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In patients with conductive hearing loss caused by middle ear disorders or atresia of the ear canal, a Bonebridge implantation can improve hearing by providing vibratory input to the temporal bone. The expected results are improved puretone thresholds and speech recognition. In the European Union, approval of the Bonebridge implantation was recently extended to children. We evaluated the functional outcome of a Bonebridge implantation for eight adults and three children. We found significant improvement in the puretone thresholds, with improvement in the air-bone gap. Speech recognition after surgery was significantly higher than in the best-aided situation before surgery. The Bonebridge significantly improved speech recognition in noisy environments and sound localization. In situations relevant to daily life, hearing deficits were nearly completely restored with the Bonebridge implantation in both adults and children.

Cochlear implantation has become a standard therapy for children with bilateral profound hearing loss, resulting in substantial and sustainable benefits for the development of expressive and receptive and expressive language skills and cognition. During the last few years, audiologic and otologic criteria for cochlear implantation have been expanded. Recently, patients with profound single-sided deafness with or without tinnitus have received cochlear implants despite normal to near-normal hearing on the contralateral side. This indication, however, has thus far been restricted to adult patients. Although it is known that unilateral hearing has an impact on social-emotional development in children, otologic surgeons have been reluctant to treat children with single-sided deafness with a cochlear implant. We report here on a case of successful cochlear implantation in an 8-year-old boy with acute single-sided deafness due to a lateral skull-base fracture, after an MRI showed signs of imminent fibrosis of the inner ear with possible prevention of cochlear implantation at a later stage. There was normal hearing in the contralateral ear. The child showed rapid development of speech discrimination in the implanted ear, improvements in sound localization and speech perception in noise, and a high degree of patient satisfaction. This experience may encourage using this therapeutic approach in children with chronic profound single-sided deafness.

The influenza-virus M2 protein has proton channel activity required for virus uncoating and maturation of hemagglutinin (HA) through low-pH compartments. The proton channel is cytotoxic in heterologous expression systems and can be blocked with rimantadine. In an independent, rimantadine-resistant function, M2, interacting with the M1 protein, controls the shape of virus particles. These bud from cholesterol-rich membrane rafts where viral glycoproteins and matrix (M1)/RNP complexes assemble. We demonstrate that M2 preparations from influenza virus-infected cells and from a baculovirus expression system contain 0.5-0.9 molecules of cholesterol per monomer. Sequence analyses of the membrane-proximal M2 endodomain reveal interfacial hydrophobicity, a cholesterol-binding motif first identified in peripheral benzodiazepine receptor and human immunodeficiency virus gp41, and an overlapping phosphatidylinositol 4,5-bisphosphate-binding motif. M2 induced rimantadine-reversible cytotoxicity in intrinsically cholesterol-free E. coli, and purified E. coli-expressed M2 functionally reconstituted into cholesterol-free liposomes supported rimantadine-sensitive proton translocation. Therefore, cholesterol was nonessential for M2 ion-channel function and cytotoxicity and for the effect of rimantadine. Only about 5-8% of both M2 preparations, regardless of cholesterol content, associated with detergent-resistant membranes. Cholesterol affinity and palmitoylation, in combination with a short transmembrane segment suggest M2 is a peripheral raft protein. Preference for the raft/non-raft interface may determine colocalization with HA during apical transport, the low level of M2 incorporated into the viral envelope and its undisclosed role in virus budding for which a model is presented. M2 may promote clustering and merger of rafts and the pinching-off (fission) of virus particles.

Human herpesvirus-8 (HHV-8) is the etiological agent of Kaposi’s sarcoma (KS), which primarily affects human immunodeficiency virus (HIV)-infected adults with advanced immunodeficiency. Currently, only limited prevalence data for HHV-8 infection in HIV-infected children living in non-endemic areas are available. This multicenter cross-sectional study was conducted in four university hospitals in Germany specializing in pediatric HIV care. Stored serum specimens obtained from 207 vertically HIV-1-infected children and adolescents were tested for antibodies against lytic and latent HHV-8 antigens. Logistic regression was used to assess independent risk factors associated with HHV-8 seropositivity. The overall HHV-8 seroprevalence was 24.6 % ( n  = 51/207) without significant differences related to sex, age, or ethnicity. In univariate analysis, HHV-8 seropositivity was significantly associated with a child having being born outside Germany, maternal origin from sub-Saharan Africa, a history of breastfeeding, CDC immunologic category 3, and deferred initiation of antiretroviral therapy (>24 months of age). In multivariate analysis, a child’s birth outside Germany was the only significant risk factor for HHV-8 seropositivity (odds ratio 3.98; 95 % confidence interval 1.27–12.42). HHV-8-associated malignancies were uncommon; only one patient had a history of KS. Serum specimen of vertically HIV-infected children and adolescents living in Germany showed a high HHV-8 seroprevalence. These findings suggest that primary HHV-8 infection—a risk factor for KS and other HHV-8-associated malignancies—occurs early in life. Thus, management of perinatally HIV-infected children should include testing for HHV-8 coinfection and should consider future risks of HHV-8-associated malignancies.

We study the functioning and possible breakdown of the interbank market in the presence of counterparty risk. We allow banks to have private information about the risk of their assets. We show how banks' asset risk affects funding liquidity in the interbank market. Several interbank market regimes can arise: i) normal state with low interest rates; ii) turmoil state with adverse selection and elevated rates; and iii) market breakdown with liquidity hoarding. We provide an explanation for observed developments in the interbank market before and during the 2007-09 financial crisis (dramatic increases of unsecured rates and excess reserves banks hold, as well as the inability of massive liquidity injections by central banks to restore interbank activity). We use the model to discuss various policy responses.

We study the functioning and possible breakdown of the interbank market in the presence of counterparty risk. We allow banks to have private information about the risk of their assets. We show how banks' asset risk affects funding liquidity in the interbank market. Several interbank market regimes can arise: i) normal state with low interest rates; ii) turmoil state with adverse selection and elevated rates; and iii) market breakdown with liquidity hoarding. We provide an explanation for observed developments in the interbank market before and during the 2007-09 financial crisis (dramatic increases of unsecured rates and excess reserves banks hold, as well as the inability of massive liquidity injections by central banks to restore interbank activity). We use the model to discuss various policy responses. JEL Classification: G01, G21, D82