[Exposure of Pupils to Recreational Noise from Portable Listening Devices and Possible Preventive Measures]. / Freizeitlärmbelastung durch tragbare Musikabspielgeräte bei Schülern und Präventionsmöglichkeiten.

Background and Objectives: Exposure to recreational noise is becoming increasingly important due to a change in leisure behavior amongst children and adolescents. The aim of this pilot study was to assess exposure of 6th grade pupils to recreational noise from portable listening devices (PLD). Furthermore, preventive measures to reduce recreational noise exposure should be identified. Methods: In "Ohrkan Kids", 38 Bavarian pupils aged 11 to 14 were interviewed regarding their music listening behavior using a standardized questionnaire. In addition, measurements of commonly used volume settings on the children's portable listening devices were carried out. Furthermore, the German Social Accident Insurance (DGUV), health insurance companies as well as health and education ministries of the German federal states were surveyed regarding their activities in the prevention of recreational noise exposure. Results: Based on the questionnaire data for weekly usage, 10 out of 31 children (32.3%) exceeded the upper exposure value of 85 dB recommended by labor protection law. Taking actually measured values, 9 out of 31 children (29%) exceeded this level. The DGUV and some federal states carry out specific projects for the prevention of recreational noise exposure. Conclusion: The large number of children with hazardous music consumption indicates that measures for the prevention of noise-induced hearing loss are already required for 11 to 14 year olds. To maximize the number of children addressed, age-appropriate and target-group-specific preventive measures are needed. As there are only few studies which examined the effectiveness of awareness campaigns for the prevention of recreational noise, any future prevention projects should be evaluated with an increased focus on estimating their effectiveness.

Multivalent bonds in self-assembled bundles of ultrathin gold nanowires.

Ultrathin gold nanowires are unusual colloidal objects that assemble into bundles with line contacts between parallel wires. Each molecule in the contact line interacts with many ligand and solvent molecules. We used X-ray scattering and electron microscopy to study how these interactions control assembly.

Comparison of chromosome banding analysis, interphase- and hypermetaphase-FISH, qualitative and quantitative PCR for diagnosis and for follow-up in chronic myeloid leukemia: a study on 350 cases.

For the diagnosis of CML and for monitoring of treatment response the detection of the t(9;22)(q34;q11) or the BCR-ABL rearrangement is necessary. Chromosome banding analysis (CA) is still the gold standard but other techniques like Southern blot, fluorescence in situ hybridization (FISH) and polymerase chain reaction (PCR) are available. We analyzed 350 CML patients at different stages of disease in parallel with CA, interphase-FISH (IP-FISH), hypermetaphase-FISH (HM-FISH) and RT-PCR. In 20 cases with no Ph(+) metaphases in CA, HM-FISH detected 0.2 to 10% BCR-ABL(+)metaphases. After IP-FISH 107 samples were judged as negative. However, in 17 of these samples HM-FISH detected BCR-ABL(+) metaphases (0.3-11%), and in eight cases CA detected Ph(+) metaphases (2.5-25%). A comparison of IP-FISH performed on uncultivated cells vs cells cultivated for 48 h in 70 cases revealed a higher proportion of BCR-ABL+ cells in the cultivated samples. If nested PCR was negative, all other methods were negative in all cases too. In addition, 94 cases were evaluated using real-time PCR (LightCycler technology). The BCR-ABL/cABL ratio measured showed a high correlation with all other methods. Interestingly, a wide range in the BCR-ABL/ABL ratio was observed especially in patients who showed 100% Ph-positive metaphases in CA. In conclusion, CA, IP-FISH, HM-FISH and real-time PCR give reliable results but differences due to measurement of different target structures have to be kept in mind when using these data for definition of remission status.

Effect of macrophage-specific colony-stimulating factor (CSF-1) on swine monocyte/macrophage susceptibility to in vitro infection by African swine fever virus.

Swine cells of the monocyte/macrophage lineage (MM) proliferate and survive for several weeks in vitro in medium supplemented with the murine macrophage-specific hematopoietic growth factor, colony-stimulating factor 1 (CSF-1). The extent to which MM, cultured in CSF-1, supported African swine fever virus (ASFV) growth in vitro was investigated. MM, cultured in medium with CSF-1, were sensitive to infection and viral-induced cytopathogenic damage by both natural field isolates of ASFV and fibroblast-adapted ASFV strains, as were primary MM (P-MM). Without CSF-1, blood mononuclear leukocytes (MNL), containing lymphocytes and MM, and P-MM could be reliably used in microculture for ASFV titration when inoculated at times limited to no more than 3 to 5 days after culture inception; inclusion of CSF-1 in the media stimulated continued MM survival and growth, and allowed for the use of MNL and P-MM for ASFV titration when inoculated as long as 2 to 3 weeks after microculture inception. MM that were propagated beyond 1 week in secondary culture in medium with CSF-1 (MM-CSF) were useful in microcultures for infective-ASFV titration, only when the cells were kept in medium with CSF-1 and inoculated no later than 3 days of culture inception. In vitro studies of ASFV infection in P-MM and in MM-CSF showed comparable kinetics in ASFV-induced hemadsorption (HAd), cytopathogenic effect (CPE), cytoplasmic viral antigens and nucleic acid material. Compared to P-MM in culture without CSF-1, relatively minor delays in CPE onset induced by some ASFV strains were noticed in MM-CSF and in P-MM that were placed in media with CSF-1. The effects of ASFV on DNA synthesis in the virus-susceptible MM, cultured with or without CSF-1, were also examined at different times of infection by measurement of 3H-thymidine (3H-TdR) incorporation into total precipitable culture material. ASFV-infection of P-MM, placed in culture medium with CSF-1, caused a pronounced transient increase in total 3H-TdR incorporation at the early onset of CPE and HAd. When compared to uninfected P-MM that were stimulated by CSF-1 to synthesize DNA, infected P-MM failed to incorporate 3H-TdR after CPE was fully evident. For P-MM that were cultured without CSF-1 and for MM-CSF, that were kept in culture with CSF-1, transient increases in 3H-TdR incorporation at the onset of CPE and HAd by ASFV-infection were evident, but were much less pronounced.

In vitro induction of swine peripheral blood monocyte proliferation by the fibroblast-derived murine hematopoietic growth factor CSF-1.

The addition of conditioned medium from murine L929 fibroblasts (MGF) to cultures of swine peripheral blood mononuclear cells (MNL) resulted in growth of cells of macrophage/monocyte lineage (MO). Glass-adherent swine MNL, shown to be greater than 95% phagocytic MO, grew in the presence of MGF, whereas swine blood granulocytes and lymphocytes were not MGF-responsive. Primary and secondary MO growth were directly dependent on MGF presence and concentration. MGF-stimulated MO synthesized DNA, as measured by cellular incorporation of tritium-labeled thymidine (3H-TdR). This mitogenic response was maximal by 5 to 6 days in primary MO cultures and declined thereafter to a lower magnitude in secondary MO cultures. In the presence of MGF, viable MO numbers increased with an approximate population doubling time of 5 to 7 days in primary culture. This growth rate was prolonged, to about 10 to 12 days, for MGF-stimulated MO in secondary cultures. MGF removal from primary and secondary MO cultures resulted in rapid growth cessation and cell death. MGF-stimulated MO could not be sustained in secondary culture beyond 7 weeks. MGF-cultured MO were positive for latex phagocytosis, non-specific esterase, Fc-receptor expression, and could mediate antibody-dependent cell-mediated cytotoxicity. The MO-mitogenic principle of MGF was identified as the murine, macrophage-specific colony-stimulating factor, CSF-1 (M-CSF). The swine MO-proliferative response to MGF was inhibited by addition of monospecific goat antisera to M-CSF. Purified M-CSF stimulated the growth of swine MO from cultures of MNL and primary glass-adherent MO.

Inhibition of African swine fever virus in cultured swine monocytes by phosphonoacetic acid (PAA) and by phosphonoformic acid (PFA).

The use of phosphonoacetic (PAA) and phosphonoformic acid (PFA) as inhibitors of African swine fever virus (ASFV) replication in porcine monocytes/macrophages (MO) was investigated. At concentrations sufficient to inhibit replication, hemadsorption, and cytopathogenic damage by high inocula of ASFV, both antiviral agents were cytostatic and suppressed the DNA-synthetic growth response of porcine MO to the MO-specific colony-stimulating factor-1 (CSF-1). PAA and PFA inhibited ASFV-associated DNA-synthesis in the cytoplasm of infected swine MO. Using ASFV-specific monoclonal antibodies in immunebinding assays and in immunoprecipitation analysis of radiolabeled proteins of infected MO, PAA and PFA inhibited the synthesis of ASFV proteins of 13, 73, and 150/220 kDa, and caused a variable inhibition in the synthesis of a 12 kDa ASFV protein. These antiviral drugs, however, did not prevent the appearance of an early 32 kDa ASFV protein. The cytostatic and virus-suppressive effects of PAA and PFA could be reversed. ASFV resumed growth in infected MO cultures, if the cells maintained in medium with CSF-1 were removed from the antivirals before 1 week of drug exposure. With prolonged exposure to PAA or PFA (beyond 1 week), ASFV could not be recovered from infected MO cultures.