Introduction: Women's sexual health is a vital and important part of life at any age. In particular, pregnancy and childbirth bring biological, psychological, and social changes which may influence sexual health. It has been shown that sexual function declines during pregnancy and does not return to its baseline levels during the postpartum period. Despite the complexity and significance of this subject, health providers often neglect sexual aspects during pregnancy and postpartum. Aim: We believe that clarifying the risk factors will help open conversations and improvements in sexual function. Methods: In this review, we focus on how postpartum sexual function is affected by mode of delivery, perineal trauma during delivery, episiotomy, and lactation. Concclusions: We conclude that the mode of delivery has no significant effect on short-and long-term postpartum sexual function. On the other hand, 3rd and 4th degree tears are strongly associated with postpartum sexual dysfunction. We found that episiotomy does not adversely affect sexual function, and lactation has a slightly negative effect. We believe that shedding light on this topic will lead to a better understanding for pregnant and postpartum women and the obstetrician. Further studies may elucidate more useful treatment approaches.

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Introduction Preterm infants with necrotizing enterocolitis (NEC) are at increased risk of cerebral injury and neurodevelopmental dysfunction. N‐acetyl‐cysteine (NAC) is a known anti‐inflammatory and antioxidant agent. Currently, there is no prophylactic treatment in clinical use to prevent NEC and its neurodevelopmental sequelae. We sought to determine whether brain inflammation/apoptosis accompanies NEC systemic inflammation, and whether it can be attenuated by maternal NAC treatment during pregnancy and/or in the neonatal period in a rat model. Material and methods An established NEC newborn model (hypoxia 5% O2 for 10 min and formula feeding thrice daily, beginning on day 1 for 4 days) was used in Sprague‐Dawley rat pups (n = 32). An additional group of pups (n = 33) received NAC (300 mg/kg intraperitoneal thrice daily) in addition to NEC conditions (NEC‐NAC). Control pups (n = 33) were nursed and remained with the dam in room air. Two additional groups included pups of dams treated once daily with NAC (300 mg/kg intravenous) in the last 3 days of pregnancy. After birth, pups were randomized into NAC‐NEC (n = 33) with NEC conditions and NAC‐NEC‐NAC (n = 36) with additional postnatal NAC treatment. Pups were sacrificed on the fifth day of life. Pup serum interleukin (IL)‐6 protein levels, and brain nuclear factor kappa B (NF‐κB) p65, neuronal nitric oxide synthase (nNOS), Caspase 3, tumor necrosis factor alpha (TNF‐α), IL‐6 and IL‐1β protein levels were determined by ELISA, western blot and TUNEL staining, and the groups were compared using analysis of variance (ANOVA). Results NEC pups had significantly increased serum IL‐6 levels compared with the control group as well as increased neuronal apoptosis and brain protein levels of NF‐κB, nNOS, Caspase 3, TNF‐α, IL‐6 and IL‐1β compared with control. In all NAC treatment groups, levels of serum IL‐6, neuronal apoptosis and brain NF‐κB, nNOS, Caspase 3, TNF‐α, IL‐6 and IL‐1β protein levels were significantly reduced compared with the NEC group. The most pronounced decrease was demonstrated within the NAC‐NEC‐NAC group. Conclusions NAC treatment can attenuate newborn inflammatory response syndrome and decrease offspring brain neuroapoptosis and inflammation in a rat model of NEC by inhibition of NF‐κB, nNOS and Caspase 3 pathways.

Background and Objectives: Vaginal fractional carbon dioxide (CO 2 ) laser treatment has emerged in the past two decades as a non-surgical option for vaginal tightening. Mounting evidence supports the effectiveness and safety of this treatment for female sexual dysfunction. A newly developed vaginal tactile imaging (VTI) technique accurately evaluates the biomechanical parameters of the female pelvic floor and vagina, including tissue elasticity, pelvic support, and pelvic muscle function in high definition. In the current study, we evaluated changes in objective biomechanical parameters using VTI, following vaginal CO 2 laser treatment for vaginal tightening and sexual dysfunction. Study Design/Materials and Methods: We conducted a prospective cohort between June 2018 and January 2020. Inclusion criteria were vaginal looseness, decreased local sensation during sexual intercourse, and sexual dysfunction. All the participants were treated with a vaginal carbon dioxide laser. They underwent a gynecological evaluation based on the Vaginal Health Index (VHI) and sexual function assessment according to the Female Sexual Function Index (FSFI). Vaginal biomechanical parameters were assessed by VTI. Initial evaluations were performed at the pre-treatment consult visit, 1 week prior to the first treatment and at a 6-month post-treatment follow-up visit. Results: Twenty-five women were included in the final analysis. Compared with baseline, the post-treatment mean scores for vaginal elasticity and tightening were higher (54.8 ± 5.2 vs. 41.5 ± 6.3, P = 0.0027 and 1.97 ± 0.25 vs. 1.32 ± 0.31, P = 0.0014, respectively). Post-treatment increases were demonstrated in pelvic muscle contraction strength (25.9 ± 3.5 vs. 16.5 ± 4.2, P = 0.0011) and in reflex pelvic muscle contraction (2.93 ± 0.44 vs. 2.12 ± 0.47,

Progesterone has been shown to regulate immunity during pregnancy, and progesterone administration may reduce inflammation-induced preterm labor. We sought to determine the maternal brain immune response to LPS-induced inflammation in pregnant and non-pregnant mice and whether additional progesterone supplementation attenuates this response. Pregnant (P: n = 9) and non-pregnant mice (NP: n = 9) were randomized to pretreatment with vaginal progesterone/carrier (Replens), daily from days 13 to 16. On days 15 and 16, LPS/saline was administered by intraperitoneal injection (Replens + saline n = 3; Replens + LPS n = 3; progesterone + LPS n = 3). Mice were sacrificed on day 16 and maternal serum analyzed for IL-6 levels and brains analyzed for nNOS, NF-kB, IL-6 protein levels and for immature myeloid cells (IMCs) and microglial activity. LPS significantly increased brain nNOS, NF-kB, and IL-6 in both NP and P mice, with significantly greater responses in P mice. In both NP and P groups, progesterone significantly attenuated LPS-induced increase of nNOS and NF-kB, however with no effect on serum IL-6. In the NP brains, LPS significantly increased IMC population and progesterone reduced the IMC phenotype to levels similar to controls. In P mice, neither LPS nor LPS + progesterone altered the brain IMC population. LPS significantly increased the microglial activity in both NP and P groups, which was attenuated by progesterone. Progesterone attenuates brain inflammatory response to LPS in both NP and P mice although it has no effect on systemic inflammation. In NP mice, progesterone attenuated the increase in brain IMC following LPS administration. Our results suggest that endogenous progesterone during pregnancy may protect the brain from LPS-induced inflammation.

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