Biomedical subjects

Gerhard Huber

Publications and source records attributed to Gerhard Huber.

4 recordsLinked to original sources

PubMed2006

Spatially resolved ultra-trace analysis of elements combining resonance ionization with a MALDI-TOF spectrometer.

A combined setup for spatially resolved mass analysis of trace amounts of elements and macromolecules is presented. Using a MALDI-TOF mass spectrometer, a laser spectroscopic setup for resonant ionization of neutral atoms has been implemented. This allows for an efficient and selective detection of trace elements by means of resonance ionization mass spectrometry (RIMS). The instrumental scheme is described, and methodological developments are presented. In a first application pure, laser desorption/ionization with TOF-MS was used to measure mass distributions of cosmic nanodiamonds. For further applications regarding the spatially resolved ultra-trace analysis of elements in solid samples, an implanted target was used to characterize both laser desorption/ionization and laser desorption/resonance ionization for the detection of trace elements within. A perspective of the setup is given and future investigations are outlined.

Journal Article↗

PubMed2006

Complete deterministic linear optics Bell state analysis.

We show how hyperentanglement allows us to deterministically distinguish between all four polarization Bell states of two photons. In this proof-of-principle experiment, we employ the intrinsic time-energy correlation of photon pairs generated with high temporal definition in addition to the polarization entanglement obtained from parametric down-conversion. For the identification, no nonlinear optical elements or auxiliary photons are needed. The new possibilities this complete Bell measurement offers are demonstrated by realizing an optimal dense coding protocol.

Journal Article↗

PubMed2003

Oral prion infection requires normal numbers of Peyer's patches but not of enteric lymphocytes.

Prion pathogenesis following oral exposure is thought to involve gut-associated lymphatic tissue, which includes Peyer's patches (PPs) and M cells. Recruitment of activated B lymphocytes to PPs requires alpha(4)beta(7) integrin; PPs of beta 7(-/-) mice are normal in number but are atrophic and almost entirely devoid of B cells. Here we report that minimal infectious dose and disease incubation after oral exposure to logarithmic dilutions of prion inoculum were similar in beta 7(-/-) and wild-type mice, and PPs of both beta 7(-/-) and wild-type mice contained 3-4 log LD(50)/g prion infectivity > or =125 days after challenge. Despite marked reduction of B cells, M cells were present in beta 7(-/-) mice. In contrast, mice deficient in both tumor necrosis factor and lymphotoxin-alpha (TNF alpha(-/-) x LT alpha(-/-)) or in lymphocytes (RAG-1(-/-), mu MT), in which numbers of PPs are reduced in number, were highly resistant to oral challenge, and their intestines were virtually devoid of prion infectivity at all times after challenge. Therefore, lymphoreticular requirements for enteric and for intraperitoneal uptake of prions differ from each other. Although susceptibility to prion infection following oral challenge correlates with the number of PPs, it is remarkably independent of the number of PP-associated lymphocytes.

Animals↗

PubMed2003

Human prion diseases: epidemiology and integrated risk assessment.

Human prion diseases are devastating and incurable, but are very rare. Fears that the bovine spongiform encephalopathy epizootic would lead to a large epidemic of its presumed human counterpart, variant Creutzfeldt-Jakob disease (vCJD), have not been realised. Yet a feeling of uncertainty prevails in the general public and in the biomedical world. The lack of data on the prevalence of asymptomatic carriers of vCJD compounds this uncertainty. In addition to this problem, Switzerland is currently faced with another issue of major public concern: a recent rise in the incidence of CJD. Here we examine the plausibility of several scenarios that may account for the increase in CJD incidence, including ascertainment bias due to improved reporting of CJD, iatrogenic transmission, and transmission of a prion zoonosis. In addition, we present the design and current status of a Swiss population-wide study of subclinical vCJD prevalence.

Creutzfeldt-Jakob Syndrome↗