IC Formation Research Articles

Seven Segment Display Circuit Simulation using Electronics Workbench

A seven segment display, or in Indonesian it is called a seven segment display, is an electronic device consisting of segments that are used to display decimal numbers or numbers. This journal will explain how to simulate a seven segment display circuit using computer software called Electronics Workbench. This simulation is done to help understand how a seven segment display circuit can work, and because this is a simulation, there is no need to be afraid of failure, or making mistakes. This simulation is done by connecting a seven segment display with a 74 series Digital IC, you can use a 7447 or 7448 IC, because the function is still the same, and the IC formation is still the same, and is suitable for connecting seven segment displays. Then the IC is controlled via a switch / button that is connected directly to the IC, and the switch and IC are also connected to a power source, so that the circuit simulation can run. The results of this simulation show that the simulation can be done well in the Electronics Workbench software, can be a medium of learning about how seven segment displays work, and so that we can more easily understand how electronic devices work.

A Complementary Mechanism of Bacterial mRNA Translation Inhibition by Tetracyclines.

Tetracycline has positively impacted human health as well as the farming and animal industries. Its extensive usage and versatility led to the spread of resistance mechanisms followed by the development of new variants of the antibiotic. Tetracyclines inhibit bacterial growth by impeding the binding of elongator tRNAs to the ribosome. However, a small number of reports indicated that Tetracyclines could also inhibit translation initiation, yet the molecular mechanism remained unknown. Here, we use biochemical and computational methods to study how Oxytetracycline (Otc), Demeclocycline (Dem), and Tigecycline (Tig) affect the translation initiation phase of protein synthesis. Our results show that all three Tetracyclines induce Initiation Factor IF3 to adopt a compact conformation on the 30S ribosomal subunit, similar to that induced by Initiation Factor IF1. This compaction was faster for Tig than Dem or Otc. Furthermore, all three tested tetracyclines affected IF1-bound 30S complexes. The dissociation rate constant of IF1 in early 30S complexes was 14-fold slower for Tig than Dem or Otc. Late 30S initiation complexes (30S pre-IC or IC) exhibited greater IF1 stabilization by Tig than for Dem and Otc. Tig and Otc delayed 50S joining to 30S initiation complexes (30S ICs). Remarkably, the presence of Tig considerably slowed the progression to translation elongation and retained IF1 in the resulting 70S initiation complex (70S IC). Molecular modeling of Tetracyclines bound to the 30S pre-IC and 30S IC indicated that the antibiotics binding site topography fluctuates along the initiation pathway. Mainly, 30S complexes show potential contacts between Dem or Tig with IF1, providing a structural rationale for the enhanced affinity of the antibiotics in the presence of the factor. Altogether, our data indicate that Tetracyclines inhibit translation initiation by allosterically perturbing the IF3 layout on the 30S, retaining IF1 during 70S IC formation, and slowing the transition toward translation elongation. Thus, this study describes a new complementary mechanism by which Tetracyclines may inhibit bacterial protein synthesis.

Electrospinning of dexamethasone/cyclodextrin inclusion complex polymer fibers for dental pulp therapy

Beta-cyclodextrin (β-CD) is an oligosaccharide commonly used to improve the aqueous solubility of lipophilic drugs (e.g., dexamethasone, DEX). Here we present the development of a drug delivery system to provide sustained release of DEX by β-CD-inclusion complex (IC) to amplify the mineralization capacity of stem cells from human-extracted deciduous teeth (SHEDs) as a potential direct pulp capping strategy. First, IC of DEX (DEX-CD-IC) was synthesized with β-CD. To confirm DEX-CD-IC complex formation, X-ray diffraction (XRD) and Fourier transform infrared spectroscopy (FTIR) analyses were performed. XRD data indicated that IC formation was achieved due to formation of a new crystalline structure, whereas FTIR revealed the presence of the IC from the shifting of the peaks of each component in DEX-CD-IC. Then, electrospun poly(lactic-co-glycolic acid, PLGA) fibers (PLGA/DEX-CD-IC) were processed by varying the concentration of DEX-CD-IC (5%, 10 %, and 15 %). The release of DEX from fibers was determined by ultraperformance liquid chromatography for 28 days. Thanks to the solubility enhancement of DEX by IC, electrospun PLGA/DEX-CD-IC fibers released DEX in a more sustained fashion compared to PLGA/DEX fibers. No deleterious effect was found in terms of SHEDs’ proliferation when cultured with or on electrospun fibers, regardless of the IC presence. Importantly, a more pronounced odontogenic differentiation was stimulated by electrospun fibers loaded with the lowest DEX-CD-IC concentration (5%), as a result of the sustained DEX release. In sum, PLGA/DEX-CD-IC fibers have great potential in vital dental pulp therapy, owing to its sustained DEX release, cytocompatibility, and odontogenic differentiation capacity.

A reverse translational study on the effect of rituximab, rituximab plus belimumab, or bortezomib on the humoral autoimmune response in SLE

ObjectivesSLE is a severe autoimmune disease characterized by autoreactive B cells and IC formation, which causes systemic inflammation. B cell–targeted therapy could be a promising treatment strategy in SLE patients; nevertheless, randomized clinical trials have not always been successful. However, some groups have demonstrated beneficial effects in severe SLE patients with off-label rituximab (RTX) with belimumab (BLM), or bortezomib (BTZ), which targeted different B cells subsets. This study assembled sera from SLE cohorts treated with RTX+BLM (n = 15), BTZ (n = 11) and RTX (n = 16) to get an in-depth insight into the immunological effects of these therapies on autoantibodies and IC formation.MethodsAutoantibodies relevant for IC formation and the avidity of anti-dsDNA were determined by ELISA. IC-mediated inflammation was studied by complement levels and ex vivo serum-induced neutrophil extracellular trap formation.ResultsReductions in autoantibodies were observed after all approaches, but the spectrum differed depending upon the treatment. Specifically, only RTX+BLM significantly decreased anti-C1q. Achieving seronegativity of ≥1 autoantibody, specifically anti-C1q, was associated with lower disease activity. In all SLE patients, the majority of anti-dsDNA autoantibodies had low avidity. RTX+BLM significantly reduced low-, medium- and high-avidity anti-dsDNA, while RTX and BTZ only significantly reduced medium avidity. IC-mediated inflammation, measured by C3 levels and neutrophil extracellular trap formation, improved after RTX+BLM and RTX but less after BTZ.ConclusionThis study demonstrated the impact of different B cell–targeted strategies on autoantibodies and IC formation and their potential clinical relevance in SLE.

INCORPORACIÓN DEL COMPLEJO DE EXCUSIÓN DE CIPROFLOXACINO/BETA CICLODEXTRINA A FIBRAS ELECTROHILADAS DE ÁCIDO POLILÁCTICO Y EL MODELAMIENTO DEL COMPORTAMIENTO DE LIBERACIÓN

The fluoroquinolone ciprofloxacin (CIP) hidrophobic drug and its inclusion complex, β-cyclodextrin-CIP (IC) were encapsulated into micro- and nano-fibers of polylactic acid (PLA) via electrospinning technique to evaluate CIP release. The IC was characterized by 13C solid-state nuclear magnetic resonance (SSNMR) and thermogravimetric analysis (TGA) to investigate the inclusion complex formation and fiber encapsulation. The PLA-IC and PLA-CIP fibers were characterized by TGA, Raman spectroscopy and scanning electron microscopy (SEM). The release behavior of CIP and loading efficiency percentage (LE%)were evaluated via UV-Vis at 276 nm. The LE% of CIP was higher to PLA-IC with respect to the fibers with only CIP. IC release behavior was more sustained from PLA-IC fibers versus PLA-CIP as an effect of the IC formation. The CIP was released in a more prolonged and sustained manner from PLA-IC fibers versus PLA-CIP fibers. Different PLA-CIP and PLA-IC fiber diameters did not affect the release profile. The experimental results of CIP and IC were approximated with three commonly used semi-empirical models: Korsmeyer-Peppas, zero-order, and first-order kinetic equation to explain the release mechanism.

EIF5 and eIF5B together stimulate 48S initiation complex formation during ribosomal scanning.

48S initiation complex (48S IC) formation is the first stage in the eukaryotic translation process. According to the canonical mechanism, 40S ribosomal subunit binds to the 5′-end of messenger RNA (mRNA) and scans its 5′-untranslated region (5′-UTR) to the initiation codon where it forms the 48S IC. Entire process is mediated by initiation factors. Here we show that eIF5 and eIF5B together stimulate 48S IC formation influencing initiation codon selection during ribosomal scanning. Initiation on non-optimal start codons—following structured 5′-UTRs, in bad AUG context, within few nucleotides from 5′-end of mRNA and CUG start codon—is the most affected. eIF5-induced hydrolysis of eIF2-bound GTP is essential for stimulation. GTP hydrolysis increases the probability that scanning ribosomal complexes will recognize and arrest scanning at a non-optimal initiation codon. Such 48S ICs are less stable owing to dissociation of eIF2*GDP from initiator tRNA, and eIF5B is then required to stabilize the initiator tRNA in the P site of 40S subunit. Alternative model that eIF5 and eIF5B cause 43S pre-initiation complex rearrangement favoring more efficient initiation codon recognition during ribosomal scanning is equally possible. Mutational analysis of eIF1A and eIF5B revealed distinct functions of eIF5B in 48S IC formation and subunit joining.

Immune complex formation in human diabetic retina enhances toxicity of oxidized LDL towards retinal capillary pericytes

Recently it has been shown that levels of circulating oxidized LDL immune complexes (ox-LDL-ICs) predict the development of diabetic retinopathy (DR). This study aimed to investigate whether ox-LDL-ICs are actually present in the diabetic retina, and to define their effects on human retinal pericytes versus ox-LDL. In retinal sections from people with type 2 diabetes, costaining for ox-LDL and IgG was present, proportionate to DR severity, and detectable even in the absence of clinical DR. In contrast, no such staining was observed in retinas from nondiabetic subjects. In vitro, human retinal pericytes were treated with native LDL, ox-LDL, and ox-LDL-IC (0-200 mg protein/l), and measures of viability, receptor expression, apoptosis, endoplasmic reticulum (ER) and oxidative stresses, and cytokine secretion were evaluated. Ox-LDL-IC exhibited greater cytotoxicity than ox-LDL toward retinal pericytes. Acting through the scavenger (CD36) and IgG (CD64) receptors, low concentrations of ox-LDL-IC triggered apoptosis mediated by oxidative and ER stresses, and enhanced inflammatory cytokine secretion. The data suggest that IC formation in the diabetic retina enhances the injurious effects of ox-LDL. These findings offer new insights into pathogenic mechanisms of DR, and may lead to new preventive measures and treatments.

Direct Monitoring of Initiation Factor Dynamics through Formation of 30S and 70S Translation-Initiation Complexes on a Quartz Crystal Microbalance

Translation initiation is a dynamic and complicated process requiring the building a 70S initiation complex (70S-IC) composed of a ribosome, mRNA, and an initiator tRNA. During the formation of the 70S-IC, initiation factors (IFs: IF1, IF2, and IF3) interact with a ribosome to form a 30S initiation complex (30S-IC) and a 70S-IC. Although some spectroscopic analyses have been performed, the mechanism of binding and dissociation of IFs remains unclear. Here, we employed a 27 MHz quartz crystal microbalance (QCM) to evaluate the process of bacterial IC formation in translation initiation by following frequency changes (mass changes). IFs (IF1, IF2, and IF3), N-terminally fused to biotin carboxyl carrier protein (bio-BCCP), were immobilized on a Neutravidin-covered QCM plate. By using bio-BCCP-IF2 immobilized to the QCM, three steps of the formation of ribosomal initiation complex could be sequentially observed as simple mass changes in real time: binding of a 30S complex to the immobilized IF2, a recruitment of 50S to the 30S-IC, and formation of the 70S-IC. The kinetic parameters implied that the release of IF2 from the 70S-IC could be the rate-limiting step in translation initiation. The IF3-immobilized QCM revealed that the affinity of IF3 for the 30S complex decreased upon the addition of mRNA and fMet-tRNA(fMet) but did not lead to complete dissociation from the 30S-IC. These results suggest that IF3 binds and stays bound to ICs, and its interaction mode is altered during the formation of 30S-IC and 70S-IC and is finally induced to dissociate from ICs by 50S binding. This methodology demonstrated here is applicable to investigate the role of IFs in translation initiation driven by other pathways.

Synthesis and characterization of inclusion complexes of aliphatic-aromatic poly(Schiff base)s with β-cyclodextrin (highlight)

This paper describes the formation of polymer inclusion complexes(polymer-CD-ICs) between β-cyclodextrin(β-CD) and aliphatic-aromatic poly(Schiff base)s. Fourier transform infrared(FTIR) spectroscopy, 1H nuclear magnetic resonance spectroscopy(1H-NMR), thermogravimetric analysis(TGA) and X-ray diffraction(XRD) have been used to observe the formation of polymer-CD-ICs. In FTIR spectra, the characteristic peaks of β-CD at 3391 cm−1 shifted to 3418 cm−1 and the intense peak at 1602 cm−1 due to the –C = N– stretching vibration diminished after formation of inclusion complexes. Compared the 1H-NMR of polymer-CD-ICs with β-CD, the chemical shift of the protons H-3, H-5 have shifted to higher field after the formation of inclusion complexes, which is perhaps due to the interaction of these protons with polymers. The TGA analysis revealed that the polymer-CD-ICs had better thermal stability than β-CD, suggesting that the polymer increased the stability of β-CD. The X-ray diffraction patterns displayed that the strong peak for both polymer-CD-ICs at approximately 20.0° (2θ) may confirm their IC formation.

Measurements of the vapor pressure of cubic ice and their implications for atmospheric ice clouds

Under conditions commonly found in Earth's atmosphere, water can form two solid phases; hexagonal ice (Ih) and cubic ice (Ic). Recent reports have suggested that Ic may form in the atmosphere under a wider range of conditions than previously believed. In light of these reports, the formation of Ic has been suggested as one contributing factor for in‐situ observations of persistent in‐cloud supersaturations in cold cirrus. However, an accurate evaluation of the contribution of Ic formation to the observed supersaturations requires knowledge of the saturation vapor pressure of Ic, which has not been measured. In this manuscript, we report direct measurements of the vapor pressure of Ic over the temperature range 180–190 K. Over this temperature range, the vapor pressure of the cubic phase is 10.5 ± 2.5% higher than that of the hexagonal phase. Field measurements of in‐cloud supersaturations made during CRYSTAL‐FACE are also re‐analyzed and discussed.

Effect of Methylated Cyclodextrins on the Crystallization of Poly(3‐hydroxybutyrate)

AbstractSummary: The effects of methylated CDs, α‐ and β‐DMCD and α‐ and β‐TMCD on the crystallization behavior of P(3HB) have been investigated by employing DSC and polarized optical microscopy (POM). The crystallization and nucleation of P(3HB) was improved by an addition of appropriate amount of each methylated CD, while negative effect of miscible blend was observed when the amount of addition exceeds the optimum value for the maximum nucleating effect. β‐TMCD was shown to be the most effective for the enhancement of the P(3HB) crystallization, thought to be due to the possibility of IC formation with P(3HB).Plots of log{−ln [1 − X(t)]} versus log (t) for mixtures of P(3HB) with different CDs or talc, respectively.imagePlots of log{−ln [1 − X(t)]} versus log (t) for mixtures of P(3HB) with different CDs or talc, respectively.

The Immunogenicity of Modified Lipoproteins

The immunogenicity of modified low-density lipoprotein (mLDL) has been demonstrated both in laboratory animals and humans. Circulating human mLDL antibodies, purified by affinity chromatography, are predominantly of the IgG isotype, subclasses 1 and 3. The purified antibodies react with malondialdehyde-lysine and carboxymethyl-lysine epitopes, but also recognize minimally modified forms of LDL that do not contain significant amounts of those two epitopes. The quantitative assays of mLDL and mLDL antibodies in serum samples by enzymoimmunoassay (EIA) are unreliable owing to the interference of preformed circulating immune complexes (CICs). Isolation of CICs by precipitation with low concentrations of polyethylene glycol followed by analysis of antigens and antibodies contained in the precipitates is a technically complex approach, but one that yields valuable data. With this approach we have confirmed that the IgG antibodies involved in IC formation belong to the proinflammatory IgG1 and IgG3 isotypes, have a higher avidity than those that remain unbound in the supernatant after CIC precipitation, and are of higher avidity in diabetic patients with macroalbuminuria than in those with normal albuminuria. We have also developed capture assays for different forms of mLDL. These assays have shown a significant enrichment in mLDL of the precipitated ICs. The enrichment is also more pronounced in the CICs obtained from diabetic patients with macroalbuminuria. In conclusion, isolation and characterization of LDL-ICs appears to yield information of significant value that is not derived from other approaches to measure LDL modifications and their corresponding antibodies in humans.

Differential Role of Three Major New Zealand Black-Derived Loci Linked with Yaa-Induced Murine Lupus Nephritis

By assessing the development of Y-linked autoimmune acceleration (Yaa) gene-induced systemic lupus erythematosus in C57BL/6 (B6) x (New Zealand Black (NZB) x B6.Yaa)F(1) backcross male mice, we mapped three major susceptibility loci derived from the NZB strain. These three quantitative trait loci (QTL) on NZB chromosomes 1, 7, and 13 differentially regulated three different autoimmune traits: anti-nuclear autoantibody production, gp70-anti-gp70 immune complex (gp70 IC) formation, and glomerulonephritis. Contributions to the disease traits were further confirmed by generating and analyzing three different B6.Yaa congenic mice, each carrying one individual NZB QTL. The chromosome 1 locus that overlapped with the previously identified Nba2 (NZB autoimmunity 2) locus regulated all three traits. A newly identified chromosome 7 locus, designated Nba5, selectively promoted anti-gp70 autoantibody production, hence the formation of gp70 IC and glomerulonephritis. B6.Yaa mice bearing the NZB chromosome 13 locus displayed increased serum gp70 production, but not gp70 IC formation and glomerulonephritis. This locus, called Sgp3 (serum gp70 production 3), selectively regulated the production of serum gp70, thereby contributing to the formation of nephritogenic gp70 IC and glomerulonephritis, in combination with Nba2 and Nba5 in NZB mice. Among these three loci, a major role of Nba2 was demonstrated, because B6.Yaa Nba2 congenic male mice developed the most severe disease. Finally, our analysis revealed the presence in B6 mice of an H2-linked QTL, which regulated autoantibody production. This locus had no apparent individual effect, but most likely modulated disease severity through interaction with NZB-derived susceptibility loci.

The covalent interaction of C3 with IgG immune complexes

Antigens (Ags) are converted into immune complexes (antigen-antibody complexes, IC) as soon as they encounter their specific antibodies (Abs). In fluids containing complement, the process of IC formation and fixation of complement components occur simultaneously. Hence, the formation of Ag-Ab-complement complexes is the normal way of eliminating Ags from a host. C3b-C3b-IgG covalent complexes are immediately formed on interaction of serum C3 with IgG-IC. These C3b-C3b dimers constitute the core for the assembly of C3/C5-convertase on the IC, which are subsequently converted into iC3b-iC3b-IgG by the complement regulators. These complexes are detected on SDS–PAGE by two bands of molecular composition, C3 α65-C3 α43 (band A) and C3 α65-heavy chain of the Ab (band B), which correspond to C3b-C3b and C3b-IgG covalent interaction respectively, and that identify opsonized IC (C3b-IC). C3b can attach to Fab and Fc regions of the Ab molecule with similar efficiency. The presence of multiple C3b binding regions on IgG is considered an advantageous characteristic that facilitates the elimination of Ags in the form of C3b n-IC. Ab molecules on the IC recognize the Ag, and also serve as a very good acceptor for C3b binding. In this way, Ags, even if they have no acceptor sites for C3b, can be efficiently processed and removed. When C3 is activated in serum by IC or other activators, secondary C3b-IgG covalent complexes are generated, with bystander monomeric circulating IgG, and thus constitute, physiological products of complement activation. These complexes gain importance when IgG concentration is extremely high as in cases of infusion of intravenous IgG (IVIG) in several pathologies. The covalent attachment of activated complement C3 (C3b, iC3b, C3 d,g) to Ags or IC links innate and adaptative immunity by targeting Ags to different cells of the immune system (follicular dendritic cells, phagocytes, B cells). Hence C3b marks Ags definitively, from the earliest contact with the innate immune system until their complete elimination from the host.

Stable icosahedral nanostructure in gold-copper alloy clusters

Different formation rates of stable icosahedral nanostructures were observed for the clusters of four different Au- 13, 25, 39 and 57 at.% Cu alloys. The rate was found to be maximum, 80%, for Au-25 at.% Cu alloy clusters and decrease with increasing and decreasing the Cu content from 25 at.%. The icosahedral structures along 5-, 3- and 2-fold axes were identified clearly by high resolution transmission electron microscope. The critical size for the Ic formation was found to be 6 nm in diameter for all the alloys. Cu content in the alloys plays an important role to form the stable Ic and controls the formation rate.

Nephritogenic antibodies in lupus nephritis.

A critical discussion of data on the possible role of IgG3 cryoglobulins, cross-reactive anti-DNA antibodies and anti-DNA idiotypes in the pathogenesis of lupus nephritis is included. A further possibility involving cationic nuclear autoantigens is presented in detail. Histone was employed as a model antigen, representative of this group. Histones were shown to have high affinity for the rat GBM; they could also act as planted antigen and induce IC formation; furthermore they were able to mediate the binding of highly anionic DNA. The demonstration of histones in glomerular deposits in both lupus mice and patients with SLE is important evidence, linking such molecules with the kidney lesions.

Studies on the pathogenic roles of antigens isolated from renal tubular cells in the classical Heymann nephritis

In order to analyze the antigens (Ags) which cause Heymann nephritis (HN) and mechanisms of IC formation in the subepithelial site of GBM, we isolated two Ags from renal tubular epithelium (RTE) from Wistar rats and prepared rabbit antiserum against these Ags. Classical HN was induced by immunization with crude renal tissue suspension by the method of Heymann et al. Immunofluorescence method in normal rat kidney revealed that the Ag with MW of 65 KD (= beta) existed not only in RTE, but also in the glomerular capillary wall. On the other hand, the Ag with MW of 35 KD (= gamma) only existed in RTE. Circulating Abs and glomerular eluted Abs from the kidney of classical HN, reacted to RTE only by indirect immunofluorescence. Soluble Fx1A, beta and gamma were electrophoresed on SDS-PAGE gels and transblotted onto nitrocellulose membrane, anti beta Abs reacted to several bands including 330 KD band of Fx1A and beta Ag. However anti gamma Abs reacted to only 330 KD band of Fx1A and gamma Ags. On the other hand, Glomerular eluted Abs from the kidney of classical HN reacted to several bands of Fx1A and gamma Ag, but not to beta Ag. These facts suggest that beta and gamma are components of 330 KD protein of Fx1A. The gamma Ag is thought to be one of the major pathogenic Ag in HN.

Biological Activities Residing in the Fc Region of Immunoglobulin

This chapter discusses studies involving lymphocyte activation and immune regulation by peptides derived from IC and Fc fragments of immunoglobulin (Ig). The cellular and subcellular events involved in lymphocyte activation by these biologically active peptides are discussed. There are five major classes of mammalian Ig: IgG, IgM, IgA, IgD, and IgE. The fundamental structure of the Ig molecule consists of two identical light (L) and two identical heavy (H) chains. IgG can be cleaved into smaller fragments by a variety of enzymes other than papain. Pepsin cleaves Ig on the carboxy terminal side of the inter-H chain disulfide bonds, resulting in the formation of a large F (ab')2 fragment. The Fc fragment is degraded by pepsin into heterogeneous peptides. The Fc region of the Ig molecule is involved in a wide variety of biological effector functions that include control of catabolic rate, C fixation, binding to FcR, anaphylaxis, opsonization, placental and gut transfer, and immune regulation. Because the cellular events in lymphocyte activation by Fc fragments and IC appear to be identical, perhaps immunoregulation by these agents occurs via similar pathways. The release of biologically active peptides derived from the Fc fragment of antibody may be part of a potent nonspecific in vivo immunoregulatory network. In addition to the release of Fc region peptides, IC formation also results in C activation with the subsequent release of C fragments (C3a and C5a) that possess immunoregulatory properties.

Prebiotic synthesis of imidazole-4-acetaldehyde, imidazole-4-glycol and imidazole-4-ethanol

A wide var iety of chemical processes have been used for the synthesis of amino acids from prebiot ic molecular precursors under plausible pr imi t ive Earth conditions (M i l l e r , 1982). The prebiot ic formation of a l l protein-type amino acids has been demonstrated except for three amino acids: h is t id ine , lys ine, and arginine (Weber and Mi l l e r , 1981). As a continuation of our work on the prebiot ic synthesis of imidazole, 2-methylimidazole, and 4-methylimidazole (Or6 et a l . , 1984), th is paper reports the prebiot ic synthesis of other imidazoles (l~-4-acetaldehyde, Im-4-glycol, and Im-4-ethanol), which are among the intermediate products in the proposed prebiot ic synthet ic pathway of h is t id ine.

Circulating immune complexes in uveitis

The serum of 63 patients suffering from various clinical types of endogenous uveitis with unknown etiology was investigated for the presence of circulating immune complexes (CIC). None of the patients was suffering from a systemic disease usually associated with CIC. Significantly elevated CIC levels were detected in 2 women with chronic cyclitis. One of them was also suffering from paresis of the facial nerve. The investigation reported here indicates that C1q-binding CIC are of no importance in the pathogenesis of endogenous uveitis. On the one hand one should consider the possibility of local IC formation, on the other hand one should be aware of the fact that IC does not always represent a pathogenic factor but that it may also occur as a secondary phenomenon after non-immunologic tissue destruction.