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The paper is the first, introductory part to the description of an interdisciplinary research project in the modernization of laboratories at The Faculty of Civil Engineering, The Silesian University of Technology. The scope of the paper is to disseminate the current state of knowledge of ergonomics and issues involved in the technology of laboratory processes, describing the methodology of experiments carried out in geotechnical laboratories, their equipment and spatial requirements in view of the users – research staff. The course and results of the pre-design studies are presented in: PRE-DESIGN STUDIES ON THE EXAMPLE OF THE MODERNIZATION OF GEOTECHNICAL LABORATORIES

Enterovirus (EV) infections are frequent and predominantly affect children. Neurological manifestations are rare but can induce severe consequences. Since 2014 a global rise in EV-D68 and EV-71 infections manifesting with neurological complications, namely rhombencephalitis (EV-71) and acute flaccid myelitis (EV-D68), has been observed with an increased distribution in Europe and isolated occurrences in Germany. Typically prodromes with respiratory infections and gastrointestinal conditions precede neurological symptoms. In these cases, an EV infection should be considered as the underlying cause and appropriate diagnostic tests should be performed. Other than the typical inflammatory signs in cerebrospinal fluid (CSF), the changes on magnetic resonance imaging (MRI) in particular are seminal; however, confirmation of the virus is often not possible in the CSF so that other specimens from, e.g. feces or the respiratory tract are required. To date there are no causal therapies for either of these EV infections; therefore, a comprehensive supportive therapy is of major significance. In Taiwan some beneficial effects could be observed by administration of intravenous immunoglobulins; however, a reliable study has not yet been published.

Progressive multifocal leukoencephalopathy (PML) is a disease of immunosuppressed patients caused by the JC polyomavirus (JCPyV). Due to the elevated risk in patients treated with natalizumab for multiple sclerosis (MS) and also treatment with other biologicals for different indications, the relevance of PML has increased in recent years. This article summarizes the published knowledge on the biology and pathogenesis of PML with a focus on the role of cerebrospinal fluid diagnostics in the work-up for PML and the current PML case definition. Current recommendations regarding risk management are discussed, as are possible therapies and prevention.

With the approval of various substances for the immunotherapy of multiple sclerosis (MS), treatment possibilities have improved significantly over the last few years. Indeed, the choice of individually tailored preparations and treatment monitoring for the treating doctor is becoming increasingly more complex. This is particularly applicable for monitoring for a treatment-induced compromise of the immune system. The following article by members of the German Multiple Sclerosis Skills Network (KKNMS) and the task force "Provision Structures and Therapeutics" summarizes the practical recommendations for approved immunotherapy for mild to moderate and for (highly) active courses of MS. The focus is on elucidating the substance-specific relevance of particular laboratory parameters with regard to the mechanism of action and the side effects profile. To enable appropriate action to be taken in clinical practice, any blood work changes that can be expected, in addition to any undesirable laboratory findings and their causes and relevance, should be elucidated.

Chronisch immunvermittelte Polyneuropathien, wie die CIDP [chronisch inflammatorische (entzundliche) demyelinisierende Polyneuropathie] und die multifokal motorische Neuropathie (MMN), stellen im klinischen Alltag eine diagnostische und therapeutische Herausforderung dar. Die Heterogenitat in der klinischen Prasentation als auch die nur wenigen klinischen Therapiestudien stellen Limitationen im Umgang mit diesen Krankheitsbildern dar. In den letzten Jahren wurden auf diesem Gebiet jedoch Fortschritte erzielt: Einerseits gibt es neue diagnostische Kriterien und Leitfaden, die im klinischen Alltag die differenzialdiagnostische Einordnung erleichtern, andererseits gibt es fur die CIDP inzwischen eine klinische Studie hochster Evidenzklasse, die sowohl die Kurz- als auch Langzeitwirksamkeit von intravenosen Immunglobulinen demons­triert. In dem folgenden Ubersichtsartikel werden die rezenten diagnostischen und therapeutischen Erkenntnisse fur die CIDP als auch die MMN zusammengestellt.

History and findings A 29-year-old man presented in another hospital because of discoordination of all extremities with sudden onset. After fast reversal of the symptoms, he was discharged without a clear diagnosis. Because of remaining discrete dysarthria, computed tomography and magnetic resonance imaging were performed which demonstrated bilateral cerebellar infarcts. The cause was assumed to be a transient embolic occlusion of the distal basilar artery. Treatment and course Intravenous heparin was started to prevent further occlusions. Because no source for emboli or other causes were found, the patient was discharged after 14 days on acetylic acid (250 mg/d) as secondary prevention therapy. Conclusions A vascular or neurological cause is often not considered when neurological symptoms are quickly reversible after a transient occlusion of the basilar artery. In these cases, the suspected diagnoses of psychiatric illness, alcohol abuse, drug intoxication, infection or myocardial infarction do not lead to the necessary investigations. Thus, a potentially life-threatening situation may be disregarded.

Over the past decade we have observed considerable advances in the treatment of autoimmune-mediated disorders affecting the nervous system. Part of this development was the introduction of high-dose polyclonal intravenous immunoglobulins (IVIg). On the basis of randomised, placebo-controlled, double-blind clinical trials, IVIg has become the first line treatment for Guillain-Barre syndrome, chronic idiopathic inflammatory demyelinating polyneuropathy (CIDP) and multifocal motor neuropathy (MMN). Furthermore, IVIg can serve as a rescue therapy for patients with rapidly worsening myasthenia gravis, and is a second-line therapy for dermatomyositis, stiff-person syndrome, and pregnancy- or post-partum-associated multiple sclerosis attacks. Due to the excellent safety profile and its uncomplicated administration, IVIg has been used very liberally for most diseases with a suspected autoimmune pathology or where there is no treatment available. This, and the strict licensing requirements, has led to a shortage in IVIg supply and a dramatic increase in costs. Therefore, IVIg should principally be used according to available data from controlled clinical trials. Here we review the clinical applications and recommendations for the use of IVIg in neurological diseases.

In recent years the approval of new substances has led to a substantial increase in the number of course-modifying immunotherapies available for multiple sclerosis. Therapy conversion therefore represents an increasing challenge. The treatment options sometimes show complex adverse effect profiles and necessitate a long-term and comprehensive monitoring. This article presents an overview of therapy conversion of immunotherapies for multiple sclerosis in accordance with the recommendations of the Disease-Related Competence Network for Multiple Sclerosis and the German Multiple Sclerosis Society as well as the guidelines on diagnostics and therapy for multiple sclerosis of the German Society of Neurology and the latest research results. At the present point in time it should be noted that no studies have been carried out for most of the approaches for therapy conversion given here; however, the recommendations are based on theoretical considerations and therefore correspond to recommendations at the level of expert consensus, which is currently essential for the clinical daily routine.

Multiple sclerosis (MS) is characterized by oligodendrocyte death and myelin sheath destruction of the central nervous system (CNS) in response to autoinflammatory processes. Besides demyelination axonal degeneration constitutes the second histopathological hallmark of this disease. A large number of immunomodulatory and targeted immunosuppression treatments have been approved for relapsing remitting (RR) MS where they effectively reduce relapse rates; however, currently no treatment options exist to repair injured axonal tracts or myelin damage that accumulates over time particularly in progressive MS. In light of the growing available therapeutic repertoire of highly potent immunomodulatory medications there is an increasing interest in the development of therapies aimed at neutralizing neurodegenerative damage. Endogenous remyelination processes occur mainly as a result of oligodendrocyte precursor cell (OPC) activation, recruitment and maturation; however, this repair activity appears to be limited and increasingly fails during disease progression. Based on these observations OPCs are considered as promising targets for the regenerative treatment of all stages of MS. This article presents an overview of approved medications with a suggested role in regeneration, regenerative treatments that are currently being tested in clinical trials, as well as promising future therapeutic approaches derived from basic glial cell research aiming at the promotion of the endogenous repair activity of the brain.

Intravenous immunoglobulin (IVIg) is an efficacious treatment for immune-mediated neuropathies like Guillain-Barré syndrome (GBS), chronic inflammatory demyelinating neuropathy (CIDP), and multifocal motor neuropathy (MMN). In the pathogenesis of immune-mediated neuropathies chemokines and their receptors play a crucial role. Using flow cytometry we examined whether IVIg modulates chemokine expression repertoires of T cells and monocytes. The expression of inflammatory chemokine receptors CCR1, CCR2, CCR4, CCR5, CCR6 and CXCR3 was investigated on circulating T-cell subsets, and CCR1, CCR2 and CCR5 on circulating monocytes before and after IVIg treatment in patients with immune-mediated neuropathies (MMN, n = 7; GBS, n = 1; CIDP, n = 2). Furthermore, the homing potential of T cells was analyzed by the expression of CCR7, a chemokine receptor known to be utilized by mature T cells to recirculate into secondary lymphoid organs. In contrast to studies in chronic heart failure, no differences in expression patterns before and after IVIg treatment of any of the investigated chemokine receptors were found. Furthermore, the proportion of CD45RO-positive CD4+ or CD8+ T-cell subsets was not changed by IVIg treatment. Thus, we concluded that modulation of the expression of chemokine receptors on circulating leukocytes by IVIg is not a mode of action in immune-mediated neuropathies.

For centuries extracts from the Cannabis sativa plant have been used for recreational use and as remedies. Anecdotal reports from patients with multiple sclerosis (MS) experiencing relief of their spasticity and pain after smoking marihuana have prompted discussions about a potential therapeutic application of cannabis preparations in MS. Only recently the first large, multicenter, double-blind, placebo controlled study was conducted evaluating the use of cannabinoids for treatment of spasticity and other symptoms related to MS. Based on this trial and previous uncontrolled observations together with insights from basic research and animal experiments there is reasonable evidence for the therapeutical employment of cannabinoids in the treatment of MS related symptoms. Furthermore, data are arising that cannabinoids have immunomodulatory and neuroprotective properties. However, results from clinical trials do not allow the recommendation for the general use of cannabinoids in MS. This article summarizes the present knowledge of clinical and experimental research regarding the therapeutic potential of cannabinoids for the treatment of MS.

Diese Kasuistik beschreibt eine Patientin mit spatem Erkrankungsbeginn einer Multiplen Sklerose. Trotz des hoheren Manifestationsalters war die Erkrankung anfangs klar schubformig, aber eine immunmodulatorische Therapie mit Interferon β-1b wurde erst beim Ubergang in die sekundar chronisch progrediente Phase begonnen. Bei noch klar vorhandener Schubaktivitat bewirkte die Therapie mit Interferon β-1b eine Stabilisierung des Krankheitsverlaufs.

We report on a patient with atypical first manifestation of multiple sclerosis (MS) with autonomous functional disorder. Neurological tests were not performed earlier than 3 years after the occurrence of first signs and symptoms in association with erectile dysfunction and voiding disorders when sensory disturbances occurred. MS was finally diagnosed. No further clinical attack was observed in the 3 years following the initiation of therapy with interferon β-1b.

Objective: Intravenous immunoglobulin (IVIg) has been widely used in neurological diseases during the last decade. The current indications for IVIg in the acute management of neuromuscular disorders, often similar to the indications for plasma exchange, are reviewed and discussed on the basis of the available clinical and experimental data. Data Sources and Selection Criteria: Original papers and reviews on IVIg, covered by repeated MEDLINE searches from 1981 to 1996 and some significant papers from other sources. Results: Compared to plasma exchange, that has been used for some of the indications treated with IVIg, the latter is more widely available and has only few side effects with a small risk of transmission of infectious agents. Good clinical evidence for the efficacy of IVIg is available for Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy, and multifocal motor neuropathy. In conditions like myasthenia gravis and myositis, favorable effects were reported, but future studies have to be awaited. Conclusions: IVIg is a promising therapy, that has been shown to be effective in some neuromuscular disorders. Routine use in the acute management of these diseases should be restricted to conditions for which a positive effect has been proven in controlled trials.

Inflammatory bowel diseases, such as Crohn's disease, ulcerative colitis, autoantibody driven celiac disease and infectious Whipple's disease can all be associated with neurological symptoms. The neurological manifestation may occur even before the gastrointestinal symptoms or the enteropathic symptoms can even be absent as in celiac disease. These diseases can be caused by malresorption and lack of vitamins due to enteral inflammation as well as (auto-)immunological mechanisms and drug-associated side effects. Thus, inflammatory bowel diseases have to be considered in the differential diagnosis. In this review the most common neurological manifestations of these diseases will be described as well as the diagnostic approach.

Human immunoglobulins (IG, mostly IgG) are used as replacement therapy in patients with inherited primary immunodeficiencies, and in patients with secondary immuno-deficiencies often observed in multiple myeloma or chronic lymphocytic leukemia. Ig are also approved as immunomodulatory therapy in neurological autoimmune diseases (NAID) such as Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP) and multifocal motor neuropathy (MMN). 16 different Ig preparations for intravenous and subcutaneous use are at the moment available in Germany. The SIGNS study (Assessment of immunoglobulins in a long-term non-interventional study) investigates the clinical use of these drugs under clinical practice conditions. In this non-interventional prospective open-label cohort study, 550 patients with new or maintenance Ig therapy are observed with respect to drug utilization, effectiveness, (i. e. number of infections in PID and SID, functionality in NAID), tolerability, quality of life and costs in approximately 50 sites throughout Germany (neurologists, pediatricians, oncologists, other) for at least two years. This largest study of its kind is expected to contribute to optimization of Ig therapy in the postmarketing setting.

Our knowledge on the clinical efficacy of intravenous immunoglobulins (IVIg) in neurological diseases has greatly increased in the last 5 years. Liquid formulations with a higher concentration of IVIg have simplified administration. Despite a worldwide increase in plasma production it is still a valuable biological product which is why current indications must be continuously validated. Long-term efficacy of the preparation Gamunex could be demonstrated in patients with chronic inflammatory demyelinating polyneuropathy (CIDP). In acute myasthenic worsening a dose of 1 g IVIg/kg body weight appears to be sufficient for clinical stabilization. New indications, such as the postpolio syndrome or Alzheimer's disease are being explored in clinical trials. In addition to the consensus statement from 2004 the evidence for clinical use of IVIg has been re-evaluated and recommendations are given.

Long-term treatment of immune-mediated polyneuropathies remains difficult. For acute polyneuritis, or Guillain-Barré syndrome, the established standard therapy utilizes high doses of polyvalent intravenous immunoglobulins (IVIG). A recently published randomized placebo-controlled study of patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) showed IVIG to be clinically effective also for this disorder in both short and long term. This survey presents data of this so-called ICE study ("Intravenous immune globulin for the treatment of chronic inflammatory demyelinating polyradiculoneuropathy"). It also discusses the value of IVIG in the treatment of immune-mediated polyneuropathies.

The currently licensed medications for relapsing-remitting multiple sclerosis (RRMS) are only partially effective and require a parenteral route of administration. Thus there is a need for new, preferably orally available therapeutics. Such a substance could be fumaric acid and its esters (FAE). These compounds are already in use for treatment of psoriasis and are known to have an immunomodulatory effect. In addition there is a potential for neuroprotective effects as suggested by in vitro studies and experiments in the animal model of experimental autoimmune encephalomyelitis. A phase II clinical study in RRMS patients with the modified fumaric acid ester BG-12 showed as "proof of principle" in a frequent MRI design that FAE significantly reduce the number of gadolinium-enhancing lesions after 24 weeks of treatment. Further phase III studies have been started to explore the long-term efficacy of this substance. The results of these studies will show if FAE can be another treatment option, maybe for combination therapy, in patients with MS.

For centuries extracts from the Cannabis sativa plant have been used for recreational use and as remedies. Anecdotal reports from patients with multiple sclerosis (MS) experiencing relief of their spasticity and pain after smoking marihuana have prompted discussions about a potential therapeutic application of cannabis preparations in MS. Only recently the first large, multicenter, double-blind, placebo controlled study was conducted evaluating the use of cannabinoids for treatment of spasticity and other symptoms related to MS. Based on this trial and previous uncontrolled observations together with insights from basic research and animal experiments there is reasonable evidence for the therapeutical employment of cannabinoids in the treatment of MS related symptoms. Furthermore, data are arising that cannabinoids have immunomodulatory and neuroprotective properties. However, results from clinical trials do not allow the recommendation for the general use of cannabinoids in MS. This article summarizes the present knowledge of clinical and experimental research regarding the therapeutic potential of cannabinoids for the treatment of MS.

The immunomodulatory treatment of multiple sclerosis (MS) with high-dose intravenous immunoglobulins (IVIg) has been discussed with some controversy in the context of evidence-based medicine. The recent publication of eight trials investigating several aspects of MS has shed some more light on the role of IVIg treatment in MS. Here we summarize and critically discuss the new data in the context of previous studies on this treatment. In relapsing-remitting MS, IVIg remain a second-line treatment when other licensed treatments are not possible. Currently there is no role for IVIg in secondary progressive MS. Similarly, the use of IVIg during an acute relapse shows no benefit in addition to standard steroid treatment. The initiation of IVIg therapy after a clinically isolated syndrome has delayed the occurrence of definite MS, and this may become a new indication. Furthermore, previous data suggesting that IVIg can reduce the incidence of postpartal relapses have been substantiated. However, those trials unfortunately lack appropriate internal control groups. By and large, previous recommendations for the use of IVIg in MS are supported by the new data.

Intravenous immunoglobulins (IVIg) have become an alternative immunomodulatory treatment for neurological autoimmune disorders. On the basis of several well conducted placebo-controlled trials evidence is available supporting the efficacy of IVIg. However, of all neurological diseases, IVIg is currently only licensed for Guillain-Barré syndrome. Thus, the off-label use of IVIg has to be focussed although an effective treatment must be made available for the patients, in particular when there is no other treatment alternative. The consensus paper presented here critically discusses the modern studies investigating the use of IVIg in neurological diseases. On the basis of this evidence recommendations for the treatment with IVIg were developed. To achieve a broad and valid consensus, numerous German speaking experts in the field were involved. It is expected that this manuscript will help to ascertain a rational use of IVIg in the future.

Recent clinical studies in multiple sclerosis (MS) provide new data on the treatment of clinically isolated syndromes, on secondary progression, on direct comparison of immunomodulatory treatments and on dosing issues. All these studies have important implications for the optimized care of MS patients. The multiple sclerosis therapy consensus group (MSTCG) critically evaluated the available data and provides recommendations for the application of immunoprophylactic therapies. Initiation of treatment after the first relapse may be indicated if there is clear evidence on MRI for subclinical dissemination of disease. Recent trials show that the efficacy of interferon beta treatment is more likely if patients in the secondary progressive phase of the disease still have superimposed bouts or other indicators of inflammatory disease activity than without having them. There are now data available, which suggest a possible dose-effect relation for recombinant beta-interferons. These studies have to be interpreted with caution, as some potentially important issues in the design of these studies (e. g. maintenance of blinding in the clinical part of the study) were not adequately addressed. A meta-analysis of selected interferon trials has been published challenging the value of recombinant IFN beta in MS. The pitfalls of that report are discussed in the present review as are other issues relevant to treatment including the new definition of MS, the problem of treatment failure and the impact of cost-effectiveness analyses. The MSTCG panel recommends that the new diagnostic criteria proposed by McDonald et al. should be applied if immunoprophylactic treatment is being considered. The use of standardized clinical documentation is now generally proposed to facilitate the systematic evaluation of individual patients over time and to allow retrospective evaluations in different patient cohorts. This in turn may help in formulating recommendations for the application of innovative products to patients and to health care providers. Moreover, in long-term treated patients, secondary treatment failure should be identified by pre-planned follow-up examinations, and other treatment options should then be considered.

Accumulation and activation of mononuclear cells (lymphocytes and monocytes) in the CNS is one of the crucial steps in the pathogenesis of multiple sclerosis (MS). Chemokines and their receptors govern physiological and pathological leukocyte trafficking and may also be pertinent in hematogenous leukocyte infiltration of the CNS. Due to broad pharmacological interest in the chemokine system, peptide antagonists and small molecular antagonists are now available for clinical therapeutic trials. For the treatment of MS in particular, the chemokine receptors CCR1, CCR2, CCR5, and CXCR3 are possible targets in a chemokine-based therapeutic approach. In this review, we summarize current knowledge of the roles of chemokines and chemokine receptors in the pathogenesis of MS. Furthermore, options for possible therapeutic intervention through the chemokine system are outlined. Clinical studies in MS patients applying this knowledge are expected soon.

In this paper we examine several aspects of performance and connection management during handoffs and interface switching in mobile computing environments. We demonstrate the insufficiency of network layer mobility protocols to preserve high-performance operation of reliable transport protocols such as TCP under certain circumstances. We also introduce a mobility-aware transport, Mobile TCP, that maintains robust operation despite lossy mobile activity. Experimental results are presented and discussed.

Currently available therapies for multiple sclerosis (MS) delay disease progression via immunomodulation or immunosuppression. A persisting neurological deficit is mostly irreversible. Thus, a reparative treatment is urgently warranted. After positive results in animal models, clinical trials to promote endogenous remyelination with intravenous immunoglobulins (IVIg) or the growth factor IGF-1 were performed, unfortunately without clinical improvement. Another possibility to achieve remyelination is the transplantation of myelinating cells into the central nervous system. Proof of principle and demonstration of the functionality were shown in numerous experiments, and a first clinical trial in patients with MS has started. Although there are still several open questions, many are specific to MS and can not be answered in an animal model. This first trial will show if cell transplantation is a feasible concept in MS and whether the transplanted cells will survive and form new myelin. Schwann cells are currently the most promising cells to be transplanted, due to the advantages of an autologous transplantation from the patient's sural nerve biopsy, possibility to expand the cells in culture, and the possibility that they may escape the ongoing inflammatory reaction in MS. Other cell types are available, including stem cells, which are in the centre of a lively discussion. The results of the ongoing trial must be awaited before other transplant studies are performed to tackle other yet unresolved problems. At the time, it seems unlikely that cell transplantation will become clinical practice in the near future.

There is no doubt about the immunomodulatory capacity of intravenous immunoglobulins (IVIg). This also holds true for multiple sclerosis (MS), where clinical trials have shown a reduction in relapse rate and number of active lesions on MRI after IVIg treatment. Experimental data in the model of murine Theiler's virus encephalomyelitis (TMEV) gave rise to the hypothesis that IVIg may also promote remyelination. Unfortunately, recent trials were unable to demonstrate clinically relevant remyelination in MS patients treated with IVIg. A possible explanation could lie in the fact that IVIg do not influence the function of oligodendrogilial cells in vitro. In contrast, IVIg can protect oligodendrocytes against complement-mediated injury and thus provide more cells that could engage in remyelination. In addition, IVIg can modulate microglial functions in vitro, thus creating a microenvironment permissive for remyelination. Should such mechanisms also be operative in vivo, they would have escaped detection in the treatment protocols used to date. It would appear that IVIg need to be administered while the inflammatory process is still ongoing, whereas the published trials included only patients with a stable deficit when there is probably little or no active inflammation. Despite new studies on IVIg, its role in the management of MS remains elusive.

Mit der groser werdenden Anzahl von Indikationen und dem zunehmenden Einsatz von intravenosen Immunglobulinen (IVIg) im klinischen Alltag werden auch mehr unerwunschte Wirkungen berichtet. Ursprunglich wurde die Haufigkeit von Nebenwirkungen mit 5–10% angegeben [29, 78]. Einige neuere Untersuchungen haben jedoch teilweise wesentlich hohere Komplikationsraten bis zu 81% berichtet [10, 17, 102]. Die haufigen Nebenwirkungen sind dabei allerdings milde und komplett reversibel, wahrend schwerwiegende unerwunschte Reaktionen nur sehr selten auftreten [79, 101]. Fur die tagliche Praxis und den behandelnden Arzt bedeutet dies, dass bei Indikationsstellung zur Gabe von IVIg Benefit und Risiko gut abgewogen werden sollten und die Therapie uberwacht werden muss, um potentielle Nebenwirkungen zu vermeiden bzw. rechtzeitig zu erkennen.

Septo-optic dysplasia (or de Morsier syndrome) is a congenital disorder characterised by anomalies in cerebral midline structures, optic nerve hypoplasia, and hormonal deficiencies. Diagnosis should be made early, due to the possibility of treating the hormonal disturbances. We describe here a case with decreased visual acuity, one-sided hemianopia, nystagmus und agenesis of the septum pellucidum and discuss the heterogeneous appearance of this syndrome. There are two theories regarding its pathogenesis. The first postulates simultaneous damage to both cerebral structures and optic nerve development around the 6th week of gestation, while the other favours secondary degeneration of optic nerve fibres due to a cerebral lesion.

Small and large vessel occlusive disease leading to chronic cerebral ischemia and brain atrophy is a concept originating in the last century. The modern notion of acute brain infarct, however, appears to have eclipsed the idea of chronic hypoperfusion as an important factor in ischemic cerebral damage. We present a patient history featuring recurrent episodes of acute posterior circulation infratentorial ischemia in addition to a progressive cerebellar syndrome over a course of several years. Laboratory work-up including cerebral angiography, repeated CT and MR scanning revealed basilar artery occlusion, a pontine infarct and a subsequently developing cerebellar atrophy without signs of cerebellar infarction. Findings indicating causes of cerebellar atrophy other than ischemia could not be elicited. We offer the hypothesis that basilar artery occlusion, inducing subsequent chronic ischemia, is the most likely cause of the cerebellar atrophy observed in our case.

A 29-year-old man presented in another hospital because of discoordination of all extremities with sudden onset. After fast reversal of the symptoms, he was discharged without a clear diagnosis. Because of remaining discrete dysarthria, computed tomography and magnetic resonance imaging were performed which demonstrated bilateral cerebellar infarcts. The cause was assumed to be a transient embolic occlusion of the distal basilar artery.Intravenous heparin was started to prevent further occlusions. Because no source for emboli or other causes were found, the patient was discharged after 14 days on acetylic acid (250 mg/d) as secondary prevention therapy.A vascular or neurological cause is often not considered when neurological symptoms are quickly reversible after a transient occlusion of the basilar artery. In these cases, the suspected diagnoses of psychiatric illness, alcohol abuse, drug intoxication, infection or myocardial infarction do not lead to the necessary investigations. Thus, a potentially life-threatening situation may be disregarded.

The complete amino-acid sequence of the AL Bence-Jones protein was determined from amyloidosis patient EZI. The protein was isolated from the urine by ammoniumsulfate precipitation, ion exchange chromatography, reduced, aminoethylated or carboxymethylated, and digested with either trypsin or staphylococcal protease. The peptides were separated using RP-HPLC and characterized by amino-acid sequence analysis and amino-acid analysis. The EZI polypeptide consists of 216 amino acids. It has a N-terminus blocked by PCA and amino-acid residues specific for the lambda 1.1 subgroup. Wit Ala, Ser, Ser, Thr, and Arg in pos. 112, 114, 163, and 190 the constant part belongs to the K(-), Oz(-), Mcg (-) isotype. An alanine was identified in position 90. This replaces the hydrophilic threonine or serine residues determined in the other lambda 1.1 L-chains and represents the only hydrophilic/hydrophobic substitution.

The immunoglobulin Kol was the first intact antibody molecule which was characterized by high-resolution X-ray crystallography. Furthermore the complete amino-acid sequence of the heavy (H)-chain is known. Here we report the complete amino-acid sequence of the light (L)-chain of the monoclonal immunoglobulin Kol (IgG1). The polypeptide has an Mr of 22,781, consists of 216 amino acids and due to its structure is of the lambda-type. With the characteristic amino acids threonine, asparagine, threonine, glycine and lysine in positions 101, 114, 116, 154, and 165, respectively the Kol L-chain is of the Mcg isotype. With the proteins Mcg, Mot, Bur, Loc and Mem six myeloma-derived amino-acid sequences of the same isotype are known. The amino-acid sequence of the N-terminal variable part is characteristic of subgroup 1. This contribution completes the primary structure of IgG1 Kol.