Kenya is made up of two normal alpha-globin chains and two (A)gammabeta-fusion globin chains. The latter are the product of an (A)gammabeta-hybrid globin gene formed as a result of misalignment during meiosis and nonhomologous crossing over. It is associated with a deletion of 22.7 kb including the delta-globin gene, between the (A)gamma- and beta-globin genes. Hb Kenya is found in Kenyans and Ugandans. Heterozygotes have moderately increased Hb F, and this mutation has been known as an ((A)gammabeta)(+) hereditary persistence of fetal hemoglobin (HPFH). Compound heterozygotes for Hb Kenya/Hb S are thought to be asymptomatic, but reports of long term follow-up of these patients are lacking. The correct identification of Hb Kenya is sometimes problematic. In cation exchange high performance liquid chromatography, Hb Kenya elutes in similar position as Hb A(2), Hb Lepore, Hb E, and several other variant hemoglobins. Definitive diagnosis that is necessary for proper patient management is best done by DNA-based gap-PCR tests.

Cutaneous leishmaniasis in Texas: A northern spread of endemic areas.

Leishmaniasis, an infection caused by various species of Leishmania protozoa, is usually transmitted by the bite of phlebotomine sandflies. The clinical presentations are extremely diverse and dependent on a variety of host and parasitic factors. Although rare in the United States, cutaneous leishmaniasis is endemic in south-central Texas. At this time, no autochthonous cases of cutaneous leishmaniasis are known to have been reported in north Texas. We report 9 autochthonous cases of cutaneous leishmaniasis obtained in residents of north Texas. None of these patients had any travel history to areas known to be endemic for Leishmania.

Laser assisted topical 'biofilm' chemoprevention of oral cancer.

This study examines whether a combination of laser microvascular targeting, mucosal adhesive film (MAF) and retinoic acid (RA) techniques would improve the efficacy for oral cancer chemoprevention. The cheek pouches of 48 hamsters were painted with 7,12-dimethlbenz[a]nthrancene to produce premalignant lesions. There were four groups of 12 each: (1) control; (2) pulsed dye laser (PDL) treatment; (3) topical MAF/RA patch treatment; and (4) combined treatment of PDL and MAF/RA. The treatments were conducted for 27 days. Our findings indicate that this new combined treatment is safe and effective for oral cancer chemoprevention, and warrants further study.