Melgaardmcgowan5946

treatment for SE is associated with shorter duration of SE, ICU and hospital stays compared to the use of a second-line non-anesthetic antiseizure drug instead or prior to anesthetics, without an associated increase in complications.

To investigate sex and race differences in the association between fasting blood glucose (FBG) and risk of ischemic stroke (IS).

This prospective longitudinal cohort study included adults age ≥45 years at baseline in the Reasons for Geographic And Racial Differences in Stroke Study, followed for a median of 11.4 years. The exposure was baseline FBG (mg/dL); suspected IS events were ascertained by phone every 6 months and were physician-adjudicated. Cox proportional hazards were used to assess the adjusted sex/race-specific associations between FBG (by category and as a restricted cubic spline) and incident IS.

Of 20,338 participants, mean age was 64.5(SD 9.3) years, 38.7% were Black, 55.4% were women, 16.2% were using diabetes medications, and 954 IS events occurred. Compared to FBG <100, FBG ≥150 was associated with 59% higher hazards of IS (95%CI 1.21-2.08) and 61% higher hazards of IS among those on diabetes medications (95%CI 1.12-2.31). The association between FBG and IS varied by race/sex (HR, FBG ≥ 150 vs. FBG <100 White women 2.05 (95% CI 1.23-3.42), Black women 1.71 (95%CI 1.10-2.66), Black men 1.24 (95%CI 0.75-2.06), White men 1.46 (95%CI 0.93-2.28), p

=0.004). Analyses using FBG splines suggest that sex was the major contributor to differences by race/sex subgroups.

Sex differences in the strength and shape of the association between FBG and IS are likely driving the significant differences in the association between FBG and IS across race/sex subgroups. These findings should be explored further and may inform tailored stroke prevention guidelines.

Sex differences in the strength and shape of the association between FBG and IS are likely driving the significant differences in the association between FBG and IS across race/sex subgroups. These findings should be explored further and may inform tailored stroke prevention guidelines.

To assess whether neuronal signals in patients with genetic generalized epilepsy (GGE) are heritable, we examined magnetoencephalography resting-state recordings in patients and their healthy siblings.

In a prospective, cross-sectional design, we investigated source-reconstructed power and functional connectivity in patients, siblings, and controls. We analyzed 5 minutes of cleaned and awake data without epileptiform discharges in 6 frequency bands (1-40 Hz). We further calculated intraclass correlations to estimate heritability for the imaging patterns within families.

Compared with controls (n = 45), patients with GGE (n = 25) showed widespread increased functional connectivity (θ to γ frequency bands) and power (δ to γ frequency bands) across the spectrum. Siblings (n = 18) fell between the levels of patients and controls. Heritability of the imaging metrics was observed in regions where patients strongly differed from controls, mainly in β frequencies, but also for δ and θ power. Network connectivity in GGE was heritable in frontal, central, and inferior parietal brain areas and power in central, temporo-parietal, and subcortical structures. Presence of generalized spike-wave activity during recordings and medication were associated with the network patterns, whereas other clinical factors such as age at onset, disease duration, or seizure control were not.

Metrics of brain oscillations are well suited to characterize GGE and likely relate to genetic factors rather than the active disease or treatment. High power and connectivity levels co-segregated in patients with GGE and healthy siblings, predominantly in the β band, representing an endophenotype of GGE.

Metrics of brain oscillations are well suited to characterize GGE and likely relate to genetic factors rather than the active disease or treatment. check details High power and connectivity levels co-segregated in patients with GGE and healthy siblings, predominantly in the β band, representing an endophenotype of GGE.

A systematic literature search has been performed to identify potential confounders for outcome prediction using pupillary light reflex in adult critically ill patients, as measured by handheld automated pupillometry devices.

Three digital databases (PubMed, EmBase, Cochrane) were systematically searched. Articles published between 1990-2019 in adult patients, using monocular automated handheld devices were considered. Studies were classified according to the OCEBM classification (level 1 represents the highest, level 5 the lowest level of evidence). Case reports, original research and systematic reviews were included and cross-referenced.

Using 202 search terms, 58 eligible articles reporting on the use of handheld pupillometry in the critically ill could be identified, considering 3246 patients. The highest level of evidence came from 10 randomized trials and 19 prospective observational studies. The level of evidence was mostly 2 to 3 and highest with studies regarding the potential confounding effecl confounding effects on outcome and pupillary reflexes. When treatment is guided by pupillary metrics, such confounders put patients at risk of over- or undertreatment. Future research should validate and identify additional confounders, as our review suggests that even more unexplored confounders may exist.We previously proposed that the dopamine D2 receptor-interacting protein S100B binds to a putative S100B-binding motif at residues R233-L240 towards the N-terminus of the 3rd cytoplasmic loop. We used in vitro pull-down assays with FLAG-tagged fragments of the rat D2 receptor third cytoplasmic loop and in vitro-synthesized S100B to evaluate this hypothesis. Our results indicate that the putative S100B-binding motif is neither necessary nor sufficient for strong binding of S100B. Instead, two residues at the junction of the 5th membrane-spanning domain and the cytoplasmic extension of that a-helical domain, K211-I212, are required for robust, calcium-sensitive binding of S100B. This is also the approximate location of previously identified determinants for the binding of arrestin and calmodulin. A D2 receptor mutation converting I212 to phenylalanine has been described in patients with a hyperkinetic movement disorder. Significance Statement S100B is a small calcium-binding protein that modulates signaling by the dopamine D2 receptor.