Blood laboratory findings in patients suffering from self‐perceived electromagnetic hypersensitivity (EHS)

Risks from electromagnetic devices are of considerable concern. Electrohypersensitive (EHS) persons attribute a variety of rather unspecific symptoms to exposure to electromagnetic fields. The pathophysiology of EHS is unknown and therapy remains a challenge. We hypothesized that some electrosensitive individuals are suffering from common somatic health problems. Toward this end we analysed clinical laboratory parameters including thyroid‐stimulating hormone (TSH), alanine transaminase (ALT), aspartate transaminase (AST), creatinine, hemoglobine, hematocrit and c‐reactive protein (CRP) in subjects suffering from EHS and in controls that are routinely used in clinical medicine to identify or screen for common somatic disorders. One hundred thirty‐two patients (n = 42 males and n = 90 females) and 101 controls (n = 34 males and n = 67 females) were recruited. Our results identified laboratory signs of thyroid dysfunction, liver dysfunction and chronic inflammatory processes in small but remarkable fractions of EHS sufferers as potential sources of symptoms that merit further investigation in future studies. In the cases of TSH and ALT/AST there were significant differences between cases and controls. The hypotheses of anaemia or kidney dysfunction playing a major role in EHS could be unambiguously refuted. Clinically it is recommended to check for signs of treatable somatic conditions when caring for individuals suffering from self‐proclaimed EHS. Bioelectromagnetics 30:299–306, 2009. © 2009 Wiley‐Liss, Inc.     

分子系统发育对中国芸香科分类的贡献

The treatment of Rutaceae in the Chinese flora chose to follow Engler in recognizing Rutoideae and Toddalioideae as two separate subfamilies. Morphological and chemical comparisons, however, suggested grouping those two subfamilies in one subfamily, Rutoideae. This move has received support from molecular phylogenetic analyses, which also showed that the Chinese taxa in Euodia should be placed in Tetradium and Melicope following Hartley. Investigations into the chemistry and molecular phylogeny of Murraya also indicated that the species in the section Bergera without yuehchukene should be removed from Murraya. These findings clearly show the value of molecular cladistics to the taxonomy of Rutaceae in China and also directions for further investigations. Key words Bergera, Euodia, Melicope, Murraya, Rutaceae, Rutoideae, Tetradium, Toddalioideae.     

Phylogeny and biogeography of the genus Illadopsis (Passeriformes: Timaliidae) reveal the complexity of diversification of some African taxa

African jungle babblers or illadopsises, genus Illadopsis Heine, 1859, are small shy babblers which occupy the undergrowth of African humid forest habitats. The taxonomy of Illadopsis as well as its biogeography are currently poorly known because the morphological differentiation is rather subtle and no phylogenetic analysis has been undertaken. To investigate these issues, we sequenced four loci (mitochondrial ND2 and ND3, and nuclear myoglobin intron 2 and β-fibrinogen intron 5) for the seven species of Illadopsis . Our analyses retrieve the monophyly of Illadopsis and suggest that I. albipectus and I. cleaveri , I. puveli and I. rufescens , some individuals of I. rufipennis and I. pyrrhoptera are sister taxa respectively. I. fulvescens appears to be an isolated taxon and our data reveal several cases of "incipient speciation" among its populations. Our dating analyses, using a Bayesian relaxed-clock method, reveal that most splits in Illadopsis occurred synchronously around the Plio-Pleistocene transition, suggesting that some diversification events in African forest taxa took place before the onset of the large-amplitude climatic cycles of the Pleistocene epoch. Thus, the diversification of African taxa in time and space to be more complex than the Pleistocene time frame traditionally associated with the diversification of African forest taxa. Instead we observe a process of differentiation which roughly corresponds to the broadly hypothesised lowland refugia of upper Guinea, eastern and western Guinea-Congolia, although the time frame of this divergence well predates the Pleistocene epoch. Our results also suggest that deep genetic divergences do exist among species complexes of African birds which differ only slightly in morphological characters. As such, molecular analyses are powerful and essential tools if we are to construct the evolutionary history of such lineages in a meaningful manner.     

Soluble polyphenols: Synthesis and bioavailability of 3,4′,5-tri(α-d-glucose-3-O-succinyl) resveratrol

We report the development of a chemical modification method of general applicability to polyphenols, which increases solubility to influence absorption. Glucosyl groups were added to the resveratrol kernel via a succinate linker, yielding 3,4′,5-tri-(α-d-glucose-3-O-succinyl) resveratrol. The construct was only slowly hydrolyzed in acid and at pH 6.8, but it was destroyed by blood esterases in less than 1 h. In rats its administration resulted in a blood concentration versus time curve shifted to longer times in comparison to resveratrol, a useful modulation of pharmacokinetics. The area-under-curve parameter and the metabolite mix were similar to those of resveratrol. The method may be advantageously employed to solubilize other polyphenols and to make them more palatable.     

PPIB Mutations Cause Severe Osteogenesis Imperfecta

Deficiency of cartilage-associated protein (CRTAP) or prolyl 3-hydroxylase 1(P3H1) has been reported in autosomal-recessive lethal or severe osteogenesis imperfecta (OI). CRTAP, P3H1, and cyclophilin B (CyPB) form an intracellular collagen-modifying complex that 3-hydroxylates proline at position 986 (P986) in the α1 chains of collagen type I. This 3-prolyl hydroxylation is decreased in patients with CRTAP and P3H1 deficiency. It was suspected that mutations in the PPIB gene encoding CyPB would also cause OI with decreased collagen 3-prolyl hydroxylation. To our knowledge we present the first two families with recessive OI caused by PPIB gene mutations. The clinical phenotype is compatible with OI Sillence type II-B/III as seen with COL1A1/2, CRTAP, and LEPRE1 mutations. The percentage of 3-hydroxylated P986 residues in patients with PPIB mutations is decreased in comparison to normal, but it is higher than in patients with CRTAP and LEPRE1 mutations. This result and the fact that CyPB is demonstrable independent of CRTAP and P3H1, along with reported decreased 3-prolyl hydroxylation due to deficiency of CRTAP lacking the catalytic hydroxylation domain and the known function of CyPB as a cis-trans isomerase, suggest that recessive OI is caused by a dysfunctional P3H1/CRTAP/CyPB complex rather than by the lack of 3-prolyl hydroxylation of a single proline residue in the α1 chains of collagen type I.     

Missense Mutations in a Retinal Pigment Epithelium Protein, Bestrophin-1, Cause Retinitis Pigmentosa

Bestrophin-1 is preferentially expressed at the basolateral membrane of the retinal pigmented epithelium (RPE) of the retina. Mutations in the BEST1 gene cause the retinal dystrophies vitelliform macular dystrophy, autosomal-dominant vitreochoroidopathy, and autosomal-recessive bestrophinopathy. Here, we describe four missense mutations in bestrophin-1, three that we believe are previously unreported, in patients diagnosed with autosomal-dominant and -recessive forms of retinitis pigmentosa (RP). The physiological function of bestrophin-1 remains poorly understood although its heterologous expression induces a Cl⁻-specific current. We tested the effect of RP-causing variants on Cl⁻ channel activity and cellular localization of bestrophin-1. Two (p.L140V and p.I205T) produced significantly decreased chloride-selective whole-cell currents in comparison to those of wild-type protein. In a model system of a polarized epithelium, two of three mutations (p.L140V and p.D228N) caused mislocalization of bestrophin-1 from the basolateral membrane to the cytoplasm. Mutations in bestrophin-1 are increasingly recognized as an important cause of inherited retinal dystrophy.