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Thruster-assisted position mooring (PM) systems use both mooring lines and thrusters for station keeping of marine structures in ocean environments. To operate in an energy-efficient manner in moderate sea conditions, setpoints need to be appropriately chosen for the setpoint controller, so that the mooring system counteracts main environmental loads, while the thrusters reduce oscillatory motions of the marine structure. In this paper, reinforcement learning is used to design a decision-making agent for setpoint selection. In particular, a deep deterministic policy gradient (DDPG) approach is adopted with the powerful actor–critic architecture to continuously modify the setpoint setting at an optimal position. Extensive numerical experiments demonstrated that with the DDPG-based PM system, the intelligent agent is able to successfully identify the optimal positioning region in an unknown and stochastic environment, and the power consumption of the thrusters is maintained at a considerably low level.

The obstacle avoidance problem of autonomous surface vessels (ASV) has attracted the attention of the marine control research community for long years. Out of safety consideration, it is important for ASV to avoid all kinds of obstacles like shores, cliffs, floaters and other vessels. Developing a heading and path planning strategy for ASV is the main task and the remaining challenge. Traditional obstacle avoidance algorithms lead to too much computing in working environment. The issue of computation cost can be solved by training obstacle avoidance models with reinforcement learning (RL). By using the RL method, the ASV will choose the most efficient action according to the ASV’s experience it learned from the past. In this paper, RL is adopted to design a decision-making agent for obstacle avoidance. To train the obstacle avoidance model under a sparse feedback environment, hierarchical reinforcement learning (HRL) method is applied. Using this algorithm, better obstacle avoidance performance and longer survival time can be achieved. Memory pool modification and target network modification are also used to smooth the training process of the ASV. Simulation results demonstrate that HRL can make the learning process of un-manned ship’s obstacle avoidance smoother and more effective. Also, the living time of ASVs is improved.

Protein folding in the cell is regulated by several quality-control mechanisms. Correct folding of glycoproteins in the endoplasmic reticulum (ER) is tightly monitored by the recognition of glycan signals by lectins in the ER-associated degradation (ERAD) pathway. In mammals, mannose trimming from N-glycans is crucial for disposal of misfolded glycoproteins. The mannosidases responsible for this process are ER mannosidase I and ER degradation–enhancing α-mannosidase–like proteins (EDEMs). However, the molecular mechanism of mannose removal by EDEMs remains unclear, partly owing to the difficulty of reconstituting mannosidase activity in vitro. Here, our analysis of EDEM3-mediated mannose-trimming activity on a misfolded glycoprotein revealed that ERp46, an ER-resident oxidoreductase, associates stably with EDEM3. This interaction, which depended on the redox activity of ERp46, involved formation of a disulfide bond between the cysteine residues of the ERp46 redox-active sites and the EDEM3 α-mannosidase domain. In a defined in vitro system consisting of recombinant proteins purified from HEK293 cells, the mannose-trimming activity of EDEM3 toward the model misfolded substrate, the glycoprotein T-cell receptor α locus (TCRα), was reconstituted only when ERp46 had established a covalent interaction with EDEM3. On the basis of these findings, we propose that disposal of misfolded glycoproteins through mannose trimming is tightly connected to redox-mediated regulation in the ER.

Soybean isoflavones (SIs) are phytoestrogens that competitive with estrogens in body. Although SIs play an important role in reproduction, their role in testicular development in roosters is unknown. This study was conducted to investigate the effect of SIs on testicular development and serum reproductive hormone profiles in young breeder roosters (70-133days old). Gene expression of steroidogenic acute regulatory protein (StAR), cholesterol side-chain cleavage enzyme (P450scc), and 3β-hydroxysteroid dehydrogenase (3β-HSD), which are related to testosterone synthesis, in rooster testis were also evaluated after treatment with different SI doses. Although SIs had no significant effect on body weight, 5mg/kg SIs significantly increased the testis index and serum levels of reproductive hormones (gonadotropin releasing hormone, follicle- stimulating hormone, luteinizing hormone, and testosterone).To further investigate whether SIs regulate hormone synthesis via StAR, p450scc, 3β-HSD, real time-PCR was performed to measure the mRNA levels of the corresponding genes. The results showed that 5mg/kg of SIs significantly increased StAR mRNA levels. However, there were no significant effects on p450scc or 3β-HSD mRNA levels. Moreover, the spermatogonial development and the number of germ cell layers were increased by treatment with 5mg/kg of SIs. These results suggest that SIs promote testicular growth by increasing reproductive hormone secretion, which is closely related to StAR expression, to positively regulate reproduction in young roosters.

Thyroid hormone (TH) is important for normal reproductive functions and dysregulation of TH support is associated with reproductive disorders. We have previously reported that 3,5,3'-triiodothyronine (T₃) increases follicle stimulating hormone (FSH)-induced preantral follicle growth in vitro. Interaction of hormones with apoptosis and proliferation of granulosa cells is poorly understood. The present study investigated the role and the mechanism of T₃ and/or FSH on granulosa cell apoptosis and proliferation. Granulosa cells harvested from DES-primed immature rats were exposed to T₃ (1 nM) and/or FSH (100 ng/ml) for 24-48 h. We demonstrated by TUNEL assays that the hormones prevented cells from C8-ceramide-induced apoptosis. The Src/PI3K/Akt pathway was involved in the regulation of granulosa cell survival. While ineffective alone, T₃ significantly enhanced the proliferating cell nuclear antigen (PCNA) content of FSH-induced granulosa cells, consistent with the cell number pattern after treatment. Moreover, the action of the hormones on cell proliferation was also shown to be mediated by the Src/PI3K/Akt pathway. Taken together, these results suggest that T₃ potentiates the cell survival action of FSH through inhibiting cell apoptosis and promoting cell proliferation. Moreover, the protective and survival effects of hormones are mediated by the activation of Src/PI3K/Akt pathway.