[Treatment of carbon monoxide poisoning in Germany : A retrospective single center analysis]. / Behandlung von Kohlenmonoxidvergiftungen in Deutschland : Eine retrospektive Single-Center-Analyse.

BACKGROUND: The symptoms of acute carbon monoxide (CO) poisoning are unspecific, ranging from headaches to unconsciousness and death. In addition to acute symptoms, delayed severe neurological sequelae may occur. While a total of 440 deaths by CO poisoning were registered in Germany in 1999, a total of 594 patients died (0.73 per 100,000 inhabitants) in 2014 and in 2015 the number even increased to 648 deaths. A national database on clinical symptoms, course of illness or quality of care concerning CO poisoning does not yet exist. METHODS: The treatment data of patients admitted to the Hyperbaric Emergency Centre Wiesbaden (HEC) from 2013 to 2017 with CO poisoning formed the basis of the study. This was a comparative evaluation of patient demographics, poisoning sources, symptom spectrum, course of treatment and time intervals registered on the preclinical and clinical levels. RESULTS: From 2013 to 2017 a total of 476 patients (282 men and 194 women) with an average non-invasively measured CO-Hb of 15% (Q0.25 = 7.6%, Q0.75 = 22.3%) were treated with hyperbaric oxygen. Heaters (n = 131), charcoal barbecues (n = 93), fires (n = 90), hookahs (n = 78) and combustion engines (n = 37) were the most frequent CO sources identified. Headaches, vertigo, nausea and syncope were the most prevalent symptoms. A median of 91 min (Q0.25 = 53 min; Q0.75 = 147 min) passed between first medical contact and BGA-validated diagnosis. In total, 151 patients were transferred directly to the HEC, whereas 325 patients were secondarily transferred. The delay in this subgroup took 183 min (median Q0.25 = 138 min; Q0.75 = 248 min). After receiving the first hyperbaric treatment, 80% were free of symptoms. Remaining symptoms included headache (10%), fatigue (8%), vertigo (5%) and nausea (3%) and 45 patients terminated further treatment. Of the patients 417 received a second hyperbaric treatment and 370 patients were treated 3 times. After the third treatment, 89% were free of symptoms and 5% still reported headaches, 3% vertigo and 2% fatigue. In total, 6 patients died and 430 patients were symptom-free after treatment. CONCLUSION: Commonly known sources (fire, charcoal grills) aside, many poisonings by smoking a hookah were observed. This study highlights the importance of considering CO poisoning as a differential diagnosis when encountering patients, especially of younger age, with non-specific neurological symptoms, as well as the importance of early initiation of treatment. A direct correlation between CO-Hb values (whether measured noninvasively or by invasive BGA) and the initial symptoms could not be demonstrated. In total, substantial time expired between the diagnosis and start of treatment of patients transported to a primary care hospital compared to those transported directly to the HEC. Although analysis showed adequate treatment with oxygen in the preclinical interval, administration of oxygen during primary hospital stay showed room for improvement. Introducing a national CO poisoning register and uniform treatment guidelines could improve in-house clinical processes. Multicenter studies are needed to close the gaps identified in the quality of care in Germany.

Multilevel blazed gratings in resonance domain: an alternative to the classical fabrication approach.

In this paper we present a novel technological approach for the fabrication of multilevel gratings in the resonance domain. A coded chromium mask is used to avoid alignment errors in electron beam lithography, which typically occur within the standard multistep binary micro-optics technology. The lateral features of all phase levels of the grating are encoded in a single chromium mask. The final profile of the structure is obtained by selective etching process for each level. This new technological method is applied for the fabrication of two different three-level gratings in resonance domain. The corresponding optical response as well as structural characterizations are presented and discussed. In particular, a first order diffraction efficiency of 90% is demonstrated for a grating period twice the wavelength at normal incidence.

Cartesian oval representation of freeform optics in illumination systems.

The geometrical method for constructing optical surfaces for illumination purpose developed by Oliker and co-workers [Trends in Nonlinear Analysis (Springer, 2003)] is generalized in order to obtain freeform designs in arbitrary optical systems. The freeform is created by a set of primitive surface elements, which are generalized Cartesian ovals adapted to the given optical system. Those primitives are determined by Hamiltonian theory of ray optics. The potential of this approach is demonstrated by some examples, e.g., freeform lenses with collimating front elements.

Rewetting does not return drained fen peatlands to their old selves.

Peatlands have been drained for land use for a long time and on a large scale, turning them from carbon and nutrient sinks into respective sources, diminishing water regulation capacity, causing surface height loss and destroying biodiversity. Over the last decades, drained peatlands have been rewetted for biodiversity restoration and, as it strongly decreases greenhouse gas emissions, also for climate protection. We quantify restoration success by comparing 320 rewetted fen peatland sites to 243 near-natural peatland sites of similar origin across temperate Europe, all set into perspective by 10k additional European fen vegetation plots. Results imply that rewetting of drained fen peatlands induces the establishment of tall, graminoid wetland plants (helophytisation) and long-lasting differences to pre-drainage biodiversity (vegetation), ecosystem functioning (geochemistry, hydrology), and land cover characteristics (spectral temporal metrics). The Paris Agreement entails the rewetting of 500,000 km2 of drained peatlands worldwide until 2050-2070. A better understanding of the resulting locally novel ecosystems is required to improve planning and implementation of peatland rewetting and subsequent management.

Differential expression of perforin in muscle-infiltrating T cells in polymyositis and dermatomyositis.

Polymyositis (PM) and dermatomyositis (DM) are the prototypical inflammatory diseases of skeletal muscle. In PM, CD8+ T cells invade and destroy muscle fibers, whereas humoral effector mechanisms prevail in DM. We studied the expression of the cytotoxic mediator perforin in inflammatory cells in PM and DM muscle by semiquantitative PCR, immunohistochemistry and confocal laser microscopy. Similar levels of perforin mRNA were expressed in PM and DM, and abundant perforin-expressing CD3+CD8+ and CD3+ CD4+ T cells were observed in both diseases. However, there was a striking difference in the intracellular localization of perforin. In DM, perforin was distributed randomly in the cytoplasm of the inflammatory T cells. In contrast, 43% of the CD8+ T cells that contacted a muscle fiber in PM showed perforin located vectorially towards the target muscle fiber. The results suggest (a) that the random distribution of perforin in the cytoplasm of muscle-infiltrating T cells observed in DM reflects nonspecific activation, and (b) that the vectorial orientation observed only in PM reflects the specific recognition via the T cell receptor of an antigen on the muscle fiber surface, pointing to a perforin- and secretion-dependent mechanism of muscle fiber injury.

Plasmonic Purcell effect reveals obliquely ordered phosphorescent emitters in Organic LEDs.

The non-isotropic alignment of molecules can increase the interaction efficiency with propagating light fields. This applies to both emissive and absorptive systems and can be exploited for achieving unprecedented efficiencies of organic opto-electronic devices such as organic light-emitting diodes. Optical analysis has revealed certain phosphorescent emitters to align spontaneously in an advantageous orientation. Unfortunately, established approaches only determine an average orientation because emission patterns solely depend on the second moments of the transition dipole vector distribution. In order to resolve further details of such a distribution, additional differences in the emission characteristics of parallel and perpendicularly oriented emitters need to be introduced. A thin metal layer near the emitters introduces plasmon mediated losses mostly for perpendicular emitters. Then, analyzing the emission at different polarizations allows one to measure emission lifetimes of mostly parallel or mostly perpendicular oriented emitters. This should alter the transient emission when observing the temporal phosphorescence decay under different directions and/or polarizations. The angular width of the orientation distribution can be derived from the degree of such lifetime splitting. Our results suggest a narrow but obliquely oriented molecular ensemble of Ir(MDQ)2(acac) doped into the α-NPD host inside an Organic LED stack.

Aberrant activation of CD8+ T-cell and CD8+ T-cell subsets in patients with newly diagnosed IDDM.

Two- and three-color cytofluorimetric techniques were used to study the expression patterns of the activation antigen HLA-DR on peripheral blood immunoregulatory T-cells from 25 patients with newly diagnosed insulin-dependent diabetes mellitus (IDDM) and 14 age- and sex-matched control subjects. The mean percentage of total activated (CD3+HLA-DR+) T-cells was significantly elevated in the IDDM group compared with the control group (P < 0.001). In control subjects, basal activation of CD4+ and CD8+ lymphocytes accounted for the low percentage levels of activated T-cells. In contrast, the majority of IDDM patients showed an unbalanced activation of CD4+ and CD8+ lymphocytes with predominant activation of the CD8+ lymphocyte subset. The composition of the activated T-cell fraction was dependent on the composition of the total (activated + nonactivated) T-cell population, as indicated by the positive correlation between the CD4+/CD8+ T-cell ratios in these two cell populations (r = 0.714; P < 0.001). Excessive activation of CD8+ T-cells was attributable to similar increases in the proportions of CD8+ CD45RA+HLA-DR+ (naive) and CD8+CD45RA-HLA-DR+ (memory) cells. Analysis of the CD11b-defined subsets revealed predominant activation of CD8+ CD11b- (cytotoxic) T-cells; CD8+ CD16+ HLA-DR+ natural killer cells were unchanged. The distribution of HLA-DR+ cells among subsets of CD4+ T-cells differed from the pattern in the CD8+ population in that selective activation of CD4+ CD45RA- (memory, helper-inducer) cells accounted for the small increase in activated CD4+ cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Ising-Bloch transition for the parametric Ginzburg-Landau equation with rapidly varying perturbations.

We study the effects of rapid periodic and stochastic modulations of parameters in systems described by the complex parametric Ginzburg-Landau equation. Amplitude equations, which govern the dynamics of the field averaged over the rapid modulations, are derived. For temporal modulations of the linear detuning the threshold for the transition from Ising to Bloch walls is shifted depending on the strength of the perturbation. In contrast to this, rapid perturbations of the linear gain lead only to a decrease of the amplitude of both wall types leaving the bifurcation point of the Ising-Bloch transition unchanged. Stochastic perturbations of the detuning lead to a Brownian motion of the Bloch wall beyond bifurcation where the velocity is given analytically. All theoretical predictions are confirmed by numerical simulations of the full stochastic Ginzburg-Landau equation.

Mumps infection and insulin-dependent diabetes mellitus (IDDM).

In order to select a population at risk for the development of diabetes for a prospective study of the relationship of islet cell antibodies (ICA), islet cell surface antibodies ( ICSA ), and glucose tolerance after mumps infection, we carried out a screening program for diabetes. A diabetic survey was conducted among 1581 children (less than 16 yr of age) with mumps infection 14 mo before the survey, using a brief questionnaire combined with urinary glucose analysis. Responses to the screening program were obtained from 68.4% (N = 1080) of the children. Out of a total of 1080 subjects, 1069 (99%) had no diabetes mellitus, diabetic symptoms, or glucosuria. A "positive urine glucose screen" was obtained in 11 subjects (1%) of the study group. These individuals all had a normal oral glucose tolerance test according to the new WHO definition. A group of 86 children was randomly selected from the total group of 1080 children for follow-up glucose tolerance, ICA, and ICSA . Irrespective of the negative urine glucose screen impaired glucose tolerance was diagnosed in 3.5% (N = 3) of the 86 children. The prevalence of ICA and ICSA was 78% and 36%, respectively. The simultaneous prevalence of ICA and ICSA was 33%. The pathogenetic role of mumps infection and ICA/ ICSA and their possible relationship to slow progressive beta cell destruction remain to be elucidated.

Constitutive and cytokine-induced production of interleukin-6 by human myoblasts.

Several recent studies have shown that some inflammatory myopathies are autoimmune diseases. It is possible that certain alterations in the muscle-immune cell microenvironment and in the local production of cytokines could take part in the pathogenesis of inflammatory myopathies. In the present study we investigated the effects of tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) on the secretion of interleukin-6 (IL-6) by myoblasts. Purified human myoblasts from normal subjects and from patients with polymositis were cultured in the presence of TNF-alpha and IFN-gamma at two concentrations (100 and 200 U/ml), alone or in combination, for 12, 24 and 48 h. The supernatants were collected and the IL-6 concentrations tested by ELISA (Genzyme). We found that myoblasts secrete IL-6 constitutively. The secretion of IL-6 was greatly increased by TNF-alpha; the increase was both time- and dose-dependent. IFN-gamma caused a moderate increase in IL-6 secretion, but this effect was not significant, despite a slight positive trend over time. There was no synergism in the effect of IFN-gamma and TNF-alpha. It is known that inflammatory myopathies are characterized by mononuclear cell infiltration and muscle regeneration: myoblasts are present in infiltrated tissues. Thus, the local production of cytokines that characterizes the inflammatory reaction, could stimulate myoblasts to secrete IL-6, which might add to the pro-inflammatory effects of IL-6 produced by activated macrophages and T cells.

Co-expression of ICAM-1, VCAM-1, ELAM-1 and Hsp60 in human arterial and venous endothelial cells in response to cytokines and oxidized low-density lipoproteins.

T-cells and monocytes are the first cells infiltrating the arterial intima during the early stages of atherogenesis. Recently our laboratory has provided evidence that T-cells isolated from atherosclerotic intima reacts against heat shock protein 60 (Hsp60). Transmigration of activated T-cells into the intima is mediated by adhesion molecules (ICAM-1; VCAM-1; ELAM-1) expressed on activated endothelial cells. Here we studied the potential of cytokines (TNF-alpha, IFN-gamma, IL-1). Escherichia coli lipopolysaccharide (LPS), native and oxidized low-density lipoprotein (LDL; oxLDL) and high temperature to induce adhesion molecules as well as Hsp60 and Hsp70 expression in human endothelial cells (EC). On Northern blots, a strong signal for ICAM-1, VCAM-1 and ELAM-1 was detected after 4 h, which thereafter declined, but did not reach the basal level of untreated control cells. Heat shock induced the expression of Hsp60 and Hsp70 but not of adhesion molecules. EC were cultivated in serum-free medium, which led to the expression of adhesion molecule transcripts. Addition of LDL or oxLDL to these ECs did not alter the expression of these transcripts. The production of adhesion molecule proteins was analysed by flow cytometry. In human venous endothelial cells (HVEC) and human arterial endothelial cells (HAEC) ICAM-1 and VCAM-1 production was permanently highly induced, whereas the high level of ELAM-1 production at 4 h disappeared after 24 h. Furthermore, only HAEC, but not HVEC, produced ICAM-1, VCAM-1 and ELAM-1 after stress by moderately and highly oxLDL. LDL and oxLDL did not induce the production of Hsp60 and Hsp70. The present study demonstrates the co-expression of Hsp60 and adhesion molecules in arterial and venous EC in response to cytokine and LPS exposure, and that oxLDL is an efficient inducer of adhesion molecules in arterial EC and not in venous EC. These features provide the prerequisites for a cellular immune reaction against Hsp60 expressed by stressed EC in the initial stages of atherosclerosis.

Detection of autoantibodies to the 65-kD isoform of glutamate decarboxylase by radioimmunoassay.

Autoantibodies (AAb) to glutamate decarboxylase (GAD) occur with a high prevalence in sera of newly diagnosed type I (insulin-dependent) diabetic patients. The aim of this study was to establish a GAD-AAb radioimmunoassay using 125I-labelled GAD65 and to evaluate this assay in a cross-sectional study with newly diagnosed type I diabetic patients (diabetes duration < 6 weeks). Furthermore, subjects at high risk of developing type I diabetes and individuals suffering from other autoimmune diseases were examined in this assay. For GAD-AAb detection, 125I-labelled GAD65 was incubated with 10 microliters of human serum overnight on ice. Thirty of 51 (59%) type I diabetic patients but none of the 54 healthy blood donors tested were found to be positive. A displacement step using 100,000 g supernatant from rat brain containing or not containing GAD showed the specificity of the binding of 125I-GAD65. Concerning the individuals at high risk of developing diabetes. 9/12 (75%) islet cell antibody (ICA)-positive non-diabetic and 4/34 (12%) ICA-negative subjects with metabolic abnormalities were GAD-AAb positive. These results show the association between type I (insulin-dependent) diabetes mellitus and the occurrence of GAD65-AAb, which possibly predicts a risk of developing the disease.

Autoantibodies against GAD65 rather than GAD67 precede the onset of type 1 diabetes.

The enzyme glutamate decarboxylase (GAD) is considered one of the major Beta cell antigens in Type 1 diabetes mellitus. The GAD autoantibody (GAD-AAb) prevalence in newly diagnosed Type 1 diabetic patients has been described up to 80%, depending on the detection method used. The aim of this study was to evaluate a simple, specific, and sensitive radioimmunoassay (RIA) method for detection of AAb against both isoforms of the enzyme, GAD65 and GAD67, in a cross-sectional study using sera from newly diagnosed Type 1 diabetic patients and in a longitudinal study using sera from prediabetic patients and individuals at risk of developing the disease. The 125I-labelled full-length human recombinant proteins of GAD65 and GAD67 expressed in SF9 cells were used as the antigen source. The prevalence of GAD65-AAb in newly diagnosed Type 1 diabetic patients was found to be 73% (112/153), in contrast to 19% (14/72) of GAD67-AAb. Only one patient produced AAb restricted to GAD67. Furthermore, GAD65-AAb could also be detected in 73% (11/15) of prediabetic patients (up to 122 months before clinical manifestation of the disease), whereas only 27% (4/15) of them were positive for GAD67-AAb. In the group at risk of developing Type 1 diabetes, these prevalences were 77% (10/13) and 46% (6/13), respectively. In all GAD67-AAb-positive patients investigated in the longitudinal study, AAb to GAD65 were detectable. In 47% of patients positive for both GAD65-AAb and ICA, the GAD65-AAb appeared by up to 46 months before the occurrence of ICA was detected. The data illustrated that GAD65 is the main immunogenic isoform of the enzyme in the preclinical and clinical stages. The RIA detecting AAb against this isoform may facilitate the screening for individuals at risk of developing the disease.

Alterations of purine metabolism in mononuclear cells of individuals at risk of developing type I (insulin-dependent) diabetes mellitus.

For the metabolic characterization of immunocompetent cells which are involved in the development of an insulin-dependent diabetes, a method for measurement of adenine uptake by mononuclear and macrophage-depleted mononuclear cell populations and of incorporation rates into the ATP, ADP, AMP and hypoxanthine fractions of these cells is presented and examined for its informative value in a cross-sectional study of individuals at risk of developing insulin-dependent diabetes. Values of 30 controls were compared with those of 53 risk persons. In controls and in 28 of the risk persons the adenine uptake by mononuclear cells was two to three times higher than that by the macrophage-depleted mononuclear cell population, suggesting high adenine metabolic activity of phagocytic cells. This activity was significantly decreased in the phagocytic cells of the remaining 25 risk persons. Additionally, the adenine incorporation rates into the adenine nucleotides of mononuclear cells were reduced by approximately 50% in these 25 risk persons. The alterations of purine metabolism were found associated with clinical symptoms of transient alterations of glucose tolerance and in the case of manifestation with a mild (HLA DR 3) type of insulin-dependent diabetes.

Alterations of purine metabolism in mononuclear cell populations of first degree relatives of insulin-dependent diabetic individuals with disturbed glucose tolerance.

In a T lymphocyte and macrophage-depleted mononuclear cell population of the peripheral venous blood of 10 of 41 first degree relatives of insulin-dependent diabetic individuals who had or had had disturbed glucose tolerance adenine uptake rates were significantly increased, the relative adenine incorporation rates into the adenine nucleotides, however, were diminished. Values were compared with those of 30 controls. In 7 of 9 investigated individuals with increased adenine uptake rates antibody-dependent cellular cytotoxicity against rat Langerhans islets (ADCC) was increased in the same cell population. In these individuals the number of diabetes manifestations was relatively high. Adenine uptake rates, ADCC and glucose tolerance changed with time.

Glucose tolerance behaviour before the onset of type I (insulin-dependent) diabetes in young people as a predictor of the further course of the disease: a retrospective analysis of 33 cases.

A study was made of glucose tolerance and insulin secretion in 33 persons who later developed insulin-dependent diabetes (aged 4-24 years) and observation continued further in the first years after manifestation. Patients who developed the typical labile type of diabetes were of normal weight and had either normal glucose tolerance tests before diagnosis or had impaired glucose tolerance (IGT) for a short interval of 2-16 months. Subjects with IGT over a significantly (p less than 0.01) longer period of 32.30 +/- 6.25 (normal body weight) or 94.71 +/- 20.62 (obese) months developed a milder form of diabetes with retarded insulin dependency in obese subjects. The severe and mild form of IDDM are distinct with respect to insulin requirement (0.75 +/- 0.03 or 0.28 +/- 0.04 U/kg b.w., P less than 0.01) and glucagon stimulated C-peptide (0.18 +/- 0.05 or 1.41 +/- 0.27, P less than 0.01) in the first 2.5-3.5 years after onset. The two forms were not different regarding HLA-DR antigens. Islet cell surface antibodies investigated in 15 probands at 27 occasions before diabetes onset had no prognostic value. The development of a mild form of IDDM may be expected in cases with pre-existing IGT for more than one year. The insulin secretion is of low predictive value under these conditions. The observation is of practical use and theoretical interest.

No association between anti-bovine serum albumin antibodies and islet cell reactive antibodies in newly diagnosed type 1 diabetic patients.

Serological findings have suggested that antibodies (Ab) to bovine serum albumin (BSA-Ab) are associated with type 1 diabetes mellitus. The aim of our study was to evaluate a competitive fluid-phase radioimmunoassay for detecting BSA-Ab using different incubation times and to study a possible association of these BSA-antibodies with autoantibodies (AAb) frequently detected in type 1 diabetic patients. For the overnight incubation time, there was an enormous overlap in the [125I]BSA binding by serum samples between 52 newly diagnosed type 1 diabetic patients (mean [125I]BSA binding 23.6 +/- 17.4%) and 54 healthy blood donors (mean [125I]BSA binding 10.2 +/- 15.7%). By an incubation time of only 3 min the BSA-antibody prevalence was found to be 15.4% (8/52) for type 1 diabetic patients and 3.7% (2/54) for control subjects. However, there was no association between BSA-Ab and type 1 diabetes-associated antibodies as cytoplasmic islet cell antibodies (ICA), or glutamate decarboxylase autoantibodies. Our results confirm that (i) BSA-Ab occur more frequently in newly diagnosed type 1 diabetic patients compared with a healthy control group and (ii) that the BSA-Ab detected by the fluid-phase radioimmunoassay with an incubation time of 3 min are more disease-associated than the [125I]BSA binding after an overnight incubation. The competitive BSA-Ab fluid-phase radioimmunoassay described is a simple and rapid method to detect antibodies specifically reactive with BSA. It is suggested that the humoral immune reactivity to BSA in type 1 diabetic patients probably reflects an unspecific defect of the immune system and gives no additionally diagnostic value about the type 1 diabetes.

Increased prevalence of elevated urinary albumin excretion rate in type 2 diabetic patients suffering from ischemic foot lesions.

UNLABELLED: Present cross-sectional clinical study was aimed at the evaluation the prevalence of cardiovascular risk factors in Type 2-diabetics suffering from different clinical manifestations of diabetic foot lesions due to peripheral vascular disease and/or diabetic neuropathy. 1025 non-insulin-dependent (Type 2) diabetics (NIDDM) of both sexes were investigated. Patients were classified in Type II diabetes without peripheral vascular disease and foot lesions (group 0, controls), with macroangiopathic related foot lesions (group 2), with neuropathic foot lesions (group 3), and with mixed neuropathic-ischemic foot lesions (group 4). Apart from urinary albumin excretion rate (UAE), the following micro- and macroangiopathic risk factors and diseases were taken into account: Hypertension, degree of metabolic control (HbA1c), lipid concentrations, duration of diabetes, retinopathy, clinical nephropathy. RESULTS: In the total population the UAE was significantly (p < 0.01) correlated with duration of diabetes, serum creatinine, hypertension, age, lipid concentrations, HbA1c and insulin requirement. In comparison to Type II diabetic patients without peripheral vascular disease (group 0) and with neuropathic foot lesions (group 3), subjects with ischemic (group 2) and mixed neuropathic-ischemic foot lesions demonstrated an increased prevalence of pathological UAE, which was associated with a higher frequency of clinical nephropathy, retinopathy, an older age and longer duration of diabetes. It is concluded that microalbuminuria in Type 2 diabetes reflects both the existence of diabetic nephropathy and peripheral vascular disease which is often associated with the insulin resistance syndrome.

Characterization of monoclonal islet cell reactive autoantibodies from the diabetic biobreeding (BB/OK) rat.

Two fusion experiments using the heteromyeloma cell line CB-F7 and splenocytes from two diabetes-prone BB (BioBreeding) rats at the onset of diabetes resulted in 128 islet cell reactive autoantibodies primarily detected with permeabilized insulin-producing rat insulinoma cells (RIN) by a cellular enzyme-linked immunosorbent assay. Seventy-nine (62%) of 128 RIN cell reactive supernatants exhibited a cross-reactivity with rat splenic lymphocytes. Six stable hybridomas secreting monoclonal ICSA (islet cell surface antibodies) were established, but only one monoclonal antibody, R4B10, showed preferential beta-cell binding. Six monoclonal antibodies showed a dual reactivity as ICA (islet cell cytoplasmic antibodies) detected by immunostaining of pancreatic islet cryosections and as ICSA on the surface of viable islet cells, whereas two reacted only with an ICA-like pattern. One monoclonal ICSA was specifically displaced from the RIN cell surface by sera of type 1 diabetic patients.

Reciprocity theorem and perturbation theory for photonic crystal waveguides.

Starting from Maxwell's equations we derive a reciprocity theorem for photonic crystal waveguides. A set of strongly coupled discrete equations results, which can be applied to the simulation of perturbed photonic crystal waveguides. As an example we analytically study the influence of the dispersion of a two level system on the band structure of a photonic crystal waveguide. In particular, the formation of polariton gaps is discussed.