Selective induction of neural tumors in the rat by single-dose exposure of the immature nervous system to ethylnitrosourea (EtNU) is a model for the study of cell lineage-, differentiation stage-, and carcinogen-dependent mechanisms in neuro-oncogenesis. Overall yields and relative frequencies of different types of neural tumors vary with the developmental window chosen for the EtNU-pulse. Precursor cells belonging to different neural lineages and targeted by the carcinogen at distinct developmental stages may thus bear a differential risk of malignant conversion. To specify subpopulations of neural precursors in fetal (prenatal day 18) BDIX-rat brain, four monoclonal antibodies (mAbs) recognizing cell surface differentiation antigens were used: mAb RB 13-2 directed against 0-acetylated gangliosides and binding to approximately 36% of fetal brain cells (FBC); mAb RB 13-6 recognizing a 130 kDa glycoprotein (expressed by approximately 8% of FBC); and mAbs RB21-7 and RB21-15 which bind, respectively, to embryonal neural cell adhesion molecules (N-CAM) and a 24 kDa protein (expressed by approximately 55% and 12% of FBC). Antigen expression profiles were compared with those of 14 primary brain tumors and 16 malignant neural cell lines, all of which had been induced by EtNU on prenatal day 18 in vivo. Monoclonal antibodies RB13-2 and RB21-7 did not bind to any of the tumors or cell lines. In contrast, mAbs RB13-6 and RB21-15 both reacted with 14/14 tumors, and with 16/16 and 10116 cell lines, respectively. Expression of the latter antigens might thus specify lineage-specific stages of FBC development/differentiation particularly susceptible to EtNU-induced malignant transformation. Two-color fluorescence analyses revealed three subsets of FBC binding mAb RB13-6 (RB13-2+/ RB13-6+/ RB2 1-1 5-; RB 13-2-mB 13-6+mB2 1-1%; and RB 13-2-/
The article only touches on the fact that the so called nocebo effect is known but that barely any research has been conducted to find out more about this effect. In my opinion this constitutes a wide gap in research, because the nocebo effect can occur even if the instructions for use of medications are known and information has been provided-for example, about the risks of surgery. This means that possible side effects of a medication or operation may be caused primarily by the nocebo effect. This presents jurisdiction with difficult situation: on the one hand, it is a legal requirement that patients who have reached the age of consent are fully informed about their treatment. If, however, such nocebo effects develop around the treatment then a legal dilemma arises. It needs to be clarified whether not passing on information about a defined medication weighs more heavily in the balance than a possible nocebo effect. In order to gain an understanding of the frequency of nocebo effects, one might compare, say, the frequency of adverse effects before and after the now legally compulsory information about defined adverse effects was introduced. On the other hand, one might compare the rate of adverse effects associated with a particular treatment in Germany-where a high degree of information about certain adverse effects is a legal requirement-with the rate of adverse effects in countries where German physicians work but where the legal requirement for information about medical therapies is less stringent. The United Arab Emirates is one such example.
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