Impact of Chromosomal Structural Rearrangements on IVF Laboratory Outcomes in PGT-SR Cycles: A Propensity Score Matching-Based Study.

Chromosomal structural rearrangements (SR) can impair gametogenesis, increasing the risk of embryos carrying unbalanced chromosomal content (i.e., with a gain or loss of chromosomal material).

Trafficking of luteinizing hormone receptor directs the differential signal activation between luteinizing hormone and chorionic gonadotropin.

Luteinizing hormone (LH) and human choriogonadotropin (hCG) support distinct reproductive events via differential activation of the luteinizing hormone receptor (LHCGR). LH-mediated LHCGR trafficking is known to be key in activating and regulating its signal responses, yet whether LH and hCG differentially direct LHCGR trafficking is unknown. Bioluminescence resonance energy transfer (BRET) trafficking biosensors and high-resolution TIRF imaging demonstrated that LH induces rapid internalization and recycling via an APPL1-linked very early endosomal pathway, while hCG-mediated receptor trafficking and recycling is slower, and preferentially involves β-arrestins and accumulation in endocytic compartments positive for early and late endosomal markers.

Long-Term Postoperative Recurrence Rates and Fertility Outcomes After Endometrioma CO-Laser Vaporization: A Five-Year Follow-Up Experience.

Study Objective: Although cystectomy remains the gold standard for the surgical treatments of endometriomas, concerns about the negative effect on ovarian reserve are rising. Laser-CO vaporization of endometriomas has shown encouraging data on ovarian reserve preservation, postoperative pregnancy rates, and recurrence. The aim of this study was to assess postoperative recurrence rate and pregnancy rate in patients with endometriomas managed by CO fiber laser vaporization after at least 5 years following surgery.

Differential pathogenetic mechanisms of mutations in helix 2 and helix 6 of rhodopsin.

Variants in rhodopsin (RHO) have been linked to autosomal dominant congenital stationary night blindness (adCSNB), which affects the ability to see in dim light, and the pathogenetic mechanism is still not well understood. In this study we report two novel RHO variants found in adCSNB families, p.W265R and p.

Endometriosis and Adenomyosis: Modern Concepts of Their Clinical Outcomes, Treatment, and Management.

Endometriosis and adenomyosis are complex gynecological conditions characterized by diverse clinical presentations, including superficial peritoneal endometriosis (SPE), ovarian endometrioma (OMA), and deep infiltrating endometriosis (DIE). The hallmark features of these pathologies involve the manifestation of pain symptoms and infertility, and approximately 30% of patients are asymptomatic. Despite ongoing research, definitive treatments for these conditions remain elusive, and clinical management primarily revolves around medical or surgical interventions.

Minimally invasive surgery for ovarian endometriosis as a mean of improving fertility: Cystectomy vs. CO2 fiber laser ablation what do we know so far?

Minimally invasive surgery emerged in the 1980s as a safe and effective technique which requires smaller incisions and, usually, a shorter hospital stay compared to traditional surgery. Since then, minimally invasive surgery has expanded in many surgical specialties. One of its newest application in gynecology stands in the infertility management of young women with unexplained infertility or suspected endometriosis.

Intracellular cGMP increase is not involved in thyroid cancer cell death.

Introduction: Type 5 phosphodiesterase (PDE5) inhibitors (PDE5i) lead to intracellular cyclic-guanosine monophosphate (cGMP) increase and are used for clinical treatment of erectile dysfunction. Studies found that cGMP may up/downregulate the growth of certain endocrine tumor cells, suggesting that PDE5i could impact cancer risk.

Aim: We evaluated if PDE5i may modulate thyroid cancer cell growth in vitro.

LH increases the response to FSH in granulosa-lutein cells from sub/poor-responder patients in vitro.

Study Question: Does LH addition to FSH in vitro recover the human primary granulosa lutein cell (hGLC) sub/poor-response?

Summary Answer: A picomolar concentration of LH may recover the FSH-induced cAMP and progesterone production of hGLC from sub/poor-responder women.

What Is Known Already: Clinical studies suggested that FSH and LH co-treatment may be beneficial for the ovarian response of sub/poor-responders undergoing ovarian stimulation during ART.

Study Design, Size, Duration: hGLC samples from 286 anonymous women undergoing oocyte retrieval for ART were collected from October 2017 to February 2021.

Regulation of antral follicular growth by an interplay between gonadotropins and their receptors.

Knowledge of the growth and maturation of human antral follicles is based mainly on concepts and deductions from clinical observations and animal models. To date, new experimental approaches and in vitro data contributed to a deep comprehension of gonadotropin receptors' functioning and may provide new insights into the mechanisms regulating still unclear physiological events. Among these, the production of androgen in the absence of proper LH levels, the programming of follicular atresia and dominance are some of the most intriguing.

Endocrine Disruption of the Follicle-Stimulating Hormone Receptor Signaling During the Human Antral Follicle Growth.

An increasing number of pollutants with endocrine disrupting potential are accumulating in the environment, increasing the exposure risk for humans. Several of them are known or suspected to interfere with endocrine signals, impairing reproductive functions. Follicle-stimulating hormone (FSH) is a glycoprotein playing an essential role in supporting antral follicle maturation and may be a target of disrupting chemicals (EDs) likely impacting female fertility.

Phosphodiesterase (PDE) 5 inhibitors sildenafil, tadalafil and vardenafil impact cAMP-specific PDE8 isoforms-linked second messengers and steroid production in a mouse Leydig tumor cell line.

Type 5 phosphodiesterase (PDE5) blockade by inhibitors (PDE5i) results in intracellular cyclic guanosine monophosphate (cGMP) increase and smooth muscle relaxation and are used for the treatment of men erectile dysfunction. Although they have high specificity for PDE5, these inhibitors are suspected to cross-interact also with cyclic adenosine monophosphate (cAMP)-specific PDEs, inducing the intracellular accumulation of this cyclic nucleotide and related testosterone increase, positively impacting male reproductive parameters. However, the link between the use of PDE5i and the activation of cAMP-mediated steroidogenesis is still unclear.

A longitudinal DTI and histological study of the spinal cord reveals early pathological alterations in G93A-SOD1 mouse model of amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by selective motor neuron degeneration in the motor cortex, brainstem and spinal cord. It is generally accepted that ALS is caused by death of motor neurons, however the exact temporal cascade of degenerative processes is not yet completely known. To identify the early pathological changes in spinal cord of G93A-SOD1 ALS mice we performed a comprehensive longitudinal analysis employing diffusion-tensor magnetic resonance imaging alongside histology and electron microscopy, in parallel with peripheral nerve histology.

Up-regulation of neural and cell cycle-related microRNAs in brain of amyotrophic lateral sclerosis mice at late disease stage.

Background: Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by selective motor neuron degeneration in motor cortex, brainstem and spinal cord. microRNAs (miRNAs) are small non-coding RNAs that bind complementary target sequences and modulate gene expression; they are key molecules for establishing a neuronal phenotype, and in neurodegeneration. Here we investigated neural miR-9, miR-124a, miR-125b, miR-219, miR-134, and cell cycle-related miR-19a and -19b, in G93A-SOD1 mouse brain in pre-symptomatic and late stage disease.