Retinal Cell Death Caused by Sodium Iodate Involves Multiple Caspase-Dependent and Caspase-Independent Cell-Death Pathways

Herein, we have investigated retinal cell-death pathways in response to the retina toxin sodium iodate (NaIO₃) both in vivo and in vitro. C57/BL6 mice were treated with a single intravenous injection of NaIO₃ (35 mg/kg). Morphological changes in the retina post NaIO₃ injection in comparison to untreated controls were assessed using electron microscopy. Cell death was determined by TdT-mediated dUTP-biotin nick end labeling (TUNEL) staining. The activation of caspases and calpain was measured using immunohistochemistry. Additionally, cytotoxicity and apoptosis in retinal pigment epithelial (RPE) cells, primary retinal cells, and the cone photoreceptor (PRC) cell line 661W were assessed in vitro after NaIO₃ treatment using the ApoToxGlo™ assay. The 7-AAD/Annexin-V staining was performed and necrostatin (Nec-1) was administered to the NaIO₃-treated cells to confirm the results. In vivo, degenerating RPE cells displayed a rounded shape and retracted microvilli, whereas PRCs featured apoptotic nuclei. Caspase and calpain activity was significantly upregulated in retinal sections and protein samples from NaIO₃-treated animals. In vitro, NaIO₃ induced necrosis in RPE cells and apoptosis in PRCs. Furthermore, Nec-1 significantly decreased NaIO₃-induced RPE cell death, but had no rescue effect on treated PRCs. In summary, several different cell-death pathways are activated in retinal cells as a result of NaIO₃.     

Stratification Dynamics and Geothermal Potential of a Deep Shaft in the Flooded Wolf Mine,Siegerland/Germany

Mine Water and the Environment - Mine water hydraulics and geothermal potential of a deep shaft of the flooded Wolf mine in the Siegerland ore district of the Rhenish Massif in Germany were...     

The Müller (glial) cell in normal and diseased retina: a case for single-cell electrophysiology

In the retina of most vertebrates there exists only one type of macroglia, the Müller cell. Müller cells express voltage-gated ion channels, neurotransmitter receptors and various uptake carrier systems. These properties enable the Müller cells to control the activity of retinal neurons by regulating the extracellular concentration of neuroactive substances such as K+, GABA and glutamate. We show here how electrophysiological recordings from enzymatically dissociated mammalian Müller cells can be used to study these mechanisms. Müller cells from various species have Na(+)-dependent GABA uptake carriers, but only cells from primates have additional GABA receptors that activate Cl- channels. Application of glutamate analogues causes enhanced membrane currents recorded from Müller cells in situ but not from isolated cells. We show that mammalian Müller cells have no ionotropic glutamate receptors but respond to increased K+ release from glutamate-stimulated retinal neurons. This response is involved in extracellular K+ clearance and is mediated by voltage-gated (inwardly rectifying) K+ channels which are abundantly expressed by healthy Müller cells. In various cases of human retinal pathology, currents through these channels are strongly reduced or even extinguished. Another type of voltage-gated ion channels, observed in Müller cells from many mammalian species, are Na+ channels. In Müller cells from diseased human retinae, voltage-dependent Na+ currents were significantly increased in comparison to cells from control donors. Thus, the expression of glial ion channels seems to be controlled by neuronal signals. This interaction may be involved in the pathogenesis of retinal gliosis which inevitably accompanies any degeneration of retinal neurons. In particular, Müller cell proliferation may be triggered by mechanisms requiring the activation of Ca(2+)-dependent K+ channels. Ca(2+)-dependent K+ currents are easily elicitable in Müller cells from degenerating retinae and can be blocked by 1 mM TEA (tetraethylammonium). In purified Müller cell cultures, the application of 1 mM TEA greatly reduces the proliferative activity of the cells. These data clearly show that Müller cells are altered in cases of neuronal degeneration and may be crucially involved in pathogenetic mechanisms of the retina.     

The influence of sodium dodecyl sulfate from different sources on the separation of virus proteins in polyacrylamide gel electrophoresis

Bacteriophage 7-7-1 is shown to adsorb specifically to the complex flagella of its host Rhizobium lupini H13-3. Deflagellation of motile cells before the addition of phage leads to a complete inhibition of phage propagation for at least 60 min. Among phage-resistant mutants, many non-motile (mot) and non-flagellated (fla) derivatives of R. lupini H13-3 have been selected. Electron microscopic observations indicate that bacteriophage 7-7-1 attaches with its short tail fibres to the conspicuous helical filament of R. lupini flagells. This attachment is reversible; irreversible phage adsorption takes place at the flagellar base. It is postulated that phage 7-7-1 moves along the rotating flagellum towards a final receptor next to the insertion site of the flagellum, where tail contraction and injection of phage nucleic acid occurs.     

Towards Certificate-Based Authentication for Future Mobile Communications

Certificate-based authentication of parties provides a powerful means for verifying claimed identities, since communicating partners do not have to exchange secrets in advance for authentication. This is especially valuable for roaming scenarios in future mobile communications where users authenticate to obtain network access—service access may potentially be based thereon in integrated approaches—and where the number of access network providers and Internet service providers is expected to increase considerably. When dealing with certificates, one must cope with the verification of complete certificate paths for security reasons. In mobile communications, additional constraints exist under which this verification work is performed. These constraints make verification more difficult when compared to non-mobile contexts. Mobile devices may have limited capacity for computation and mobile communication links may have limited bandwidth. In this paper, we propose to apply PKI servers—such as implemented at FhG-SIT—that allow the delegation of certificate path validation in order to speed up verification. Furthermore, we propose a special structure for PKI components and specific cooperation models that force certificate paths to be short, i.e., the lenghts of certificate paths are upper-bounded to certain small values depending on the conditions of specific cases. Additionally, we deal with the problem of users who do not have Internet access during the authentication phase. We explain how we solved this problem and show a gap in existing standards.     

Autonomic nervous function during haemodialysis assessed by spectral analysis of heart-rate variability

To investigate the effect of neuronal differentiation on the capacity of antisense oligonucleotides (AS-ODNs) to suppress the production of acetylcholinesterase (AChE) in rat pheochromocytoma cells, we tested seven 3'-phosphorothioated AS-ODNs targeted to ACHEmRNA and two control ODNs. Three different administration protocols were used: oligonucleotides were added at 1 microM for 24 hours to nondifferentiated PC12 cells, together with nerve growth factor (NGF) or 24 hours following NGF-induced cholinergic differentiation. The content of free thiol groups in lysed cells was measured to evaluate cell number, therefore, survival, and the rate of acetylthiocholine hydrolysis was the measure of AChE activity. Among nondifferentiated cells, over 95% survived treatment with 8 of 9 of the ODNs. Moreover, two AS-ODN suppressed AChE activity in non-differentiated PC12 cells by 16%-20% as compared with 10% suppression by control ODNs (P < or = 0.01). When added concurrently with NGF, one other AS-ODN suppressed AChE activity significantly better (28%) than the control ODNs (16%). Moreover, when added following NGF treatment, which induced a significant increase in AChE activity, four different AS-ODNs but not the control ODNs suppressed 20%-35% of the enhanced AChE activity (p < or = 0.01). Reduced levels of AChE mRNA but no difference in actin mRNA levels were observed by following the kinetics of RT-PCR amplification in differentiated PC12 cells treated with these four AS-ODNs, as compared with control cells. Our findings demonstrate a differentiation-related increase in the susceptibility of PC12 cells to inhibition by specific AS-ODNs, suggesting the use of this model system to select AS-ODNs for suppression of AChE levels in the treatment of neurodegenerative diseases associated with cholinergic malfunction.     

Evaluation of Bioelectromethanogenesis Part I: Energy Calculations

Bioelectromethanogenesis, a technology to convert electrical energy into CH₄, is on the transition from lab-scale to industrial application. But the question arises if it is really a sustainable technology or just another scientific artifact. Especially the energy efficiency is a crucial aspect to allow conclusions about the applicability. In this paper, the basics of energy calculations are applied to literature data to model the energy efficiency. Different scenarios were calculated, showing that further research has to be conducted to turn bioelectromethanogenesis into a feasible technology.     

Computed tomography in Graves' ophthalmopathy

The CT scan with the 160 x 160 matrix demonstrated both the normal orbital anatomy and the abnormal orbital anatomy of Graves' ophthalmopathy in great detail. In Graves' ophthalmopathy, the cardinal pathologic feature of extraocular muscle enlargement was accurately reflected on the CT scan and was a distinctive, diagnostically reliable finding. Enlargement of the medial and lateral rectus muscles and of the apex of the muscle cone were the most consistent findings. The severity of the CT scan abnormalities correlated well with clinical severity. Because muscle cone abnormality was observed characteristically in those patients with sight loss, we suggest that pressure by the extraocular muscles on the optic nerve may contribute to visual acuity loss in this disease.