Additional file 1: of Changes in lipoprotein lipase and endothelial lipase mass in familial hypercholesterolemia during three-drug lipid-lowering combination therapy

Associations between the changes in LPL/EL mass and those in lipids. (PPTX 2501 kb

Histological characteristics of fibrosis in biopsy specimens in the 21 patients with HCM.

<p>Interstitial fibrosis; increased interstitial collagen without evidence of myocyte loss. Myocardial scarring; increased interstitial collagen with evidence of myocyte loss <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0101465#pone.0101465-Seidman1" target="_blank">[9]</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0101465#pone.0101465-John1" target="_blank">[22]</a>. The presence of islands of surviving cardiomyocyte among fibrotic tissues was considers as evidence of cardiomyocyte loss <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0101465#pone.0101465-Basso1" target="_blank">[23]</a>. HCM as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0101465#pone-0101465-t001" target="_blank">Table 1</a>.</p

Predictors of the collagen fraction in biopsied specimens (unadjusted and multivariate-adjusted regression analyses).

<p>CI  =  confident interval. AF, EF, HCM, LGE, LVDD, MWT and PWT as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0101465#pone-0101465-t001" target="_blank">Tables 1</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0101465#pone-0101465-t003" target="_blank">3</a>.</p

Characteristics of LGE-CMR in the 21 patients with HCM.

<p>CMR  =  cardiac magnetic resonance imaging; LGE  =  late gadolinium enhancement. HCM as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0101465#pone-0101465-t001" target="_blank">Table 1</a>.</p

Diagnostic values of LGE for detecting microscopic myocardial scarring or interstitial fibrosis in biopsied specimens in the HCM patients (N = 21).

<p>NPV  =  negative predictive value; PPV  =  positive predictive value. HCM as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0101465#pone-0101465-t001" target="_blank">Table 1</a>.</p

Characteristics of the 21 patients with HCM.

<p>AF  =  atrial fibrillation; ASH  =  asymmetrical septal hypertrophy; CLBBB  =  complete left bundle branch block; CRBBB  =  complete right bundle branch block; HCM  =  hypertrophic cardiomyopathy; IVST  =  intraventricular septal wall thickness; LAD  =  left atrial dimension; LVDD  =  left ventricular end-diastolic dimension; LVEF  =  left ventricular ejection fraction; MWT  =  maximal wall thickness; PWT  =  posterior wall thickness.</p

Relationships between the microscopic fibrosis fraction and the LGE fraction in the HCM patients.

<p>(<b>A</b>) A fair correlation was found between the LGE fraction and the total fibrosis fraction in biopsied specimens (N  =  21). (<b>B</b>) To examine whether the LGE fraction correlated with the microscopic collagen fraction in HCM with preserved LV systolic function, 5 end-stage HCM patients were excluded from analyses. In the remaining 16 HCM patients, a correlation between the LGE fraction in the whole heart and the microscopic collagen fraction in biopsied specimens was observed (r  =  0.62, p  =  0.011). Abbreviations as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0101465#pone-0101465-g001" target="_blank">Figure 1</a>.</p

Qualitative and quantitative assessments of myocardial fibrosis in endomyocardial biopsy and LGE-CMR in the HCM patients.

<p>(<b>A</b>–<b>C</b>) Typical histology from endomyocardial biopsy. Upper panels; no pathological fibrosis (<b>A</b>), increased interstitial fibrosis (<b>B</b>), and severe myocardial scarring (<b>C</b>). Slides were stained with Azan dye. Interstitial fibrosis was defined as increased interstitial collagen without evidence of cardiomyocyte loss <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0101465#pone.0101465-Seidman1" target="_blank">[9]</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0101465#pone.0101465-John1" target="_blank">[22]</a>. Lower panels: areas of fibrosis visualized by ImageJ software. Fibrosis volume fraction determined by digital planimetry was 2% (<b>A</b>), 15% (<b>B</b>) and 45% (<b>C</b>), respectively. Myocardial scarring was defined as increased interstitial collagen with evidence of cardiomyocyte loss <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0101465#pone.0101465-Seidman1" target="_blank">[9]</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0101465#pone.0101465-John1" target="_blank">[22]</a>. The presence of islands of surviving cardiomyocyte among fibrotic tissues was considers as evidence of cardiomyocyte loss <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0101465#pone.0101465-Basso1" target="_blank">[23]</a>. (<b>D</b>) Islands of surviving cardiomyocyte (arrows) among fibrotic tissues observed with high magnification of Image C. (<b>E and F</b>) Defining and quantifying LGE. Representative HCM patients with no LGE (<b>E</b>) and with positive LGE (<b>F</b>). Areas of LGE (traced by yellow lines) were quantified by manual planimetry and presented as percentage of left ventricular areas (traced by blue lines). Total of 6 short axes views were analyzed in each HCM patient. The LGE volume fraction was 0% in Case D, and 16% in Case E. Scale bars represent 200 µm. CMR  =  cardiac magnetic resonance imaging, HCM  =  hypertrophic cardiomyopathy, LGE  =  late gadolinium enhancement.</p

Concordant and discordant appearance of fibrosis in LGE-CMR and endomyocardial biopsy in the HCM patients.

<p>(<b>A</b>) Myocardial scarring was observed both in CMR and endomyocardial biopsy. (<b>B</b>) LGE was present in CMR, but there was no evidence of microscopic myocardial scarring. Scale bars represent 200 µm. Abbreviations as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0101465#pone-0101465-g001" target="_blank">Figure 1</a>.</p

موسى بن محمد قاضي زاده الرومي. أشكال التأسيس

Numérisation effectuée à partir d'un document de substitution.Commentaire des Aškāl al-ta'sīs de Muḥammad ibn Ašraf al-Samarqandī. Titre au f. 2. Inc. (f. 2v) : الحمد لله الذي خلق كل شيء بقدر وقدر له ما يليق من أشكال وصور... وبعد فإن الهندسة مع متانة مسائلها Exp. (f. 50v) : وهذه الأشكال الخمسة الأخيرة من ثانية كتاب الأصول لأقليدس وليكن هذا آخر الكلام وقد تم الكتاب Copie achevée par ʿAbd al-Qādir ibn Muṣṭafā al-Ḥallāq le 12 šawwāl 1176 h. / 26 avril 1763.Cachet et marque du commanditaire de la copie : Muḥammad ʿĀrif, mudarris à Dār al-Sulṭana, Marque de possession de Muḥammad ibn Ḥusayn (?) (f. 1). Indication de prix : 15 piastres (f. 1). Marque à l'encre violette datée du 3 šaʿbān 1361 h. / 16 août 1942, au nom de Muḥammad al-Amīn ibn Muḥammad ʿAbd Allāh (f. 1v