Lymphangioleiomyomatosis and pregnancy: a mini-review.

Lymphangioleiomyomatosis(LAM) is a slow progressive, rare cystic lung disease in women of reproductive age, associated with infiltration of the lung by atypical smooth muscle like cells, leading to the cystic destruction of the lung parenchyma. As LAM exclusively affects women of childbearing age, it can arise or exacerbate during pregnancy. Many patients with LAM are discouraged from pregnancy, although there is not much objective evidence effect on fertility. Patients diagnosed with LAM during pregnancy experience worse outcomes, so the safety of pregnancy is a vexing problem. What was worse, treatment strategies are limited on the effects of LAM on pregnancy outcomes. Pregnancy could be considered in LAM patients. Successful delivery in women with LAM depends on the condition of the LAM, which is in turn dependent on obstetricians and respiratory physicians. In this review, we describe the epidemiology, pathogenesis, diagnosis, clinical features and the treatment strategies of LAM during pregnancy.

Rac1 promotes the lipopolysaccharide-induced inflammatory response and contraction-associated proteins (CAPs) expression in mouse uterine smooth muscle cells.

Activation of the maternal immune system leads to a downstream cascade of proinflammatory events that culminate in the activation of spontaneous uterine contractions, which is associated with preterm birth. Ras-related C3 botulinum toxin substrate 1 (Rac1) is a crucial protein related to cell contraction and inflammation. The main purpose of this study was to explore the role and function of Rac1's regulation of inflammation through in- vivo and in-vitro experiments. Rac1 inhibitor was used in animal model of preterm birth and cells isolated from the uterine tissues of pregnant mice on gestational day 16 were transfected with adenovirus to knockdown or overexpress Rac1 and treated with the Calcium-calmodulin-dependent protein kinase II (CaMKII) inhibitor KN93. The expression of Rac1, uterine contraction-associated proteins (CAPs) (COX-2 and Connexin43), and inflammatory cytokines, were assessed by Western blotting and RTPCR. LPS upregulated Rac1, COX-2 and Connexin43 expression in uterine smooth muscle cells (USMCs). The expression of inflammatory cytokines, COX-2, and Connexin43 was significantly decreased in shRac1-transfected cells compared with cells stimulated with LPS only. Rac1 overexpression led to an increase in the expression of inflammatory cytokines, COX-2, and Connexin43. Furthermore, after Rac1 overexpression, KN93 reduced the expression of uterine contraction-associated proteins and inflammatory cytokines. It is thought that the effect of Rac1 on inflammatory cytokine and contraction-associated protein expression in USMCs is mediated by CaMKII. Rac1 can modulate the expression of contraction-associated proteins and inflammatory cytokines through the CaMKII pathway. Rac1 could be an effective therapeutic target for improving the outcome of preterm birth.

A Systematic Review and Meta-analysis of the Analgesic Effects of Lidocaine Administered Intravenously or Intraperitoneally Post-Abdominal Surgery.

BACKGROUND: Reducing postoperative pain is still a tremendous challenge for perioperative clinicians. Lidocaine is a local anesthetic that belongs to the amide class and has anti-inflammatory, anti-hyperalgesic, and analgesic effects. Extensive research has been conducted to determine the optimal route for its administration. OBJECTIVE: To compare the efficacy of perioperative intravenous lidocaine with that of intraperitoneal lidocaine on postoperative analgesia in patients undergoing abdominal surgery. STUDY DESIGN: EMBASE, PubMed, and The Cochrane Library were searched for randomized controlled trials published through December 2022 that compared patients receiving perioperative intravenous lidocaine with those receiving intraperitoneal lidocaine. The primary outcome measures included the pain score, as evaluated by the Visual Analog Scale, and opioid analgesia requirements. The secondary outcome measures were hospitalization length, gastrointestinal function recovery, etc. The data were acquired and recorded in electronic spreadsheets that had been designed for this purpose. METHODS: This systematic review's design was based on the Cochrane Handbook for Systematic Reviews of Interventions and was reported in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) statement. The Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) method was used to examine the certainty of the evidence. Furthermore, we examined the dependability of the calculated (favorable) treatment effects through considerations of information size and modified significance thresholds (trial sequential analysis). RESULTS: Seven trials including 478 patients were included. Our meta-analysis demonstrates that compared with intravenous lidocaine, patients who received intraperitoneal lidocaine had lower pain scores at 4 hours (mean difference [MD] 1.40; 95% CI, 0.22 to 2.59); 12 hours (MD 0.18; 95% CI, 0.06 to 0.30); and 24 hours (MD -0.12; 95% CI -0.40 to 0.17) postsurgery. However, no obvious difference in opioid consumption (P > 0.05) was found. In addition, the intraperitoneal lidocaine group had a longer postsurgery hospital stay than the intravenous lidocaine group (95%CI, -0.17 to -0.00; I2 = 0%). Intravenous lidocaine was more beneficial for achieving gastrointestinal return than intraperitoneal lidocaine (95% CI, -0.26 to -0.10; I2 = 2%). LIMITATIONS: The sample size of enrolled RCTs was small, which could potentially result in an overestimation or underestimation of the treatment effect in the collected data. There was high heterogeneity among the studies. CONCLUSION: This meta-analysis suggests that post-abdominal surgery intraperitoneal lidocaine administration has a better analgesic effect than intravenous lidocaine, with a lower pain score. However, intravenous lidocaine is more beneficial for gastrointestinal recovery after abdominal surgery.

Effect of carbamylated erythropoietin on neuronal apoptosis in fetal rats during intrauterine hypoxic-ischemic encephalopathy

BACKGROUND: Hypoxic-ischemic encephalopathy (HIE) is a common disease that occurs during the perinatal period. The primary cause of neonatal HIE is related to fetal intrauterine anoxia. Carbamylated erythropoietin (CEPO), a derivative of erythropoietin (EPO), does not exert any erythropoietic effect; however, the neuroprotective effects resemble those of EPO. Previous studies have shown the potential benefits of CEPO on the central nervous system. The present study aimed to investigate the role of CEPO in neuronal apoptosis during intrauterine HIE and the underlying mechanisms. RESULTS: To validate our hypothesis, we established an intrauterine HIE model by occluding the bilateral uteroovarian arteries of pregnant Sprague-Dawley rats. Compared to the I/R group, neuronal apoptosis in the CEPO group was significantly lower at 4, 12, 24, and 48 h (P < 0.05). CEPO significantly inhibited CC3 expression (P < 0.05) during the early-stages after ischemia-reperfusion (0.5, 4, 8, 12 and 24 h), upregulated Bcl-2 expression, and downregulated Bax expression at 4, 8, 12, and 24 h (P < 0.05). CONCLUSIONS: Carbamylated erythropoietin pretreatment inhibited the expression of proapoptotic protein CC3 in brain and regulated the Bcl-2/Bax ratio, resulting in reduced neuronal apoptosis and thus resulting in a protective effect on intrauterine HIE.