Empfehlungen zu Ernährung und Bewegung von Kleinkindern

Monatsschrift Kinderheilkunde -     

Lymphadenectomy in Bladder Cancer

Pelvic lymphadenectomy is widely accepted as an essential part of radical cystectomy. It provides important information (number of lymph nodes involved, tumor volume, capsular perforation) for prognosis, which may help identify patients at increased risk for progression. More important, there is a growing body of evidence indicating that meticulous, extended pelvic lymphadenectomy may cure a substantial number of patients who would otherwise develop local recurrences or distant metastases. Furthermore, extended bilateral lymph node dissection facilitates cystectomy, makes it safer to perform and does not substantially alter morbidity of the operation.     

Cellular‐FLIP,Raji isoform (c‐FLIPR) modulates cell death induction upon T‐cell activation and infection

Dysregulation of apoptosis caused by an imbalance of pro‐ and anti‐apoptotic protein expression can lead to cancer, neurodegenerative, and autoimmune diseases. Cellular‐FLIP (c‐FLIP) proteins inhibit apoptosis directly at the death‐inducing signaling complex of death receptors, such as CD95, and have been linked to apoptosis regulation during immune responses. While the isoforms c‐FLIP_L and c‐FLIP_S are well characterized, the function of c‐FLIP_R remains poorly understood. Here, we demonstrate the induction of endogenous murine c‐FLIP_R in activated lymphocytes for the first time. To analyze c‐FLIP_R function in vivo, we generated transgenic mice expressing murine c‐FLIP_R specifically in hematopoietic cells. As expected, lymphocytes from c‐FLIP_R transgenic mice were protected against CD95‐induced apoptosis in vitro. In the steady state, transgenic mice had normal cell numbers and unaltered frequencies of B cells and T‐cell subsets in lymphoid organs. However, when challenged with Listeria monocytogenes, c‐FLIP_R transgenic mice showed less liver necrosis and better bacterial clearance compared with infected wild‐type mice. We conclude that c‐FLIP_R expression in hematopoietic cells supports an efficient immune response against bacterial infections.     

Microstructure and long-term stability of solder joints on nickel-plated aluminium formed during short soldering times

Within this work, we demonstrate that an easy soldering process in combination with wet chemical coating is suitable to realize a strong and reliable solder interconnection of Al substrates, even at short soldering times <5 s in ambient air. The microstructure of solder joints on wet chemically treated aluminum foils is investigated. A single and double zincate pre-treatment are compared to activate the Al surface, followed by electroless Ni plating. The quality of the solderable Ni surface is characterized by contact angle measurements, yielding good wettability (<60°), which is also achieved after isothermally heating (250 °C) the Ni-coated Al foils for 100 min. The microstructure of the Sn62Pb36Ag2 solder joints is investigated by SEM and EDX of cross sections, directly after soldering as well as after isothermal aging at 85 °C. Under the used soldering conditions, with a soldering temperature at about 280 °C, diffusion zones <500 nm were identified. Nonetheless, high peel forces after soldering >5 N mm⁻¹ show stable values under aging conditions of 85 °C for 1000 hours. This could be correlated to a mixed fracture pattern, promoting the high adhesion due to the absence of a dominant failure mechanism.

High mechanical reliability of tin-based solder joints processed by joining copper and nickel-coated aluminium with short soldering times in ambient air.     

Inhibition of interferon γ induced interleukin 12 production: A potential mechanism for the anti-inflammatory activities of tumor necrosis factor

Inflammation is associated with production of cytokines and chemokines that recruit and activate inflammatory cells. Interleukin (IL) 12 produced by macrophages in response to various stimuli is a potent inducer of interferon (IFN) γ production. IFN-γ, in turn, markedly enhances IL-12 production. Although the immune response is typically self-limiting, the mechanisms involved are unclear. We demonstrate that IFN-γ inhibits production of chemokines (macrophage inflammatory proteins MIP-1α and MIP-1β). Furthermore, pre-exposure to tumor necrosis factor (TNF) inhibited IFN-γ priming for production of high levels of IL-12 by macrophages in vitro. Inhibition of IL-12 by TNF can be mediated by both IL-10-dependent and IL-10-independent mechanisms. To determine whether TNF inhibition of IFN-γ-induced IL-12 production contributed to the resolution of an inflammatory response in vivo, the response of TNF^+/+ and TNF^−/− mice injected with Corynebacterium parvum were compared. TNF^−/− mice developed a delayed, but vigorous, inflammatory response leading to death, whereas TNF^+/+ mice exhibited a prompt response that resolved. Serum IL-12 levels were elevated 3-fold in C. parvum-treated TNF^−/− mice compared with TNF^+/+ mice. Treatment with a neutralizing anti-IL-12 antibody led to resolution of the response to C. parvum in TNF^−/− mice. We conclude that the role of TNF in limiting the extent and duration of inflammatory responses in vivo involves its capacity to regulate macrophage IL-12 production. IFN-γ inhibition of chemokine production and inhibition of IFN-γ-induced IL-12 production by TNF provide potential mechanisms by which these cytokines can exert anti-inflammatory/repair function(s).     

In Vitro Activity of wALADin Benzimidazoles against Different Life Cycle Stages of Plasmodium Parasites

wALADin1 benzimidazoles are specific inhibitors of δ-aminolevulinic acid dehydratase from Wolbachia endobacteria of filarial nematodes. We report that wALADin1 and two derivatives killed blood stage Plasmodium falciparum in vitro (50% inhibitory concentrations, 39, 7.7, and 12.8 μM, respectively). One of these derivatives inhibited gliding motility of Plasmodium berghei ANKA infectious sporozoites with nanomolar affinity and blocked invasion into hepatocytes but did not affect intrahepatocytic replication. Hence, wALADin1 benzimidazoles are tools to study gliding motility and potential antiplasmodial drug candidates.     

Biometrical analysis of the shoulder joint regarding glenoid implant dimensions for arthroplasty

Purpose

Reduced bone stock and difficult intraoperative orientation are challenges in glenoid replacement surgery. New implant designs and methods for fixation, such as locking screws, extra-long central pegs and/or central compression screws are targeting these issues. The objective of this study is the analysis of the glenoid dimension regarding maximum central peg diameter and peg length (PL), and maximum screw length (SL) for glenoid fixation.

Methods

Retrospective analysis of magnetic resonance imaging (n = 50) scans. Measurement of the maximum inferior glenoid diameter (GD), SL, maximum length of a 9.9, 10 and 11.4 mm central peg (PL) in the transverse plane; glenoid version (GV), humeral head diameter (HHD). Two independent measurements.

Results

Mean age: 49.0 ± 15.7 years (17–80) (n = 20 female, 49.6 ± 16.0; n = 30 male, 48.6 ± 15.7). Mean values of measurement were GD: 28.9 ± 3.7 mm (21–39); SL: 34.1 ± 4.9 mm (26–44); PL 9.9 mm: 19.4 ± 4.3 mm (9–30); PL 10 mm: 19.0 ± 4.4 mm (8–30); PL 11.4 mm: 16.5 ± 4.1 mm (7–26) with significant gender differences (p = 0.001; p = 0.022; p = 0.001); GV: ?0.6° ± 4.9° (?10 to 11); HHD: 50.0 mm ± 4.9 (41–61). There was good correlation between PL and SL (r = 0.32, p = 0.024) and for GD and PL (r = 0.61, p = 0.001; r = 0.57, p = 0.001; r = 0.96, p = 0.001). The ratio of HHD and GD was very constant with 0.6 ± 0.07.

Conclusions

These data indicate the high interindividual variability of glenoid morphology including significant gender-related differences. The good correlation between humeral head size and GD and maximum central PL can be helpful for cases with reduced bone stock in decision-making about implant size and bone grafting.