The phosphatidylinositol 3-kinase (Pi3K)/protein kinase B (aKT) signaling pathway is involved in the regulation of multiple cellular physiological processes by activating downstream corresponding effector molecules, which serve an important role in the cell cycle, growth and proliferation. This is a common phenomenon; overactivation of the pathway is present in human malignancies and has been implicated in cancer progression, hence one of the important approaches to the treatment of tumors is rational drug design using molecular targets in the Pi3K/aKT signaling pathway. in brief, the present review analyzed the effects of the Pi3K/aKT signaling pathway on certain gynecological cancer types. Contents 1. introduction 2. composition and function of the Pi3K/aKT signaling pathway 3. association between Pi3K/aKT and endometrial cancer 4. association between Pi3K/aKT and cervical cancer 5. association between Pi3K/aKT and ovarian cancer 6. current status of treatment for the Pi3K/aKT signaling pathway 7. conclusion

Ammonia stress can inhibit the survival and growth, and even cause mortality of shrimp. In this study, ammonia-metabolizing enzyme activities and gene expression were compared between two strains of L. vannamei under different ammonia-N (NH4+) concentrations (3.4, 13.8, and 24.6 mg/L). The results showed that elevated ammonia concentrations mainly increased glutamine synthetase (GSase) activities while inhibiting transglutaminase (TGase) activities in the muscle of both strains. Thus, we concluded that L. vannamei could accelerate the synthesis of glutamine from glutamate and NH4+ to alleviate ammonia stress. Compared with the muscle, the hepatopancreas plays a major role in ammonia stress and might be a target tissue to respond to the ammonia stress. Compared to the control group, the treatment of high ammonia concentrations reduced the hepatopancreas TGase (TG) gene expression and increased the gene expression rates of glutamate dehydrogenase-β (GDH-β) and GSase (GS) in both the muscle and the hepatopancreas of the two strains (p < 0.05). These genes (GDH-β and GS) in strain B were not only expressed earlier but also at levels higher than the expression range of strain A. At the gene level, strain B showed a more rapid and positive response than strain A. These data might help reveal the physiological responses mechanisms of shrimp adapt to ammonia stress and speed up the selective breeding process in L. vannamei.

This study aimed to evaluate the clinical significance of pretreatment red cell distribution width (RDW), monocyte/lymphocyte ratio (MLR), neutrophil/lymphocyte ratio (NLR), and platelet/lymphocyte ratio (PLR) in patients with urothelial carcinoma of the bladder (UCB).Hematological parameters of 127 consecutive patients with UCB and 162 healthy controls were retrospectively analyzed. Receiver operating characteristic curve was plotted to determine the optimal cut-off value of RDW, MLR, NLR, and PLR to predict UCB. Whether these parameters could be independent predictors of UCB and had an association with the demographics and clinical characteristics of patients were also assessed.Patients with UCB had higher pretreatment RDW, MLR, NLR, and PLR compared with the healthy controls. With the tumor progression, MLR, NLR, and PLR rose consistently, whereas no significant difference was observed in RDW across tumor stages. NLR and PLR were associated with tumor size and tumor grade, while MLR was correlated with tumor size only. The best threshold of RDW, MLR, NLR, and PLR to predict UCB was 13.50%, 0.26, 2.16, and 128.46, respectively. Multivariate logistic regression model identified NLR ≥ 2.16 (odds ratio [OR] = 2.914; P < .001) and PLR ≥ 128.46 (OR = 2.761; P < .001) as independent predictors of UCB. High NLR and PLR were also associated with tumor markers, such as carcinoembryonic antigen and α-fetoprotein.Pretreatment NLR and PLR could be significant independent predictors of UCB. These simple and readily available inflammatory markers therefore might be used to manage the disease.

Taurine‐upregulated gene 1 (TUG1), a kind of long non‐coding RNAs (lncRNAs), was up‐regulated in ischaemic stroke (IS) with the function of promoting neuron apoptosis. In this study, we aimed to investigate the association of TUG1 polymorphisms with IS risk. The TUG1 polymorphisms were genotyped using a custom‐by‐design 48‐Plex SNPscan kit. The promoter activity was measured using the dual luciferase reporter assay. Relative expression of TUG1 in IS patients was analysed using quantitative PCR and the binding of TUG1 https://www.ncbi.nlm.nih.gov/SNP/snp_ref.cgi?type=rs%26rs=rs2240183 polymorphism to transcription factor was analysed using chromatin immunoprecipitation (ChIP) assay. The https://www.ncbi.nlm.nih.gov/SNP/snp_ref.cgi?type=rs%26rs=rs2240183 CT/CC genotypes and C allele in the promoter of TUG1 were associated with an increased risk of IS (CT/CC vs. TT: adjusted OR = 1.70, 95% CI, 1.16‐2.49, P = 0.006; C vs. T: adjusted OR = 1.47, 95% CI, 1.12‐1.93, P = 0.005). Logistic regression analysis showed that the https://www.ncbi.nlm.nih.gov/SNP/snp_ref.cgi?type=rs%26rs=rs2240183 was a risk factor of IS besides TC, TG, HDL‐C, LDL‐C, VLDL‐C, Apo‐A1, Apo‐B and NEFA. Further functional analysis revealed that the TUG1 https://www.ncbi.nlm.nih.gov/SNP/snp_ref.cgi?type=rs%26rs=rs2240183 C allele exhibited higher transcriptional activity and TUG1 expression levels (P < 0.01). The ChIP assay showed that the https://www.ncbi.nlm.nih.gov/SNP/snp_ref.cgi?type=rs%26rs=rs2240183 C allele binds to transcriptional factor GATA‐1. These findings indicate that the https://www.ncbi.nlm.nih.gov/SNP/snp_ref.cgi?type=rs%26rs=rs2240183 C allele was associated with a higher risk of IS possibly by binding to GATA‐1 and elevating TUG1 levels.