Pregnancy outcomes in infertile patients with endometrial hyperplasia with or without atypia undergoing in vitro fertilization: the early-follicular long protocol is superior to midluteal long protocol.

Background: Although in vitro fertilization (IVF) in infertile patients with endometrial hyperplasia is common after drug treatment, the pregnancy outcomes are often unsatisfactory. Till date, no studies have reported the outcome of patients with endometrial hyperplasia treated using early-follicular long (EL) protocol and midluteal long (ML) protocol. Objective: To evaluate the pregnancy outcomes and disease prognosis of patients with endometrial hyperplasia with or without atypia undergoing IVF treatment with EL protocol or ML protocol. Methods: This was a retrospective study in university-affiliated reproductive medical center. A total of 138 patients with endometrial hyperplasia undergoing IVF treatment were included to compare the pregnancy outcomes and disease prognosis between EL and ML protocols. We further matched 276 patients with normal endometrium to compare the pregnancy outcomes between patients with endometrial hyperplasia and patients with normal endometrium under different controlled ovarian stimulation (COS) protocol. Results: In patients with endometrial hyperplasia, the clinical pregnancy rate (CPR) and live birth rate (LBR) were significantly higher in EL protocol than in ML protocol (61.8% vs. 43.5%, P=0.032; 50.0% vs. 30.6%, P= 0.022). In the ML protocol, patients with endometrial hyperplasia had significantly lower CPR and LBR than those with normal endometrium (43.5% vs. 59.7%, P=0.037; 30.6% vs. 49.2%, P=0.016). While in the EL protocol, they achieved similar CPR and LBR as patients with normal endometrium (61.8% vs. 69.7%, P=0.232; 50.0% vs. 59.9%, P=0.156). In patients with endometrial hyperplasia, COS protocol was an independent factor affecting clinical pregnancy (adjusted odds ratio [OR] 2.479; 95% confidence interval [CI] 1.154-5.327) and live birth (adjusted OR 2.730; 95% CI 1.249-5.966). After 1-10 years of follow-up, no significant difference was found in the recurrence rate of endometrial lesions between both treatment groups. Conclusions: For patients with endometrial hyperplasia undergoing IVF treatment, the EL protocol is superior to ML protocol, and in the EL protocol, they can achieve similar pregnancy outcomes as patients with normal endometrium.

Leaf cuticular lipids on the Shandong and Yukon ecotypes of saltwater cress, Eutrema salsugineum, and their response to water deficiency and impact on cuticle permeability.

The impact of water-deficit stress on leaf cuticular waxes and cutin monomers, and traits associated with cuticle permeability were examined in Shandong and Yukon ecotypes of Eutrema salsugineum (syn. Thellungiella salsuginea). Although Shandong exhibits glaucous leaves, and Yukon is non-glaucous, wax amounts on non-stressed Yukon leaves were 4.6-fold higher than on Shandong, due mainly to Yukon's eightfold higher wax fatty acids, especially the C22 and C24 acid homologues. Water deficit caused a 26.9% increase in total waxes on Shandong leaves, due mainly to increased C22 and C24 acids; and caused 10.2% more wax on Yukon, due mainly to an increase in wax alkanes. Total cutin monomers on non-stressed leaves of Yukon were 58.3% higher than on Shandong. Water deficit caused a 28.2% increase in total cutin monomers on Shandong, whereas total cutin monomers were not induced on Yukon. With or without stress, more abundant cuticle lipids were generally associated with lower water loss rates, lower chlorophyll efflux rates and an extended time before water deficit-induced wilting. In response to water deficit, Shandong showed elevated transcription of genes encoding elongase subunits, consistent with the higher stress induction of acids by Shandong. Yukon's higher induction of CER1 and CER3 transcripts may explain why alkanes increased most on Yukon after water deficit. Eutrema, with its diverse cuticle lipids and responsiveness, provides a valuable genetic resource for identifying new genes and alleles effecting cuticle metabolism, and lays groundwork for studies of the cuticle's role in extreme stress tolerance.

Relationship between the autoantibody and expression of ß3-adrenoceptor in lung and heart.

BACKGROUND: Evidences suggest that ß3 -adrenoceptor (ß3-AR) plays an important role in heart failure (HF), although no data is reported indicating how these effects may change with the increasing age. Pulmonary congestion and edema are the major life-threatening complications associated with HF. The purpose of this study is to explore the relationship between the anti-ß3-AR autoantibody and the expression of ß3-AR in the lungs and heart for both aged patients and rats with HF. METHODS: Synthetic ß3-AR peptides served as the target antigens in ELISA were used to screen the anti-ß3-AR autoantibody in aged patients and rats. Two aged rat models were constructed based on aortic banding and sham-operation. The expression of ß3-AR mRNA and protein in the lung and heart was measured in intervention and non-intervention groups by Western blot analysis at the baseline, 5(th), 7(th), 9(th) and 11(th) week, respectively. RESULTS: The frequency and titer of anti-ß3-AR autoantibody in aged patients and rats with HF were higher than those in the control group (p<0.05). The expression of ß3-AR mRNA and protein in pulmonary tissues decreased continually from the 7(th) week (p<0.05), followed by HF observed during the 9(th) week. The expression of ß3-AR in myocardial tissues continued to increase after the 9(th) week (p<0.05), and the expression of both ß3-AR mRNA and protein in the BRL group [HF group with BRL37344 (4-[-[2-hydroxy-(3-chlorophenyl)ethyl-amino] phenoxyacetic acid) (a ß3-AR agonist) injection] was positively correlated with BRL37344 when compared with non-BRL group (HF group without BRL37344 injection) (p<0.05). CONCLUSION: Anti-ß3-AR autoantibody was detected in aged patients and rats with HF. The expression of ß3-AR mRNA and protein in pulmonary tissues decreased continually, and began earlier than in the heart, but its expression in myocardial tissues increased continually and could be further promoted by ß3-AR agonist.

Inhibition of ubiquitin protein expression and 20S proteasome activity by irbesartan prevents post-infarction ventricular remodeling and decreases TNF-α generation.

Myocardial infarction (MI) may induce severe alterations of the cardiac contractile function that may, in turn, lead to heart failure (HF). The ubiquitin-proteasome system (UPS) plays a critical role in cardiac remodeling following MI. Angiotensin II type 1 receptor (AT1R) blockers effectively prevent left ventricular (LV) remodeling. However, it has not been elucidated whether the preventive effect of AT1R-blockers on LV remodeling is mediated through the UPS pathway. In the present study, with the use of cardiac morphometric parameters, haemodynamic measurements and enzyme-linked immunosorbent assay, we demonstrated that post-ischemic HF rats exhibited a significant increase in ventricular remodeling and irbesartan was effective in reversing cardiac remodeling. The expression of TNF-α, ubiquitin protein and 20S proteasome were significantly increased in the MI control group and irbesartan was shown to dose-dependently inhibit the expression of TNF-α, ubiquitin protein and 20S proteasome. In conclusion, it was hypothesized that UPS signaling is involved in ventricular remodeling following MI and the mechanism underlying the effect of irbesartan on ventricular remodeling may be associated with the downregulation of the expression of TNF-α, ubiquitin protein and 20S proteasome.