Correspondence analysis between different congenital abnormalities and amniotic fluid volumes.

<p>The correspondence analysis visualizes the contingency between the different types of congenital abnormalities and amniotic fluid volumes. The closer groups are located to each other, the stronger the correlation between the groups is. The horizontal-axis accounts for 70.7% of the variation and the vertical-axis for 19.9%. The significance of relationships between types of amniotic fluid volumes and congenital abnormalities is calculated using chi-squared tests. Oligohydramnios (OH) and anhydramnios (AH) associate significantly with urogenital defects (UG) and polyhydramnion (PH) with muscular system malformations (MUS), but not significantly after bonferroni adjustment. Normal amniotic fluid volumes associate with nervous system defects, but not significantly after bonferroni adjustment. No associations are found between cardiovascular defects (CV), skeletal defects (SK), craniofacial defects (CF), limb development abnormalities (LD), digestive system defects (DS), and ventral body wall defects (VBW) and the different types of amniotic fluid volume.</p

Examples of fetuses that should be excluded and included from FA measurements.

<p>A: Fetus with limb deformities (indicated by arrows), which include bowing of the radius and ulna, bowing of the digits, bowing and hypoplasia of the femur, tibia and fibula. B: Fetus with limb deformities including bowing of the digits, bowing and hypoplasia of the femur, tibia and fibula, and talipes equinovarus (clubfeet). The deformed traits in fetus A and B should be excluded from FA measurements. C: Non-deformed, representative fetus, that allows FA measurements: the limbs are properly positioned and no deformities are present. Here, fetuses A and B developed with reduced amniotic fluid volumes and fetus C developed with a normal amniotic fluid volume.</p

Relationships between age, FA and amniotic fluid volumes.

<p>Mean size-corrected fluctuating asymmetry decreases with age (in weeks on a log-transformed scale) for human deceased fetuses that developed in normal amniotic volumes and with polyhydramnios (PH) and increased with age for fetuses with oligohydramnios (OH) and anhydramnios (AH). Slopes of regression lines are not significantly different from each other, but are when AH/OH and normal volumes/PH are grouped together.</p

Additional file 7: of Proteomics analysis identifies new markers associated with capillary cerebral amyloid angiopathy in Alzheimer’s disease

Figure S6. Protein expression of males versus females. Quantitative data on several CAA selective data was plotted with males represented as triangles and females as dots. No clear relationship between gender and protein abundance was observed. (TIF 24739 kb

Additional file 6: of Proteomics analysis identifies new markers associated with capillary cerebral amyloid angiopathy in Alzheimer’s disease

Figure S5. Protein expression of CAA case #5 relative to the experimental groups and individual cases. (A) On the left the expression profile of case #5 compared to the average expression profile of the control group (2nd row), AD group (3rd row) and the CAA group (4th row). Green, expression below the overall mean; red, above the overall mean. The expression profile of case #5 is largely similar to that of the control groups but some proteins show a similar expression as in the AD and/or CAA groups. (B) Expression values (LFQ values) of several CAA specific proteins identified in this study with case #5 indicated as empty triangle pointing down. Case #5 does not differ from the CAA group in these markers. (TIF 1835 kb

Additional file 5: of Proteomics analysis identifies new markers associated with capillary cerebral amyloid angiopathy in Alzheimer’s disease

Figure S4. Clustering analysis of experimental groups and individual cases. Clustering analysis and heat maps of the different experimental groups (A) and individual cases (B) based on proteins with a significant difference (ANOVA, p < 0.05) in expression between any of the groups. (TIF 709 kb

Additional file 8: of Proteomics analysis identifies new markers associated with capillary cerebral amyloid angiopathy in Alzheimer’s disease

Figure S7. Immunoreactivity for COL6A2 is equally present in leptomeningeal vessels in control, AD and CAA tissue. (TIF 3794 kb

Additional file 4: of Proteomics analysis identifies new markers associated with capillary cerebral amyloid angiopathy in Alzheimer’s disease

Table S1. Complete dataset, containing log2 transformed quantitative values (LFQ values) of all quantified proteins per individual case. (XLSX 665 kb

Additional file 1: of Proteomics analysis identifies new markers associated with capillary cerebral amyloid angiopathy in Alzheimer’s disease

Figure S1. Coomassie blue staining of the SDS PAGE gels containing the microdissected tissue lysates. (TIF 478 kb

Additional file 2: of Proteomics analysis identifies new markers associated with capillary cerebral amyloid angiopathy in Alzheimer’s disease

Figure S2. Total protein fluorescent signal from blots used for immunoblot analysis. Total protein load was visualized using a chemidoc EZ (Bio-Rad) after electroblotting and used to obtain densitometric values which were then used to normalize for total protein input. (TIF 553 kb