ABSTRACT
MR images of infants and fetuses allow non-invasive analysis of the brain. Quantitative analysis of brain development requires automatic brain tissue segmentation that is typically preceded by segmentation of the intracranial volume (ICV). Fast changes in the size and morphology of the developing brain, motion artifacts, and large variation in the field of view make ICV segmentation a challenging task. We propose an automatic method for segmentation of the ICV in fetal and neonatal MRI scans. The method was developed and tested with a diverse set of scans regarding image acquisition parameters (i.e. field strength, image acquisition plane, image resolution), infant age (23-45 weeks post menstrual age), and pathology (posthaemorrhagic ventricular dilatation, stroke, asphyxia, and Down syndrome). The results demonstrate that the method achieves accurate segmentation with a Dice coefficient (DC) ranging from 0.98 to 0.99 in neonatal and fetal scans regardless of image acquisition parameters or patient characteristics. Hence, the algorithm provides a generic tool for segmentation of the ICV that may be used as a preprocessing step for brain tissue segmentation in fetal and neonatal brain MR scans.
Subject(s)
Brain/diagnostic imaging , Fetus/diagnostic imaging , Head/diagnostic imaging , Algorithms , Deep Learning , Humans , Image Processing, Computer-Assisted , Magnetic Resonance Imaging , Neural Networks, Computer , Organ SizeABSTRACT
The histopathological diagnosis and treatment of borderline epithelial tumors of the ovary (BTO) still pose problems to both pathologists and gynecologists. BTO is a disease of younger, fertile females and generally has an excellent prognosis. A minority of patients, however, succumb to this disease. A review of the literature is given addressing aspects of epidemiology, histology, treatment and prognosis, resulting in a proposal for the management of serous and mucinous borderline tumors of the ovary.
ABSTRACT
Incubation of RSU 1069 in the presence of biologically active double-stranded phi X174 DNA resulted in, depending on pH, ionic strength and concentration of drug, inactivation of the DNA. A variety of lesions are induced including a high number of single-strand breaks and alkali-labile lesions, which are at most partly lethal. The main inactivating damage consists probably of base damage, induced by alkylation. A considerable part of the damage induced by RSU 1069 can be repaired by the various repair enzymes of the bacterial host of the phi X174 DNA. Finally the damage (pattern) depends considerably on the ionic composition of the reaction solution, which can be explained by an equilibrium model presented in this paper.
Subject(s)
Antineoplastic Agents/toxicity , DNA Damage , DNA Repair , DNA, Viral/drug effects , DNA/drug effects , Misonidazole/analogs & derivatives , Radiation-Sensitizing Agents/toxicity , Alkalies , Antineoplastic Agents/chemistry , Bacteriophage phi X 174/drug effects , Bacteriophage phi X 174/genetics , Electrolytes/chemistry , Hydrogen-Ion Concentration , Misonidazole/chemistry , Misonidazole/toxicity , Radiation-Sensitizing Agents/chemistryABSTRACT
We have examined the capacity of the nitroimidazole aziridine antitumour drug RSU 1069 to react with DNA in vitro in order to get a better understanding of its mechanism of action. Moreover, we have utilized biologically active phi X174 DNA to investigate the biological relevance of the chemical DNA modification induced by the drug. Incubation of RSU 1069 in the presence of single-stranded phi X174 DNA resulted in extensive inactivation of the DNA, which is dependent on the concentration of drug and temperature. Only about 2% of the inactivating damage can be attributed to strand breakage. The main damage most probably consists of base damage, of which a part is non-lethal and alkali-labile which in turn can be converted into lethal lesion and subsequently into a break applying a post-incubation alkali treatment. Furthermore, from the dependence of the inactivation and also the formation of breaks on pH and ionic strength, it is concluded that the reaction most probably takes place between a protonated RSU 1069 and a negative DNA coil and that the damage pattern reflects the difference in reactivity of RSU 1069 with the phosphate groups and the bases in DNA. Comparison between RSU 1069 and its ring-open hydrolysis product RSU 1137 revealed that (lethal) damage induced in the DNA must be ascribed to the alkylating properties of the aziridine moiety.
