Calcium channel blocker prevents stress-induced activation of renin and aldosterone in conscious pig

A considerable amount of data suggest the involvement of calcium-mediated processes in the activation of the renin-angiotensin-aldosterone (RAA) cascade. To investigate the effect of calcium-channel inhibition on the RAA system, we studied 21 conscious pigs. Blood renin and aldosterone levels increased by subjecting animals to 24 hours of immobilization stress. Renin and aldosterone levels were repeatedly measured by radio-immunoassay in blood samples taken periodically over 24 hours from a chronically implanted arterial cannula. Pretreatment of the animals (N = 11) with nisoldipine, 2 x 20 mg p.o. daily for 2 days before and on the day of immobilization, transiently attenuated the stress-induced increase of plasma renin activity and completely prevented the rise of aldosterone, as compared to nontreated controls (N = 10). The finding that nisoldipine suppresses RAA activation induced by a nonpharmacologic stimulus in the conscious intact animal may have clinical implications.     

Observation and analysis of junior OB/GYNs’ workflow in German hospitals

Purpose  

Over the past few years the numbers of German physicians choosing to work abroad or leaving the medical profession have been growing. Main reasons for physicians’ dissatisfaction are the lack of autonomy and the subsequent workload. Studies have employed subjective instruments of evaluation to investigate levels of occupational stress. However, there is a lack of objective work task analysis. The aim of this study is to monitor the workflow of German obstetrician/gynecologists (OB/GYN) through an objective, computer-based analysis.     

Hürden und Aussichten neuer antimikrobieller Konzepte in Forschung und Entwicklung

Bundesgesundheitsblatt - Gesundheitsforschung - Gesundheitsschutz - Antimikrobielle Resistenzen (AMR) entwickeln sich weltweit zum ernsten Problem für das Gesundheitswesen. Über...     

Impact of chemotherapeutic agents on the immunostimulatory properties of human 6‐sulfo LacNAc+ (slan) dendritic cells

Chemotherapy is an important treatment modality for many patients with advanced cancer. Recent data revealed that certain chemotherapeutic agents differentially affect maturation, cytokine production and T‐cell stimulatory capacity of dendritic cells (DCs), which play a crucial role in the induction of antitumor immunity. Whereas most reports are based on mouse or human monocyte‐derived DCs, studies investigating the direct effect of chemotherapeutic drugs on native human DCs are rather limited. Here, we evaluated the impact of various chemotherapeutic drugs on the immunostimulatory properties of 6‐sulfo LacNAc⁺ (slan) DCs, representing a major subpopulation of human blood DCs. Because of their various antitumor effects, slanDCs may essentially contribute to the immune defense against tumors. We demonstrated that doxorubicin and vinblastine significantly impair the release of tumor necrosis factor‐α, interleukin (IL)‐6 and IL‐12 by slanDCs. Functional data revealed that both drugs inhibit slanDC‐mediated proliferation of T lymphocytes and their capacity to differentiate naive CD4⁺ T cells into proinflammatory T‐helper type I cells. Furthermore, these agents markedly suppressed the ability of slanDCs to stimulate interferon‐γ secretion by natural killer (NK) cells. In contrast, paclitaxel, mitomycin C and methotrexate sustained the ability of slanDCs to produce proinflammatory cytokines and their potential to activate T‐lymphocytes and NK cells. These results indicate that doxorubicin and vinblastine impair the ability of native human DCs to stimulate important immune effector cells, whereas methotrexate, mitomycin C and paclitaxel maintain their immunostimulatory properties. These novel findings may have implications for the design of treatment modalities for tumor patients combining immunotherapeutic strategies and chemotherapy.     

Control of proven pulmonary and suspected CNS aspergillus infection with itraconazole in a patient with chronic granulomatous disease

An 11-year-old boy with chronic granulomatous disease caused by cytochrome b deficiency developed right upper lung lobe aspergillosis. Intracerebral lesions developed on maximum doses of flucytosine and amphotericin B. Treatment with 16 mg/kg oral itraconazole was followed by a dramatic clinical improvement and almost complete disappearance of the intracerebral lesions. Plasma itraconazole levels were between 40 and 3440 ng/ml depending on concomitant medication. Toxicity was restricted to transient elevation of alkaline phosphatase and gamma glutamyl transferase. We conclude that further trials with itraconazole are justified in high risk patients in whom conventional therapy has failed.