Optimisation of the Hull Steel Weight considering Ice Class for the Design of an Electric Ferry

Alternative propulsion systems are becoming increasingly important in the maritime industry due to climate change. For this reason, the FUSE project aims to reduce CO2 emissions by investigating design options for electric RoPax vessels. For vessels in this order of magnitude, the power requirement for the engine needs to be reduced in order to minimise the demand on batteries. Therefore, one key challenge of the project is to reduce the mass of the vessel. In this context, ice-going ships have a significant proportion of the steel weight located in the ice belt. This offers the opportunity to reduce weight at this point. This thesis deals with the optimisation of the ice belt structure to answer the question if steel weight can be significantly reduced by lowering the ice class and accounting for recent data of ice conditions. It also considers possible compromises that a ship owner would have to accept when reducing the ice class. In addition, the effect of the steel grade on the steel weight of the ice belt is discussed. The structural analysis of the ice belt is realised by using a parametric finite element model, which is created with the software Abaqus. The ice load is applied according to the Finnish-Swedish Ice Class Rules, which are based on an elastic limit state. The steel structure is optimised using a Particle Swarm Optimisation (PSO). The PSO is carried out in three optimisation steps, which are referred to as the ice class study, the ice condition study and the steel grade study. The results of the PSO are compared with an analytical approach. This method is applied to the case study of an electric ferry. The results indicate that the steel weight reduction is more efficient for a steel structure with the highest ice class IA Super and the lowest steel grade S235. By lowering the ice class, it is possible to save up to 17.0 % of the ice belt steel weight and 1.57 % of the total steel weight. When the steel grade is increased, the percentage rates of mass reduction correspond to 22.8 % and 2.57 % respectively. Another result is that a ship with an ice class IB cannot operate on the ferry route for 0.8 % of the design life and for ice class IC it is 1.6 %. In contrast, ice class IA Super and IA have no operational restrictions. This study can be used as a guide for the selection of an ice class

Rezension zu Timo Feldhaus: Mary Shelleys Zimmer. Als 1816 ein Vulkan die Welt verdunkelte

Sophie Blasig rezensiert Timo Feldhaus' „Mary Shelleys Zimmer. Als 1816 ein Vulkan die Welt verdunkelte“ (Rowohlt 2022)

Raman tweezers provide the fingerprint of cells supporting the late stages of KSHV reactivation

Kaposi's sarcoma-associated herpesvirus (KSHV) has both latent and lytic phases of replication. The molecular switch that triggers a reactivation is still unclear. Cells from S phase of cell cycle provide apt conditions for an active reactivation. In order to specifically delineate the Raman spectra of cells supporting KSHV reactivation, we followed a novel approach where cells were sorted based on the state of infection (latent Vs lytic) by a flow cytometer and then analyzed by the Raman tweezers. The Raman bands at 785, 813, 830, 1095, and 1128 cm-1 are specifically altered in cells supporting KSHV reactivation. These 5 peaks make up the Raman fingerprint of cells supporting KSHV reactivation. The physiological relevance of the changes in these peaks with respect to KSHV reactivation is discussed in the following report. Originally published Journal of Cellular and Molecular Medicine, Vol. 13, No. 8b, Aug 200

S100B is increased in mood disorders and may be reduced by antidepressive treatment

Previous studies have reported alterations of glial cells and particularly astrocytes in mood disorders. Therefore, serum concentration of the astrocytic marker S100B was ascertained with an immunoluminometric assay in 20 patients with mood disorder and 12 healthy age-matched controls. Serum S100B was elevated in major depression (median after admission 410 ng/l, at discharge < 100 ng/l) and mania (130, 160 ng/l), when compared with controls (< 100 ng/l; rho< 0.01). Antidepressive treatment reduced S100B in conjunction with severity of depressive symptoms ( rho< 0.01). The severity of depression (Hamilton Depression Rating Scale) was positively correlated with S100B (r(s) = 0.51, rho< 0.005). Elevated serum S100B during depressive and manic episodes of mood disorders may indicate alterations of astrocytes, which are reversed by antidepressive treatment

Claudin‐derived peptides are internalized via specific endocytosis pathways

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/91364/1/j.1749-6632.2012.06567.x.pd

Dendritic cells: Key players in human herpesvirus 8 infection and pathogenesis

Human herpesvirus 8 (HHV-8; Kaposi's sarcoma-associated herpesvirus) is an oncogenic gammaherpesvirus that primarily infects cells of the immune and vascular systems. HHV-8 interacts with and targets professional antigen presenting cells and influences their function. Infection alters the maturation, antigen presentation, and immune activation capabilities of certain dendritic cells (DC) despite non-robust lytic replication in these cells. DC sustains a low level of antiviral functionality during HHV-8 infection in vitro. This may explain the ability of healthy individuals to effectively control this virus without disease. Following an immune compromising event, such as organ transplantation or human immunodeficiency virus type 1 infection, a reduced cellular antiviral response against HHV-8 compounded with skewed DC cytokine production and antigen presentation likely contributes to the development of HHV-8 associated diseases, i.e., Kaposi's sarcoma and certain B cell lymphomas. In this review we focus on the role of DC in the establishment of HHV-8 primary and latent infection, the functional state of DC during HHV-8 infection, and the current understanding of the factors influencing virus-DC interactions in the context of HHV-8-associated disease

Mood Disorders Are Glial Disorders: Evidence from In Vivo Studies

It has recently been suggested that mood disorders can be characterized by glial pathology as indicated by histopathological postmortem findings. Here, we review studies investigating the glial marker S100B in serum of patients with mood disorders. This protein might act as a growth and differentiation factor. It is located in, and may actively be released by, astro- and oligodendrocytes. Studies consistently show that S100B is elevated in mood disorders; more strongly in major depressive than bipolar disorder. Successful antidepressive treatment reduces S100B in major depression whereas there is no evidence of treatment effects in mania. In contrast to the glial marker S100B, the neuronal marker protein neuron-specific enolase is unaltered. By indicating glial alterations without neuronal changes, serum S100B studies confirm specific glial pathology in mood disorders in vivo. S100B can be regarded as a potential diagnostic biomarker for mood disorders and as a biomarker for successful antidepressive treatment

Serum S100B is increased during early treatment with antipsychotics and in deficit schizophrenia

Previous studies reported controversial results concerning alterations of astrocytes in schizophrenia. Because S100B may be regarded as a marker for astrocytes, the objective of this study was to examine S100B serum concentrations in 30 patients with schizophrenia with a monoclonal two-site immunoluminometric assay that specifically detects S100B. An ANOVA revealed medication (p0.05). Patients with deficit (250.6±154.9 ng/l) had higher S100B levels than patients with nondeficit schizophrenia (146.7±107.2 ng/l, p<0.05) or controls (p<0.005). S100B was positively correlated with the subscore ‘thought disturbance’ of the Brief Psychiatric Rating Scale (p<0.05). In summary, increased serum levels of S100B may indicate alterations of astrocytes during early treatment with antipsychotics and in deficit schizophrenia. Whether S100B is elevated due to injured astrocytes and a disrupted blood–brain barrier, or by active secretion of S100B by astrocytes, has to be clarified by further studies

A strategy for enrichment of claudins based on their affinity to Clostridium perfringens enterotoxin

<p>Abstract</p> <p>Background</p> <p>Claudins, a family of protein localized in tight junctions, are essential for the control of paracellular permeation in epithelia and endothelia. The interaction of several claudins with <it>Clostridium perfringens </it>enterotoxin (CPE) has been exploited for an affinity-based enrichment of CPE-binding claudins from lysates of normal rat cholangiocytes.</p> <p>Results</p> <p>Immunoblotting and mass spectrometry (MS) experiments demonstrate strong enrichment of the CPE-binding claudins -3, -4 and -7, indicating specific association with glutathione-S-transferase (GST)-CPE_116–319fusion protein. In parallel, the co-elution of (non-CPE-binding) claudin-1 and claudin-5 was observed. The complete set of co-enriched proteins was identified by MS after electrophoretic separation. Relative mass spectrometric protein quantification with stable isotope labeling with amino acids in cell culture (SILAC) made it possible to discriminate specific binding from non-specific association to GST and/or matrix material.</p> <p>Conclusion</p> <p>CPE_116–319provides an efficient tool for single step enrichment of different claudins from cell lysates. Numerous proteins were shown to be co-enriched with the CPE-binding claudins, but there are no indications (except for claudins -1 and -5) for an association with tight junctions.</p