RÉSUMÉ
Due to its unique intensity distribution, self-acceleration, and beam self-healing properties, Airy beam holds great potential for optical wireless communications in challenging channels, such as underwater environments. As a vital part of 6G wireless network, the Internet of Underwater Things requires high-stability, low-latency, and high-capacity underwater wireless optical communication (UWOC). Currently, the primary challenge of UWOC lies in the prevalent time-varying and complex channel characteristics. Conventional blue Gaussian beam-based systems face difficulties in underwater randomly perturbed links. In this work, we report a full-color circular auto-focusing Airy beams metasurface transmitter for reliable, large-capacity and long-distance UWOC links. The metasurface is designed to exhibits high polarization conversion efficiency over a wide band (440-640 nm), enabling an increased data transmission rate of 91% and reliable 4 K video transmission in wavelength division multiplexing (WDM) based UWOC data link. The successful application of this metasurface in challenging UWOC links establishes a foundation for underwater interconnection scenarios in 6G communication.
RÉSUMÉ
Bone morphogenetic protein and activin membrane-bound inhibitor (BAMBI) regulates mammalian ovarian follicle growth and maturation; however, its effect on luteinized granulosa cells (LGCs) in sheep ovarian follicles remains unknown. Here we explored the regulatory role of LGC functions and steroid hormone synthesis by BAMBI. Multiple sequence alignment revealed that the sheep BAMBI gene sequence was relatively conserved. Sheep LGCs were strongly positive for BAMBI. LGC proliferation increased when BAMBI was silenced and decreased when BAMBI was overexpressed. After BAMBI overexpression, the expression of CASP3, CASP8, CASP9, and BAX significantly increased, whereas that of BCL2 and the ratio of BCL2/BAX expression decreased. The opposite was observed after BAMBI silencing. CDKN1A, CCND1, and CCND2 were downregulated with BAMBI overexpression and upregulated with BAMBI silencing. Expression of steroid hormone-related genes (CYP11A1, STAR, and 3BHSD), except CYP19A1, significantly increased after BAMBI overexpression. Moreover, estrogen and progesterone secretion increased after BAMBI overexpression and decreased after BAMBI interference. The effect of the exogenous addition of bone morphogenetic protein 2 (BMP2) on GCs was similar to that of BAMBI overexpression. In conclusion, BAMBI can regulate the proliferation and steroid hormone synthesis of sheep LGCs, and BMP2 can affect LGCs as an activator of BAMBI. These findings provide a basis for further research on the physiological role of BAMBI.
Sujet(s)
Cellules de la granulosa , Stéroïdes , Femelle , Animaux , Ovis , Protéine Bax/métabolisme , Cellules cultivées , Cellules de la granulosa/métabolisme , Stéroïdes/métabolisme , Progestérone/métabolisme , Prolifération cellulaire , MammifèresRÉSUMÉ
BACKGROUND: Polyethylene glycol loxenatide (PEX-168) is a new antidiabetic drug; as such, there are not yet any reports on its weight loss effect. Therefore, this trial was designed to investigate the effect of PEX-168 on simple obese mice. METHODS: Thirty healthy male C57BL/6 mice were randomly selected and divided into a control group (NC) and an obesity model group. The high-fat diet-induced simple obesity mice were divided into a model control group (HF) and three intervention groups. The intervention groups were injected with different doses of PEX-168 intraperitoneally once a week for 12 weeks (low (LD), medium (MD) and high (HD)). Fasting blood glucose (FBG), body weight and food intake were measured from 1 to 12 weeks after PEX-168 injection. The serum insulin (INS), C-reactive protein (CRP), chemerin and omentin levels were measured after 12 weeks. RESULTS: Compared with the HF group, the low dose of PEX-168 reduced the body weight of the mice in a short period of time (8 weeks), and the mice in the MD and HD groups showed a significant decrease in body weight (P < 0.05). The low dose of PEX-168 could effectively improve the blood glucose and homeostasis model assessment of insulin resistance (Homa-IR) of the mice (FBG P < 0.05 INS, Homa-IR P < 0.001), but there was no significant difference between different doses (P > 0.05). CRP levels in the MD and HD groups were significantly improved (P < 0.05). The levels of serum chemerin and omentin in the intervention groups were also significantly improved (P < 0.01), but there was no significant difference between the different doses (P > 0.05). CONCLUSIONS: PEX-168 significantly reduced the body weight of simple obese mice and improved the insulin resistance. PEX-168 may regulate the expression of chemerin and omentin through its hypoglycaemic effect, and the weight-reducing effect of PEX-168 is unlikely to be the reason for the changes in both.
Sujet(s)
Adipokines/métabolisme , Hyperinsulinisme/traitement médicamenteux , Hypoglycémiants/pharmacologie , Inflammation/traitement médicamenteux , Obésité/traitement médicamenteux , Peptides/pharmacologie , Polyéthylène glycols/pharmacologie , Animaux , Alimentation riche en graisse , Modèles animaux de maladie humaine , Hypoglycémiants/administration et posologie , Insulinorésistance/physiologie , Mâle , Souris , Souris de lignée C57BL , Souris obèse , Peptides/administration et posologie , Polyéthylène glycols/administration et posologieRÉSUMÉ
BACKGROUND: At present, there is a lack of drug treatment for obese patients, so it is needed to find a drug that is effective and has few side effects to treat obesity. PEX-168 is a novel long-acting glucagon-like peptide-1 receptor agonist for T2DM. It improves blood glucose with fewer side effects. The aim of the present study was to investigate the effect of PEX-168 on blood glucose and body weight of mice with simple obesity. METHODS: Thirty healthy and 6-week-old C57BL/6 male mice were randomly divided into a normal control group (NC, n = 6) and obesity model group (n = 24). The obesity model mice were randomly divided into a high-fat diet group (HF) and intervention groups with different doses of PEX-168 (0.03 mg/kg, 0.1 mg/kg, and 0.3 mg/kg). Each group includes 6 mice. Body weight, food intake, and fasting blood glucose (FBG) were evaluated after intraperitoneal injection, and the intervention was performed weekly for 12 weeks. Fasting insulin (FINS) levels were measured at the 12th week. RESULTS: Compared with HF, the food intake of mice in the intervention groups decreased transiently, but there was no difference between different doses (P > 0.05). The body weight of mice in the middle and high dose of PEX-168 intervention groups decreased significantly, and the differences were statistically significant (P < 0.05). The administration of PEX-168 can effectively improve the blood glucose of obese mice, the difference was statistically significant (P < 0.05), but there was no difference between different doses (P > 0.05). At the 10th week, the incidence of transient hypoglycemia was 67% and 50% in the middle- and high-dose groups, respectively. The levels of serum FINS in the intervention groups were significantly lower than those in the HF group, and the differences were statistically significant (P < 0.05), but there was no difference between different doses (P > 0.05). CONCLUSIONS: PEX-168 showed significant improvement in the FBG and FINS levels of simple obese mice. Middle and high doses of PEX-168 could reduce the weight of simple obese mice, but there was a certain risk of hypoglycemia.
RÉSUMÉ
A variety of effector proteins contribute to host defense in Caenorhabditis elegans. However, beyond lytic enzymes and antimicrobial peptides and proteins, little is known about the exact function of these infection-related effectors. This study set out to identify pathogen-dependent cytokine-like molecules, focusing on C-type lectin domain-containing proteins (CLECs). In total, 38 CLECs that are differentially regulated in response to bacterial infections have been previously identified by microarray and transcriptome sequencing (RNA-seq) analyses in C. elegans. We successfully cloned 18 of these 38 CLECs and chose to focus on CLEC-47 because, among these 18 cloned CLECs, it was the smallest protein and was recombinantly expressed at the highest levels in prokaryotic cells examined by SDS-PAGE. Quantitative real-time PCR (qRT-PCR/qPCR) showed that the expression of clec-47 was induced by a variety of Gram-positive bacterial pathogens, including Enterococcus faecium, Staphylococcus aureus, and Cutibacterium acnes, but was suppressed by the Gram-negative bacteria Klebsiella pneumoniae and Pseudomonas aeruginosa. By expressing CLEC-47 in HEK 293 cells, we showed that CLEC-47 is released into the culture media, which the Golgi apparatus inhibitors (brefeldin A [BFA] and GolgiStop) could block. Purified recombinant CLEC-47 (maltose binding protein [MBP]-CLEC-47-His) did not display antimicrobial activity against ESKAPE pathogen isolates but bound directly to murine macrophage J774A.1 cells. Recombinant CLEC-47 attracted and recruited J774A.1 cells in a chemotaxis assay. In addition, qPCR studies and enzyme-linked immunosorbent assays (ELISAs) showed that CLEC-47 activates J774A.1 cells in a dose- and time-dependent manner to express the proinflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin-1ß (IL-1ß), IL-6, and Macrophage Inflammatory Protein 2 (MIP-2). Moreover, C. elegans, fed with CLEC-47-expressing Escherichia coli, demonstrated enhanced expression of several antimicrobial proteins (CNC-1, CNC-2, CPR-1, and CPR-2) as well as the detoxification protein MTL-1. These data suggest that CLEC-47 functions as a novel cytokine-like signaling molecule and exemplify how the study of infection-related effectors in C. elegans can help elucidate the evolution of immune responses. IMPORTANCE A variety of effector proteins contribute to host defense in the nematode Caenorhabditis elegans. However, little is known about the exact function of these infection-related effectors beyond lytic enzymes and antimicrobial peptides and proteins. This study set out to identify pathogen-dependent cytokine-like molecules, and we focus on the C-type lectin domain-containing proteins (CLECs). Our data suggest that CLEC-47 functions as a novel cytokine-like signaling molecule and exemplify how the study of infection-related effectors in nematodes can help elucidate the evolution of immune responses.