Additional file 1 of Longitudinal observational study of boxing therapy in Parkinson’s disease, including adverse impacts of the COVID-19 lockdown

Additional file 1. Supplementary Table 1: Analysis of GEE Parameter Estimates: Empirical Standard Error Estimates. Modeling was based on the absolute number of falls per month, excluding those who reported no falls at any time during the study period. Supplementary Table 2: Analysis of GEE Parameter Estimates: Contrast Estimate Results. Modeling was based on the absolute number of falls per month, excluding those who reported no falls at any time during the study period. Supplementary Table 3: Analysis of GEE Parameter Estimates: Empirical Standard Error Estimates. Modeling was based on the number of months in which at least one fall occurred, excluding those who reported no falls at any time during the study period. Supplementary Table 4: Analysis of GEE Parameter Estimates: Contrast Estimate Results. Modeling was based on the number of months in which at least one fall occurred, excluding those who reported no falls at any time during the study period

Two-way ANOVA analyses of <i>in vitro</i> proliferation of IDH^wt and IDH^mut tumor cells in varying glucose and ketogenic culture conditions.

Two-way ANOVA analyses of in vitro proliferation of IDHwt and IDHmut tumor cells in varying glucose and ketogenic culture conditions.</p

Summary of cell lines used.

Summary of cell lines used.</p

The effect of unrestricted cycling KD on patient-derived IDH1^wt and IDH1^mut flank xenograft growth.

Tumor volumes for mice subcutaneously engrafted with IDH1mut GBM164 at 21 days, IDH1mut GBM 196 at 14 days, and IDH1wt GBM12 at 14 days, either on SD or cycling KD (initiated 3 days after engraftment). Time points differed due to differing rates of tumor growth. Bars = means, P values calculated by unpaired t-tests.</p

Basic metabolic parameters of mice on an unrestricted cycling KD.

Saphenous vein blood samples tested for glucose (A) and ketones (B) at the end of each week. Mouse body weights are shown in (C). Green bars indicate weeks in which mice were on KD.</p

Summary of macronutrient composition of standard and experimental diets presented as proportion of total kilocalories.

Summary of macronutrient composition of standard and experimental diets presented as proportion of total kilocalories.</p

Effect of ketones on patient-derived IDH1^wt and IDH1^mut tumor cell proliferation <i>in vitro</i>.

Absolute cell counts over 14 days of culture in either normal glucose (NG) or low glucose (LG), with or without 10 mM β-hydroxybutyrate (BHB). Each data point is shown as mean ±SEM. Two-way ANOVA analyses of the final time points are described in the Results text and Table 3.</p

Additional file 1 of The efficacy of DNA mismatch repair enzyme immunohistochemistry as a screening test for hypermutated gliomas

Additional file 1: Table S1. Detailed clinical and pathologic data for the full cohort of 100 gliomas. Tumors 1–9 are hypermutated and are also shown in Table S1. of the main manuscript. The following tumors are from the same patients: 1 and 2; 5, 11, and 12; 7 and 94. Pre-TMZ gliomas were designated as N/A in the TMZ dose and duration columns. Records on temozolomide dosage and cycles were incomplete for many post-TMZ patients, because they had been treated at outside institutions prior to re-resection at Northwestern. “D Astro” = diffuse astrocytoma; “A Astro” = anaplastic astrocytoma; “A Oligo” = anaplastic oligodendroglioma; N/A = not available or not applicable. Table S2. Correlation matrix. N = 93 tumors (cases without MGMT data were excluded, as well as hypermutated tumor #2 since it came from the same patient as tumor #1, see Fig. 2 and Additional file 1: Table S1). Each value represents Spearman ρ (rho) correlation coefficients, with 1 = perfect direct correlation, 0 = no correlation, and − 1 = perfect inverse correlation. *P < 0.05. TMZ = temozolomide

The effect of unrestricted cycling KD on patient-derived IDH1^wt and IDH1^mut intracranial xenograft growth.

Kaplan-Meier survival curves of mice engrafted with (A) IDH1wt NPA or (B) IDH1mut NPAC1, either on SD or cycling KD (initiated 3 days after engraftment).</p

Cells previously Lgr5+ remain lineage restricted.

<p>In addition to tdTomato+ cells staining positive for Gabra6 (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0114433#pone-0114433-g003" target="_blank">Fig. 3b</a>), neither Lgr5+ cells nor cells previously Lgr5+ are positive for other lineage markers. Sections from <i>Lgr5^EGFP-CreERT2; R26R^tdTomato</i> mice that were lineage traced from P4 to P10 or P7 to P14 were stained for <b>a</b>) BLBP to identify Bergmann glia, <b>b</b>) Calb1 to identify Purkinje neurons and <b>c</b>) Olig2 to identify cell of the oligodendrocyte lineage. Representative images shown. Sections were also stained for Lgr5-EGFP and DAPI, while tdTomato marks lineage traced cells. <b>d</b>) Cells staining positive for a lineage marker or tdTomato were counted. Numbers shown are aggregated from all sections analyzed (≥4 per marker). There was no overlap of tdTomato and any lineage marker analyzed. Yellow arrows indicate examples of cells that are Lgr5+/tdTomato+ but lineage marker negative, while red arrows indicate examples of cells Lgr5-/tdTomato+ that are lineage marker negative. Scale bars, <i>top 3 panels</i>: 100 microns, <i>bottom 9 panels</i>: 25 microns. ML – molecular layer; PL – Purkinje layer; IGL – internal granule layer; WM – white matter tract.</p