data_sheet_1_Alterations of Brain Structural Network in Parkinson’s Disease With and Without Rapid Eye Movement Sleep Behavior Disorder.docx

Background and objective<p>Rapid eye movement sleep behavior disorder (RBD) has a strong association with alpha synucleinpathies such as Parkinson’s disease (PD) and PD patients with RBD tend to have a poorer prognosis. However, we still know little about the pathogenesis of RBD in PD. Therefore, we aim to detect the alterations of structural correlation network (SCN) in PD patients with and without RBD.</p>Materials and methods<p>A total of 191 PD patients, including 51 patients with possible RBD (pRBD) and 140 patients with non-possible RBD, and 76 normal controls were included in the present study. Structural brain networks were constructed by thresholding gray matter volume correlation matrices of 116 regions and analyzed using graph theoretical approaches.</p>Results<p>There was no difference in global properties among the three groups. Significant enhanced regional nodal measures in limbic system, frontal-temporal regions, and occipital regions and decreased nodal measures in cerebellum were found in PD patients with pRBD (PD-pRBD) compared with PD patients without pRBD. Besides, nodes in frontal lobe, temporal lobe, and limbic system were served as hubs in both two PD groups, and PD-pRBD exhibited additionally recruited hubs in limbic regions.</p>Conclusion<p>Based on the SCN analysis, we found PD-pRBD exhibited a reorganization of nodal properties as well as the remapping of the hub distribution in whole brain especially in limbic system, which may shed light to the pathophysiology of PD with RBD.</p

Epigenetic Changes in Individuals with Arsenicosis

Inorganic arsenic (iAs) is an environmental toxicant currently poisoning millions of people worldwide, and chronically exposed individuals are susceptible to arsenicosis or arsenic poisoning. Using a state-of-the-art technique to map the methylomes of our study subjects, we identified a large interactome of hypermethylated genes that are enriched for their involvement in arsenic-associated diseases, such as cancer, heart disease, and diabetes. Notably, we have uncovered an arsenic-induced tumor suppressorome, a complex of 17 tumor suppressors known to be silenced in human cancers. This finding represents a pivotal clue in unraveling a possible epigenetic mode of arsenic-induced disease

NIPT T21 Modeled Performance at Low Fetal Fractions.

<p>In figure, 27,824 samples that passed all laboratory quality criteria with fetal fractions between 4 and 8% were fitted into two normal distributions, one for euploids and one for T21 positives. The fitted distribution was used to estimate specificity and sensitivity.</p

Breakdown of the NIPT Final Results.

<p>Trisomy 13 and 18 began reporting in February 2012.</p><p>Breakdown of the NIPT Final Results.</p

NIPT Laboratory Performance.

<p>The table shows key laboratory performance indicators. Business days are defined as Monday through Friday excluding federal holidays. Canceled tests are samples that are inappropriate for testing primarily those with no indication for testing. Amended reports primarily include reports amended for typographical errors.</p><p>NIPT Laboratory Performance.</p

Impact of BMI on Final Results.

<p>This figure shows a breakdown of final results when binned by maternal BMI. The number of patients in each bin is displayed above their respective bin.</p

Average NIPT Patient Demographics (n = 100,000).

<p>Gestational age was determined by LMP or ultrasound. Maternal height and weight are not required for testing and not provided for all samples, n = 86,734.</p><p>Average NIPT Patient Demographics (n = 100,000).</p