Nucleon Sigma Terms with N_{f}=2+1 Flavors of O(a)-Improved Wilson Fermions.

We present a lattice-QCD based analysis of the nucleon sigma terms using gauge ensembles with N_{f}=2+1 flavors of O(a)-improved Wilson fermions, with a complete error budget concerning excited-state contaminations, the chiral interpolation as well as finite-size and lattice spacing effects. We compute the sigma terms determined directly from the matrix elements of the scalar currents. The chiral interpolation is based on SU(3) baryon chiral perturbation theory using the extended on-mass shell renormalization scheme. For the pion nucleon sigma term, we obtain σ_{πN}=(43.7±3.6) MeV, where the error includes our estimate of the aforementioned systematics. The tension with extractions based on dispersion theory persists at the 2.4-σ level. For the strange sigma term, we obtain a nonzero value, σ_{s}=(28.6±9.3) MeV.

Strange Electromagnetic Form Factors of the Nucleon with N_{f}=2+1 O(a)-Improved Wilson Fermions.

We present results for the strange contribution to the electromagnetic form factors of the nucleon computed on the coordinated lattice simulation ensembles with N_{f}=2+1 flavors of O(a)-improved Wilson fermions and an O(a)-improved vector current. Several source-sink separations are investigated in order to estimate the excited-state contamination. We calculate the form factors on six ensembles with lattice spacings in the range of a=0.049-0.086 fm and pion masses in the range of m_{π}=200-360 MeV, which allows for a controlled chiral and continuum extrapolation. In the computation of the quark-disconnected contributions, we employ hierarchical probing as a variance-reduction technique.

Review of lattice results concerning low-energy particle physics: Flavour Lattice Averaging Group (FLAG).

We review lattice results related to pion, kaon, D- and B-meson physics with the aim of making them easily accessible to the particle-physics community. More specifically, we report on the determination of the light-quark masses, the form factor [Formula: see text], arising in the semileptonic [Formula: see text] transition at zero momentum transfer, as well as the decay constant ratio [Formula: see text] and its consequences for the CKM matrix elements [Formula: see text] and [Formula: see text]. Furthermore, we describe the results obtained on the lattice for some of the low-energy constants of [Formula: see text] and [Formula: see text] Chiral Perturbation Theory. We review the determination of the [Formula: see text] parameter of neutral kaon mixing as well as the additional four B parameters that arise in theories of physics beyond the Standard Model. The latter quantities are an addition compared to the previous review. For the heavy-quark sector, we provide results for [Formula: see text] and [Formula: see text] (also new compared to the previous review), as well as those for D- and B-meson-decay constants, form factors, and mixing parameters. These are the heavy-quark quantities most relevant for the determination of CKM matrix elements and the global CKM unitarity-triangle fit. Finally, we review the status of lattice determinations of the strong coupling constant [Formula: see text].

Early magnetic resonance imaging of brainstem lesions after severe head injury.

OBJECT: The availability of magnetic resonance (MR) imaging data obtained in comatose patients after head injury is scarce, because MR imaging is somewhat cumbersome to perform in patients requiring ventilation and because, in the first hours after injury, its relevance is clearly inferior to computerized tomography (CT) scanning. The authors assessed the value of MR imaging in the early postinjury period. METHODS: In this prospective study MR imaging was performed in 61 consecutive patients within 7 days after they suffered a severe head injury. An initial CT scan had already been obtained. To understand the clinical significance of the lesions whose morphological appearance was identified with MR imaging, brainstem function was assessed by registration of somatosensory and auditory evoked potentials. Brainstem lesions were visualized in 39 patients (64%). Bilateral pontine lesions proved to be 100% fatal and nonbrainstem lesions carried a mortality rate of 9%. In singular cases circumstances allowed for a clear clinical distinction between primary and secondary brainstem lesions. On MR imaging all lesions were hyper- and hypointense after intervals longer than 2 days. Within shorter intervals (< 2 days) after the injury, primary lesions appeared isointense on MR imaging. In one secondary brainstem lesion there were no traces of blood. CONCLUSIONS: Because mean intracranial pressure (ICP) levels in patients without brainstem lesions were similar to those in patients with brainstem lesions, the authors conclude that it was not mainly increased ICP that accounted for the high mortality rates in patients with brainstem lesions. The authors also conclude that brainstem lesions are more frequently found in severe head injury than previously reported in studies based on neuropathological or CT scanning data. Early MR imaging after head injury has a higher predictive value than CT scanning.

Expression of the plasminogen activator system and the inhibitors PAI-1 and PAI-2 in posttraumatic lesions of the CNS and brain injuries following dramatic circulatory arrests: an immunohistochemical study.

Plasminogen activators as inducible extracellular serine proteases are involved in a variety of processes, such as the degradation of brain structures. In regions of brain degradation, an increase in the expression of genes encoding cytokines and proteinases has recently been demonstrated. We tested the hypothesis, whether the plasminogen activator system as well as the plasminogen activator inhibitors are expressed and possibly involved in a proteolytic cascade that breaks down the extracellular matrix as a result of ischemic or posttraumatic brain destructions. To study this supposition, we investigated immunohistochemically the expression of tPA, uPA and its receptor, the plasminogen activator inhibitors PAI-1 and PAI-2, tetranectin as well as the laminin breakdown as an event of secondary brain injury. Brain tissue from 21 autopsy cases with severe brain injuries, material from 14 ischemic infarcts and 11 controls with acute hypoxia were used. All components of the plasminogen activator system studied were over-expressed immunohistochemically in reactive astrocytes, microglia and endothelial cells around the lesion zone. Tetranectin showed an analogous distribution to the plasminogen activator system. A reduced immunoreactivity of laminin within the identical region of destruction was detected concomitant with laminin remnants in perivascular macrophages, so that a remarkable role of the plasmin cascade in the degradation of extracellular matrix proteins in the brain is taken into consideration.

Stiff-man syndrome: possible autoimmune etiology targeted against GABA-ergic cells.

We report the case of a female patient, who died at the age of 66 years. Besides an insulin-dependent diabetes mellitus (IDDM) she had developed the clinical symptoms of stiff-man-syndrome (SMS) and harbored autoantibodies against glutamate-decarboxylase (GAD) in blood and liquor. GAD catalyzes the biosynthesis of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). The autopsy revealed typical alterations observed in diabetes mellitus including an incomplete fibrosis of pancreatic Langerhans islets. A decrease of GABA-ergic cells in the cerebellar cortex was observed, and a size reduction of Renshaw cells in the spinal cord. Furthermore, a dilution series of a polyclonal GABA antibody delivered a reduced immunofluorescence in the cerebellum. In skeletal muscle a neurogenic atrophy was observed. As described in literature, the clinical symptoms decayed following clonazepam administration. We suggest that this case including GAD autoantibodies, dramatic loss of GAD-expressing pancreatic cells, and loss or atrophy of GABA secretory neurons, supports the hypothesis that SMS may be an autoimmune disease directed against GABA-ergic cells. Furthermore, we suggest a neuronal hypersensitivity at the spinal cord level caused by the atrophic Renshaw cells.

Comparative regression analysis of concurrent elimination-phase blood and breath alcohol concentration measurements to determine hourly degradation rates.

Following the introduction of limit values for blood alcohol and breath alcohol concentrations of 0.5 g/kg and 0.25 mg/L, respectively, as provided under s. 24 a of the German Road Traffic Act the question is whether also breath alcohol concentrations can be back calculated to the time of the traffic offence in cases where it is definite that the person to be examined is in the period of alcohol elimination. To this end, a study was performed in which 56 healthy volunteers consumed 0.5, 0.8 and 1.0 g of ethanol mixed with fruit juice per kilogram of body weight over a period of 10-20 min. Calculations included all 391 pairs of concurrent blood alcohol and breath alcohol concentration values obtained after 2 h following the end of drinking. All volunteers exceeded the peak value of the alcohol curve. The measured values included were above 0.1 g/kg and 0.05 mg/L. For an average intake of alcohol of 0.88 g/kg the following regression lines were calculated for the period starting 2 h after the end of drinking: blood alcohol concentration [g/kg] = 1.318 - 0.172 h and breath alcohol concentration [mg/L] = 0.589 - 0.079 h. Subtracting the simple standard deviation from the mean value yielded hourly degradation rates above 0.1 g/kg and above 0.05 mg/L, respectively. Subtracting two standard deviations, the values fell below this level in both cases. In fact, back calculation of breath alcohol concentrations based on 0.05 mg/h seems to be possible for traffic offences if certain conditions are complied with, such as the use of Evidential 7110, a calibrated breath alcohol analyser approved by the Federal Physical-Technical Laboratory for measuring the breath alcohol concentration.

LC-MS/MS analysis of pholedrine in a fatal intoxication case.

Pholedrine (4'-hydroxymethamphetamine) is a cardiovascular agent exerting hypertensive and adrenergic effects. High doses may cause a drop in the peripheral circulation blood flow and increase blood pressure, heart rate and body temperature up to a state of central respiratory paralysis. A 15-year-old girl who suffered from heavy agitation and hallucinations was admitted to the intensive care unit in a comatose state. The clinical findings included a maximum heart rate of 170 bpm and a body temperature of 43.8 degrees C. Resuscitation measures were in vain and abandoned after approximately 2h. A toxicological emergency analysis using GC/MS revealed a considerable amount of pholedrine in blood and urine. A method for determining pholedrine in human body fluids utilizing high-performance liquid chromatography (HPLC)/tandem mass spectrometry (LC-MS/MS) with a turbo ion-spray source was developed, using D11-methamphetamine and D5-methylenedioxymethamphetamine as internal standards. Samples were prepared by SPE extraction using SPEC-C18AR/MP3((R)) columns, which yielded the best extraction recovery (67%). Chromatographic separation was achieved at pH 5 on an RP-18 stationary phase applying gradient elution from 50 to 70% of B (methanol/acetonitrile 3/1 (v/v), 0.02% acetic acid) in A (5mM ammonium acetate/acetonitrile 95/5 (v/v), 0.02% acetic acid). Supra-pure acetic acid was added to the post-column effluent with a flow rate of 0.2 microl/min to optimize ionization. Detection was carried out in the positive ionization, multiple reaction monitoring (MRM) mode. The chromatograms showed no interference from other substances. The limit of detection (LOD, S/N=3) of pholedrine was 0.8 ng/ml and its lower limit of quantification (LLOQ, S/N=10) 3ng/ml. The calibration curve was linear (r=0.999) in the range 1-100 ng/ml. Samples with higher concentrations were diluted to suit the working range. The intra-day R.S.D. between 5 and 80 ng/ml were 3.8-8.7% and the inter-day R.S.D. between 5 and 100 ng/ml were 6.7-10.7%. The pholedrine concentrations in blood and urine collected when the girl was still alive were 16.1 microg/ml (R.S.D. 10.5%) and 1120 microg/ml (R.S.D. 8%), respectively. In post-mortem samples, they were 23.0 microg/ml (R.S.D. 5.1%) in heart blood and 27.3 microg/g (R.S.D. 6.6%) in the liver.

A systematic regional study of dopamine and dopamine-derived salsolinol and norsalsolinol levels in human brain areas.

Dopamine and the dopamine-derived tetrahydroisoquinoline alkaloids salsolinol and norsalsolinol were measured by high-performance liquid chromatography with electrochemical detection in 15 regions of the human brain. The regional distribution of dopamine in 32 brains was similar to previous reports with highest concentrations in the basal ganglia, especially in the striatum, followed by the substantia nigra and the hypothalamus. Significant amounts of salsolinol and norsalsolinol were only found in these dopamine-rich areas, whereas in the other regions no alkaloids were detected. These findings suggest that the concentration of the substrate dopamine may determine the alkaloid level during in vivo formation.

Is it possible to differentiate mtDNA by means of HVIII in samples that cannot be distinguished by sequencing the HVI and HVII regions?

The mitochondrial control region includes three so-called hypervariable (HV) regions, in which the polymorphic positions show a particularly high frequency. According to a population study of 200 unrelated individuals from Germany, HVI (positions 16,024-16,365, according to Anderson) showed 88 variable positions in a total length of 342 bp (26%) and HVII (positions 73-340) displayed 65 mutable sites in 268 bp (24%). HVIII (positions 438-574) exhibited a slightly lower variability, with 25 polymorphic sites within 137 bp (18%), but contrasted clearly with the background, which showed variability rates of only 7% (positions 16,366-16,569, 1-72) and 3% (positions 341-437), respectively. At present, the displacement (D)-loop database in Magdeburg comprises 904 sequences of the mitochondrial HVI region and HVII region from Germans, Austrians and Swiss. By means of this material, the extent to which the mtDNA sequences that do not differ in the HVI and HVII regions can be differentiated by additionally sequencing HVIII was investigated.

Mitochondrial DNA in the Central European population. Human identification with the help of the forensic mt-DNA D-loop-base database.

Sequencing of mtDNA is an advanced method for the individualisation of traces. Disadvantages of this method are expensive and time-consuming analysis and evaluation procedures as well as the necessary stock of population-genetic data which is still insufficient. Central European institutes of forensic medicine from Germany, Austria, and Switzerland have been working together since the beginning of 1998 to establish a mtDNA database. The aim is to build up a large stock of forensically established data and provide population-genetic data for frequency investigations, which will serve as a basis for expert opinions and scientific research. Good data quality is ensured by using original sequences only. Ring tests, which have been conducted to enhance analytical reliability, revealed a high correspondence rate of the analytical results obtained by the individual member institutes. Today 1410 sequences are available for comparison, of which 1285 sequences in the HV1 and HV2 regions cover the full ranges from 16051 to 16365 and from 73 to 340 (according to Anderson). The major part is formed by Central European sequences comprising 1256 data sets from Germany, Austria, and Switzerland. Today the database contains sequences from a total of 12 European, six African and three Asian countries including 100 sequences from Japan. This paper is aimed at discussing the individualisation potentials of mtDNA as well as the possibilities and limits of ethnic differentiation by means of pairwise sequence differences on the basis of the data stock available.

Effect of Epiphytic Fungi on Brown Rot Blossom Blight and Latent Infections in Sweet Cherry.

Antagonistic effects of Aureobasidium pullulans, Epicoccum purpurascens, and Gliocladium roseum on establishment of Monilinia fructicola infections on cv. Royal Anne cherry blossoms were assessed in a mist chamber and under field conditions. Conidia of each fungus were applied to blossoms that were subsequently inoculated with conidia of M. fructicola. Mist chamber experiments on forced blossoms demonstrated that incidence of recovery of M. fructicola from blossoms was significantly reduced (P ≤ 0.05) to similar levels when either E. purpurascens or the fungicide benomyl had been applied 24 h prior to inoculation with M. fructicola. In field trials in 1990, 1991, and 1993, application of E. purpurascens reduced blossom blight relative to nontreated blossoms by 47, 58, and 45%, respectively; whereas application of A. pullulans caused reductions of 54, 13, and 47%, respectively. Comparable reductions in blossom blight for the fungicide iprodione were 80, 95, and 98%, respectively. Latent M. fructicola infections were evaluated by dipping immature green cherries in a dilute solution of the herbicide paraquat. Applications of E. purpurascens and A. pullulans to blossoms reduced the number of latent M. fructicola infections in green cherries by 24 and 48%, respectively, in 1990; 57 and 62%, respectively, in 1991; and 19 and 16%, respectively, in 1993. This compares with reductions of 95, 91, and 17% in 1990, 1991, and 1993, respectively, with the fungicide iprodione. E. purpurascens and G. roseum also were recovered from surface-disinfested, paraquat-dipped cherry fruit. Percent recovery of these fungi was significantly (P ≤ 0.05) higher from treatments where they had been applied to blossoms compared with the nontreated control.

Review of lattice results concerning low-energy particle physics.

We review lattice results related to pion, kaon, [Formula: see text]- and [Formula: see text]-meson physics with the aim of making them easily accessible to the particle-physics community. More specifically, we report on the determination of the light-quark masses, the form factor [Formula: see text], arising in semileptonic [Formula: see text] transition at zero momentum transfer, as well as the decay-constant ratio [Formula: see text] of decay constants and its consequences for the CKM matrix elements [Formula: see text] and [Formula: see text]. Furthermore, we describe the results obtained on the lattice for some of the low-energy constants of [Formula: see text] and [Formula: see text] Chiral Perturbation Theory and review the determination of the [Formula: see text] parameter of neutral kaon mixing. The inclusion of heavy-quark quantities significantly expands the FLAG scope with respect to the previous review. Therefore, we focus here on [Formula: see text]- and [Formula: see text]-meson decay constants, form factors, and mixing parameters, since these are most relevant for the determination of CKM matrix elements and the global CKM unitarity-triangle fit. In addition we review the status of lattice determinations of the strong coupling constant [Formula: see text].

QCD and strongly coupled gauge theories: challenges and perspectives.

We highlight the progress, current status, and open challenges of QCD-driven physics, in theory and in experiment. We discuss how the strong interaction is intimately connected to a broad sweep of physical problems, in settings ranging from astrophysics and cosmology to strongly coupled, complex systems in particle and condensed-matter physics, as well as to searches for physics beyond the Standard Model. We also discuss how success in describing the strong interaction impacts other fields, and, in turn, how such subjects can impact studies of the strong interaction. In the course of the work we offer a perspective on the many research streams which flow into and out of QCD, as well as a vision for future developments.