Trophic and spatial patterns of contaminants in fishes from the Republic of the Marshall Islands in the equatorial Pacific.

The Republic of the Marshall Islands (RMI) has been affected by marine pollution from militarization and urbanization. To address concerns raised by the Marshall Islands Marine Resources Authority, this study examined concentrations of dissolved contaminants in reef and pelagic fishes in the RMI and assessed potential associated risks. Metals, organochlorine pesticides, polychlorinated biphenyls (PCBs), and polycyclic aromatic hydrocarbons (PAHs) were examined in reef and pelagic fishes from six atolls: Kwajalein, Majuro, Jaluit, Utirik, Rongelap, and Wotje. Clear trophic patterns emerged for metals. Total arsenic was highest in higher trophic level reef fishes, particularly in the camouflage grouper (Epinephelus polyphekadion) (>100 µg g-1 total As), but inorganic arsenic was negligible in higher trophic levels and showed an inverse trend with the highest percentages present in parrotfishes and herbivores. Copper and mercury were elevated in higher trophic level reef and pelagic fishes, respectively, and the maximum mercury concentrations (6.45 µg g-1 in Gymnosarda unicolor) were among the highest reported in the Pacific. Conversely, cadmium and lead were highest in lower trophic levels, like surgeonfishes and parrotfishes. PCBs were more clearly linked to locations and were highest at two atolls with military history (Kwajalein and Jaluit) (>U.S. EPA Screening Value of 2.5 ppb). PAHs were ubiquitous across taxa (detected in 97% of samples), but the highest concentrations were in lower trophic levels. Organochlorine pesticides were detected at very low concentrations that do not likely pose a risk. We compare concentrations to established thresholds for human health and find that - for specific locations and species - contaminant concentrations may pose a risk to fish and other marine taxa, as well as human consumers. This study provides baseline information that aids the development of marine conservation and public health recommendations and addresses a data gap that persists for marine pollution throughout the Pacific Islands.

Low rate of intracerebral hemorrhage after cardiac catheterization in patients with acute ischemic stroke in a large case series.

BACKGROUND AND AIMS: Myocardial infarction complicating acute ischemic stroke (IS) is associated with high mortality, but evidence guiding the acute management is scarce. In particular, data on the risk of intracerebral hemorrhage (ICH) due to early cardiac catheterization including the peri-procedural application of antithrombotic drugs in patients with acute ischemic stroke are limited. Here, we aimed to evaluate the incidence and patient characteristics of ICH after cardiac catheterization in acute stroke patients to help to govern the risk of intracranial bleeding versus the benefits of myocardial reperfusion via cardiac catheterization. METHODS: We screened a consecutive cohort of n = 126 patients with acute ischemic stroke (IS) who underwent cardiac catheterization during the same hospital stay at a large German neurovascular center (LMU Munich). Eventually, we identified n = 42 patients with cardiac catheterization after acute stroke. N = 22/42 patients did not receive neuroimaging post cardiac catheterization and were discharged without any new neurological deficits, n = 20/42 had neuroimaging after cardiac catheterization and were included for final analysis. RESULTS: Cardiac catheterization was performed within a median of 3,6 days after ischemic stroke (No-ICH 7,3 days (IQR, 3,8-16,2) vs. ICH 1,1 days (IQR, 0,8-74,6), p = 0,40), One patient showed new neurological deficits after cardiac procedures (n = 1/42, 2,4 %). New or progressive ICH was ultimately found in 15 % (3/20) of cases. They were classified as HT1, PH1 and PH2 according to ECASS II criteria, respectively. With regards to the coronary catheterization, 85 % of all patients undergoing catheterization ultimately received percutaneous cardiac intervention. ICH was not significantly associated with any of the independent variables. Intrahospital death due to either ischemic stroke, ICH or cardiovascular events did not occur. CONCLUSION: The incidence of ICH in ischemic stroke followed by early cardiac catheterization and application of antithrombotic drugs was comparable to studies reporting on the incidence of ICH in ischemic stroke patients without catheterization. This study's results strengthen the hypothesis that in presence of both, acute myocardial infarction and acute ischemic stroke, the general risk for ICH is not prohibitive of cardiac catheterization.

Surface effects of vapour-liquid-solid driven Bi surface droplets formed during molecular-beam-epitaxy of GaAsBi.

Herein we investigate a (001)-oriented GaAs1-xBix/GaAs structure possessing Bi surface droplets capable of catalysing the formation of nanostructures during Bi-rich growth, through the vapour-liquid-solid mechanism. Specifically, self-aligned "nanotracks" are found to exist trailing the Bi droplets on the sample surface. Through cross-sectional high-resolution transmission electron microscopy the nanotracks are revealed to in fact be elevated above surface by the formation of a subsurface planar nanowire, a structure initiated mid-way through the molecular-beam-epitaxy growth and embedded into the epilayer, via epitaxial overgrowth. Electron microscopy studies also yield the morphological, structural, and chemical properties of the nanostructures. Through a combination of Bi determination methods the compositional profile of the film is shown to be graded and inhomogeneous. Furthermore, the coherent and pure zincblende phase property of the film is detailed. Optical characterisation of features on the sample surface is carried out using polarised micro-Raman and micro-photoluminescence spectroscopies. The important light producing properties of the surface nanostructures are investigated through pump intensity-dependent micro-PL measurements, whereby relatively large local inhomogeneities are revealed to exist on the epitaxial surface for important optical parameters. We conclude that such surface effects must be considered when designing and fabricating optical devices based on GaAsBi alloys.

Effects of AlGaAs cladding layers on the luminescence of GaAs/GaAs1-xBix/GaAs heterostructures.

The structural and optical properties of GaAs1-xBix quantum wells (QWs) symmetrically clad by GaAs barriers with and without additional confining AlGaAs layers are studied. It is shown that a GaAs/GaAs1-xBix/GaAs QW with x ~ 4% and well width of ~ 4 nm grown by molecular beam epitaxy demonstrates efficient photoluminescence (PL) that becomes significantly more thermally stable when a cladding AlGaAs layer is added to the QW structure. The PL behavior for temperatures between 10 and 300 K and for excitation intensities varying by seven orders of magnitude can be well described in terms of the dynamics of excitons including carrier capture in the QW layer, thermal emission and diffusion into the cladding barriers. Understanding the role of these processes in the luminescence of dilute GaAs1-xBix QW structures facilitates the creation of highly efficient devices with reduced thermal sensitivity and low threshold current.

X-ray diffraction from nonperiodic layered structures with correlations: analytical calculation and experiment on mixed Aurivillius films.

X-ray diffraction from films consisting of layers with different thicknesses, structures and chemical contents is analysed. The disorder is described by probabilities for different sequences of layers. Closed analytical expressions for the diffracted X-ray intensity are obtained when the layers form a stationary Markov chain. The proposed model is applied to the diffraction data from epitaxial sodium bismuth titanate thin films with Aurivillius structure possessing such one-dimensional disorder. In this case, the disorder is caused by a random stacking of three and four perovskite units separated by bismuth oxide interlayers. The results of analytical calculations are in good agreement with the experimental data and indicate that the incorporation of sodium in the Bi(4)Ti(3)O(12) phase causes the formation of a fourth perovskite unit.

Optical evidence of a quantum well channel in low temperature molecular beam epitaxy grown Ga(AsBi)/GaAs nanostructure.

A Ga(AsBi) quantum well (QW) with Bi content reaching 6% and well width of 11 nm embedded in GaAs is grown by molecular beam epitaxy at low temperature and studied by means of high-resolution x-ray diffraction, photoluminescence (PL), and time-resolved PL. It is shown that for this growth regime, the QW is coherently strained to the substrate with a low dislocation density. The low temperature PL demonstrates a comparatively narrow excitonic linewidth of ∼ 40 meV. For high excitation density distinct QW excited states evolve in the emission spectra. The origins of peculiar PL dependences on temperature and excitation density are interpreted in terms of intra-well optical transitions.

A novel multi-detection technique for three-dimensional reciprocal-space mapping in grazing-incidence X-ray diffraction.

A new scattering technique in grazing-incidence X-ray diffraction geometry is described which enables three-dimensional mapping of reciprocal space by a single rocking scan of the sample. This is achieved by using a two-dimensional detector. The new set-up is discussed in terms of angular resolution and dynamic range of scattered intensity. As an example the diffuse scattering from a strained multilayer of self-assembled (In,Ga)As quantum dots grown on GaAs substrate is presented.

Late-onset metachromatic leukodystrophy: genotype strongly influences phenotype.

BACKGROUND: P426L and I179S are the two most frequent mutations in juvenile and adult metachromatic leukodystrophy (late-onset MLD), which, in contrast to infantile MLD, show marked phenotypic heterogeneity. OBJECTIVE: To search for genotype-phenotype correlations in late-onset MLD. METHODS: The authors reviewed the clinical course of 22 patients homozygous for mutation P426L vs 20 patients heterozygous for mutation I179S, in which the second arylsulfatase A (ASA) mutation had also been determined. RESULTS: P426L homozygotes principally presented with progressive gait disturbance caused by spastic paraparesis or cerebellar ataxia; mental disturbance was absent or insignificant at the onset of disease but became more apparent as the disease evolved. In contrast, compound heterozygotes for I179S presented with schizophrenia-like behavioral abnormalities, social dysfunction, and mental decline, but motor deficits were scarce. Reduced peripheral nerve conduction velocities and less residual ASA activity were present in P426L homozygotes vs I179S heterozygotes. CONCLUSION: The characteristic clinical differences between homozygous P426L and compound heterozygous I179S patients establish a distinct genotype-phenotype correlation in late-onset metachromatic leukodystrophy.

Controlling planar and vertical ordering in three-dimensional (In,Ga)As quantum dot lattices by GaAs surface orientation.

Anisotropic surface diffusion and strain are used to explain the formation of three-dimensional (In,Ga)As quantum dot lattices. The diffusion characteristics of the surface, coupled with the elastic anisotropy of the matrix, provides an excellent opportunity to influence the dot positions. In particular, quantum dots that are laterally organized into long chains or chessboard two-dimensional arrays vertically organized with strict vertical ordering or vertical ordering that is inclined to the sample surface normal are accurately predicted and observed.

[Unusual course of alpha-mannosidosis with symptoms of paranoid-hallucinatory psychosis]. / Ungewöhnlicher Verlauf einer alpha-Mannosidose mit Symptomen einer paranoid-halluzinatorischen Psychose.

We report the case of a 27-year-old female with recurrent paranoid-hallucinatory episodes who was initially diagnosed as suffering from schizophrenic psychosis. After 10 years of treatment under this diagnosis, alpha-mannosidosis was identified to be the underlying cause of her psychiatric symptoms. alpha-Mannosidosis is a rare autosomal recessive lysosomal storage disorder associated with decreased activity of the enzyme mannosidase. In the present case, diagnosis was made late in the illness after failure of a response to antipsychotic treatment and with the patient additionally showing progressive cognitive decline. Only after extensive investigation was the diagnosis made by showing decreased alpha-mannosidase enzyme activity in serum and blood leukocytes. This case demonstrates that an unusual clinical course or striking symptom patterns, especially in association with somatic comorbidity, in psychotic patients should lead to diagnostic consideration of inherited metabolic disease.

Expression of major histocompatibility complex class I molecules on the different cell types in multiple sclerosis lesions.

Multiple sclerosis is considered to be an immune-mediated disease of the central nervous system, characterized by chronic inflammation, primary demyelination and axonal damage. The mechanisms of demyelination and axonal injury are heterogeneous and complex. One possible mechanism is direct damage of oligodendrocytes and neurons by Class I MHC restricted cytotoxic T-cells. In this study we analyzed the expression of functional MHC class I molecule complex, consisting of alpha-chain and beta2-microglobulin, in a large sample of human autopsy material, containing 10 cases of acute MS, 10 cases of chronic active MS, 10 cases of chronic inactive MS and 21 controls. To examine the expression of MHC class I and II molecules on the different cell-types in brain, we used quantitative immunohistochemical techniques, double staining and confocal laser microscopy scans on paraffin embedded sections. We found constitutive expression of MHC class I molecule on microglia and endothelial cells. A hierarchical up-regulation of MHC class I was present on astrocytes, oligodendrocytes, neurons and axons, depending upon the severity of the disease and the activity of the lesions. MHC class II molecules were expressed on microglia and macrophages, but not on astrocytes. These data indicate that in MS lesions all cells of the central nervous system are potential targets for Class I MHC restricted cytotoxic T-cells.

Guillain-Barré syndrome with marked pleocytosis or a significant proportion of polymorphonuclear granulocytes in the cerebrospinal fluid: neuropathological investigation of five cases and review of differential diagnoses.

In cases with otherwise clinically typical Guillain-Barré syndrome (GBS), pronounced cerebrospinal fluid (CSF) pleocytosis or the mere presence of CSF-polymorphonuclear granulocytes should alert the physician to consider alternative diagnoses. Therefore, we retrospectively studied the neuropathology of central and peripheral nervous system in two cases with a CSF cell count of more than 50/microl and in three cases with a significant proportion of polymorphonuclear granulocytes in the CSF sediment. All cases fulfilled the required criteria for the diagnosis of GBS, the duration from onset to death ranged from 4 to 100 days. Neuropathological investigations included routine staining procedures and immunohistochemistry for antigens of glial and haematopoetic cells as well as for products of relevant neurotropic viruses. Demyelinating polyradiculitis was present in four cases, in one patient with a survival time of 4 days the type of damage to myelinated fibres was unclassifiable. In the central nervous system a consistent finding was diffuse activation of microglia, only one case showed mild meningeal and lower brainstem inflammation. Viral products were generally absent. In summary, the neuropathological findings confirm that marked CSF pleocytosis or the presence of polymorphonuclear granulocytes does not rule out the diagnosis of GBS.

Lethal fulminate S. aureus sepsis in M. Behçet overnight cold exposure.

Whether patients with Behçet's disease (BD) and immunosuppressive therapy are generally prone to acquire severe infectious diseases is unknown. A 48-year-old man under corticosteroids and azathioprine for BD since 1995 was admitted because of a transitory ischemic attack. Between the third and fourth hospital day he was accidentally locked up, insufficiently dressed, in the hospital's chapel over night. On the following day, he developed fever and deteriorating consciousness until he became comatose. CT scans of the brain were normal and there was only a slight pleocytosis. Despite adequate therapy, the patient's condition further deteriorated such that he died. Responsible for his decline was a fulminate sepsis, diagnosed upon fever, increased C-reactive protein, thrombocyte decline, multi-organ failure, rhabdomyolysis, growth of S. aureus on blood culture, and autopsy. Patients with BD and immunosuppressive therapy, may be more vulnerable to infections and may develop lethal overwhelming sepsis already after overnight cold exposure.

Altered expression of voltage-dependent calcium channel alpha(1) subunits in temporal lobe epilepsy with Ammon's horn sclerosis.

Voltage-dependent calcium channels, the initial components in the calcium signalling cascade, are increasingly being recognised as relevant factors in the pathology of epilepsy. To further characterise their role in temporal lobe epilepsy associated with Ammon's horn sclerosis, we investigated the immunohistochemical distribution of five different voltage-dependent calcium channel alpha(1) subunits (alpha(1A), alpha(1B), alpha(1C), alpha(1D), alpha(1E)) in 14 hippocampal specimens of patients with Ammon's horn sclerosis in comparison with eight autopsy control cases. In epilepsy specimens an increased immunoreactivity was observed for alpha(1A), alpha(1B), alpha(1D) and alpha(1E) in the neuropil of the dentate gyrus molecular layer. Dentate gyrus granule cells and residual CA3 pyramidal neurones showed enhanced immunoreactivity for alpha(1A), while labelling of these neurones was decreased for alpha(1C). Astrocytes in Ammon's horn sclerosis specimens were strongly immunoreactive for the alpha(1C) subunit contrasting with an absent astrocytic alpha(1C) labelling in controls. Our results suggest that the expression of calcium channels in neurones and glial cells is dynamically regulated in temporal lobe epilepsy, supporting the relevance of calcium signalling pathways for this disease.

Distribution of a calcium channel subunit in dystrophic axons in multiple sclerosis and experimental autoimmune encephalomyelitis.

Multiple sclerosis and experimental autoimmune encephalomyelitis (EAE) are immune-mediated diseases of the CNS. They are characterized by widespread inflammation, demyelination and a variable degree of axonal loss. Recent magnetic resonance spectroscopy studies have indicated that axonal damage and loss are a reliable correlate of permanent clinical disability. Accordingly, neuropathological studies have confirmed the presence and timing of axonal injury in multiple sclerosis lesions. The mechanisms of axonal degeneration, however, are unclear. Since calcium influx may mediate axonal damage, we have studied the distribution of the pore-forming subunit of neuronal (N)-type voltage-gated calcium channels in the lesions of multiple sclerosis and EAE. We found that alpha(1B), the pore-forming subunit of N-type calcium channels, was accumulated within axons and axonal spheroids of actively demyelinating lesions. The axonal staining pattern of alpha(1B) was comparable with that of beta-amyloid precursor protein, which is an early and sensitive marker for disturbance of axonal transport. Importantly, within these injured axons, alpha(1B) was not only accumulated, but also integrated in the axoplasmic membrane, as shown by immune electron microscopy on the EAE material. This ectopic distribution of calcium channels in the axonal membrane may result in increased calcium influx, contributing to axonal degeneration, possibly via the activation of neutral proteases. Our data suggest that calcium influx through voltage-dependent calcium channels is one possible candidate mechanism for axonal degeneration in inflammatory demyelinating disorders.

[Development of academic clinical neurology in Europe; a successful concept and its consequences]. / Die Entwicklung der schulmedizinischen Neurologie in Europa, ein Erfolgskonzept und seine Konsequenzen.

Clinical medicine in the 18th century is devoted to Hippocratic tradition. Pathology is not a requisite in this concept. The viewpoint of the pathologists is obscured by traditional philosophy and hampered by insufficient methods. In the 19th century, concepts of correlation between clinical signs and local organ pathology occur. The catastrophic increase of traumatic injury of the nervous system during world war I results in better concepts of clinical localization. At the beginning of the 21st century, the traditional view of the neurological science has changed the image of the patient profoundly, by the emergence of new diseases, disappearance of others and an altered view of the traditional neurologist.

Multiple sclerosis and chronic autoimmune encephalomyelitis: a comparative quantitative study of axonal injury in active, inactive, and remyelinated lesions.

Recent magnetic resonance (MR) studies of multiple sclerosis lesions indicate that axonal injury is a major correlate of permanent clinical deficit. In the present study we systematically quantified acute axonal injury, defined by immunoreactivity for beta-amyloid-precursor-protein in dystrophic neurites, in the central nervous system of 22 multiple sclerosis patients and 18 rats with myelin-oligodendrocyte glycoprotein (MOG)-induced chronic autoimmune encephalomyelitis (EAE). The highest incidence of acute axonal injury was found during active demyelination, which was associated with axonal damage in periplaque and in the normal appearing white matter of actively demyelinating cases. In addition, low but significant axonal injury was also observed in inactive demyelinated plaques. In contrast, no significant axonal damage was found in remyelinated shadow plaques. The patterns of axonal pathology in chronic active EAE were qualitatively and quantitatively similar to those found in multiple sclerosis. Our studies confirm previous observations of axonal destruction in multiple sclerosis lesions during active demyelination, but also indicate that ongoing axonal damage in inactive lesions may significantly contribute to the clinical progression of the disease. The results further emphasize that MOG-induced EAE may serve as a suitable model for testing axon-protective therapies in inflammatory demyelinating conditions.

Central nervous system pathology in patients with the Guillain-Barré syndrome.

Thirteen autopsy cases of patients with clinical criteria of the Guillain-Barré syndrome were investigated for pathological changes and cellular composition of inflammatory infiltrates in the CNS and PNS. The survival times from the onset of neurological symptoms until death ranged from 1 day to 12 months. In the CNS, degeneration of spinal posterior tracts was seen in three cases. Mononuclear infiltrates consisted of evenly proportioned lymphocytes and macrophages in cases with survival of 1 and 2 days, whereas macrophages predominated in cases with survival of 5 days and longer. Infiltrates presented as nodular clusters around blood vessels and neurons, or were scattered diffusely. They were found within the spinal cord in eight out of 13 cases, within the medulla oblongata in eight out of 12 cases, within the pons in five out of nine cases, and in one out of four midbrains. Activation of microglia, either focal or diffuse, was found in various degrees in 11 out of 13 cases, involving the spinal cord (six out of 13 cases), the medulla oblongata (10 out of 12 cases), the pons (five out of nine cases) or as subependymal rims along the walls of the ventricular system and the central canal of the spinal cord (seven out of 13 cases). In the PNS, myelin loss (12 out of 13 cases), axonal degeneration (six out of 13 cases) and mononuclear cell infiltrates (13 out of 13 cases) were seen in segmental and cranial nerves, spinal ganglia and spinal roots in varying distribution and severity. Mononuclear cell infiltrates were composed of macrophages and T lymphocytes, with even distribution in cases with short survival (1 and 2 days), and predominance of macrophages in cases with protracted clinical course. T lymphocytes were equally composed of OPD4+ and CD8+ cells without obvious differences between cases of short and long duration, or between PNS and CNS infiltrates in 11 out of 12 cases, whilst two cases had a dominant OPD4+ subset. We conclude that CNS pathology is frequent in patients with Guillain-Barré syndrome. It involves axons with secondary myelin impairment, microglial activation and inflammatory infiltration. In this series, primary demyelination is not found in the CNS. Changes such as degeneration of spinal posterior tracts are secondary to pathology in the PNS. Inflammatory cell reactions in the CNS are similar to those in the PNS and to CNS pathology in experimental allergic neuritis. This inflammation might reflect CNS immune activation in the absence of the relevant antigen, in addition to cellular reactions accompanying secondary CNS changes. The presence of distinct pathology in the CNS is in contrast with other recent studies on the pathology of Guillain-Barré syndrome which, unlike this study, may have been influenced by recently introduced treatments.