Soledad Sánchez-Mateos

Three-dimensional printing has been progressively integrated into various industries, particularly the medical sector, where its significance in tissue engineering for transplantation is growing exponentially. The purpose of this systematic review is to ascertain whether the bioprinting of scaffolds holds the potential to provide treatment for pathologies within the female reproductive system. The inclusion criteria applied were the bioimprinting of the ovary, uterus, endometrium, or vagina, intended for surgical implantation in the patient. Articles employing printing methods that do not incorporate cells embedded in the material, those that generate tissue other than that of the female reproductive system, and those that print structures with in vitro applications were excluded from the review. The search for relevant articles was conducted until 3 April 2025. After analyzing 667 articles extracted from PubMed, Scopus and Web of Science, 13 articles were included in this review. The analysis of the results encompassed aspects related to the bioprinting technology employed, the hydrogels and cells utilized, as well as the bioprinted structure and the corresponding target tissue. Few studies investigated the creation of a multicellular scaffold and in none of the cases was it implanted in a large animal model, only in murine and rabbit models. These articles reaffirm the feasibility of employing 3D bioprinting to fabricate tissues and functional organs in the present and future. This advancement will revolutionize the future demand for organs for transplantation.

The present study evaluated whether the administration of cereals enriched with nutrients that are facilitators of sleep could help improve the sleep of infants who had sleep disorders at night time. Thirty infants aged 8-16 months with sleep disorders involving at least three nocturnal waking episodes took part in the study. They were given a night-time 'sleep facilitating cereal' product containing 225 mg tryptophan, 5.3 mg adenosine-5'-P, and 6.3 mg uridine-5'-P per 100 g of product. These cereals were given in a double-blind procedure lasting 5 weeks, with ingestion of the cereal between 18:00 and 06:00. In the control week, the children received a standard cereal (75 mg tryptophan/100 g product without nucleotides) dissolved in a standard formula milk (231.5 mg tryptophan, 2.6 mg adenosine-5'-P, 5 mg uridine-5'-P, per 100 g product). In one experimental week, the children received the night-time sleep facilitating cereal together with the standard formula milk. In another week, they received the sleep facilitating cereal together with a night milk specially formulated to attain the sleep rhythm (480 mg tryptophan, 8.8 mg uridine-5'-P, and 7.6 mg adenosine-5'-P per 100 g product). The three experimental weeks were separated by two wash-out weeks in which the milk and cereal administered was identical in composition to that of the control week. All the infants received a programmed writer actimeter which they wore continually, attached to their ankles, to record their motor activity. The recorded activity was used to calculate information about the time in bed, assumed sleep, actual sleep, sleep efficiency, sleep latency, immobility, and total activity. The infants receiving the enriched cereal during the time of darkness showed improvements in their sleep parameters, regardless of whether the milk they took at night was standard or enriched with tryptophan, adenosine-5'-P, and uridine-5'-P. In summary, the administration of enriched cereals led to an improvement in sleep, regardless of the type of infant milk used. These results support the concept of chrononutrition since they confirm that the sleep/wake rhythm can be influenced by diet.

Abstract: Serotonin, one of the most important neurotransmitters in the central nervous system, is synthesized by the amino acid, tryptophan. Given that this essential amino acid is consumed in the diet, the aim of this study was to evaluate the effect of orally administered L‐tryptophan (125 mg/kg) on circadian variations in the levels of serotonin in brain and plasma. We used male Wistar rats of 14 ± 2 weeks of age (n = 240), maintained under conditions of a 12‐hr light:dark cycle, and food and waterad libitum. Tryptophan administration was by gavage in a daily single dose at 7 p.m. for 7 days. The serotonin levels were measured by ELISA every hour at night (8 p.m. to 8 a.m.) and every 4 hr during daytime (8 a.m. to 8 p.m.). The results show that in both the tryptophan‐treated and untreated groups the highest values appeared during the beginning of the darkness with a peak at 9, 10 and 11 p.m. in controls, and at 9 p.m. in the tryptophan‐treated group. After tryptophan administration, the levels of serotonin were significantly higher in the plasma and all the brain regions analysed than in the control group. This increase of serotonin levels was greater in the pineal gland than in other brain regions, and the least in plasma. In conclusion, oral administration of tryptophan during 7 days enhances serotonin levels over a 24‐hr period, and produces an advance in the peak of serotonin in both plasma and different brain regions.

Since the tryptophan-derived metabolites serotonin and melatonin have been shown to possess reinforcing and/or antioxidant properties in the immune system, this investigation was aimed at determining the possible effect of a 7-day administration of tryptophan (125 mg/kg b.w.), the precursor of both the neurotransmitter and the indole, on the phagocytosis and free radical scavenging of peritoneal macrophages from adult male Wistar rats. Phagocytosis was measured by the latex-bead phagocytosis index (PI), i.e., the number of latex beads ingested by 100 macrophages, the phagocytosis percentage (PP), i.e., the percentage of cells that had phagocytosed at least one latex bead, and the phagocytosis efficiency (PE), i.e., the ratio PI:PP which indicates how effectively the phagocytes ingested the particles. Oxidative metabolism was measured by the nitroblue tetrazolium (NBT) reduction test. In control conditions, PI, PP, and PE significantly increased during the dark period, while the superoxide anion levels underwent a significant reduction. Tryptophan treatment significantly raised the phagocytosis parameters in a general fashion, as well as decreasing the oxidative metabolism with respect to the control values. Also, there was a significant rise in the MESORs of the PI and PE (of around 16% and 12%, respectively), the MESOR of the percentage of NBT reduction was significantly reduced (19%). Orally administered tryptophan enhanced the phagocytic response and detoxification of superoxide anion radicals derived from this immune function in the peritoneal macrophages of rats, very probably through its conversion to the immunoregulatory molecules, serotonin and melatonin.

The most physiological processes that take place in the body have a circadian rhythm which is controlled by an internal biological clock located in the suprachiasmatic nucleus. The indole melatonin synthesized in the pineal gland, acts to sync...

Abstract:  Melatonin exerts oncostatic effects on different kinds of neoplasias, especially on estrogen‐dependent mammary tumors. Current knowledge about the mechanisms by which melatonin inhibits the growth of breast cancer cells point to an interaction of melatonin with estrogen‐responsive pathways. The intratumoral production of estrogens in breast carcinoma tissue plays a pivotal role in the proliferation of mammary tumoral cells and its blockade is one of the main objectives of the treatment of breast cancer. The aim of the present work is centered on the study of the role of melatonin in the control of some enzymes involved in the formation and transformation of estrogens in human breast cancer cells. The present study demonstrates that melatonin, at physiologic concentrations, modulates the synthesis and transformation of biologically active estrogens in MCF‐7 cells, through the inhibition of sulfatase (STS) and 17β‐hydroxysteroid dehydrogenase type 1 (17β‐HSD1) activity and expression, enzymes involved in the estradiol formation in breast cancer cells. Physiologic concentrations of melatonin also stimulate the activity and expression of estrogen sulfotransferase (EST), the enzyme responsible for the formation of the biologically inactive estrogen sulfates. The level of EST mRNA steady‐state of cells treated with melatonin was three times higher than that in control cells. These findings which document that melatonin has an inhibitory effect on STS and 17β‐HSD1 and a stimulatory effect on EST, in combination with its previously described antiaromatase effect, can open up new and interesting possibilities in clinical applications of melatonin in breast cancer.