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Chronic diseases and illnesses associated with unspecific symptoms are on the rise. In addition to chronic stress in social and work environments, physical and chemical exposures at home, at work, and during leisure activities are causal or contributing environmental stressors that deserve attention by the general practitioner as well as by all other members of the health care community. It seems certainly necessary now to take "new exposures" like electromagnetic field (EMF) into account. Physicians are increasingly confronted with health problems from unidentified causes. Studies, empirical observations, and patient reports clearly indicate interactions between EMF exposure and health problems. Individual susceptibility and environmental factors are frequently neglected. New wireless technologies and applications have been introduced without any certainty about their health effects, raising new challenges for medicine and society. For instance, the issue of so-called non-thermal effects and potential long-term effects of low-dose exposure were scarcely investigated prior to the introduction of these technologies. Common EMF sources include Wi-Fi access points, routers and clients, cordless and mobile phones including their base stations, Bluetooth devices, ELF magnetic fields from net currents, ELF electric fields from electric lamps and wiring close to the bed and office desk. On the one hand, there is strong evidence that long-term-exposure to certain EMF exposures is a risk factor for diseases such as certain cancers, Alzheimer's disease and male infertility. On the other hand, the emerging electromagnetic hypersensitivity (EHS) is more and more recognized by health authorities, disability administrators and case workers, politicians, as well as courts of law. We recommend treating EHS clinically as part of the group of chronic multisystem illnesses (CMI) leading to a functional impairment (EHS), but still recognizing that the underlying cause remains the environment. In the beginning, EHS symptoms often occur only occasionally, but over time they may increase in frequency and severity. Common EHS symptoms include headaches, concentration difficulties, sleeping problems, depression, lack of energy, fatigue and flu-like symptoms. A comprehensive medical history, which should include all symptoms and their occurrences in spatial and temporal terms and in the context of EMF exposures, is the key to the diagnosis. The EMF exposure can be assessed by asking for typical sources like Wi-Fi access points, routers and clients, cordless and mobile phones and measurements at home and at work. It is very important to take the individual susceptibility into account. The primary method of treatment should mainly focus on the prevention or reduction of EMF exposure, that is, reducing or eliminating all sources of EMF at home and in the workplace. The reduction of EMF exposure should also be extended to public spaces such as schools, hospitals, public transport, and libraries to enable persons with EHS an unhindered use (accessibility measure). If a detrimental EMF exposure is reduced sufficiently, the body has a chance to recover and EHS symptoms will be reduced or even disappear. Many examples have shown that such measures can prove effective. Also the survival rate of children with leukemia depends on ELF magnetic field exposure at home. To increase the effectiveness of the treatment, the broad range of other environmental factors that contribute to the total body burden should also be addressed. Anything that supports a balanced homeostasis will increase a person's resilience against disease and thus against the adverse effects of EMF exposure. There is increasing evidence that EMF exposure has a major impact on the oxidative and nitrosative regulation capacity in affected individuals. This concept also may explain why the level of susceptibility to EMF can change and why the number of symptoms reported in the context of EMF exposures is so large. Based on our current understanding, a treatment approach that minimizes the adverse effects of peroxynitrite - as has been increasingly used in the treatment of multisystem disorders - works best. This EMF Guideline gives an overview of the current knowledge regarding EMF-related health risks and provides concepts for the diagnosis and treatment and accessibility measures of EHS to improve and restore individual health outcomes as well as for the development of strategies for prevention.

Background: Vasoactive intestinal peptide (VIP) exerts immune-modulatory actions mainly via VPAC1 receptor stimulation. VPAC1 may be a treatment target of inflammatory diseases, but little is known about the receptor expression profile in immune-competent cells in vivo., Material and Methods: 20 male healthy subjects received a single intravenous bolus of 2 ng/kg body weight Escherichia coli endotoxin (LPS). Receptor status was evaluated in peripherial blood cells before and 3, 6 and 24 h after LPS by FACS analysis and q-PCR. VIP plasma concentrations were measured by ELISA., Results: Granulocytes accounted for 51% of leukocytes at baseline and 58 ± 37% were positive for VPAC1. The granulocyte population increased 2.6 fold after LPS, and a transient down-regulation of VPAC1 to 28 ± 23% was noted at 3 h (p < 0.001), which returned to baseline at 24 hours. Baseline VPAC1 expression was low in lymphocytes (6.3 ± 3.2%) and monocytes (11 ± 9.6%). In these cells, LPS up-regulated VPAC1 at 6 h (13.2 ± 4.9%, p < 0.001) and 24 h (31.6 ± 20.5%, p = 0.001), respectively. Consistent changes were noted for the VIP-receptors VPAC2 and PAC1. VPAC1, VPAC2 and PAC1 mRNA levels were unchanged in peripheral blood mononuclear cells (PBMC). VIP plasma concentration increased from 0.5 ± 0.3 ng/ml to 0.7 ± 0.4 ng/ml at 6 h after LPS (p < 0.05) and returned to baseline within 24 h., Conclusion: The time profile of VPAC receptor expression differs in granulocytes, monocytes and lymphocytes after LPS challenge in humans. Changes in circulating VIP concentrations may reflect innate immune responses.

Perinatal asphyxia remains a major cause of acute mortality and of permanent neurodevelopmental disability in infants and children. However, the pathophysiologic features of hypoxic-ischemic encephalopathy are still incompletely understood. Animal studies have been focussing on grey matter pathology but information on white matter lesions is limited. The aim of the study was to investigate white matter lesions after three months following graded perinatal asphyxia in the rat using a well-documented, reproducible, clinically relevant and simple animal model of perinatal asphyxia. Brains of rat pups (n=10 per group) exposed to asphyctic periods of 10 and 20 minutes were examined histologically and compared to normoxic brain using Kluever-Barrera myelin staining, immunohistochemically with antibodies against myelin basic protein, 2',3'-cyclic-nucleotide'-phosphodiesterase as markers for myelination, antibodies against neurofilaments for the evaluation of axonal density and antibodies against glial fibrillary acidic protein as a marker for astrocytic gliosis. Morphometry three months after perinatal asphyxia showed significant reduction of corpus callosum in asphyctic brains. Patchy myelination deficits were found in hippocampal fimbriae and cerebellum, lobulus L 8, accompanied by reduced axonal density. Hypothalamus and striatum did not show any myelination deficit. Up to now only short term effects of perinatal asphyxia on myelination have been reported and this communication reveals long-term myelination deficit in three brain regions after three months following perinatal asphyxia. As myelination deficit was regularly accompanied by reduction of neurofilament immunoreactivity, we suggest that white matter lesions are paralleling grey matter damage, a subject still controversial in pathophysiology of brain damage in perinatal asphyxia.

Chromosomes from ten human male fibroblast metaphases were completely reconstructed from electron micrographs of serially sectioned material. Chromosome centromere positions were determined by finding the three-dimensional coordinates of the centromere midpoint. The data set showed the identity of nine chromosome types (chromosomes 1, 2, 3, 6, 9, 16, 17, 18 and the Y chromosome) preserved as they are positioned in vivo. The results indicate that there is (1) no significant association of the homologous chromosomes examined, (2) a significant tendency for a central location of the Y chromosome and of chromosome 18, (3) a significant tendency for a peripheral location of chromosome 6, (4) no significant tendency for homologous chromosomes to reorganize as metaphase advances and (5) no significant differential condensation across the metaphase plate. Therefore, the only organization pattern observed for the centromeres of the homologous chromosomes studied is some sorting by size across the metaphase plate. These results may be typical of dividing cell types. Different chromosome arrangements are found in some non-dividing cell types (e.g. mammalian brain cells). The different distributions of chromosomes in different cell types can be considered as forms of "nuclear differentiation". It is postulated that nuclear differentiation may be related to cell differentiation.

Satellite nucleoli of lymphocytes were studied to provide additional information on the cytochemistry of these nucleoli particularly with respect to the presence of rDNA and RNA polymerase I. According to the results of the in situ hybridization satellite nucleoli contain rDNA similarly as characteristic nucleoli. Immunostaining demonstrated that satellite nucleoli similarly as characteristic nucleoli possess RNA polymerase I in addition to proteins B23, C23 and fibrillarin. RNA of satellite nucleoli was detected in satellite as well as in characteristic nucleoli with buffered toluidine or methylene blue. The cytochemical evidence and morphology of satellite nucleoli strongly supports the supposition that these nucleoli represent solitary small nucleoli containing nucleolus organizer regions which did not participate in the formation of characteristic nucleoli.

Bronchial epithelial cells obtained by brush biopsy during fiberoptic bronchoscopy performed in 12 patients with chronic bronchitis and 12 healthy control subjects, were investigated for HLA-DR antigen expression and nucleolar silver staining patterns. In all patients with chronic bronchitis the number of bronchial epithelial cells positive to HLA-DR antigen was highly increased (> 90%), whereas in the controls only a few epithelial cells (< 10%) showed a weak HLA-DR antigen expression. Patients with chronic bronchitis showed an increased lymphocytic reaction compared to the control subjects. Both in the patients with chronic bronchitis and in the healthy controls the number of nucleoli was the same. The number of silver stained dots per nucleus was significantly higher in patients with chronic bronchitis than in the control subjects (7.70 +/- 0.87 as against 5.11 +/- 0.52; p < 0.0001). The intensity of the lymphocytic reaction correlated with the HLA-DR antigen expression and the increase in silver staining (Spearman's r = 0.543; p < 0.01). This indicates the influence of inflammation on the activation of epithelial cells derived from the respiratory tract.

The physical location of the rDNA repeating units (25 S, 18 S and 5.8 S rRNA genes and the intergenic spacer sequences) was investigated in rye (Secale cereale L.) and wheat (Triticum aestivum L.) root tip meristematic cells by in situ hybridization using light and electron microscopy. The rDNA sequences are organized differently in the two related and intercrossable species. In rye (2n = 14, one pair of chromosomes with nucleolar organizing regions, NORs), two condensed blocks of rDNA-containing chromatin occurred in each interphase nucleus. The blocks were associated with the periphery of nucleoli and a single-labelled, decondensed rDNA fibre extended into the nucleolus from the block. We term this expression pattern terminal decondensation. In wheat (2n = 6x = 42, five pairs of chromosomes with NORs), inactive condensed labelled chromatin was found unassociated with nucleoli. Active NORs had some condensed rDNA associated with the nucleolar periphery, but, in contrast to rye, condensed rDNA was also found within the nucleolus. The condensed labelled rDNA in wheat nucleoli was visible as fluorescent foci in the light microscope and labelled condensed chromatin in the electron microscope. Its absence in rye shows that condensed rDNA need not be present in active plant nucleoli. Diffuse labelled sites of rDNA, likely to represent actively transcribed rDNA, were found in both rye and wheat. Active rDNA loci in wheat have many expressed segments separated by unexpressed, condensed, rDNA-fragmented decondensation-while each locus in rye has a single, unexpressed perinucleolar condensed block of rRNA genes. Thus the positions of actively transcribed genes within the tandem arrays of rDNA at each locus are fundamentally different in the two cereals. The NOR chromosome appeared to extend through the nucleolus, and active rDNA sequences did not loop out from chromatin into the nucleolus as is frequently described in nucleolar models.

In situ hybridization using biotinylated total genomic DNA and avidin detection systems was adapted for examination of thin-sectioned plant material in the light and electron microscopes. Root tip material was preserved prior to sectioning, so that the in vivo disposition of the chromatin was maintained. Use of total genomic DNA from Secale africanum as a probe enabled the chromatin from the two parental genomes in the grass hybrid Hordeum chilense x S. africanum to be distinguished. The biotinylated probe preferentially labelled the chromosomes of S. africanum origin. DNA-DNA hybrids were visualized at the light-microscope level by Texas Red fluorescence and at the electron-microscope level by the enzymic precipitation of DAB (diaminobenzidine) or by colloidal gold particles. The use of thin sections allowed the location of probe hybridization to be established unequivocally in both metaphase and interphase nuclei. Analysis of interphase nuclei showed that chromatin originating from the two parental genomes did not intermix but occupied distinct domains.

Non-stimulated human lymphocytes from peripheral blood usually contain only one ring-shaped nucleolus. Polyethyleneglycol-mediated cell fusion with mitotic Chinese hamster ovary cells induces premature chromosome condensation in human lymphocytes. Subsequent silver staining reveals that more than one nucleolus organizer region (NOR) is silver-positive and frequently participates in the formation of "satellite associations". It can therefore be concluded that more than one NOR contributes to the ring-shaped nucleoli of lymphocytes in human peripheral blood and that they may be transcriptionally active. During phytohemagglutinin (PHA) stimulation, the number of silver-positive NORs, the number of nucleoli and the number of chromosomes participating in "satellite associations" increase.