The median difference in the latency to attack prey for the novel person (day 8) minus latency for the last day familiar person (day 7) for fast and slow birds.

<p>Positive values indicate that birds took longer to attack prey when the novel observer was timing the birds compared with a familiar observer. The box indicates the first and third quartiles whilst the bars indicate the 10^th and 90^th percentiles.</p

The median latencies over the course of the 8 days of the experiment for slow birds (solid line and filled symbol) and fast birds (hashed line and unfilled symbol).

<p>The bars represent the 10^th and 90^th percentiles. It is interesting to note that the latencies for the fast birds reach an asymptote on day 2 whereas slow birds reach their asymptote on day 3 of the experiment.</p

Cerebrospinal Fluid Inflammatory Biomarkers Reflect Clinical Severity in Huntington’s Disease

<div><p>Introduction</p><p>Immune system activation is involved in Huntington’s disease (HD) pathogenesis and biomarkers for this process could be relevant to study the disease and characterise the therapeutic response to specific interventions. We aimed to study inflammatory cytokines and microglial markers in the CSF of HD patients.</p><p>Methods</p><p>CSF TNF-α, IL-1β, IL-6, IL-8, YKL-40, chitotriosidase, total tau and neurofilament light chain (NFL) from 23 mutation carriers and 14 healthy controls were assayed.</p><p>Results</p><p>CSF TNF-α and IL-1β were below the limit of detection. Mutation carriers had higher YKL-40 (p = 0.003), chitotriosidase (p = 0.015) and IL-6 (p = 0.041) than controls. YKL-40 significantly correlated with disease stage (p = 0.007), UHDRS total functional capacity score (r = -0.46, p = 0.016), and UHDRS total motor score (r = 0.59, p = 4.5*10⁻⁴) after adjustment for age.</p><p>Conclusion</p><p>YKL-40 levels in CSF may, after further study, come to have a role as biomarkers for some aspects of HD. Further investigation is needed to support our exploratory findings.</p></div

Relationship between CSF concentration of YKL-40 and measures of disease progression and clinical severity.

<p>a, disease stage; b, UHDRS total functional score; c, UHDRS total motor score. The p-values for partial Pearson’s correlation coefficient adjusted for age are shown.</p

Comparison in CSF levels of inflammatory molecules between 14 healthy controls versus 23 gene expansion carriers.

<p>The p-values for unpaired two-tailed t-test (Il-8) or Wilcoxon log-rank test (YKL-40, chitotriosidase, IL-6) are shown.</p

Characteristics of included participants by disease stage.

<p>Characteristics of included participants by disease stage.</p

Additional file 1: Table S1. of Systemic pro-inflammatory cytokine status following therapeutic hypothermia in a piglet hypoxia-ischemia model

Pro/anti-inflammatory cytokine ratios (log10 and original scale) in NT and HT groups from baseline to 48 h. (DOCX 22 kb

Additional file 2: Table S2. of Systemic pro-inflammatory cytokine status following therapeutic hypothermia in a piglet hypoxia-ischemia model

Cytokine pro/anti-inflammatory ratios versus log Lac/NAA in basal ganglia and white matter. (DOCX 14 kb

Additional file 3: Table S3. of Systemic pro-inflammatory cytokine status following therapeutic hypothermia in a piglet hypoxia-ischemia model

Pro/anti-inflammatory cytokine ratios versus mean TUNEL counts. (DOCX 14 kb

Successful quantification of mHTT in PBMCs from 8ml whole blood in HD.

<p>These data confirm that mHTT levels in leukocytes are higher at more advanced disease stages. Assay A (mHTT N-terminus assay) was used to selectively quantify mHTT: S/B, signal over background. A) Sample set 1 (mean of 2 replicates); (B) Sample set 2 (mean of 3 replicates).</p