Fastidious Gram-Negatives: Identification by the Vitek 2 Neisseria-Haemophilus Card and by Partial 16S rRNA Gene Sequencing Analysis

Taxonomy and identification of fastidious Gram negatives are evolving and challenging. We compared identifications achieved with the Vitek 2 Neisseria-Haemophilus (NH) card and partial 16S rRNA gene sequence (526 bp stretch) analysis with identifications obtained with extensive phenotypic characterization using 100 fastidious Gram negative bacteria. Seventy-five strains represented 21 of the 26 taxa included in the Vitek 2 NH database and 25 strains represented related species not included in the database. Of the 100 strains, 31 were the type strains of the species. Vitek 2 NH identification results: 48 of 75 database strains were correctly identified, 11 strains gave `low discrimination´, seven strains were unidentified, and nine strains were misidentified. Identification of 25 non-database strains resulted in 14 strains incorrectly identified as belonging to species in the database. Partial 16S rRNA gene sequence analysis results: For 76 strains phenotypic and sequencing identifications were identical, for 23 strains the sequencing identifications were either probable or possible, and for one strain only the genus was confirmed. Thus, the Vitek 2 NH system identifies most of the commonly occurring species included in the database. Some strains of rarely occurring species and strains of non-database species closely related to database species cause problems. Partial 16S rRNA gene sequence analysis performs well, but does not always suffice, additional phenotypical characterization being useful for final identification

The temporal signature of self: Temporal measures of restingâ state EEG predict selfâ consciousness

The self is the core of our mental life. Previous investigations have demonstrated a strong neural overlap between selfâ related activity and resting state activity. This suggests that information about selfâ relatedness is encoded in our brain’s spontaneous activity. The exact neuronal mechanisms of such â restâ self containment,â however, remain unclear. The present EEG study investigated temporal measures of resting state EEG to relate them to selfâ consciousness. This was obtained with the selfâ consciousness scale (SCS) which measures Private, Public, and Social dimensions of self. We demonstrate positive correlations between Private selfâ consciousness and three temporal measures of resting state activity: scaleâ free activity as indexed by the powerâ law exponent (PLE), the autoâ correlation window (ACW), and modulation index (MI). Specifically, higher PLE, longer ACW, and stronger MI were related to higher degrees of Private selfâ consciousness. Finally, conducting eLORETA for spatial tomography, we found significant correlation of Private selfâ consciousness with activity in cortical midline structures such as the perigenual anterior cingulate cortex and posterior cingulate cortex. These results were reinforced with a dataâ driven analysis; a machine learning algorithm accurately predicted an individual as having a â highâ or â lowâ Private selfâ consciousness score based on these measures of the brain’s spatiotemporal structure. In conclusion, our results demonstrate that Private selfâ consciousness is related to the temporal structure of resting state activity as featured by temporal nestedness (PLE), temporal continuity (ACW), and temporal integration (MI). Our results support the hypothesis that selfâ related information is temporally contained in the brain’s resting state. â Restâ self containmentâ can thus be featured by a temporal signature.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/147871/1/hbm24412.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/147871/2/hbm24412_am.pd

K-ras mutations in sinonasal cancers in relation to wood dust exposure

<p>Abstract</p> <p>Background</p> <p>Cancer in the sinonasal tract is rare, but persons who have been occupationally exposed to wood dust have a substantially increased risk. It has been estimated that approximately 3.6 million workers are exposed to inhalable wood dust in EU. In previous small studies of this cancer, <it>ras </it>mutations were suggested to be related to wood dust exposure, but these studies were too limited to detect statistically significant associations.</p> <p>Methods</p> <p>We examined 174 cases of sinonasal cancer diagnosed in Denmark in the period from 1991 to 2001. To ensure uniformity, all histological diagnoses were carefully reviewed pathologically before inclusion. Paraffin embedded tumour samples from 58 adenocarcinomas, 109 squamous cell carcinomas and 7 other carcinomas were analysed for K-<it>ras </it>codon 12, 13 and 61 point mutations by restriction fragment length polymorphisms and direct sequencing. Information on occupational exposure to wood dust and to potential confounders was obtained from telephone interviews and from registry data.</p> <p>Results</p> <p>Among the patients in this study, exposure to wood dust was associated with a 21-fold increased risk of having an adenocarcinoma than a squamous cell carcinoma compared to unexposed [OR = 21.0, CI = 8.0–55.0]. K-<it>ras </it>was mutated in 13% of the adenocarcinomas (seven patients) and in 1% of squamous cell carcinomas (one patient). Of these eight mutations, five mutations were located in the codon 12. The exact sequence change of remaining three could not be identified unambiguously. Among the five identified mutations, the G→A transition was the most common, and it was present in tumour tissue from two wood dust exposed adenocarcinoma patients and one patient with unknown exposure. Previously published studies of sinonasal cancer also identify the GGT → GAT transition as the most common and often related to wood dust exposure.</p> <p>Conclusion</p> <p>Patients exposed to wood dust seemed more likely to develop adenocarcinoma compared to squamous cell carcinomas. K-<it>ras </it>mutations were detected in 13% of adenocarcinomas. In this study and previously published studies of sinonasal cancer the found K-<it>ras </it>mutations, were almost exclusively G → A transitions. In conclusion, our study, based on a large representative collection of human SNC tumours, indicates that K-<it>ras </it>mutations are relatively infrequent, and most commonly occur in adenocarcinomas. Wood dust exposure alone was not found to be explanatory for the G→A mutations, but combination of exposure to tobacco, wood dust, and possibly other occupational agents may be a more likely explanation. Overall, the study suggests a limited role for K-<it>ras </it>mutations in development of sinonasal cancer.</p

Increased Risk for Malignancies in 131 Affected CTLA4 Mutation Carriers

Background: Cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) is a negative immune regulator on the surface of T cells. In humans, heterozygous germline mutations in CTLA4 can cause an immune dysregulation syndrome. The phenotype comprises a broad spectrum of autoinflammatory, autoimmune, and immunodeficient features. An increased frequency of malignancies in primary immunodeficiencies is known, but their incidence in CTLA-4 insufficiency is unknown.Methods: Clinical manifestations and details of the clinical history were assessed in a worldwide cohort of 184 CTLA4 mutation carriers. Whenever a malignancy was reported, a malignancy-specific questionnaire was filled.Results: Among the 184 CTLA4 mutation carriers, 131 were considered affected, indicating a penetrance of 71.2%. We documented 17 malignancies, which amounts to a cancer prevalence of 12.9% in affected CTLA4 mutation carriers. There were ten lymphomas, five gastric cancers, one multiple myeloma, and one metastatic melanoma. Seven lymphomas and three gastric cancers were EBV-associated.Conclusion: Our findings demonstrate an elevated cancer risk for patients with CTLA-4 insufficiency. As more than half of the cancers were EBV-associated, the failure to control oncogenic viruses seems to be part of the CTLA-4-insufficient phenotype. Hence, lymphoproliferation and EBV viral load in blood should be carefully monitored, especially when immunosuppressing affected CTLA4 mutation carriers

Annemarie Wolff to Viktor Hamburger, June 26, 1968

Typewritten letter, 1 page (signature on back)Correspondenc

Annemarie Wolff to Viktor Hamburger, February 2, 1969

Typewritten letter, 1 pageCorrespondenc