Resting frontal asymmetry and reward sensitivity theory motivational traits

The revised reinforcement sensitivity theory (rRST) of personality has conceptualized three main systems: the behavioural approach system (BAS), behavioural inhibition system (BIS), and fightflight- freeze system (FFFS). Research links greater relative left-frontal activity with BAS-related tendencies and impulsivity and greater relative right-frontal activity with “withdrawal” motivation that included both BIS and FFFS. Although rRST has addressed the separation of FFFS and BIS, much of personality neuroscience research does not indicate which system is related to right frontal activity. We administered the Reinforcement Sensitivity Theory of Personality Questionnaire (RST-PQ) to measure the BAS and its facets (goal-drive persistence, reward interest, reward reactivity, and impulsivity), BIS, and the withdrawal FFFS. We examined the association of RST-PQ traits with resting electroencephalogram (EEG) alpha-asymmetry in female participants (N = 162) by considering the influence of experimenter’s gender. In the total group, that included two subgroups with experimenters of different gender, BAS-impulsivity was related to greater left- than right-frontal activity, and FFFS, but not BIS, was related to greater relative right-frontocentral activity. These associations remained significant for the subgroup with a young same-sex experimenter, but not with opposite-sex experimenter

Electrophysiological investigations of attentional mechanisms governing emotional information processing

There is an on-going debate in the literature concerning the contribution of automatic and controlled processes underlying emotional effects on cognition. The current thesis had two objectives: (1) to investigate attentional mechanisms in the visual perception of and memory for emotional events and (2) to examine the influence of individual differences in fear, anxiety, and approach systems on emotional attention and memory. In Chapter 2 we demonstrate trait-congruency effects in emotional information processing across a range of cognitive domains. More importantly, we show that by examining trait processes underlying trait-congruency effects in emotional information processing one is able to gain valuable insight into how differences in personality traits gives rise to these trait-congruency effects. In Chapter 3 we reveal that early stage of exogenous attention to emotional stimuli are modulated by the valence-arousal interactions of the emotional stimulus, while later stages of exogenous attention appear to be driven by the arousal value of the stimulus. More importantly, individual differences in the fear system and impulsivity dimension influenced attentional biases for emotional stimuli, underlining the importance to differentiate fear from anxiety and reward components from impulsivity. In Chapter 4 we show that divided attention at encoding does not further modulate the influence of affective content on recognition memory performance, but electrophysiological results provide evidence that this is due to different underlying mechanisms. Specifically, electrophysiological results suggest that visual attentional processes play a role in the recollection based recognition of positive/high-arousal images, but not of negative images. Thus, recollection of positive/high-arousal images requires a more effortful search for the memory trace, while negative images, regardless of arousal value, are recollected less effortful, even when attention at encoding is limited. This effect mediated the negative relationship between reward reactivity and recognition performance for positive/high-arousal images presented under conditions of high perceptual load, indicating that dysfunctional reward reactivity is related to disinhibited behavior. In Chapter 5 we provide evidence that the late posterior negativity is modulated by attentional mechanisms rather than by memory specific processes. That is, instead of being modulated by the amount of information needed for the reconstruction of the study episode, we put forward that this electrocortical component reflects controlled stimulus evaluation processes that are, at least in part, modulated by task difficulty. Overall, the results of the present thesis show that emotions exert their influence on sensory information processing via automatic, bottom-up mechanisms and via controlled, top-down processes. Further, elevated activation of fear, anxiety, and approach systems are associated with dysfunctional emotion-attention interactions in sensory information processing. Clarifying the contribution of attentional mechanisms in emotional information processing will help to gain a better understanding of affective disorders characterized by attentional and memory biases, which is necessary for the development of interventions that can be useful in the regulation of dysfunctional attention allocation and memory formation

Experimental induction of a coastal spring bloom early in the year by intermittent high-light episodes

Through the use of mesocosm experiments, we show that an unusually early spring phytoplankton bloom can be induced by intermittent high-light periods. We performed mesocosm experiments where plankton assemblages from Kiel Bight (Western Baltic Sea) received a light regime based on the natural seasonal irradiance dimmed to 43% of surface irradiance of cloudless days, starting with irradiance levels of mid-January (6 mesocosms) and mid-February (6 mesocosms). After 6 d, half of the mesocosms received a ca. 2-fold increase in irradiance. In the January mesocosms, a phytoplankton bloom developed only in the treatments with the high-light episode, whereas in the February mesocosms a phytoplankton bloom also developed in the controls. Phytoplankton net growth rates, production:biomass ratios and biomass at the end of the high irradiance episodes were positively correlated to the daily light dose. The relative biomass of diatoms increased with increasing light, whereas the relative biomass of cryptophytes decreased. A bottom-up transmission to mesozooplankton (mainly copepods of the genera Acartia and Oithona) was evident by increased densities of copepod nauplii and egg production under higher light conditions, whereas copepodids and adults showed no responses during the experimental period. The taxonomic composition of the nauplii was shifted to the advantage of Acartia/Centropages (not distinguished at the naupliar stage) under higher light conditions

Neurofascin-155 IgM autoantibodies in patients with inflammatory neuropathies

Objectives Recently, IgG autoantibodies against different paranodal proteins have been detected and this has led to important advances in the management of inflammatory neuropathies. In contrast, not much is known on IgM autoantibodies against paranodal proteins. Methods In the present study, we screened a large cohort of patients (n=140) with inflammatory neuropathies for IgM autoantibodies against neurofascin-155, neurofascin-186 or contactin-1. Results IgM autoantibodies against neurofascin-155 were detected by ELISA in five patients, four with inflammatory demyelinating polyradiculoneuropathy (CIDP) and one with Guillain-Barre syndrome (GBS), and were confirmed by ELISA-based preabsorption experiments and Western blot. Titres ranged from 1:100 to 1:400. We did not detect IgM anti-neurofascin-186 or anti-contactin-1 antibodies in this cohort. All patients presented with distally accentuated tetraparesis and hypesthesia. Remarkably, tremor was present in three of the patients with CIDP and occurred in the patients with GBS after the acute phase of disease. Nerve conduction studies revealed prolonged distal motor latencies and F wave latencies. Nerve biopsies showed signs of secondary axonal damage in three of the patients, demyelinating features in one patient. Teased fibre preparations did not demonstrate paranodal damage. Conclusion In summary, IgM neurofascin-155 autoantibodies may be worth testing in patients with inflammatory neuropathies. Their pathogenic role needs to be determined in future experiments

Helios spacecraft data revisited: Detection of cometary meteoroid trails by in-situ dust impacts

Cometary meteoroid trails exist in the vicinity of comets, forming fine structure of the interplanetary dust cloud. The trails consist predominantly of cometary particles with sizes of approximately 0.1 mm to 1 cm which are ejected at low speeds and remain very close to the comet orbit for several revolutions around the Sun. When re-analysing the Helios dust data measured in the 1970s, Altobelli et al. (2006) recognized a clustering of seven impacts, detected in a very narrow region of space at a true anomaly angle of 135 deg, which the authors considered as potential cometary trail particles. We re-analyse these candidate cometary trail particles to investigate the possibility that some or all of them indeed originate from cometary trails and we constrain their source comets. The Interplanetary Meteoroid Environment for eXploration (IMEX) dust streams in space model is a new universal model for cometary meteoroid streams in the inner solar system, developed by Soja et al. (2015). Using IMEX we study cometary trail traverses by Helios. During ten revolutions around the Sun, and in the narrow region of space where Helios detected the candidate dust particles, the spacecraft repeatedly traversed the trails of comets 45P/Honda-Mrkos-Pajduvsakova and 72P/Denning-Fujikawa. Based on the detection times and particle impact directions, four detected particles are compatible with an origin from these two comets. We find a dust spatial density in these trails of about 10^-8 to 10^-7 m^-3. The in-situ detection and analysis of meteoroid trail particles which can be traced back to their source bodies by spacecraft-based dust analysers opens a new window to remote compositional analysis of comets and asteroids without the necessity to fly a spacecraft to or even land on those celestial bodies. This provides new science opportunities for future missions like Destiny+, Europa Clipper and IMAP.Comment: 13 pages, 9 Figures, 2 Tables, accepted for pubication by Astronomy and Astrophysic

Implant selection in cervical spondylodiscitis plays a non-detrimental role - a single-center retrospective case series of 24 patients [Abstract]

Oral e-Poster Presentations - Booth 3: Spine 2 (Tumors), September 26, 2023, 4:10 PM - 4:50 PM Background: Cervical spondylodiscitis is an uncommon entity, with an incidence of 0.5 to 2.5 per 100.000 population, which is potentially extremely harmful. This type of discogenic and vertebral infection might cause a high rate of neurological impairment. Radical surgical debridement of the infected segment with fusion and intravenous antibiotic regimen remains the gold standard in most spine centers. We aimed to analyze the overall outcome in a tertiary spine center. Methods: In this study, we retrospectively included all patients suffering from cervical spondylodiscitis between 01/2017 and 05/2022, treated at the university hospital of Augsburg. Clinical and radiological parameters as well as type of implant were collected and evaluated. Descriptive statistics were performed using SPSS, and relevant correlations were examined using the t-test for independent samples and the Chi-square test. Results: 24 patients were identified and included. 17 patients (71%) suffered from sepsis on admission, 17 patients (71%) were diagnosed with epidural abscess on primary imaging and 5 patients (21%) had more than one discitis focus in a distant spinal segment. The presence of epidural abscess was significantly associated with systemic sepsis (OR=6.2; p=0.03) and myelopathy symptoms (OR= 14.4; p=0.00). Septic status was significantly associated with the occurrence of discitis in other spine segments (p=0.02), higher CCI (p=0.03) and Clavien Dindo scores (p=0.01), as well as a longer ICU stay (p=0.04) and the occurrence of nonunion (p=0.06). The most commonly detected germ was a multisensitive staphylococcus aureus (10 patients, 42%). A total of 6 patients (25%) died after a median of 20 days despite antibiogram-accurate therapy. The follow-up data of 15 patients (63%) was available with the evidence of permanent neurological damage in 9 patients (38%). The type of osteosynthesis was not significantly associated with subsidence (p=0.13), nonunion (p=0.21) or revision surgery (p=0.20). However the extent of instrumentation correlated significantly with the rate of nonunion (p=0.05). Conclusions: Cervical spondylodiscitis presents a severe infectious disease that occurs in multimorbid elderly patients and, despite adequate surgical and antibiotic treatment, is often associated with permanent neurological damage or a fatal outcome. Implant selection did not play a decisive role for the clinical and radiological outcome in this study

Dermal Phospho-Alpha-Synuclein Deposition in Patients With Parkinson's Disease and Mutation of the Glucocerebrosidase Gene

Heterozygous mutations in the glucocerebrosidase gene (GBA1) represent the most common genetic risk factor for Parkinson's disease (PD) and are histopathologically associated with a widespread load of alpha-synuclein in the brain. Therefore, PD patients with GBA1 mutations are a cohort of high interest for clinical trials on disease-modifying therapies targeting alpha-synuclein. There is evidence that detection of phospho-alpha-synuclein (p-syn) in dermal nerve fibers might be a biomarker for the histopathological identification of PD patients even at premotor or very early stages of disease. It is so far unknown whether dermal p-syn deposition can also be found in PD patients with GBA1 mutations and may serve as a biomarker for PD in these patients. Skin biopsies of 10 PD patients with different GBA1 mutations (six N370S, three E326K, one L444P) were analyzed by double-immunofluorescence labeling with anti-p-syn and anti-protein gene product 9.5 (PGP9.5, axonal marker) to detect intraaxonal p-syn deposition. Four biopsy sites (distal, proximal leg, paravertebral Th10, and C7) per patient were studied. P-syn was found in six patients (three N370S, three E326K). P-syn deposition was mainly detected in autonomic nerve fibers, but also in somatosensory fibers and was not restricted to a certain GBA1 mutation. In summary, dermal p-syn in PD patients with GBA1 mutations seems to offer a similar distribution and frequency as observed in patients without a known mutation. Skin biopsy may be suitable to study p-syn deposition in these patients or even to identify premotor patients with GBA1 mutations

Hydrocephalus, cerebral vasospasm, and delayed cerebral ischemia following non-aneurysmatic spontaneous subarachnoid hemorrhages: an underestimated problem

Non-aneurysmal subarachnoid hemorrhage (NASAH) is rare and mostly benign. However, complications such as cerebral vasospasm (CV), delayed cerebral ischemia (DCI), or post-hemorrhagic hydrocephalus (HC) may worsen the prognosis. The aim of this study was to evaluate the rate of these complications comparing perimesencephalic (PM) and non-perimesencephalic (NPM) SAH. Monocentric, retrospective analysis of patients diagnosed with NASAH from 01/2010 to 01/2021. Diagnosis was set only if vascular pathologies were excluded in at least one digital subtraction angiography, and NASAH was confirmed by cranial computed tomography (cCT) or lumbar puncture (LP). One hundred patients (62 female) with a mean age of 54.9 years (27–84) were identified. Seventy-three percent had a World Federation of Neurological Surgeons (WFNS) grading scale score I, while 9% were WFNS score IV or V at the time of admission. SAH was diagnosed by cCT in 86%, in 14% by lumbar puncture. Twenty-five percent necessitated short-term CSF diversion by extraventricular drainage or lumbar drainage, whereof 7 suffered from long-term HC treated with ventriculoperitoneal shunting (VPS). One patient without a short-term CSF drainage developed long-term HC. Ten percent developed CV, four of whom received intraarterial spasmolysis. Radiological DCI was diagnosed in 2%; none of these correlated with CV. Despite a mortality of 3% occurring solely in NPM SAH, the analyzed complication rate was comparable in both groups. We observed post-hemorrhagic complications in 35% of cases during the first 3 weeks after bleeding, predominantly in patients with NPM SAH. For this reason, close observation and cranial imaging within this time may be indicated not to overlook these complications

Quantitative susceptibility mapping (QSM) as a means to measure brain iron? A post mortem validation study

AbstractQuantitative susceptibility mapping (QSM) is a novel technique which allows determining the bulk magnetic susceptibility distribution of tissue in vivo from gradient echo magnetic resonance phase images. It is commonly assumed that paramagnetic iron is the predominant source of susceptibility variations in gray matter as many studies have reported a reasonable correlation of magnetic susceptibility with brain iron concentrations in vivo. Instead of performing direct comparisons, however, all these studies used the putative iron concentrations reported in the hallmark study by Hallgren and Sourander (1958) for their analysis. Consequently, the extent to which QSM can serve to reliably assess brain iron levels is not yet fully clear. To provide such information we investigated the relation between bulk tissue magnetic susceptibility and brain iron concentration in unfixed (in situ) post mortem brains of 13 subjects using MRI and inductively coupled plasma mass spectrometry. A strong linear correlation between chemically determined iron concentration and bulk magnetic susceptibility was found in gray matter structures (r=0.84, p<0.001), whereas the correlation coefficient was much lower in white matter (r=0.27, p<0.001). The slope of the overall linear correlation was consistent with theoretical considerations of the magnetism of ferritin supporting that most of the iron in the brain is bound to ferritin proteins. In conclusion, iron is the dominant source of magnetic susceptibility in deep gray matter and can be assessed with QSM. In white matter regions the estimation of iron concentrations by QSM is less accurate and more complex because the counteracting contribution from diamagnetic myelinated neuronal fibers confounds the interpretation

Glycine receptor autoantibody binding to the extracellular domain is independent from receptor glycosylation

Glycine receptor (GlyR) autoantibodies are associated with stiff-person syndrome and the life-threatening progressive encephalomyelitis with rigidity and myoclonus in children and adults. Patient histories show variability in symptoms and responses to therapeutic treatments. A better understanding of the autoantibody pathology is required to develop improved therapeutic strategies. So far, the underlying molecular pathomechanisms include enhanced receptor internalization and direct receptor blocking altering GlyR function. A common epitope of autoantibodies against the GlyRα1 has been previously defined to residues 1 A- 33 G at the N-terminus of the mature GlyR extracellular domain. However, if other autoantibody binding sites exist or additional GlyR residues are involved in autoantibody binding is yet unknown. The present study investigates the importance of receptor glycosylation for binding of anti-GlyR autoantibodies. The glycine receptor α1 harbors only one glycosylation site at the amino acid residue asparagine 38 localized in close vicinity to the identified common autoantibody epitope. First, non-glycosylated GlyRs were characterized using protein biochemical approaches as well as electrophysiological recordings and molecular modeling. Molecular modeling of non - glycosylated GlyRα1 did not show major structural alterations. Moreover, non-glycosylation of the GlyRα1 N38Q did not prevent the receptor from surface expression. At the functional level, the non-glycosylated GlyR demonstrated reduced glycine potency, but patient GlyR autoantibodies still bound to the surface-expressed non-glycosylated receptor protein in living cells. Efficient adsorption of GlyR autoantibodies from patient samples was possible by binding to native glycosylated and non-glycosylated GlyRα1 expressed in living not fixed transfected HEK293 cells. Binding of patient-derived GlyR autoantibodies to the non-glycosylated GlyRα1 offered the possibility to use purified non-glycosylated GlyR extracellular domain constructs coated on ELISA plates and use them as a fast screening readout for the presence of GlyR autoantibodies in patient serum samples. Following successful adsorption of patient autoantibodies by GlyR ECDs, binding to primary motoneurons and transfected cells was absent. Our results indicate that the glycine receptor autoantibody binding is independent of the receptor’s glycosylation state. Purified non-glycosylated receptor domains harbouring the autoantibody epitope thus provide, an additional reliable experimental tool besides binding to native receptors in cell-based assays for detection of autoantibody presence in patient sera