Lactobacilli and Bifidobacteria enhance mucosal B cell responses and differentially modulate systemic antibody responses to an oral human rotavirus vaccine in a neonatal gnotobiotic pig disease model

B cells play a key role in generation of protective immunity against rotavirus infection, a major cause of gastroenteritis in children. Current RV vaccines are less effective in developing countries compared to developed countries. Commensals/probiotics influence mucosal immunity, but the role of early gut colonizing bacteria in modulating intestinal B cell responses to RV vaccines is largely unknown. We co-colonized neonatal gnotobiotic pigs, the only animal model susceptible to HRV diarrhea, with 2 dominant bacterial species present in the gut of breastfed infants, Lactobacillus rhamnosus strain GG and Bifidobacterium animalis lactis Bb12 to evaluate their impact on B cell responses to an attenuated (Att) human rotavirus (HRV) Wa strain vaccine. Following HRV challenge, probiotic-colonized, AttHRV vaccinated piglets had significantly lower fecal scores and reduced HRV shedding titers compared to uncolonized, AttHRV vaccinated pigs. The reduction in HRV diarrhea was significantly correlated with higher intestinal IgA HRV antibody titers and intestinal HRV-specific IgA antibody secreting cell (ASC) numbers in probiotic-colonized, AttHRV vaccinated pigs compared to uncolonized, vaccinated pigs. The significantly higher small intestinal HRV IgA antibody responses coincided with higher IL-6, IL-10 and APRIL responses of ileal mononuclear cells (MNCs) and the immunomodulatory effects of probiotics genomic DNA on TGF-β and IL-10 responses. However, serum RV IgG antibody titers and total IgG titers were significantly lower in probiotic-colonized, AttHRV vaccinated pigs compared to uncolonized, vaccinated pigs, both pre- and post-challenge. In summary, LGG and Bb12 beneficially modulated intestinal B cell responses to HRV vaccine.     

Diagnosis and non‐surgical treatment of peri‐implant diseases and maintenance care of patients with dental implants – Consensus report of working group 3

The following consensus report is based on four background reviews. The frequency of maintenance visits is based on patient risk indicators, homecare compliance and prosthetic design. Generally, a 6‐month visit interval or shorter is preferred. At these visits, peri‐implant probing, assessment of bleeding on probing and, if warranted, a radiographic examination is performed. Diagnosis of peri‐implant mucositis requires: (i) bleeding or suppuration on gentle probing with or without increased probing depth compared with previous examinations; and (ii) no bone loss beyond crestal bone level changes resulting from initial bone remodelling. Diagnosis of peri‐implantitis requires: (i) bleeding and/or suppuration on gentle probing; (ii) an increased probing depth compared with previous examinations; and (iii) bone loss beyond crestal bone level changes resulting from initial bone remodelling. If diagnosis of disease is established, the inflammation should be resolved. Non‐surgical therapy is always the first choice. Access and motivation for optimal oral hygiene are key. The patient should have a course of mechanical therapy and, if a smoker, be encouraged not to smoke. Non‐surgical mechanical therapy and oral hygiene reinforcement are useful in treating peri‐implant mucositis. Power‐driven subgingival air‐polishing devices, Er: YAG lasers, metal curettes or ultrasonic curettes with or without plastic sleeves can be used to treat peri‐implantitis. Such treatment usually provides clinical improvements such as reduced bleeding tendency, and in some cases a pocket‐depth reduction of ≤ 1 mm. In advanced cases, however, complete resolution of the disease is unlikely.     

Structural investigations of a Podoviridae streptococcus phage C1, implications for the mechanism of viral entry

The Podoviridae phage C1 was one of the earliest isolated bacteriophages and the first virus documented to be active against streptococci. The icosahedral and asymmetric reconstructions of the virus were calculated using cryo-electron microscopy. The capsid protein has an HK97 fold arranged into a T = 4 icosahedral lattice. The C1 tail is terminated with a φ29-like knob, surrounded by a skirt of twelve long appendages with novel morphology. Several C1 structural proteins have been identified, including a candidate for an appendage. The crystal structure of the knob has an N-terminal domain with a fold observed previously in tube forming proteins of Siphoviridae and Myoviridae phages. The structure of C1 suggests the mechanisms by which the virus digests the cell wall and ejects its genome. Although there is little sequence similarity to other phages, conservation of the structural proteins demonstrates a common origin of the head and tail, but more recent evolution of the appendages.     

Perceived Roles and Collaboration Between Neuropsychologists and Speech-Language Pathologists in Rehabilitation

The purpose of the current study was to determine perceptions of neuropsychologists (NPs) and speech-language pathologists (SLPs) regarding each other's roles in the rehabilitation setting, and to assess the type and extent of collaborations. Participants were 311 SLPs and 77 NPs working in a rehabilitation setting. Results indicated a great deal of overlap between the roles of SLPs and NPs. While there was much agreement about roles, misperceptions were evident with regard to some of the domains of assessment and treatment. A need for increased collaboration on planning assessments and treatment was evident. The results suggest the need for training of both disciplines in interdisciplinary collaboration and in roles of rehabilitation team members.     

Deregulated Chromatin Remodeling in the Pathobiology of Brain Tumors

Brain tumors encompass a heterogeneous group of malignant tumors with variable histopathology, aggressiveness, clinical outcome and prognosis. Current gene expression profiling studies indicate interplay of genetic and epigenetic alterations in their pathobiology. A central molecular event underlying epigenetics is the alteration of chromatin structure by post-translational modifications of DNA and histones as well as nucleosome repositioning. Dynamic remodeling of the fundamental nucleosomal structure of chromatin or covalent histone marks located in core histones regulate main cellular processes including DNA methylation, replication, DNA-damage repair as well as gene expression. Deregulation of these processes has been linked to tumor suppressor gene silencing, cancer initiation and progression. The reversible nature of deregulated chromatin structure by DNA methylation and histone deacetylation inhibitors, leading to re-expression of tumor suppressor genes, makes chromatin-remodeling pathways as promising therapeutic targets. In fact, a considerable number of these inhibitors are being tested today either alone or in combination with other agents or conventional treatments in the management of brain tumors with considerable success. In this review, we focus on the mechanisms underpinning deregulated chromatin remodeling in brain tumors, discuss their potential clinical implications and highlight the advances toward new therapeutic strategies.