Automatisierte Planung von digitalen Hochgeschwindigkeitsnetzen

Der Ausbau von digitalen Hochgeschwindigkeitsnetzen ist gekennzeichnet durch neuartige Anforderungen an den Planungsprozess. Diese Anforderungen erfordern wiederum den Einsatz von neuartigen Paradigmen, die eine effiziente und zugleich genaue Planung von flächendeckenden Glasfasernetzen ermöglichen. Hierbei können wiederkehrende Planungsaufgaben durch eine gezielte computergestützte Automatisierung effizienter und genauer ausgeführt, als es mit bisherigen Planungskonzepten möglich ist. Dieses Arbeitspapier beschreibt die computergestützte Ausführung eines Planungsprozesses auf Basis von fünf grundlegenden, iterativen Planungsschritten und gibt Empfehlungen für eine effiziente und genaue Planung von Glasfasernetzen. Der hier vorgestellte Ansatz ermöglicht es Netzbetreibern und Investoren, den Ausbau beliebiger Siedlungs- und Gewerbegebiete auf der zuverlässigen Basis von belastbarem Faktenwissen wirtschaftlich zu priorisieren

Immunohistochemical detection of NIS protein expression in 5 µM sections of selected tissues from patient cohort.

<p>(<b>a</b>) Thyroid tissue (positive control) (400×), (<b>b</b>) Antibody free Fibroadenoma (negative control) (200×), (<b>c</b>) Fibroadenoma (400×). Also shown are breast cancer epithelial subtypes Luminal A (<b>d</b>), Luminal B (<b>e</b>), Her2 (<b>f</b>) and Basal (<b>g</b>) at 400× magnification.</p

RARα and RARβ expression in breast tissue samples, and their relationship with NIS.

<p>(<b>a</b>) RARα and RARβ expression in normal, malignant and fibroadenoma breast tissue. Results have been normalised to the endogenous controls PPIA and MRPL19 and expressed relative to the lowest detectable sample. Correlations of NIS gene expression with RARα (<b>b</b>) and RARβ (<b>c</b>) with r and p values shown (* one outlier removed). (<b>d</b>) THRα and THRβ expression in normal, malignant and fibroadenoma breast tissue.</p

Effect of β-estradiol (E₂), all trans Retinoic Acid (ATRA) and L-thyroxine (T₄) on NIS expression in breast cancer cell lines.

<p>Effect of indivdual stimulants on NIS expression in (<b>a</b>) T47D and (<b>b</b>) SkBr3 cell lines. Results have been normalised to the endogenous controls PPIA and MRPL19 and expressed relative to diluent controls, with the baseline representing 2^{−(ddCt diluent control)}. (<b>c</b>) NIS expression in T47D and SkBr3 cells following 24 hr stimulation with optimal concentrations of ligands alone and in combination. (<b>d</b>) Correlation of RARβ with THRβ gene expression within patient cohort with r and p values shown.</p

Patient demographics of study cohort.

<p>Patient demographics of study cohort.</p

ERα and PI3K expression in breast tissue samples and their relationship with NIS.

<p>Expression of ERα (<b>a</b>) and PI3K (<b>b</b>) in normal, malignant and fibroadenoma breast tissue. Results have been normalised to the endogenous controls PPIA and MRPL19 and expressed relative to the lowest detectable sample. Correlation of NIS gene expression with ERα (<b>c</b>) and PI3K (<b>d</b>) with r and p values shown.</p

NIS expression in normal, fibroadenoma (“Fibro”) and malignant breast tissue.

<p>Results have been normalised to the endogenous controls PPIA and MRPL19 and expressed relative to the lowest detectable sample. Note: Results in breast cancer patients are also stratified by epithelial subtype.</p

Relative expression of MiRNAs in tumour (n = 15), lymph nodes (n = 3) and healthy tissue (n = 5).

<p>(<b>A</b>) miR-10b expression. (<b>B</b>) miR-221 expression. (<b>C</b>) Positive correlation between miR-10b and miR-221 across all tissues. (<b>D</b>) MiR- 195 expression. (<b>E</b>) miR-497 expression. (<b>F</b>) Positive correlation between miR-195 and miR-497 expression across all tissues.</p

In Vivo miRNA study timeline.

<p>This study comprises of 20 athymic nude mice of which 15 were tumour bearing (MFP = 8 and SC = 7) and 5 were controls. Blood sampling was carried out from all animals at weeks 1, 3, and 6 as highlighted with red arrows. Tumour volume and weight measurements were undertaken at a weekly basis for the 6 week duration of the project. Animals were sacrificed at week 6 following tumour induction and all primary tumours (n = 15), lungs (n = 20) and lymph nodes (n = 3) were harvested for analysis and a terminal bleed via cardiac puncture was performed.</p

Circulating miRNA expression in tumour bearing (n = 45, 15×3) and healthy animals (n = 15, 5×3).

<p>At termination of this study, 6 weeks following tumour induction no significant difference was observed between circulating miR-221 (<b>A</b>), miR-195 (<b>B</b>) and miR-497 (<b>C</b>) in tumour bearing animals compared to healthy controls.</p