Investigation on the contribution of swim bladder to hearing in crucian carp (Carassius carassius).

The swim bladder in some teleost fish functions to transfer the sound energy of acoustic stimuli to the inner ears. This study uses the auditory evoked potential tests, micro-computed tomography scanning, reconstruction, and numerical modeling to assess the contribution of the swim bladder to hearing in crucian carp (Carassius carassius). The auditory evoked potential results show that, at the tested frequency range, the audiogram of fish with an intact swim bladder linearly increases, ranging from 100 to 600 Hz. Over this frequency, the sound pressure thresholds have a local lowest value at 800 Hz. The mean auditory threshold of fish with an intact swim bladder is lower than that of fish with a deflated swim bladder by 0.8-20.7 dB. Furthermore, numerical simulations show that the received pressure of the intact swim bladders occurs at a mean peak frequency of 826 ± 13.6 Hz, and no peak response is found in the deflated swim bladders. The increased sensitivity of reception in sound pressure and acceleration are 34.4 dB re 1 µPa and 40.3 dB re 1 m·s-2 at the natural frequency of swim bladder, respectively. Both electrophysiological measurement and numerical simulation results show that the swim bladder can potentially extend hearing bandwidth and further enhance auditory sensitivity in C. carassius.

Fc Fragment of IgE Receptor Ig (FCER1G) acts as a key gene involved in cancer immune infiltration and tumour microenvironment.

Although recent studies have revealed the relationship between Fc Fragment of IgE Receptor Ig (FCER1G) and human tumours, there is still a lack of a more comprehensive pan-cancer analysis of FCER1G as an immune-related gene. In this study, we investigated the expression pattern and prognostic value of FCER1G based on multiple databases. Subsequently, we further explored the role of FCER1G in tumour proliferation and metastasis, as well as its genomic alterations and DNA methylation levels, we next assessed the association between FCER1G and the immune infiltrating cells of the tumour microenvironment in different cancers and verified it by immunohistochemical staining. The correlation between FCER1G and immune checkpoint genes expression and its predictive power in the immune checkpoint blockade treatment cohorts were used to evaluate the importance of FCER1G in immunotherapy. Enrichment analysis of FCER1G-associated partners was also performed. In addition, we substantiated the expression of FCER1G in specific cell types of different tumours using single-cell RNA sequencing data from different databases. Our research results showed that FCER1G is up-regulated in most tumour. Positive associations were found between FCER1G expression and tumour prognosis, proliferation, and metastasis, we also found that FCER1G is closely related to the tumour microenvironment and tumour immunity. Moreover, FCER1G-associated partners were enriched in pathways associated with neutrophils activation. Finally, we confirmed that FCER1G was mainly expressed in monocyte/macrophages of the tumour microenvironment. In conclusion, our findings provided a comprehensive understanding of FCER1G in oncogenesis and tumour immunology among various tumours and demonstrated its potential value in prognosis prediction and tumour immunotherapy.

Differentiation of umbilical cord mesenchymal stem cells into hepatocytes with CYP450 metabolic enzyme activity induced by a liver injury microenvironment.

The aim of this study was to observe the effect of a simulated liver tissue injury microenvironment on the directed differentiation of umbilical cord mesenchymal stem cells into hepatocytes with CYP450 metabolic activity in vitro, and to explore the mechanisms underlying this directed differentiation. Normal and damaged liver tissue homogenate supernatants (LHS and CCl4-LHS, respectively) were used as induction fluids. After induction for different durations, Western blot and RT-PCR were used to measure the protein and gene expression of the hepatocellular proteins AFP, CK18, ALB, and the CYP450 family. Simultaneously, the metabolic activity of CYP450 in hepatocytes was determined. Compared with the LHS and CCl4-LHS controls, the LHS and CCl4-LHS induction groups showed a significantly elevated protein and gene expression of AFP, CK18, ALB, CYP1A1/2, CYP2A6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4 (P < 0.05). The metabolic activity of CYP450 in hepatocytes was increased (P < 0.05). In addition, compared with the LHS group, the CCl4-LHS group induced cell differentiation more rapidly and with a higher efficiency. The results suggested that a liver injury microenvironment is conducive for the directed differentiation of umbilical cord mesenchymal stem cells into hepatocytes with metabolic enzyme activity.

PCSK9 involves in the high-fat diet-induced abnormal testicular function of male mice.

In brief: Impaired spermatogenesis resulting from disturbed cholesterol metabolism due to intake of high-fat diet (HFD) has been widely recognized, however, the role of preprotein invertase subtilin 9 (PCSK9), which is a negative regulator of cholesterol metabolism, has never been reported. This study aims to reveal the role of PCSK9 on spermatogenesis induced by HFD in mice. Abstract: Long-term consumption of a high-fat diet (HFD) is an important factor that leads to impaired spermatogenesis exhibiting poor sperm quantity and quality. However, the mechanism of this is yet to be elucidated. Disrupted cholesterol homeostasis is one of many crucial pathological factors which could contribute to impaired spermatogenesis. As a negative regulator of cholesterol metabolism, preprotein invertase subtilin 9 (PCSK9) mediates low density lipoprotein receptor (LDLR) degradation to the lysosome, thereby reducing the expression of LDLR on the cell membrane and increasing serum low-density lipoprotein cholesterol level, resulting in lipid metabolism disorders. Here, we aim to study whether PCSK9 is a pathological factor for impaired spermatogenesis induced by HFD and the underlying mechanism. To meet the purpose of our study, we utilized wild-type C57BL/6 male mice and PCSK9 knockout mice with same background as experimental subjects and alirocumab, a PCSK9 inhibitor, was used for treatment. Results indicated that HFD induced higher PCSK9 expression in serum, liver, and testes, and serum PCSK9 is negatively correlated with spermatogenesis, while both PCSK9 inhibitor treatment and PCSK9 knockout methodologies ameliorated impaired lipid metabolism and spermatogenesis in mice fed a HFD. This could be due to the overexpression of PCSK9 induced by HFD leading to dyslipidemia, resulting in testicular lipotoxicity, thus activating the Bcl-2-Bax-Caspase3 apoptosis signaling pathway in testes, particularly in Leydig cells. Our study demonstrates that PCSK9 is an important pathological factor in the dysfunction of spermatogenesis in mice induced by HFD. This finding could provide innovative ideas for the diagnosis and treatment of male infertility.

The spatial variation and driving factors of soil total carbon and nitrogen in the Heihe River source region.

Soil carbon and nitrogen levels are key indicators of soil fertility and are used to assess ecological value and safeguard the environment. Previous studies have focused on the contributions of vegetation, topography, physical and chemical qualities, and meteorology to soil carbon and nitrogen change, but there has been little consideration of landscape and ecological environment types as potential driving forces. The study investigated the horizontal and vertical distribution and influencing factors of total carbon and total nitrogen in soil at 0-20 and 20-50 cm depths in the source region of the Heihe River. A total of 16 influencing factors related to soil, vegetation, landscape, and ecological environment were selected, and their individual and synergistic effects on the distributions of total carbon and total nitrogen in soil were assessed. The results show gradually decreasing average values of soil total carbon and total nitrogen from the surface layer to the bottom layer, with larger values in the southeast part of the sampling region and smaller values in the northwest. Larger values of soil total carbon and total nitrogen at sampling points are distributed in areas with higher clay and silt and lower soil bulk density, pH, and sand. For environmental factors, larger values of soil total carbon and total nitrogen are distributed in areas with higher annual rainfall, net primary productivity, vegetation index, and urban building index, and lower surface moisture, maximum patch index, boundary density, and bare soil index. Among soil factors, soil bulk density and silt are most closely associated with soil total carbon and total nitrogen. Among surface factors, vegetation index, soil erosion, and urban building index have the greatest influence on vertical distribution, and maximum patch index, surface moisture, and net primary productivity have the greatest influence on horizontal distribution. In conclusion, vegetation, landscape, and soil physical properties all have a significant impact on the distribution of soil carbon and nitrogen, suggesting better strategies to improve soil fertility.

Activation of SGLT3a in endometrial epithelial cells induces paracrine stromal cell decidualization.

Endometrial epithelial cells (EECs) and stromal cells (ESCs) have a close functional association. During the peri-implantation period, EECs with enhanced functional activities secrete a variety of paracrine factors to promote the decidualization of ESCs. However, little is known about the specific process by which EECs secrete paracrine factors to induce the decidualization of ESCs. Some evidence suggests that the activation of sodium-glucose cotransporter 3a (SGLT3a) induces the depolarization of ESCs to affect their function. Therefore, SGLT3a acts as a sensor molecule in certain cell types. In this study, the expression of SGLT3a was investigated in EECs to determine whether its levels increased during the peri-implantation period in female mice. The activation of SGLT3a in mouse EECs induced Na+ -dependent depolarization of the cell membrane and an influx of extracellular Ca2+ , which further promoted the expression and release of the paracrine factors prostaglandin E2 (PGE2) and F2-alpha (PGF2α) by upregulating the expression of cyclooxygenase-2. In turn, PGE2 and PGF2α induced the decidualization of ESCs. Importantly, we identified SGLT3a as a key molecule involved in the cross-talk between EECs and ESCs during the process of uterine decidualization.

Investigation on whistle directivity in the Indo-Pacific humpback dolphin (Sousa chinensis) through numerical modeling.

Odontocetes have evolved special acoustic structures in the forehead to modulate echolocation and communication signals into directional beams to facilitate feeding and social behaviors. Whistle directivity was addressed for the Indo-Pacific humpback dolphin (Sousa chinensis) by developing numerical models in the current paper. Directivity was first examined at the fundamental frequency 5 kHz, and simulations were then extended to the harmonics of 10, 15, 20, 25, and 30 kHz. At 5 kHz, the -3 dB beam widths in the vertical and horizontal planes were 149.3° and 119.4°, corresponding to the directivity indexes (DIs) of 4.4 and 5.4 dB, respectively. More importantly, we incorporated directivity of the fundamental frequency and harmonics to produce an overall beam, resulting in -3 dB beam widths of 77.2° and 62.9° and DIs of 8.2 and 9.7 dB in the vertical and horizontal planes, respectively. Harmonics can enhance the directivity of fundamental frequency by 3.8 and 4.3 dB, respectively. These results suggested the transmission system can modulate whistles into directional projection, and harmonics can improve DI.

Contribution of high-fat diet-induced PCSK9 upregulation to a mouse model of PCOS is mediated partly by SREBP2.

The incidence of polycystic ovary syndrome (PCOS) due to high-fat diet (HFD) consumption has been increasing significantly. However, the mechanism by which a HFD contributes to the pathogenesis of PCOS has not been elucidated. Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a key protein that regulates cholesterol metabolism. Our previous study revealed abnormally high PCSK9 levels in serum from patients with PCOS and in serum and hepatic and ovarian tissues from PCOS model mice, suggesting that PCSK9 is involved in the pathogenesis of PCOS. However, the factor that induces high PCSK9 expression in PCOS remains unclear. In this study, Pcsk9 knockout mice were used to further explore the role of PCSK9 in PCOS. We also studied the effects of a HFD on the expression of PCSK9 and sterol regulatory element-binding protein 2 (SREBP2), a regulator of cholesterol homeostasis and a key transcription factor that regulates the expression of PCSK9, and the roles of these proteins in PCOS pathology. Our results indicated HFD may play an important role by inducing abnormally high PCSK9 expression via SREBP2 upregulation. We further investigated the effects of an effective SREBP inhibitor, fatostain, and found that it could reduce HFD-induced PCSK9 expression, ameliorate hyperlipidemia and improve follicular development in PCOS model mice. Our study thus further elucidates the important role of an HFD in the pathogenesis of PCOS and provides a new clue in the prevention and treatment of this disorder.

Lnc-STYK1-2 regulates bladder cancer cell proliferation, migration, and invasion by targeting miR-146b-5p expression and AKT/STAT3/NF-kB signaling.

BACKGROUND: Epigenetic modulation by noncoding RNAs substantially contributes to human cancer development, but noncoding RNAs involvement in bladder cancer remains poorly understood. This study investigated the role of long noncoding RNA (lncRNA) lnc-STYK1-2 in tumorigenesis in cancerous bladder cells. METHODS: Differential lncRNA and mRNA profiles were characterized by high-throughput RNA sequencing combined with validation via quantitative PCR. Bladder cancer cell proliferation was assessed through MTS, and bladder cancer cell migration and invasion were assessed through a Transwell system. The in vivo tumorigenesis of bladder cancer cells was evaluated using the cancer cell line-based xenograft model. The dual-luciferase reporter assay verified the association of miR-146b-5p with lnc-STYK1-2 and the target gene. Protein abundances and phosphorylation were detected by Western blotting. RESULTS: Alterations in lncRNA profiles, including decreased lnc-STYK1-2 expression, were detected in bladder cancer tissues compared with adjacent noncancerous tissues. lnc-STYK1-2 silencing effectively promoted proliferation, migration, and invasion in two bladder cancer cell lines, 5637 and T24, and their tumorigenesis in nude mice. lnc-STYK1-2 siRNA promoted miR-146b-5p and reduced ITGA2 expression in bladder cancer cells. Moreover, miR-146b-5p suppressed ITGA2 expression in bladder cancer cells through direct association. Also, lnc-STYK1-2 directly associated with miR-146b-5p. Finally, miR-146b-5p inhibitors abrogated the alterations in bladder cell functions, ITGA2 expression, and phosphorylation of AKT, STAT3, and P65 proteins in 5637 and T24 cells induced by lnc-STYK1-2 silencing. CONCLUSION: lnc-STYK1-2 inhibited bladder cancer cell proliferation, migration, and tumorigenesis by targeting miR-146b-5p to regulate ITGA2 expression and AKT/STAT3/NF-kB signaling.

Numerical-modeling-based investigation of sound transmission and reception in the short-finned pilot whale (Globicephala macrorhynchus).

The sound-transmission, beam-formation, and sound-reception processes of a short-finned pilot whale (Globicephala macrorhynchus) were investigated using computed tomography (CT) scanning and numerical simulation. The results showed that sound propagations in the forehead were modulated by the upper jaw, air components, and soft tissues, which attributed to the beam formation in the external acoustic field. These structures owned different acoustic impedance and formed a multiphasic sound transmission system that can modulate sounds into a beam. The reception pathways composed of the solid mandible and acoustic fats in the lower head conducted sounds into the tympano-periotic complex. In the simulations, sounds were emitted in the forehead transmission system and propagated into water to interrogate a steel cylinder. The resulting echoes can be interpreted from multiple perspectives, including amplitude, waveform, and spectrum, to obtain the acoustic cues of the steel cylinder. By taking the short-finned pilot whale as an example, this study provides meaningful information to further deepen our understanding of biosonar system operations, and may expand sound-reception theory in odontocetes.

Progesterone-induced miR-152 interferes with embryonic implantation by downregulating GLUT3 in endometrial epithelium.

To investigate the role of progesterone-induced micro-RNA (miR)-152 in early embryonic development and implantation by regulating GLUT3 in endometrial epithelium, qRT-PCR was used to detect the expression of miR-152, GLUT1, and GLUT3 in the endometrial epithelial cells of female mice. GLUT1 and GLUT3 proteins were detected by immunohistochemical staining in the mouse endometrial epithelium. Bioinformatics prediction associated with a luciferase assay was performed to determine whether GLUT1 and GLUT3 are target genes of miR-152. Specific miR-152 mimics or inhibitors were transfected into the endometrial epithelial cells to, respectively, overexpress or downregulate miR-152. Next, the glucose concentration of uterine fluid was measured by conducting high-performance liquid chromatography in vivo, and the glucose uptake of the endometrial epithelial cells was observed using a fluorometric assay in vitro. Early embryonic development and implantation were also observed after the miR-152 mimics or inhibitors had been transfected. Embryo transfer was observed after the miR-152 mimic transfection. miR-152 was found to directly target and thereby downregulate GLUT3 expression. The expressions of both miR-152 and GLUT3 in the mouse endometrial epithelium had spatiotemporal characteristics on days 1-4 of pregnancy. miR-152 affected the glucose concentration of uterine fluid and the glucose uptake of endometrial epithelial cells. The transfection of specific miR-152 mimics led to impaired embryonic development and implantation. To conclude, in endometrial epithelial cells, progesterone-induced miR-152 downregulates GLUT3 at the posttranscriptional level to maintain a proper glucose concentration in the uterine fluid, which is necessary for early embryonic development and implantation.

[Progesterone-induced microRNA-1a inhibits the proliferation of endometrial epithelial cells].

The aim of the present study was to investigate the effects of progesterone (P4)-induced microRNA-1a (miR-1a) on the proliferation of endometrial epithelial cells (EECs) and the underlying mechanism. In vivo, following subcutaneous injection of estradiol (E2) alone (E2 group) or combined injections of E2 and P4 (E2P4 group) in ovariectomized mice, quantitative real-time PCR (qPCR) was used to check the expression of miR-1a-3p in the directly isolated mouse EECs. The agomir or antagomir specific for miR-1a-3p was injected into one side of the uterine horns of ovariectomized mice pretreated with E2 alone or in combination with P4, and the non-specific control agomir or antagomir was injected into their contralateral horns. Flow cytometry was used to analyze the cell cycle of EECs. Immunohistochemistry (IHC) was used to examine the location and expression of cyclin D2, cyclin E1, and cyclin E2 in the uterine tissue sections. In vitro, primary cultured mouse EECs were pretreated with E2 alone (E2 group) or in combination with P4 (E2P4 group). qPCR was used to detect the expression of miR-1a-3p. Exogenous mimic of miR-1a-3p was transfected into E2-pretreated EECs, and EdU incorporation analysis was used to test the proliferation activity of the EECs. The result of in vivo experiment showed that the expression of miR-1a-3p in E2P4 group was significantly higher than that in E2 group (P < 0.05). The miR-1a-3p agomir arrested cell cycle at G1 to S transition in the mice injected subcutaneously with E2 alone (P < 0.05). Conversely, silencing of miR-1a-3p with transfection of miR-1a-3p antagomir promoted the entry of cells into S phase in the mice injected subcutaneously with both E2 and P4 (P < 0.05). The expressions of cyclin E1 and cyclin E2, except for cyclin D2, in uterine sections were also dramatically reduced by miR-1a-3p overexpression in the uterine epithelium (P < 0.05). In vitro, miR-1a-3p was not expressed in the cells of both E2 and E2P4 groups. The mimic of miR-1a-3p decreased EECs proliferation activity (P < 0.05). These results indicate that P4-induced miR-1a can inhibit the expression of cyclin E1 and cyclin E2, consequently suppressing the proliferation of mouse EECs by arresting cells at G1/S phase.

Relocalisation and activation of integrins induced rapidly by oestrogen via G-protein-coupled receptor 30 in mouse blastocysts.

Integrins are the dominant and final adhesion molecules in the attachment process between the blastocysts and endometrium. It is necessary for oestrogen to rapidly activate mouse blastocysts so that they attach to the endometrial epithelium. Our previous study suggested that oestrogen can rapidly induce an increase in intracellular calcium in mouse blastocysts via G-protein-coupled receptor 30 (GPR30). Thus, we deduced that integrins may be involved in GPR30 mediation of the fast effect of oestrogen on mouse blastocysts in implantation. To prove our hypothesis, we used immunofluorescence staining and in vitro coculture of mouse blastocysts and endometrial epithelial cell line (EECs), Ishikawa cells, in the present study. We found that αv and ß1 integrin clustered in mouse blastocysts, and that ß3 integrin was relocalised to the apical membrane of blastocyst cells when embryos were treated with 1 µM 17ß-estradiol (E2), 1 µM E2 conjugated to bovine serum albumin (E2-BSA) and 1 µM G-1, a specific GPR30 agonist, for 30 min respectively, whereas pretreatment with 1 µM G15, a specific GPR30 antagonist, and 5 µM 1,2-Bis(2-aminophenoxy)ethane-N,N,N'',N''-tetraacetic acid tetrakis (acetoxymethyl ester)(BAPTA/AM), a cellular Ca2+ chelator, blocked the localisation of integrins induced by oestrogen via GPR30 in mouse blastocyst cells. E2, E2-BSA and G-1 increased the fibronectin (FN)-binding activity of integrins in blastocysts, whereas G15 and BAPTA/AM blocked the activation of integrins induced by oestrogen via GPR30 in mouse blastocysts. Inhibition of integrins by Arg-Gly-Asp peptide in blastocysts resulted in their failure to adhere to EECs in vitro, even if oestrogen or G-1 was provided. Together, the results indicate the fast effect of oestrogen via the GPR30 membrane receptor further induces relocalisation and activation of integrins in mouse blastocysts, which play important roles in the adhesion of blastocysts to EECs.

[Estrogen induced rapid increase of intracellular calcium plays important role in the implantation of mouse blastocysts].

OBJECTIVE: To study the roles of the increased intracellular calcium induced rapidly by estrogen in the implantation of mouse blastocysts. METHODS: The mouse blastocysts were collected from the female mice on the pregnant day 4, divided into 3 groups: control, E2-BSA and BAPTA +E2-BSA. Immunofluorescence staining, confocal microscopy, embryo and endometrial epithenial cells co-culture and embryo transfer were used to investigate the effect of increased intracellular calcium induced by E2-BSA on the expression and localization of integrins in blastocysts and their adhesion to endometrial epithenial calls (EECs) and implantation into the endometrium. RESULTS: The increase of intracellular calcium induced rapidly by estrogen could cause the cluster and relocation of integrin av and beta3, and BAPTA might block this effect, the adhesion rate of blastocysts in contol group was 35.5%, BAPTA +E2-BSA group was 26.7% and significantly lower than 65.6% of E2-BSA group (P<0.05), and the implantation rate in BAPTA+E2-BSA group was 11.8%, which was significantly lower than 52.9% of E2-BSA group (P<0.05). CONCLUSION: The rapid increase of intracellular calcium induced by estrogen may cause the relocalization of integrin in blastocysts and their adhesion to ECCs, which is important in the process of implantation.

Effects of expression of exogenous cyclin G1 on proliferation of human endometrial carcinoma cells.

Cyclin G1 is the only cyclin that has either positive or negative effects on cell growth. Our previous study found decreased expression of cyclin G1 in human endometrial carcinoma tissues compared with normal endometrial tissues. The study aimed to evaluate cyclin G1 expression and its effect on proliferation of human endometrial carcinoma cells (ECCs). Cyclin G1-GFP (green fluorescence protein) plasmid was constructed and transfected into various differentiated human ECCs, including Ishikawa, HEC-1-B and KLE cells, and proliferation of the transfected cells was determined by the CCK-8 method. Exogenous cyclin G1 mRNA and protein were measured by RT-PCR and Western blot, respectively, and GFP signal was monitored by fluorescence microscopy. Chinese hamster ovary (CHO) cells were transfected with the same constructs as a cell control. Cyclin G1-GFP-transfected Ishikawa cells were further treated with MG132, an inhibitor of proteasome, to analyze if low expression of cyclin G1 is related to its abnormal degradation in ECCs. Ectopic expression of exogenous cyclin G1 was found to significantly suppress the proliferation of Ishikawa and HEC-1-B cells but not KLE cells. Compared with cyclin G1-transfected CHO cells, exogenous cyclin G1 protein expression was low in Ishikawa and HEC-1-B cells, and was undetectable in KLE cells. However, all ECC lines and CHO cells expressed similar levels of exogenous cyclin G1 and GFP mRNA. MG132 treatment increased cyclin G1 protein expression in cyclin G1-GFP-transfected Ishikawa cells. This is the first study to present evidence to suggest that cyclin G1 exerts negative control on proliferation of ECCs. Exogenous cyclin G1 shows different protein expression levels in ECCs with different malignancies, and cyclin G1 protein is highly unstable and is rapidly degraded in ECCs.

Identification and Characterization of Two Novel Extracellular ß-Glucanases from Chaetomium globosum against Fusarium sporotrichioides.

Chaetomium globosum can inhibit the growth of fusarium by means of their extracellular proteins. Two novel ß-glucanases, designated Cgglu17A and Cgglu16B, were separated from the supernatant of C. globosum W7 and verified to have the ability to hydrolyze cell walls of Fusarium sporotrichioides MLS-19. Cgglu17A (397 amino acids) was classified as glycoside hydrolase family 17 while Cgglu16B belongs to the family16 (284 amino acids). Recombinant protein Cgglu17A was successfully expressed in Escherichia coli, and the enzymes were purified by affinity chromatography. Maximum activity of Cgglu17A appeared at the pH 5.5 and temperature 50 °C, but Cgglu16B shows the maximum activity at the pH 5.0 and temperature 50 °C. Most of heavy metal ions had inhibition effect on the two enzymes, but Cgglu17A and Cgglu16B were respectively activated by Ba2+ and Mn2+. Cgglu17A exhibited high substrate specificity, almost only catalyzing the cleavage of ß-1,3-glycosidic bond, in various polysaccharose, to liberate glucose. However, Cgglu16B showed high catalytic activities to both ß-1,3-glycosidic and ß-1,3-1,4-glycosidic bonds. Cgglu17A was an exo-glucanase, but Cgglu16B was an endo-glucanase based on hydrolytic properties assay. Both of two enzymes showed potential antifungal activity, and the synergistic effect was observed in the germination experiment of pathogenic fungus. In conclusion, Cgglu17A (exo-1,3-ß-glucanase) and Cgglu16B (endo-1,3(4)-ß-glucanase) were confirmed to play a key role in the process of C. globosum controlling fusarium and have potential application value on industry and agriculture for the first time.

Underwater acoustic metamaterials.

Acoustic metamaterials have been widely investigated over the past few decades and have realized acoustic parameters that are not achievable using conventional materials. After demonstrating that locally resonant acoustic metamaterials are capable of acting as subwavelength unit cells, researchers have evaluated the possibility of breaking the classical limitations of the material mass density and bulk modulus. Combined with theoretical analysis, additive manufacturing and engineering applications, acoustic metamaterials have demonstrated extraordinary capabilities, including negative refraction, cloaking, beam formation and super-resolution imaging. Owing to the complexity of impedance boundaries and mode transitions, there are still challenges in freely manipulating acoustic propagation in an underwater environment. This review summarizes the developments in underwater acoustic metamaterials over the past 20 years, which include underwater acoustic invisibility cloaking, underwater beam formation, underwater metasurfaces and phase engineering, underwater topological acoustics and underwater acoustic metamaterial absorbers. With the evolution of underwater metamaterials and the timeline of scientific advances, underwater acoustic metamaterials have demonstrated exciting applications in underwater resource development, target recognition, imaging, noise reduction, navigation and communication.

Expression of aldose reductase in mouse endometrial epithelial cells and its role in sperm capacitation.

The survival, motility and capacitation of sperm in the female reproductive tract are important prerequisites for fertilization. The uterus is the main location for sperm capacitation. One of the most important physiological functions of the endometrial epithelium is to create a suitable uterine environment under the regulation of ovarian hormones, to ensure sperm capacitation. The composition of uterine fluid directly affects sperm capacitation. Fructose is an important component of semen that supports sperm viability and motility. Aldose reductase, a rate-limiting enzyme in the polyol pathway, metabolizes sorbitol and fructose, thereby supplying cells with necessary energy for functional activities. Existing studies have reported the presence aldose reductase in the endometrium, leading us to hypothesize that its expression in endometrial epithelium might promote sperm capacitation by maintaining the uterine environment. Yet, the mechanism of regulation has not been clarified. In this study, we investigated the expression of aldose reductase in mouse endometrial epithelium and its potential role in sperm capacitation. We initially investigated the periodic characteristics of glucose, fructose and sorbitol in uterine fluid. We then studied the temporal and spatial characteristics of aldose reductase in the endometrial epithelium. Next, we examined the effect of aldose reductase on glucose, fructose and sorbitol in uterine fluid. Finally, we explored the effect of aldose reductase on sperm capacitation and fertilization. The results showed that glucose and fructose content in uterine fluid and the expression of aldose reductase fluctuated periodically during physiological periods. Inhibition of aldose reductase in the endometrial epithelium interfered with sperm capacitation and fertilization by reducing the fructose levels in the uterine fluid. To conclude, the aldose reductase-mediated polyol pathway in endometrial epithelial cells is essential to maintain an appropriate fructose environment in the uterine fluid for sperm capacitation and fertilization.

Hyperandrogen-induced polyol pathway flux increase affects ovarian function in polycystic ovary syndrome via excessive oxidative stress.

AIMS: Polycystic ovary syndrome (PCOS) is a common endocrine disorder in the women of childbearing age. It is characterized by hyperandrogenism and abnormal follicular growth and ovulation. The polyol pathway is a glucose metabolism bypass pathway initiated by aldose reductase (ADR). Androgen induces the expression of ADR in the male reproductive tract, which has a general physiological significance for male reproductive function. Here we investigate whether hyperandrogenemia in PCOS leads to increased flux of the polyol pathway in ovarian tissue, which in turn affects follicular maturation and ovulation through oxidative stress. MAIN METHODS: We used clinical epidemiological methods to collect serum and granulosa cells from clinical subjects for a clinical case-control study. At the same time, cell biology and molecular biology techniques were used to conduct animal and cell experiments to further explore the mechanism of hyperandrogen-induced ovarian polyol pathway hyperactivity and damage to ovarian function. KEY FINDINGS: Here, we find that hyperandrogenism of PCOS can induce the expression of ovarian aldose reductase, which leads to the increase of the polyol pathway flux, and affects ovarian function through excessive oxidative stress. SIGNIFICANCE: Our research has enriched the pathological mechanism of PCOS and may provide a new clue for the clinical treatment of PCOS.

[PP2A is involved in the inhibitory effect of progesterone on proliferation of mouse endometrial epithelial cells].

OBJECTIVE: To study the effect of protein phosphatase 2A (PP2A) in the negative regulation of progesterone on the proliferation of mouse endometrial epithelial cells (EECs). METHODS: Mouse EECs were isolated and cultured in vitro, which were divided into four groups when they grown to confluence: control group (P4) was treated with 1 micromol/L progesterone only, group A, B and C were treated respectively with 1 micromol/L progesterone and different concentrations of okadaic acid (5 nmol/L, 10 nmol/L and 20 nmol/L). After 24 h, the numbers of cells in different phases of the cell cycle were counted with flow cytometry. RESULTS: The effect of OA on mouse EECs was concentration-dependent. Compared with control group of P4, the change of cell cycle procession in group A was not obvious. Lower proportion of cells in G1 and G2/M phase and higher proportion of cells in S phase in group B, higher proportion of cells in G1 and S phase and lower proportion of cells in G2/M phase in group C were observed. CONCLUSION: Adequate dose OA inhibiting PP2A could release the inhibitory effect of progesterone on proliferation of mouse EECs obviously, this suggested that PP2A was involved in the inhibitory effect of progesterone on proliferation of EECs by influencing the process of cell cycle.