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Die chronisch inflammatorisch demyelinisierende Polyneuropathie (CIDP) ist eine seltene Erkrankung des peripheren Nervensystems. Im Verlauf der Erkrankung kommt es zu symmetrischer, oft proximal betonter Schwache der Extremitaten. Teilweise treten auch sensorische Ausfalle auf. Wir beschreiben einen Fall, bei dem aufgrund proximal betonter Beinschwache und erhohter Entzundungsparameter zunachst eine Polymyalgia rheumatica vermutet wurde. Letztendlich wurde nach interdisziplinarer Diagnostik eine CIDP mit gleichzeitigem Vorliegen einer Endokarditis diagnostiziert.

Coronavirus disease 2019 has rapidly spread around the globe and various comorbidities, such as diabetes have been recognized as risk factors for an unfavorable outcome. We analyzed a cohort of COVID-19 patients (n = 75) treated at a German community hospital. With a focus on diabetes mellitus, we evaluated the impact of distinct comorbidities on the COVID-19 disease course. The duration of hospital stay was prolonged if diabetes was present. An older age was associated with a poor outcome. The percentage of non-survivors increased in the presence of congestive heart failure or chronic kidney disease. In the group of diabetes patients, mortality was increased if any organ complication was present and diabetic nephropathy or the combination of obesity plus diabetes were by far the most important risk factors. Taken together, an older age, congestive heart failure, and chronic kidney disease significantly influenced COVID-19 disease course and survival. Diabetic nephropathy or the combination of obesity plus diabetes had the strongest impact on patients’ outcome.

The pandemic outbreak of COVID-19 challenges medical care systems all around the world. We here describe our experiences during the treatment of COVID-19 patients (n = 42) treated from 2 March 2020 to 16 April 2020 at a German district hospital. Forty-two COVID-19 patients were hospitalized and five patients developed a severe disease, requiring intensive care. Overall, 11 out of 42 hospitalized patients died. COVID-19 caused lymphocytopenia, as well as increased d-dimer, c-reactive protein and creatine kinase, and lactate dehydrogenase levels. These changes were mostly pronounced in patients that developed a severe disease course. Radiologic findings included ground-glass opacity, bilateral/multilobular involvement, consolidation, and posterior involvement. We compared COVID-19 patients to an average population of ‘non-COVID’ patients. Interestingly, no laboratory or radiologic finding was specific for COVID-19 when standing alone, as comorbidities of ‘non-COVID’ patients certainly can mimic similar results. In common praxis, the diagnosis of COVID-19 is based on a positive PCR result. However, a false-negative result causes problems for the workflow of an entire hospital. In our clinic, the consequences of a false assumption of SARS-CoV-2 negativity in four cases had dramatic consequences, as contact persons had to be quarantined. To avoid this, a comprehensive view of lab-results, radiology, clinical symptoms and comorbidities is necessary for the correct diagnosis or exclusion of COVID-19.

The diagnosis of coronavirus disease 2019 (COVID-19) is mainly based on a positive severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) polymerase chain reaction (PCR) result. PCR samples are obtained from upper or lower respiratory tract specimens. However, the sensitivity of PCR is known to have some limitations. We report on a patient who was admitted to our hospital with dyspnea, fever, cough, and history of contact with a SARS-CoV-2 infected relative. The initial chest computed tomography (CT) showed only minimal changes and SARS-CoV-2 PCR from a nasopharyngeal swab sample was negative. PCR results obtained from further nasopharyngeal swabs, qualified sputum samples, and from a lower respiratory tract specimen also remained negative. At day 13 after admission, a second chest CT showed radiological findings suspicious for viral pneumonia. Finally, serologic results showed high levels of immunoglobulin G and immunoglobulin A antibodies against the S1 domain of the SARS-CoV-2 spike protein, and the patient was diagnosed with COVID-19 pneumonia.

Background: Coronavirus-19 disease (COVID-19) is mainly affecting the respiratory tract, causing viral pneumonia with fever, hypoxemia, and cough. Commonly observed complications include acute respiratory failure, liver or kidney injury, and cardiovascular or neurologic symptoms. In some patients, inflammatory damage results in long term complications like pulmonary fibrosis, chronic pulmonary thrombotic microangiopathy, or neurologic symptoms. The developement of spontaneous pneumothorax is reported as a rare complication mainly in consequence to mechanic ventilation in the criticall ill. Case Report: We report on two cases of COVID-19 pneumonia complicated by a spontaneous pneumothorax and bullous lesions of the lung. Bilateral giant bullae were observed in one of the cases. This complication occurred after an initial resolvement of respiratory symptoms (day 16 and day 29 after COVID-19 treatment was started). Initially, both patients had shown a rather mild course of COVID-19 pneumonia and no mechanical ventilatory support had been necessary. Why Should an Emergency Physician Be Aware of This? In both cases, COVID-19 caused alveolar damage and formation of thoracic bullae with consequent spontaneous pneumothorax as a serious complication. Emergency physicans must be aware of this complication even if the initial COVID-19 symptoms have resolved.

Expression of signaling proteins in bone cells depends on their embryological mesoderm-derived (e.g. tibia) or cranial neural crest (CNC)-derived (e.g. jaw) origin. Connexin 43 (Cx43) is a gap junction protein that plays an essential role in the mode of action of bisphosphonates (BP). This study aimed to investigate Cx43 expression and the influence of BP application on mesoderm- and CNC-derived bone. Using a rat model, molar extraction and tibia osteotomy with (Group 4) or without (Group 3) previous BP application was performed. Untreated (Group 1) and animals selectively treated with BPs (Group 2) served as controls. Cx43 expression was immunohistochemically determined 12 and 16 weeks postoperatively via a labeling index. Cx43 expression in CNC-derived bone was significantly higher compared with mesodermal bone. BP application decreased Cx43 expression; however, detected expression levels were still higher in jawbone (Group 2 tibia vs jaw: 5.83 ± 5.06 vs 23.52 ± 6.42; p = 0.007). During bone healing after surgical intervention (Group 3) there were no expression differences between tibia and jawbone. BP treatment prior to surgery resulted in significantly lower Cx43 expression in CNC-derived compared with tibia bone (Group 4 tibia vs jaw: 56.84 ± 15.57 vs 16.40 ± 5.66; p Increased Cx43 expression in jaw compared with tibia bone is in line with their embryological origins. A significant Cx43 suppression in jawbone after BP application and surgery might contribute to the selectively altered osseous turnover and development of MRONJ in CNC-derived bone.

Observation of the climate and ecosystem of ice covered polar seas is a timely task for the scientific community. The goal is to assess the drastic and imminent changes of the polar sea ice cover induced by climate change. Retreating and thinning sea ice affects the planets energy budget, atmospheric, and oceanic circulation patterns as well as the ecosystem associated with this unique habitat. To increase the observational capabilities of sea ice scientists, we equipped a remotely operated vehicle (ROV) as sensor platform for interdisciplinary research at the ice water interface. Here, we present the technical details and operation scheme of the new vehicle and provide data examples from a first campaign in the Arctic in autumn 2016 to demonstrate the vehicle's capabilities. The vehicle is designed for efficient operations in the harsh polar conditions. Redundant modular design allows operation by three scientists simultaneously operating a wide variety of sensors. Sensors from physical, chemical, and biological oceanography are combined with optical and acoustic sea ice sensors to provide a comprehensive picture of the underside of sea ice. The sensor suite provides comprehensive capabilities and can be further extended as additional ports for power and communication are available. The vehicle provides full six degrees of freedom in navigation, enabling intervention, and manipulation skills despite its simple one function manipulator arm.

Introduction: Medical imaging technology has revolutionized health care over the past 30 years. This is especially true for ultrasound, a modality that an increasing amount of medical personal is starting to use. Purpose: The purpose of this study was to develop and evaluate a platform for improving medical image interpretation skills regardless of time and space and without the need for expensive imaging equipment or a patient to scan. Methods, results and conclusions: A stable web application with the needed functionality for image interpretation training and evaluation has been implemented. The system has been extensively tested internally and used during an international course in ultrasound-guided neurosurgery. The web application was well received and got very good System Usability Scale (SUS) scores.

Objective.To analyze clinical manifestations, serum ferritin, and serum cytokine levels in patients with adult-onset Still’s disease (AOSD) or bacterial sepsis and to evaluate their potential use for differential diagnosis.Methods.Twenty-two consecutive patients with the first flare of AOSD and 6 patients with an established diagnosis of AOSD under immunosuppressive therapy were compared with 14 patients with bacterial sepsis. Clinical manifestations were scored in a Pouchot AOSD activity score including elevated serum ferritin levels to obtain a modified Pouchot score. Serum cytokine profiles were analyzed from each patient.Results.The scores of clinical manifestations using a modified Pouchot activity score were significantly higher in patients with active untreated AOSD (mean 5.60 ± 1.93) compared with patients with chronic AOSD (mean 1.16 ± 0.98; p < 0.001) and patients with sepsis (mean 2.38 ± 1.19; p < 0.001). A modified Pouchot score ≥ 4 shows a sensitivity of 92% and a specificity of 93% for active AOSD. Serum cytokine levels of interleukin 1ß (IL-1ß), IL-6, IL-8, IL-10, IL-12, IL-18, interferon-γ, tumor necrosis factor-α, and calprotectin were elevated in acute AOSD and sepsis. Significant differences were detected only in patients with sepsis who had higher levels of IL-6 and IL-8. The overlap of the 2 groups limits the use of cytokines for differential diagnosis in individual patients.Conclusion.A modified Pouchot AOSD activity score including elevated serum ferritin levels was more useful to confirm the diagnosis of AOSD compared to patients with sepsis. Elevated serum cytokines correlate with inflammation but are of limited use to differentiate between active AOSD and bacterial sepsis.

Background—Clinical studies failed to provide clear evidence for a proatherogenic role of hypercoagulability. This is in contrast to the well-established detrimental role of hypercoagulability and thrombin during acute atherosclerotic complications. These seemingly opposing data suggest that hypercoagulability might exert both proatherogenic and antiatherogenic effects. We therefore investigated whether hypercoagulability mediates a beneficial effect during de novo atherogenesis.Methods and Results—De novo atherogenesis was evaluated in 2 mouse models with hyperlipidemia and genetically imposed hypercoagulability (TMPro/ProApoE−/−and FVLQ/QApoE−/−mice). In both mouse models, hypercoagulability resulted in larger plaques, but vascular stenosis was not enhanced secondary to positive vascular remodeling. Importantly, plaque stability was increased in hypercoagulable mice with less necrotic cores, more extracellular matrix, more smooth muscle cells, and fewer macrophages. Long-term anticoagulation reversed these changes. The reduced frequency of intraplaque macrophages in hypercoagulable mice is explained by an inhibitory role of thrombin and protease-activated receptor-1 on monocyte transendothelial migration in vitro. This is dependent on phospholipase-Cβ, phosphoinositide 3-kinase, and nitric oxide signaling in monocytes but not in endothelial cells.Conclusions—Here, we show a new function of the coagulation system, averting stenosis and plaque destabilization during de novo atherogenesis. The in vivo and in vitro data establish that thrombin-induced signaling via protease-activated receptor-1, phospholipase-Cβ, phosphoinositide 3-kinase, and nitric oxide in monocytes impairs monocyte transendothelial migration. This likely accounts for the reduced macrophage accumulation in plaques of hypercoagulable mice. Thus, in contrast to their role in unstable plaques or after vascular injury, hypercoagulability and thrombin convey a protective effect during de novo atherogenesis.

We outline the procedures used to establish benchmark physical property data for the Third Industrial Fluid Properties Simulation Challenge. For both challenge problems, this involved measurement of new data, including bubble-point pressures of ethanol/HFC-227ea mixtures at 343.13 K, and the viscosity of 1,2-butanediol, 1,3-butanediol, 1,4-butanediol, 2-methyl-1,3-propanediol, and 1,2,4-butanetriol at 373 K and 0.1 and 250 MPa. When possible, measurements were compared with published literature data. Recommended values are provided with corresponding uncertainty estimates.

Die Pathogenese des systemischen Lupus erythematodes (SLE) ist bislang nur teilweise verstanden. Charakteristisch fur diese Erkrankung ist das Auftreten von Antikorpern gegen nukleare Antigene. Weiterhin ist der SLE durch eine Interferon-I-Gen-Signatur gekennzeichnet. Eine Fehlregulation von Apoptose und Phagozytose apoptotischer Zellen wird als zentraler pathogenetischer Faktor fur seine Entstehung diskutiert. In verschiedenen Publikationen der letzten Jahre wurde deutlich, dass Autoantigene in apoptotischen Zellen akkumulieren und z. T. sogar auf deren Oberflache exponiert werden. In spaten Phasen der Apoptose kommt es auserdem zu posttranslationalen Modifikationen von Autoantigenen, wodurch Neoantigene entstehen. Auch subzellulare Fragmente wie apoptotische Mikropartikel scheinen an der Pathogenese des SLE beteiligt zu sein. Es wurde gezeigt, dass Mikropartikel relevante Autoantigene enthalten und B- und T-Lymphozyten stimulieren konnen. Daruber hinaus sind apoptotische Mikropartikel in der Lage, plasmazytoide dendritische Zellen zu stimulieren und eine gesteigerte Sekretion von Interferon α zu verursachen. Durch diese Beobachtungen konnen eine Fehlregulierung von Apoptose und Phagozytose mit der bei SLE-Patienten beobachteten Interferon-I-Gen-Signatur in direkten Zusammenhang gebracht werden.

OBJECTIVE: The study aimed at comparing burnout in staff members at residential drug and alcohol detoxification wards with and without teamsupervision. METHOD: 4 times in a period of 18 month all staff members (n = 44) were assessed for burnout using a german version (Checkliste Burnoutmerkmale) of the Maslach Burnout Inventory (MBI, Maslach u. Jackson 1986) to asses the severity and the CBE (Checkliste Burnoutentstehungsmerkmale) for associated burnout risc-factors. RESULT: There was no statistical differences between the mean scores of the 3 different wards due to extreme SDs. The interpersonal differences among staff on the 4 occasions were remarkably. On repeated measurements the intraindividual changes were high. Higher scores were correlated with high workload (seen as frequent admissions). CONCLUSION: Work-related variables (admissions) turned out to be of more importance than supervision in times of chronic staff-shortage.

Autoantibodies against opsonins of dying and dead cells mediate Fcγ receptor-dependent phagocytosis of autologous apoptotic and necrotic cells and hereby tend to elicit inflammation instead of silent clearance. We analysed sera of patients with chronic autoimmune diseases for the occurrence of IgG autoantibodies recognizing galectins. These pluripotent effectors can also bind to apoptotic or necrotic cells. Patients with antiphospholipid syndrome (APS; n = 104) and systemic lupus erythematosus (SLE; n = 62) were examined, healthy donors ( n = 31) served as controls. Selected peptides of galectin (Gal)-2 were employed for peptide-based ELISAs. Levels of anti-Gal-2PEP-IgG were significantly increased in SLE and APS when compared with controls. In addition, patients with APS showed significantly higher levels of anti-Gal-2PEP-IgG compared with patients with SLE. Anti-Gal-2PEP-IgG may, therefore, be considered novel biomarkers for APS.

Antibody-based approaches have become a novel treatment modality for lymphoma patients. Humanized 1D10 (Hu1D10; Remitogen) is among the antibodies that are currently under evaluation in phase II clinical trials in lymphoma patients. The 1D10 antibody is directed against a polymorphic epitope on the beta-chain of human leucocyte antigen (HLA) class II. We found expression of the 1D10 epitope on B cells and monocytes from approximately 50% of healthy donors. Analyses of 1D10 expression on malignant cells revealed that approximately half of the HLA class II-positive haematological malignancies expressed the 1D10 epitope. In whole blood antibody-dependent cellular cytotoxicity (ADCC) assays, Hu1D10 was more effective than rituxan in killing malignant ARH-77 B cells. Interestingly, Hu1D10-mediated lymphoma cell lysis was significantly enhanced when blood from granulocyte colony-stimulating factor (G-CSF)-treated patients was compared with blood from healthy controls. Analyses of the relevant effector cell populations revealed that FcgammaRI (CD64)-positive polymorphonuclear cells were critical for enhanced Hu1D10-mediated lymphoma killing during G-CSF therapy, while the same effector cell population induced only marginal lysis with rituxan. Furthermore, Hu1D10 was highly effective in inducing apoptosis in primary lymphoma cells from B chronic lymphocytic leukaemia patients. These preclinical results form the basis for a phase I/II clinical trial of Hu1D10 in combination with G-CSF.

Mortality has often been regarded as a measure for overall outcome and both treatment and drug policy effectiveness. The number of deaths by illegal drugs from the years 1990 - 2000 in Bavaria were analysed using statistical trend tests (Spearman rho and Kendall tau). In Bavaria in general (p = 0.014) as well as in 5 out of seven counties a significant increase in drug related mortality was found. Language: de

Introduction: Parainfluenza virus (PIV) often causes self-limiting upper respiratory tract infection (URTI) in the immunocompetent host, but can result in severe and even life-threatening lower respiratory tract infection (LRTI) in patients with hematologic malignancies or following stem cell transplantation. In contrast to respiratory syncytial virus or seasonal influenza, PIV is transmitted all year round. Here we analyze clinical characteristics of PIV infection in immunocompromised patients, assess possible risk factors for severe infection and report on nosocomial transmission as well as prolonged viral shedding. Methods: From July 2013 to June 2016, 108 cases of PIV infection in patients with hematologic malignancies or following stem cell transplantation were identified at our institution. Diagnosis of PIV was done by PCR detection of viral RNA in respiratory materials (nasopharyngeal swabs or bronchoalveolar lavage). Clinical characteristics and outcome of infected patients were retrospectively evaluated. Nosocomial transmission was assumed in patients with detection of PIV ≥ 7 days after hospital admission. The impact of possible influence factors on morbidity and mortality was analyzed by Fisher's exact test. In patients with availability of consecutive tests for PIV, duration of viral shedding was assessed. Results: 108 patients were identified, 92 with PIV type 1/3, 16 with PIV type 2/4. Median age was 59 years [range 26-79], 64% were male. 75 patients had received a stem cell transplantation (36 allogeneic, 34 autologous, 5 both), 25 of them developed PIV infection before hematologic reconstitution. Nosocomial transmission was apparent in 44% of patients. Regarding outcome, 61 patients had URTI only, 47 patients (44%) developed a LRTI. A severe LRTI, defined as treatment on the intensive care unit and/or death, was present in 10 patients. Of these, 9 patients died, resulting in a mortality rate of PIV associated LRTI of 19%; 1 patient was put on extracorporeal membrane oxygenation and subsequently recovered. Neither type of PIV, underlying hematologic disease or transplant status had a significant impact on outcome. Severe leukopenia (p=0.006), uncontrolled hematologic disease (p=0.007), presence of co-infections (p=0.001) and nosocomial transmission (p Conclusions: PIV infection can cause significant morbidity and mortality in patients with hematologic malignancies and following stem cell transplantation. Despite thorough hygienic measures, nosocomial transmission was observed in many cases and was associated with an increased risk of developing PIV related LRTI. Prolonged viral shedding of up to 79 days was detected, especially in patients with LRTI, which might facilitate nosocomial spread of PIV and should be taken into account in infection control management. Disclosures No relevant conflicts of interest to declare.

The presence of autoantibodies against immunoregulatory effectors can be relevant for onset and/or the progression of autoimmune disease. Emerging insights into an immunological activity profile including a role as opsonins give reason to systematically monitor sera of patients for immunoglobulin G (IgG) autoantibodies, preferably for several galectins at the same time. Here, we report on a study of chronic inflammatory rheumatic diseases, i.e. systemic lupus erythematosus (SLE; pilot cohort p, n = 40; confirmation cohort c, n = 109), rheumatoid arthritis (RA; p, n = 32; c, n = 25) and primary antiphospholipid syndrome (APS; c, n = 64). Enzyme-linked immunosorbent assay-based series using galectin-1, -2, -3, -4, -7, -8 and -9 and natural processing products, i.e. the truncated version of galectin-3 and the N-terminal domains of galectin-4, -8 and -9, were performed. Normal healthy donors (p, n = 20; c, n = 21) and patients with paraproteins (c, n = 19) served as controls. Highly significant optical density-value readings for IgG autoantibodies were consistently detected for the proto-type galectin-7 (SLE) and the tandem repeat-type galectin-8 and -9 (SLE and RA). Their presence was independent from the autoantibody status against double-stranded DNA (for patients with SLE) or a rheumatoid factor (for patients with RA), respectively. Importantly, anti-galectin-2 autoantibodies highly significantly correlated with the appearance of a secondary APS in patients with SLE so that this parameter may serve as an additional biomarker for APS. Equally of note, the presence of IgG autoantibodies against galectins capable to act as an opsonin may contribute to a sustained immune dysregulation in patients with chronic inflammatory rheumatic diseases.

Systemic lupus erythematosus (SLE) is a complex prototypic autoimmune disease that is based on genetic factors (complement deficiencies) and is influenced by gender (female), environment (infections and UV irradiation), as well as random events (somatic mutations). The course of the disease is influenced by genes (e.g. FcgammaRIIA) and behaviour (sun-exposure). Inefficient clearance of dying cells and subsequent accumulation of apoptotic cell remnants is an intrinsic defect causing the permanent presence of cellular debris responsible for the initiation of autoimmunity. We favour the hypothesis that post-apoptotic debris accumulates in germinal centres, activates complement, and serves as a survival signal for B-cells that had stochastically become autoreactive in the process of somatic hypermutation (etiology). In the presence of autoantibodies against apoptotic cells or adaptor molecules the accumulation of post-apoptotic remnants (SNEC) causes immune complex formation and their pathological elimination, maintaining auto-inflammation. The SLE-type autoimmunity addresses nucleic acid-containing complex antigens (viromimetica). Autoantibody-protein-nucleic-acid complexes are likely to be mistaken for opsonised viruses. As a consequence, the immune system responds with the production of type-I interferons, a hallmark of SLE (pathogenesis). We conclude that the pathogenicity of autoantibodies is strongly increased if autoantigens are accessible and immune complexes are formed, which may be considered a binary pyrogen formed from less pro-inflammatory components. The accessibility of cognate autoantigens is likely to be related to impaired or delayed clearance of apoptotic cells.

While several characteristics of systemic lupus erythematosus (SLE) have been investigated, the distinct pathogenetic mechanisms leading to autoimmunity and chronic inflammation are not understood yet. A central role for apo has been implicated in the pathogenesis of SLE and an increased rate of apo or a defective clearance of apo cells have repeatedly been described in SLE patients, which show elevated levels of alpha-interferon (alphaIFN) as well as an enhanced expression of alphaIFN-alpha inducible genes referred to as alphaIFN signature. Recent publications link alphaIFN and apo: apo cell-derived microparticles can directly stimulate plasmacytoid dendritic cells to secret alphaIFN. This review highlights the role of apo material as source for AAg and as a trigger for chronic inflammation in the pathogenesis of SLE.

Szecsi J, Schiller M, Straube A, Gerling D. A comparison of functional electrical and magnetic stimulation for propelled cycling of paretic patients. Objective To compare isometric torque and cycling power, smoothness and symmetry using repetitive functional magnetic stimulation (FMS) and functional electrical stimulation (FES) in patients with paretic legs with preserved sensibility and in patients without sensibility. Design Repeated-measures design. Setting Laboratory setting. Participants Eleven subjects with complete spinal cord injury (SCI) and 29 subjects with chronic hemiparesis (16.6±5.5mo poststroke) volunteered. Interventions Using a tricycle testbed, participants were exposed to isometric measurements and ergometric cycling experiments, performed during both 20Hz FMS and FES stimulation. Subjects with hemiparesis and with complete SCI were stimulated at maximally tolerable level and maximal intensity, respectively. Main Outcome Measures Maximal isometric pedaling torque and mean ergometric power, smoothness, and symmetry were recorded for voluntary, FES, and FMS conditions. Results Two different patterns of the efficacy of FMS were identified. (1) Patients with complete SCI did not benefit (less torque and power was evoked with FMS than with FES, P −4 respectively). (2) Patients with hemiplegia and preserved sensibility could improve their torque output ( P P Conclusions FMS is a potential alternative to surface FES of the large thigh musculature in stimulation-supported cycling of patients with partially or completely preserved sensibility.

Background Systemic lupus erythematosus (SLE) is an autoimmune disease characterised by a wide range of antibodies reacting with nuclear antigens. Abnormalities in the apoptotic cell death process and apoptotic cell clearance may play an important role in generating these antibodies. Especially antibodies to histones in serum are frequently associated with SLE. Objectives The aims of this study were to evaluate the presence of histones in the cytoplasm of fresh peripheral blood mononuclear cells (PBMCs) and in activated lymphoblasts. The activated lymphoblasts cultured without IL-2 served as a model for apoptosis induction. Methods Human PBMCs were isolated from heparinized peripheral blood of normal donors (n = 6) and activated with 1 μg/ml phytohemagglutinin (PHA) and 10 U/ml IL-2 for the first 5 days. The following two days, the cells were expanded in IL-2 containing medium (0 h). Lymphoblasts were then incubated in IL-2 free medium for 8 or 24 h as well as for 24 h with IL-2 (10 U/ml). Furthermore, lymphoblasts were treated with IL-2 after 8 or 24 h IL-2 deprivation. PBMCs and lymphoblasts were lysed in a modified RIPA-buffer, 20 μg of protein were subjected to denaturing SDS-PAGE. Western blot detection was performed with antibodies against all 5 histones H1, H2A, H2B, H3 and H4 as well as against phosporylated H3 and acetylated H4. Results Only very weak signals of the histones H2A, H2B, H3 and H4 were detected in the cytoplasm of freshly isolated PBMCs, but H1 was undetectable. The activated lymphoblasts showed elevated amounts of all five histones compared to PBMCs. Furthermore, we observed an increased amount of the histones H2A, H2B, H3 and H4 in the cytoplasm in cell culture after another 8 or 24 h without IL-2. Interestingly, the signal intensity of these histones in the cytoplasm decreased significantly after addition of IL-2 to the lymphoblasts after 8 or 24 h IL-2 deprivation. However, no difference of the detectable amount of H1 was noted in activated lymphoblasts compared to preapoptotic lymphoblasts incubated for another 8 or 24 h without IL-2. In addition, for H1 no effect of addition of IL-2 was observed. Lymphoblasts activated with IL-2 for 24 h showed the same signal intensities for the histones H2A, H2B, H3 and H4 as observed for the cells at 0 h. No bands for acetylated H4 or phosporylated H3 were detected in cytoplasm samples in contrast to strong signals in nuclear preparations. Conclusion These results suggest that histones were released from the nucleus into the cytoplasm of preapoptotic human lymphoblasts. The mechanism of the transport of the histones into the cytoplasm is until now unknown. Acetylated H4 and phosporylated H3 were only detected in nuclear extracts which excludes nuclear membrane fragility and nuclear contamination as cause for our findings. In addition, our data indicate that IL-2 can reduce the release of histones from the nucleus into the cytoplasm.