University of Zurich

About: University of Zurich is a education organization based out in Zurich, Switzerland. It is known for research contribution in the topics: Population & Medicine. The organization has 50842 authors who have published 124042 publications receiving 5304521 citations. The organization is also known as: UZH & Uni Zurich.

Reduced Prefrontal Glutamate/Glutamine and γ-Aminobutyric Acid Levels in Major Depression Determined Using Proton Magnetic Resonance Spectroscopy

Abstract: Context Increasing evidence indicates that major depressive disorder (MDD) is associated with altered function of the major excitatory and inhibitory neurotransmitters glutamate and γ-aminobutyric acid (GABA), respectively. A recently developed magnetic resonance spectroscopy method allows for reliable measurement of glutamate/glutamine (Glx) and GABA concentrations in prefrontal brain regions that have been implicated in the pathophysiologic mechanisms of MDD by studies using other neuroimaging and postmortem techniques. Objective To measure Glx and GABA levels in 2 regions of the prefrontal brain tissue in unmedicated adults with MDD. Design Cross-sectional study for association. Setting Psychiatric outpatient clinic. Participants Twenty unmedicated, depressed patients with MDD and 20 age- and sex-matched controls. Intervention Participants underwent scanning using a 3-T whole-body scanner with a transmit-receive head coil, providing a homogeneous radiofrequency field and the capability of obtaining spectroscopic measurements in a dorsomedial/dorsal anterolateral prefrontal region of interest (ROI) and a ventromedial prefrontal ROI. Main Outcome Measures Glx and GABA levels derived from magnetic resonance spectroscopy signals. Results Depressed patients had reduced Glx levels in both ROIs. The GABA levels were reduced in the dorsomedial/dorsal anterolateral prefrontal ROI. Levels of GABA and Glx were positively correlated in both ROIs. Conclusions For the first time, GABA and Glx concentrations were compared between unmedicated depressed adults and controls in prefrontal ROIs. The abnormal reductions in Glx and GABA concentrations found in the MDD sample were compatible with findings from postmortem histopathologic studies, indicating that glial cell density is reduced in the same areas in MDD.

Combined results of searches for the standard model Higgs boson in pp collisions at √s = 7 TeV

Abstract: Combined results are reported from searches for the standard model Higgs boson in proton-proton collisions at sqrt(s)=7 TeV in five Higgs boson decay modes: gamma pair, b-quark pair, tau lepton pair, W pair, and Z pair. The explored Higgs boson mass range is 110-600 GeV. The analysed data correspond to an integrated luminosity of 4.6-4.8 inverse femtobarns. The expected excluded mass range in the absence of the standard model Higgs boson is 118-543 GeV at 95% CL. The observed results exclude the standard model Higgs boson in the mass range 127-600 GeV at 95% CL, and in the mass range 129-525 GeV at 99% CL. An excess of events above the expected standard model background is observed at the low end of the explored mass range making the observed limits weaker than expected in the absence of a signal. The largest excess, with a local significance of 3.1 sigma, is observed for a Higgs boson mass hypothesis of 124 GeV. The global significance of observing an excess with a local significance greater than 3.1 sigma anywhere in the search range 110-600 (110-145) GeV is estimated to be 1.5 sigma (2.1 sigma). More data are required to ascertain the origin of this excess.

Current state of knowledge on Takotsubo syndrome: a Position Statement from the Taskforce on Takotsubo Syndrome of the Heart Failure Association of the European Society of Cardiology

Abstract: Takotsubo syndrome is an acute reversible heart failure syndrome that is increasingly recognized in modern cardiology practice. This Position Statement from the European Society of Cardiology Heart Failure Association provides a comprehensive review of the various clinical and pathophysiological facets of Takotsubo syndrome, including nomenclature, definition, and diagnosis, primary and secondary clinical subtypes, anatomical variants, triggers, epidemiology, pathophysiology, clinical presentation, complications, prognosis, clinical investigations, and treatment approaches. Novel structured approaches to diagnosis, risk stratification, and management are presented, with new algorithms to aid decision-making by practising clinicians. These also cover more complex areas (e.g. uncertain diagnosis and delayed presentation) and the management of complex cases with ongoing symptoms after recovery, recurrent episodes, or spontaneous presentation. The unmet needs and future directions for research in this syndrome are also discussed.

A harmonized classification system for FTLD-TDP pathology

Abstract: In 2006, two papers were published, each describing pathological heterogeneity in cases of frontotemporal lobar degeneration (FTLD) with ubiquitin-positive, tau-negative inclusions (FTLD-U) [7, 11]. In both studies, large series of cases were evaluated and the investigators felt that they could recognize three distinct histological patterns, based on the morphology and anatomical distribution of ubiquitin immunoreactive neuronal inclusions. The findings of Sampathu et al. were further supported by differential labelling of the pathology, using a panel of novel monoclonal antibodies; whereas, Mackenzie et al. found relatively specific clinicopathological correlations. Most importantly, the pathological features that defined the subtypes in these two studies were almost identical, providing powerful validation of the results. However, because the studies were conducted simultaneously and independently, the numbering of the subtypes, used in the respective papers, did not match (Table 1). Table 1 Proposed new classification system for FTLD-TDP pathology, compared with existing systems Shortly thereafter, further work by one of the two groups led to the identification of the transactive response DNA-binding protein with Mr 43 kD (TDP-43) as the ubiquitinated pathological protein in most cases of FTLD-U as well as the majority of sporadic amyotrophic lateral sclerosis (ALS) and some familial ALS [10]. It was subsequently confirmed that most FTLD-U cases had TDP-43 pathology and that the same pathological patterns could be recognized based on the results of TDP-43 immunohistochemistry (IHC) [1, 2]. By this time, a fourth FTLD-U subtype had been described, specifically associated with the familial syndrome of inclusion body myopathy with Paget’s disease of bone and frontotemporal dementia (IBMPFD) caused by mutations in the valosin-containing protein (VCP) gene [4], and this was also shown to have TDP-43 pathology [9]. As a result, cases of FTLD with TDP-43 pathology are now designated as FTLD-TDP and the term FTLD-U is no longer recommended [8]. The two classification systems for FTLD-U/FTLD-TDP have now gained wide acceptance and have repeatedly been validated by the discovery of additional clinical, genetic and pathological correlations. However, the continued use of two discordant numbering systems proves to be an ongoing source of confusion within the field. Previous attempts, by other groups of authors, to promote one classification over the other have not been successful. To resolve this issue, the principal authors of the original two papers are now proposing a new classification for FTLD-TDP pathology, the sole purpose of which is to provide a single harmonized system that replaces the two currently in use. In developing this new classification, the following principles were adhered to: (1) different pathological subtypes are designated by letters to help distinguish this from the pre-existing number-based systems, (2) the order of subtypes should not exactly match either of the previous systems to avoid any apparent bias, and (3) the order of the subtypes should be based on their relative frequency, with “A” being the most common. The result is summarized in Table 1. Type A is equivalent to type 1 of Mackenzie et al. and type 3 of Sampathu et al., being characterized by numerous short dystrophic neurites (DN) and crescentic or oval neuronal cytoplasmic inclusions (NCI), concentrated primarily in neocortical layer 2. Moderate numbers of lentiform neuronal intranuclear inclusions (NII) are also a common but inconsistent feature of this subtype. Type B matches Mackenzie et al. type 3 and Sampathu et al. type 2, with moderate numbers of NCI, throughout all cortical layers, but very few DN. Type C is the same as Mackenzie et al. type 2 and Sampathu et al. type 1, having a predominance of elongated DN in upper cortical layers, with very few NCI. Finally, Type D refers to the pathology associated with IBMPFD caused by VCP mutations, characterized by numerous short DN and frequent lentiform NII. Based on the results of more recent studies, there are a number of other modifications that we could have considered incorporating into this new system. Additional pathological subtypes could be added; for instance, to describe the TDP-43 pathology that is found in the mesial temporal lobe in a high proportion of cases of Alzheimer’s disease and most other common neurodegenerative conditions [3]. The pathological criteria for each of the subtypes could be expanded to include characteristic findings in subcortical regions [5, 6]. The description of the pathological features could be modified to take into account the greater sensitivity and specificity of TDP-43 IHC, which may demonstrate additional findings, not recognized with the ubiquitin immunostaining techniques upon which the original classifications were based (such as neuronal “pre-inclusions”) [2]. Although these and other recent findings represent important advances in our understanding of FTLD-TDP, most have not yet been broadly replicated or completely defined. Therefore, in order to make the transition to a new classification as simple and widely acceptable as possible and, most importantly, to allow for direct translation with the currently existing systems, we are not proposing any other significant changes, beyond the coding of the subtypes. In summary, we believed that adoption of a single harmonized system for the classification of FTLD-TDP neuropathology would greatly improve communication within the rapidly advancing field of FTLD diagnosis and research. Future attempts to resolve any outstanding issues related to the practical implementation and interpretation of FTLD pathological classification should also benefit. As indicated by their inclusion as co-authors on this paper, this proposal has received the unanimous support of all of the neuropathologists involved in the original two studies [7, 11].

The soft tissue barrier at implants and teeth

Abstract: In the present animal experiment, analyses and comparisons were made between the structure and composition of clinically healthy supraalveolar soft tissues adjacent to implants and teeth. 5 beagle dogs were used. The right mandibular premolar region was selected in each dog for placement of titanium implants, while the left mandibular premolar region served as control. Extractions of the mandibular premolars were preformed, healing allowed, following which titanium fixtures were installed in the edentolous premolar region. Abutment connection was carried out 3 months later. After another 2 months of healing, plaque control was initiated and maintained for 8 weeks. At the end of the plaque control period, clinical examinations were performed and biopsies harvested from the implant site and the contralateral premolar tooth region. Following fixation and decalcification, all tissue samples were embedded in EPON and examined by histometric and morphometric means. The result from the analyses demonstrated that the periimplant mucosa which formed at titanium implants following abutment connection had many features in common with gingival tissue at teeth. Thus, like the gingiva, the peri-implant mucosa established a cuff-like barrier which adhered to the surface of the titanium abutment. Further, both the gingiva and the peri-implant mucosa had a well-keratinized oral epithelium which was continuous with a junctional epithelium that faced the enamel or the titanium surface. In the periimplant mucosa, the collagen fibers appeared to commence at the marginal bone and were parallel with the abutment surface. All gingival and periimplant units examined were free from infiltrates of inflammatory cells. It was suggested that under the conditions of study, both types of soft tissues, gingiva and periimplant mucosa, have a proper potential to prevent subgingival plaque formation.