Infertility is defined as the inability to procreate, or carry or deliver a baby naturally. The majority of specialists describe infertility as being unable to get pregnant after having tried for at least one year. The relationship between infertility and psychological stress is complex. On the one hand, infertile couples are subject to greater stress and have a greater risk of developing psychological disorders compared with normal, healthy couples. On the other hand, high levels of psychological distress have been indicated to increase infertility. Therefore, in the present review, the main factors that may lead to increased stress in couples who try to conceive, psychological stress as the reason for infertility, and the therapies that can help decrease psychological distress and increase chances of pregnancy are underlined. In addition to the psychological side effects that may occur from infertility itself, a range of other side effects can be caused by hormones and drugs used to treat infertility. Additionally, problem during erection and ejaculation can cause of psychological distress, which can lead to infertility among men. Psychotherapy is the main intervention recommended for couples who suffer from any form of infertility. Ideally, counselling should begin before patients start any medical intervention to help with their infertility.

Daily administration of low-dose aspirin during the second and third trimesters of pregnancy does not alter uteroplacental or fetoplacental hemodynamics and does not cause moderate or severe constriction of the ductus arteriosus.

We report on a case of primary pericardial teratoma detected in a 29-week-old fetus. Due to cardiac decompensation, pericardiocentesis was performed at 33 weeks of gestation, and surgical excision of the tumor was indicated shortly after birth. The present report draws attention to the impact of fetal echocardiography on perinatal management.

Endometriosis (EMS) remains, to date, an intriguing and debilitating gynecological disorder that possesses a multifactorial substrate. Recent studies with the objective of elucidating its etiology highlighted the antagonistic effect of EMS on a multiple of processes involved in homeostasis. Although the current oxidative biomarkers clearly reveal the consequences induced by EMS, its implication in the associated inflammatory reactions could be much more complex. Besides the overproduction of reactive oxygen species (ROS) that leads to an exacerbated oxidative response, it also changes the normal expression of several pro-inflammatory modulators, reflected by the fluctuating activity of several pro- and anti-apoptotic mediators whose expression is impaired. In light of this topic, several studies elucidate the involvement of apoptosis in EMS, being brought controversial findings, even reports with no significant change. Further, some authors reported an abnormal expression of multiple genes that are crucial for the overall functionality of the female reproductive system. Cumulatively, it seems that the subsequent oxidative imbalance and apoptosis process impairment could further disrupt the normal removal of unnecessary biological products. Based on all gathered evidence, we could argue that the related stress state could determine human endobiota impairment, which could further participate in the inflammatory and main antioxidant enzyme changes occurring in EMS. Moreover, a correlation between endobiota integrity, inflammation, and oxidative stress (OS) was suggested in relation to the possible predisposition to pathogen determined infections.

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