Multiple reversible MR signal changes caused by Epstein-Barr virus encephalitis.

This report presents the imaging findings of an unusual case of Epstein-Barr virus (EBV) encephalitis. A young man presented with a short-lasting history of febrile infection, neuropsychologic deficits, ataxia, and seizures. MR imaging revealed fully reversible signal intensities (T2, diffusion-weighted imaging with a decreased apparent diffusion coefficient) in the splenium of the corpus callosum and both posterior hemispheres. EBV infection must be added to the list of differential diagnoses of (reversible) splenial lesions.

Differential sensitivity to induction of spreading depression by partial disinhibition in chronically epileptic human and rat as compared to native rat neocortical tissue.

Spreading depression (SD) is characterized by a transient breakdown of neuronal function concomitant with a massive failure of ion homeostasis. It is a phenomenon that can be induced in neocortical tissue by raising excitability, e.g. injection of K(+), application of glutamatergic agonists, or blocking Na(+)/K(+) ATPase. Here we report a novel method of SD induction using minimal disinhibition with application of low concentrations (5 microM) of the GABA(A) receptor blocker bicuculline. This procedure-while subthreshold for epileptiform activity-readily induced spontaneous SDs in native rat neocortical slices, accompanied by typical depolarizations of neurons and glial cells. In contrast, in human neocortical preparations obtained from epilepsy surgery, in approximately 20% of the slices spontaneous epileptiform activity appeared with this bicuculline dosage without SDs. Raising the concentration of bicuculline to an epileptogenic dose (10 microM) in human tissue also resulted in the generation of epileptiform activity only. Likewise, in slices from pilocarpine-treated, chronically epileptic rats, bicuculline also only induced epileptiform activity without eliciting SDs. The experiments indicate that chronic epilepsy causes a differential sensitivity to partial GABA(A) receptor blockade with regard to induction of SD.

Distribution of glutamate receptor subunits in experimentally induced cortical malformations.

Electrophysiological studies in humans and animal models have revealed an intrinsic epileptogenicity of cortical dysplasias which are a frequent cause of drug-resistant epilepsy. An imbalance of inhibition and excitation has been causative related. Receptor-binding studies in rodents demonstrated reduced binding to GABA and increased binding to glutamate receptors within cortical dysplasias and increments of AMPA- and kainate-receptor binding in its surround. Immunohistochemically a differential downregulation of GABA(A) receptor subunits could be demonstrated in widespread areas within and around dysplasias. As receptor binding critically depends on receptor subunit composition the observed changes in binding properties might be related to this. Here, we immunohistochemically analyzed the regional expression of four NMDA receptor subunits and two major AMPA- and kainate-receptor complexes in adult rats after neonatal freeze lesions. These lesions are characterized by a three- to four-layered cortex and a microsulcus which mimic human polymicrogyria. Using antibodies against NR1, NR2A, NR2B, NR2D, GluR2,3, and GluR5,6,7 receptor subunits we demonstrated a pronounced disturbance of cortical immunostaining pattern in the cortical malformation. These changes reflected the structural disorganization of the microgyrus with some distortion of the apical dendrites of paramicrogyral pyramidal cells, a decrease and disorganization of cells at the bottom of the microsulcus, and an inflection of apical dendrites toward the microsulcus. The neuronal staining pattern of large pyramidal cells in the neighborhood of the dysplasia did not differ for any subunit investigated. No remote or widespread changes of glutamate-receptor subunit distribution could be detected. The lack of gross and/or widespread alterations of glutamate-receptor subunit distribution in the surround of focal cortical dysplasia suggests the presence of other or additional mechanisms underlying the increased excitatory neurotransmitter binding and excitability in cortical malformations.

Differentiation of GABA(A) receptors in subcortical heterotopias: subunit distribution of displaced cortex reflects original commitment.

Recent evidence suggests that the expression of GABA(A) receptor subunits is determined by an early innate program which can be further modified by thalamic input and local factors. We analyzed the GABA(A) subunit distribution in experimentally induced subcortical heterotopia which are a subgroup of neuronal migration disorders. Heterotopias consist of clusters of neurons which have stopped migration early, before they have reached their final commitment and well before thalamic afferents have reached their targets. Immuno- histochemical analyses of five important GABA(A) receptor subunits revealed an expression pattern typical for upper cortical layers reflecting the original commitment of the heterotopic neurons. These results point towards detailed innate determinants of cell fate which even contain information on receptor subunit distribution and are not affected by ectopic positioning.

[Radiation sensitivity for delayed reproductive death (DRD) following single or split-dose irradiation]. / Die Strahlenempfindlichkeit für verzögerten Reproduktivtod (DRD) nach Einzel- oder Splitdosisbestrahlung.

BACKGROUND: The growth kinetics of tumors after irradiation (Figure 1) is defined by cells surviving with delayed reproductive death (DRD). The prediction of radiation sensitivity of locally recurrent tumor growth is among other factors dependent on the knowledge of the impact of fractionated irradiation on these surviving cells with DRD. Short recovery effects can be estimated in vitro by comparing the difference of the medians of the distributions of clone sizes, the median clone sizes difference (MCD) after single and split exposure irradiation of the progenitor cells. MATERIALS AND METHODS: CHO-cells of a sub clone of the line T71 have a spontaneous cell loss rate of < 5%. The cells were irradiated a) by a single exposure 3 hours after synchronization and b) by a fractionated irradiation of half the exposure of a 200-kVp radiation exposure 3 hours and 6 hours after synchronization, respectively. Clone survival was determined (Figure 2). As function of dose and incubation time the distributions of clone sizes and the MCD were determined by tapping the clone cells in microscopic projections. RESULTS: The radiation sensitivity El of the DRD can be defined as the proportional factor of the linear relationship between the MCD on one side and the dose K x the cell division factor m on the other side. EI is dependent on the age of the cells during irradiation (Figure 3) and the cell line (Table 1). The slope of the dually logarithmic growth curve of the cell population is: s = 1 - El.K. Experimentally El was found to be equal for single and split dose irradiation (Figures 4 and 5) and amounted to El = 0.065 with Sd = +/- 0.004.--Literature analysis for the mathematical estimation of El.K (Figure 6) was based on reports of measurements of the local tumor recurrence growth of carcinomas and sarcomas of rodents and pulmonary metastases of sarcomas in humans, respectively, after fractional irradiation. We obtained values of 0 < or = El.K < or = 0.77 (Table 2). Values for El are independent of the dose and lie considerably below data derived from in-vitro measurements of different cell cultures. CONCLUSIONS: Since recurrence kinetics of tumors are determined by the radiation sensitivity El of the DRD, El can be used for estimating the kinetics of tumor recurrence. As lately described, MCD is linearly proportional to the micro-nucleus frequency [12]. Determinations of the micro-nucleus frequencies in tumor cell biopsies pre and post radiation onset offer the option for developing a fast predictive assay. Organ malformations of embryos after exposition to ionizing radiation can be mathematically deduced by DRD to the partial cell mortality.

Frequency of and interaction between polymorphisms in the beta3-adrenergic receptor and in uncoupling proteins 1 and 2 and obesity in Germans.

OBJECTIVE: To determine the role of polymorphisms in the genes for beta3-adrenergic receptor (beta3-AR) and in uncoupling proteins 1 and 2 (UCP-1, UCP-2) in obesity. DESIGN: Association study with three polymorphisms and obesity. SUBJECTS: Two hundred and thirty-six morbidly obese patients who underwent gastric banding surgery, 381 patients from the medical clinic and 198 healthy blood donors. MEASUREMENTS: The frequencies of the W64R in beta3-AR, the 3826A-->G in UCP-1 and the 45bp insertion in the 3 untranslated region of exon 8 in UCP-2 polymorphisms were determined. RESULTS: There were no significant differences in the frequencies of the beta3-AR and UCP-1 polymorphisms between obese (body mass index, BMI > 30 kg/m2) and lean subjects. Lean, but not obese, carriers of the R allele of beta3-AR had a significantly higher BMI. The mean age of obese subjects (excluding diabetics) who were carriers of the G allele of the UCP-1 polymorphism, 36y, was significantly younger than wild-type, 40y (P= 0.007). This effect was not seen in lean subjects. The effect of the G allele on the mean age of obese subjects was more apparent in subjects who were also carriers of the R allele of the beta3-AR polymorphism. The frequency of the ins allele of UCP-2 was significantly higher in obese subjects, 0.31, than in lean, 0.24 (P= 0.002) and carriers of the ins allele had a significantly higher BMI, 38 vs 35 (P= 0.005). There was no association between any of the polymorphisms and type II diabetes. CONCLUSION: In a German population, there was no association between the W64R in beta3-AR or the 3826A-->G in UCP-1 polymorphisms and obesity. However, they act synergistically to accelerate the development of obesity. The 45bp insertion in the 3 untranslated region of exon 8 in UCP-2 polymorphism is associated with obesity.

[Cortical dysgenesis: current classification, MRI diagnosis, and clinical review]. / Kortikale Dysgenesien. Aktuelle Klassifikation, kernspintomographische Diagnostik und klinische Ubersicht.

Cortical dysgenesis comprises a heterogenous group of genetic or acquired disturbances of cortical development which, due to progress in modern neuroimaging techniques, are increasingly recognized in association with a variety of clinical disorders. The spectrum of clinical manifestations, depending on type and extent of the alterations, includes severe mental retardation and epilepsy as well as neuropsychological deficits and psychiatric disorders. Up to now, the nomenclature of cortical malformations has been difficult and ambiguous. Recently, the understanding and terminology of these disorders has been facilitated by the proposal of a new classification scheme based on pathophysiological as well as pathogenetic mechanisms. This proposal has been elaborated by a group of experts and is not yet well-known in the German literature. Magnetic resonance imaging (MRI) allows diagnosis and classification in many cases of cortical dysgenesis during lifetime, thereby helping to identify prognostic and therapeutic options. Early diagnosis of cortical malformations is of particular importance in patients with drug-resistant epilepsy, as they can either be cured or benefit from epilepsy surgery. This review gives examples of the most relevant cortical malformations using the new classification scheme and summarizes their clinical as well as MRI characteristics. Besides routine MRI applications, some experimental techniques are discussed which may help to identify even subtle alterations.

Differential downregulation of GABAA receptor subunits in widespread brain regions in the freeze-lesion model of focal cortical malformations.

Focal cortical malformations comprise a heterogeneous group of disturbances of brain development, commonly associated with drug-resistant epilepsy and/or neuropsychological deficits. Electrophysiological studies on rodent models of cortical malformations demonstrated intrinsic hyperexcitability in the lesion and the structurally intact surround, indicating widespread imbalances of excitation and inhibition. Here, alterations in regional expression of GABA(A) receptor subunits were investigated immunohistochemically in adult rats with focal cortical malformations attributable to neonatal freeze-lesions. These lesions are morphologically characterized by a three- to four-layered cortex with microsulcus formation. Widespread regionally differential reduction of GABA(A) receptor subunits alpha1, alpha2, alpha3, alpha5, and gamma2 was observed. Within the cortical malformation, this downregulation was most prominent for subunits alpha5 and gamma2, whereas medial to the lesion, a significant and even stronger decrease of all subunits was detected. Lateral to the dysplastic cortex, the decrease was most prominent for subunit gamma2 and moderate for subunits alpha1, alpha2, and alpha5, whereas subunit alpha3 was not consistently altered. Interestingly, the downregulation of GABA(A) receptor subunits also involved the ipsilateral hippocampal formation, as well as restricted contralateral neocortical areas, indicating widespread disturbances in the neocortical and hippocampal network. The described pattern of downregulation of GABA(A) receptor subunits allows the conclusion that there is a considerable modulation of subunit composition. Because alterations in subunit composition critically influence the electrophysiological and pharmacological properties of GABA(A) receptors, these alterations might contribute to the widespread hyperexcitability and help to explain pharmacotherapeutic characteristics in epileptic patients.

Possible carcinogenic effects of X-rays in a transgenerational study with CBA mice.

A lifetime experiment using 4279 CBA/J mice was carried out to investigate whether the pre-conceptual exposure of sperm cells to X-ray radiation or urethane would result in an increased cancer risk in the untreated progeny, and/or increased susceptibility to cancer following exposure to a promoting agent. The study consisted of four main groups, namely a control group (saline), a urethane group (1 mg/g body wt) and two X-ray radiation groups (1 Gy, 2 Gy). At 1, 3 and 9 weeks after treatment, the males of these four parental groups were mated with untreated virgin females. The offspring of each parental group was divided into two subgroups: one received s.c. urethane (0.1 mg/g body wt once) as a promoter, the other saline, at the age of 6 weeks. All animals were evaluated for the occurrence of tumours. K-ras oncogene and p53 tumour suppressor gene mutations were investigated in frozen lung tumour samples. The female offspring of male parents exposed to X-rays 1 week before their mating showed a trend towards a higher tumour incidence of the haematopoietic system than the F1 controls. In addition, a higher percentage of bronchioloalveolar adenocarcinomas in male offspring born to irradiated paternals mated 1 week after X-ray treatment points to a plausible increased sensitivity of post-meiotic germ cell stages towards transgenerational carcinogenic effects. On the other hand, no increased tumour incidence and malignancy were observed in the offspring born to irradiated paternals mated 3 and 9 weeks after X-ray treatment. Paternal urethane treatment 1, 3 and 9 weeks prior to conception did not result in significantly altered incidence or malignancy of tumours of the lung, liver and haematopoietic tissue in the offspring. K-ras mutations increased during tumour progression from bronchioloalveolar hyperplasia to adenoma. Codon 61 K-ras mutations were more frequent in lung tumours of urethane-promoted progeny from irradiated parents than from control parents. P53 mutations were absent from these lung alterations.

Excitability changes and glucose metabolism in experimentally induced focal cortical dysplasias.

Malformations of cortical development are increasingly recognized in association with severe epileptic syndromes, neuropsychological disorders and mental retardation. Several clinical and experimental studies suggest that functional consequences of cortical dysplasias are not restricted to the area of the dysplastic lesion but also involve remote brain regions. In the present study cortical malformations were induced in newborn rats at day of birth by intracerebral injection of the glutamatergic agonist ibotenate. The resulting cytoarchitectonic lesion associates neuronal depopulation of deep cortical layers, ectopic neurons in superficial layers and sulcus formation, mimicking human polymicrogyria and migration disorders. Electrophysiological recordings of evoked field potentials in slice preparations of adult animals reveal hyperexcitability in widespread cortical regions surrounding the dysplasia. Low-intensity stimulation induced epileptiform activity consisting of long-lasting, multiphasic and N-methyl-D-aspartate-dependent field responses. They appeared with high variability as all-or-none events. These widespread changes in excitability were not observed in sham-operated animals with small superficial ectopias but intact deep cortical layers, indicating that focal loss of these layers induces extended alterations in cortical connectivity and imbalance of excitation and inhibition. Restricted zones of increased excitability were also found in the forelimb and hindlimb representation cortex in sham-operated and control animals, demonstrating that this activity has to be considered as an intrinsic property of specific cortical areas. Deoxyglucose autoradiography showed that the widespread hyperexcitability in ibotenate-injected animals was not accompanied by alterations in glucose metabolism, although in the area of structural abnormality a typical metabolic pattern was found, revealing an increased glucose uptake in layer I. Hypometabolism as described for many types of human dysplastic lesions was not observed. This difference between the experimental and clinical data may be due to the absence of behavioral seizures in this model. However, it can be hypothesized that in patients with developmental malformations, additional pathogenic factors contribute to the manifestation of seizure disorders.

Epileptiform discharges to extracellular stimuli in rat neocortical slices after photothrombotic infarction.

Seizures are one of the most frequent complications after cerebral ischemia in patients. Up to now it is unknown which mechanisms are responsible for this. As shown previously photothrombotic infarction in rat neocortex leads to a sweeping suppression of GABAergic inhibition. In this study we investigated whether and to what extent epileptiform discharges can be observed in this ischemia model. In neocortical slices from lesioned animals we did not find spontaneous epileptic activity or paroxysmal depolarisation shifts. However, ipsi- and contralateral to a photothrombotic lesion the frequency of double and multiple discharges was markedly increased when compared to unlesioned controls. Surprisingly, neither the drug lubeluzole which was has been shown to prevent the GABAergic disinhibition observed after photothrombotic lesioning of rat neocortex, nor the prevention of spreading depressions by the NMDA-receptor antagonist MK-801 during lesion induction significantly affected the frequency of epileptiform discharges. This indicates that the epileptiform discharges are probably caused by functional alterations of glutamatergic receptors.

Gene cloning and regulation of gene expression of the puc operon from Rhodovulum sulfidophilum.

Rhodovulum (Rhv.) sulfidophilum, unlike other nonsulfur purple bacteria, is able to synthesize the peripheral antenna complex even under fully aerobic conditions in the dark. We have obtained strong evidence that Rhv. sulfidophilum encodes only one copy of the puc operon, comprising pucB, pucA and pucC. pucB and pucA encode the beta- and alpha-polypeptides. The third ORF (pucC), downstream of pucA, has a strong homology to pucC of Rhodobacter (Rb.) capsulatus. Deletion mutation analysis indicated that the requirement for the pucC gene product for LH II expression was less strict than in Rb. capsulatus. Comparison of the deduced alpha and beta polypeptide sequences with the directly determined primary structure revealed a C-terminal processing of the alpha-subunit. Primer extension analysis showed that the pucBAC is transcribed from a sigma70-type promoter 130 bases upstream of the translational start of pucB. Transcriptional expression of the pucBAC operon in Rhv. sulfidophilum is higher, the lower the light intensity is, and is not reduced to a ground-level by the presence of oxygen. Based on lacZ fusions the relative promoter activities were, for dark aerobic:dark semiaerobic:low light anaerobic:medium light anaerobic:high light anaerobic, 5.5:7.0:2.0:1.0:0.78. Still unidentified cis-regulatory elements or binding sites of trans-regulatory elements are apparently localized in two distinct upstream regions. Furthermore, comparison of the promoter region of the Rhv. sulfidophilum pucBAC with the promoter regions of puc operons in related species showed distinct differences in the regulatory elements. The significance of these results with respect to the regulation of transcription and the oxygen-independent synthesis of LH II from Rhv. sulfidophilum is discussed.

[Dose dependence of the frequency of micronucleated clone cells and division-related median clone size difference. II]. / Dosisabhängigkeit der Frequenz mikronukleierter Klonzellen und teilungsbezogener medianer Klongrössendifferenz--Teil II.

PURPOSE: Following irradiation of the progenitor cells the clone growth of CHO cells decreases as a result of cell losses. Lethally acting expressions of micronuclei are produced by heritable lethal mutations. The dependency of the frequency of micronucleated binucleated clone cells and of the median clone sizes difference on the radiation dose was measured and compared to non-irradiated controls. METHODS: Using the cytokinesis-block-micronucleus-method binucleated cells with micronuclei were counted as ration of all binucleated cells within a clone size distribution. This ratio (shortened: micronucleus yield) was determined for all clone size distributions, which had been exposed to different irradiation doses and incubation times. The micronucleus yields were compared to the corresponding median clone sizes differences. RESULTS: The micronucleus yield is linearly dependent on the dose and is independent of the incubation time. The same holds true for the division related median clone sizes difference, which as a result is also linearly dependent on the micronucleus yield. CONCLUSIONS: Due to the inevitably errors of the cell count of micronucleated binucleated cells, an automatic measurement of the median clone sizes differences is the preferred method for evaluation of cellular radiation sensitivity for heritable lethal mutations. This value should always be determined in addition, if clone survival fractions are used as predictive test because it allows for an estimation of the remission probability of surviving cells.

Differential responsiveness of neocortical areas in the parieto-occipital region to low-intensity stimulation in vitro.

1. Extracellular recording techniques were used to map the responses to low-intensity stimuli across rat neocortical slices prepared from the parieto-occipital region. Intracellular recordings were obtained in regions of particular interest. After electrophysiological recording, slices were fixed in paraformaldehyde (4%) and Nissl-stained to allow identification of cytoarchitectonically discrete areas. 2. In most neocortical areas of the parieto-occipital region (Par1, HL, Fr1, Fr2), low-intensity stimuli applied to layer V evoked only short monophasic field excitatory postsynaptic potentials (fEPSPs) in layer II/III. In Oc2 (secondary visual cortex, rostral part), however, a long-lasting potential (up to 450 ms) consistently followed the short monophasic response seen in the other areas. 3. The late response observed in Oc2 was characterized by its inter-stimulus variability, polyphasic appearance and N-methyl-D-aspartate (NMDA)-receptor dependence. Intracellular recordings obtained from layer II/III pyramidal neurons located in Oc2 revealed short-latency, monophasic early excitatory postsynaptic potentials (eEPSPs) followed by long-lasting excitatory postsynaptic potentials (eEPSPs) followed by long-lasting excitatory postsynaptic potentials (EPSPs), which often triggered several action potentials 4. Recordings with two extracellular electrodes, one positioned directly above the stimulation electrode and the other at a variable distance (but also in layer II/III), suggested that the corresponding excitation spreads across the slice, but does not cross the cytoarchitectonic borders of Oc2. 5. Our data indicate that the electrophysiological responses to low-intensity stimuli differ within the parieto-occipital region of the rat neocortex. The type of response elicited depends on the cytoarchitectonic area in which the stimulus is applied. The results raise the question of whether further differences between neocortical subregions, with respect to basic electrophysiological properties, exist.

[The demonstration of heritable lethal mutations in the progeny of x-ray-irradiated CHO cells by micronucleus count in clone cells]. / Nachweis vererbbarer Letalmutationen in Nachkommen röntgenbestrahlter CHO-Zellen durch Mikrokernzählung in Klonzellen.

PURPOSE: Low doses of ionizing radiation reduce the growth rates of clones following irradiation of the progenitor cells. Such reductions of clone growth have been proven by means of measurements of clone size distributions. The medians of such distributions can be used to quantify the radiation damage. Prolongations of generation times and cell death as result of heritable lethal mutations have been discussed as causes for the reduction of clone growth. MATERIAL AND METHODS: The cell number of a clone of hypotetraploid CHO-cells was compared to the frequency of micronucleated binucleated cells in the same clone using the cytokinesis-block-micronucleus method. The dose dependent reduction of clone sizes is measured by the difference of the medians (after log transformation) of the clone size distributions. RESULTS: At cytochalasin-B concentrations of 1 microgram/ml and after an incubation time of 16 h a yield of binucleated cells of about 50% was obtained. Median clone size differences as a measure of clonal radiation damage increased linearly with incubation times of 76, 100, 124, and 240 h following irradiation with 3, 5, 7, and 12 Gy. The frequency of binucleated clone cells with micronuclei strongly increased with decreasing clone size by a factor up to 20 following irradiation with 3, 5, and 7 Gy. The frequency of micronucleated binucleated clone cells was found to be independent of incubation time after irradiation. CONCLUSION: Radiation induced clone size reductions result from cell losses caused by intraclonal expression of micronuclei which have its origin in heritable lethal mutations. Measurements of clone size distributions can be done automatically. They can serve as predictive test for determination of median cell loss rates of surviving cell clones.

Biochemical and spectroscopic characterization of the B800-850 light-harvesting complex from Rhodobacter sulphidophilus and its B800-830 spectral form.

We demonstrate that the B800-830 spectral form of the B800-850 peripheral light-harvesting complex of Rhodobacter sulphidophilus, which is formed at low ionic strengths in the presence of the zwitterionic detergent LDAO, results from a local modification of the bacteriochlorophyll binding site and not the dissociation of the complex. This perturbation does not result in significant changes to the interactions between the pigments as studied by circular dichroism or fluorescence spectroscopy; however, modifications in the pigment binding sites are inferred from changes in the preresonance Raman spectrum. Specifically, an alteration of the hydrogen bonding of the 2-acetyl group of at least one of the bacteriochlorophyll groups that make up the 850 nm absorbing pair is observed. This implies an alteration in the conformation of the C-terminal domain of the alpha-polypeptide, in which are located the two tyrosyl residues that are believed to act as H-bond donors to these groups, induced by the protein-bound detergent in the absence of bound cations. We suggest that the ability of this complex to form an 800-830 complex is linked to the presence of an aspartyl residue immediately upstream of the tyrosyl residues. This study therefore provides a further illustration of the importance of hydrogen bonds to the 2-acetyl group of the bacteriochlorophyll in the determination of its spectral properties; furthermore, we provide a description of a conformational change that is able to modulate chromophore binding in these complexes.

Isolation and complete amino acid sequence of the beta- and alpha-polypeptides from the peripheral light-harvesting pigment-protein complex II of Rhodobacter sulfidophilus.

The peripheral light-harvesting bacteriochlorophyll-carotenoid-protein complex B800-850 (LHII) has been isolated from membranes of semi-aerobic dark-grown cells of Rhodobacter sulfidophilus strain W4. A reversed-phase HPLC system resolved one beta- and one alpha-polypeptide in the ratio 1:1. The material obtained was of high purity and suitable for direct microsequence analysis. The primary structures of the beta- and alpha-polypeptides have been determined. The beta-polypeptide consists of 51 amino acid residues, yielding a molecular mass of 5512 Da and having 64.7% hydrophobicity. The alpha-polypeptide consists of 52 amino acid residues, with a calculated molecular mass of 5661 Da and 75% hydrophobicity. The significance of uncommon structure motives with respect to the unusual spectroscopic characteristics of this light-harvesting complex is discussed.

The light-harvesting complex II (B800-850) of Rhodobacter sulfidophilus: characterization and formation under different growth conditions.

The photosynthetic bacterium Rhodobacter sulfidophilus is able to grow chemotrophically and phototrophically at a broad range of light intensities. In contrast to other facultative phototrophs, R. sulfidophilus synthesizes reaction center and light-harvesting (LH) complexes, B870 (LHI) and B800-850 (LHII) even under full aerobic conditions in the dark. The content of bacteriochlorophyll (BChl) varied from 3.8 micrograms Bchl per mg cell protein when grown at high light intensity (20,000 lux) to 60 micrograms Bchl per mg cell protein when grown at low light intensities (6 lux). After a shift from high light to low light conditions, the size of the photosynthetic unit increased by a factor of 4. Chromatographic analysis of the LHII complex, isolated and purified from cells grown phototrophically (at high and low light intensities) and chemotrophically, could resolve only one type of alpha and one type of beta polypeptide in the purified complex, of which the N-terminal sequences have been determined.

[Dose requirements for projection techniques in x-ray diagnosis]. / Dosisbedarf für die Projektionsverfahren der Röntgendiagnostik.

The dose required in x-ray diagnosis depends upon the demands made on a diagnostically optimal x-ray film or in fluoroscopy, and upon the technical quality of the equipment. The actual dose requirement, derived from field studies, is juxtaposed on the basis of representative examples with the maximum permissible dose requirement in accordance with the prescribed minimum sensitivity values of the x-ray film. The ideal dose requirement has been stated by Cohen et al. (1981) by a formula basing on parallel beam, maximum quantum yield and Bucky grid effect depending on the signal to noise ratio and object contrast. This was checked by means of contrast detail diagrams measured at the hole phantom, and was additionally compared with measurement results obtained by Wust et al. (1989) with acrylic glass phantoms. The optimal dose requirement is obtained by the maximum technically possible approach to the ideal requirement level. Examples are given, besides for x-ray equipment with Gd2 O2 S screen film systems for grid screen mammography, and new thoracic examination systems for mass screenings. Finally, a few values concerning the dose requirement or the analogous time required for fluorescent screening in angiography and interventional radiology, are stated, as well as for dentistry and paediatric x-ray diagnostics.