Growth Hormone Cotreatment for Low-Prognosis Patients According to the POSEIDON Criteria.

Background: Poor ovarian response (POR) remains one of the most challenging conditions in assisted reproduction technology. Previous studies seemed to indicate that growth hormone (GH) was a potential solution for the dilemma of POR; however, the role GH played on the low-prognosis patients diagnosed and stratified by the POSEIDON criteria remains indistinct. Methods: This retrospective study was performed among women with POR according to the POSEIDON criteria who failed a previous in vitro fertilization (IVF)/intracytoplasmic sperm injection (ICSI) cycle, and the subsequent cycle was under GH cotreatment and conducted within 12 months. These participants were stratified into four groups according to the POSEIDON criteria. The comparison was implemented between the failed cycle and the cycle treated with GH. Generalized estimating equation (GEE) multivariate regression was applied for data analysis. Results: A total of 428 low-prognosis women were included in this study. GH supplementation improved the live birth rates (47.66%, 28.33%, 45.45%, and 24.07%; in groups 1, 2, 3, and 4, respectively) and the clinical pregnancy rates (OR 19.16, 95% CI 7.87-46.63, p < 0.001; OR 7.44, 95% CI 1.65-33.55, p = 0.009; OR 10.19, 95% CI 2.39-43.52, p = 0.002; OR 27.63, 95% CI 4.46-171.11, p < 0.001; in groups 1, 2, 3, and 4, respectively) in all four POSEIDON groups. The number of oocytes retrieved was significantly elevated in the subgroups with normal ovarian reserve (IRR 1.47, 95% CI 1.36-1.59, p < 0.001; IRR 1.31, 95% CI 1.15-1.49, p < 0.001; in groups 1 and 2, respectively). The number of day-3 good-quality embryos was significantly elevated in the subgroups with either normal ovarian reserve or aged young (IRR 2.13, 95% CI 1.78-2.56, p < 0.001; IRR 1.54, 95% CI 1.26-1.89, p < 0.001; IRR 1.47, 95% CI 1.10-1.98, p = 0.010; in groups 1, 2, and 3, respectively). Conclusion: Growth hormone cotreatment could ameliorate the pregnancy outcome for women with POR under the POSEIDON criteria who failed a previous IVF/ICSI cycle. The application of growth hormone for low-prognosis women who experienced a failed cycle might be considered and further studied.

Gas6/Axl signaling pathway promotes proliferation, migration and invasion and inhibits apoptosis in A549 cells.

Several studies have demonstrated that growth arrest-specific protein 6 (Gas6) and Axl are highly expressed in various tumor tissues, such as renal cell and esophageal carcinoma. However, the effect of the Gas6/Axl signaling pathway on lung adenocarcinoma is still unclear. The aim of the present study was to investigate the effect of the Gas6/Axl signaling pathway on lung adenocarcinoma cells and its mechanism of action, which may provide a novel target for the clinical treatment of lung adenocarcinoma. Human lung adenocarcinoma tissues were used to examine the activation of the Gas6/Axl signaling pathway. In addition, the human lung adenocarcinoma cell line A549 was employed to study the effects of the Gas6/Axl signaling pathway on the proliferation, migration, invasion and apoptosis of lung adenocarcinoma cells. Recombinant human Gas6 protein and inhibitor TP-0903 were used to activate and inhibit the Gas6/Axl signaling pathway, respectively. The results revealed that Gas6 and Axl expression level was increased in human lung adenocarcinoma tissues compared with adjacent healthy tissues. After inhibition of the Gas6/Axl signaling pathway with TP-0903, p21, p53, caspase 3, caspase 8 and caspase 9 exhibited higher expression level in A549 cells. The opposite effect was observed when the Gas6/Axl signaling pathway was activated. In addition, the migratory and invasive ability of A549 cells was determined via wound-healing and Transwell invasion assays. The results indicated that the migratory and invasive ability of A549 cells was significantly increased when the Gas6/Axl signaling pathway was activated and inhibition of Gas6/Axl signaling pathway caused the opposite results. Activity of Gas6/Axl signaling pathway was shown to be positively associated with cell proliferation by Cell Counting Kit 8 and clone formation assays. In conclusion, the Gas6/Axl signaling pathway was revealed to promote the proliferation, migration and invasion and inhibit the apoptosis of lung adenocarcinoma cells, which serve important roles in the progression of lung adenocarcinoma.

The Effect of Placing Flow-Diverting Stents in Intracranial Collateral Arteries of Miniature Pig.

BACKGROUND Flow-diverting stent (FDS) has been suggested as an effective intracranial aneurysm treatment. However, the effects of FDS on collateral branches of an aneurysm parent artery still remain unknown. Thus, the present study aimed to comprehensively evaluate the effects of placing a FDS in the intracranial collateral artery, using a miniature pig animal model. MATERIAL AND METHODS Ten healthy miniature pigs were included in the study: one pig was reserved as a control and the remaining nine pigs were placed in three experimental groups: FDS (i.e., Pipeline), LVIS, and Solitaier-AB stent groups. Pigs in the experimental groups were examined by cerebral angiography immediately after stent placement, followed by hemodynamic analyses. In addition, magnetic resonance imaging (MRI) of the brain of pigs in the experimental groups was performed to inspect the brain for obstruction and blood flow. Stents were examined for the growth of neointimas. RESULTS The results showed that neointimas, consisting of smooth muscle cells, collagenous fibers, and macrophages, were 0.67 mm thick on average and partially covered the stent wires. The thickness of neointimas in the FDS group was significantly higher than in the two conventional intracranial stent groups. There was no obvious obstruction identified in collateral arteries where the FDS was placed. CONCLUSIONS These results indicated that neointimas in collateral arteries of a miniature pig would be slightly thickened after one month of FDS placement; and FDS was shown to be safe for collateral arteries.