The late effects of cancer treatment have recently gained a worldwide interest among reproductive endocrinologists, oncologists, and all health-care providers, and the protection against iatrogenic infertility caused by chemotherapy assumes a high priority. Here, we summarize the case for and against using GnRH-agonist for fertility preservation and minimizing chemotherapy-induced gonadotoxicity. The rationale and philosophy supporting its use is that preventing premature ovarian failure (POF) is preferable to treating it, following the dictum: 'an ounce of prevention is worth a pound of cure'. Despite many publications on this subject, there are many equivocal issues necessitating summary. Until now, 20 studies (15 retrospective and 5 randomized, controlled trials) have reported on 1837 patients treated with GnRH-a in parallel to chemotherapy, showing a significant decrease in POF rate in survivors versus 9 studies reporting on 593 patients, with results not supporting GnRH-a use. Patients treated with GnRH-a in parallel to chemotherapy preserved their cyclic ovarian function in 91% of cases when compared with 41% of controls, with a pregnancy rate of 19-71% in the treated patients. Furthermore, seven meta-analyses have concluded that GnRH-a are beneficial and may decrease the risk of POF in survivors. However, controversy still remains regarding the efficiency of GnRH-a in preserving fertility. Since not all the methods involving fertility preservation are unequivocally successful and safe, these young patients deserve to be informed of all the various modalities to minimize gonadal damage and preserve ovarian function and future fertility. Combining several methods for a specific patient may increase the odds for minimally invasive fertility preservation.

The optimum thermal environment for naked babies. The optimum thermal environment in which to nurse a baby naked in an incubator has been defined from a knowledge of the magnitude of the factors affecting thermal balance. MethodsThe data on heat production and heat loss on which the present analysis is based were obtained using a specially constructed metabolic chamber at The London Hospital. 123 healthy premature and full-term infants of known gestation have been studied with the consent of their parents. Many of the smaller infants were studied at least twice a week throughout the first month of life. The babies weighed between 0 -96 and 4-76 kg. at birth. We have studied the range of control that these naked babies exerted over evaporative and nonevaporative heat loss, and measured average heat production while the babies lay at rest in warm surroundings free of thermal stress. We have then combined these findings in order to establish estimates of what constitutes a neutral thermal environment.Heat production was calculated from measured oxygen consumption on the assumption that the consumption of 1 litre of 02 at S.T.P. (dry) liberates 4-83 kilocalories of heat. Evaporative heat loss was calculated from measured water loss on the assumption that the evaporation of 1 g. water results in the loss of 0-6 kilocalories of heat from the body. Estimates of nonevaporative heat loss were obtained indirectly from measurements of heat production and heat storage, 328

When assembling a nephron during development a multipotent stem cell pool becomes restricted as differentiation ensues. A faulty differentiation arrest in this process leads to transformation and initiation of a Wilms’ tumor. Mapping these transitions with respective surface markers affords accessibility to specific cell subpopulations. NCAM1 and CD133 have been previously suggested to mark human renal progenitor populations. Herein, using cell sorting, RNA sequencing, in vitro studies with serum-free media and in vivo xenotransplantation we demonstrate a sequential map that links human kidney development and tumorigenesis; In nephrogenesis, NCAM1+CD133− marks SIX2+ multipotent renal stem cells transiting to NCAM1+CD133+ differentiating segment-specific SIX2− epithelial progenitors and NCAM1−CD133+ differentiated nephron cells. In tumorigenesis, NCAM1+CD133− marks SIX2+ blastema that includes the ALDH1+ WT cancer stem/initiating cells, while NCAM1+CD133+ and NCAM1−CD133+ specifying early and late epithelial differentiation, are severely restricted in tumor initiation capacity and tumor self-renewal. Thus, negative selection for CD133 is required for defining NCAM1+ nephron stem cells in normal and malignant nephrogenesis.