Clinical prognostic significance of xeroderma pigmentosum group C and IFN­Î³ in non­small cell lung cancer.

Lung cancer is the most common cancer in the world due to its high incidence and recurrence. Genetic instability is one of the main factors leading to its occurrence, development and poor prognosis. Decreased xeroderma pigmentosum group C (XPC) expression notably enhances the stem cell properties of lung cancer cells and increases their proliferation and migration. Additionally, patients with lung cancer and low XPC expression had a poor prognosis. The purpose of the present study was to analyze the effect of XPC and IFN-γ on the clinical prognosis of patients with non-small cell lung cancer (NSCLC). Lung adenocarcinoma specimens were collected from a total of 140 patients with NSCLC. Additionally, from these 140 patients, 48 paracarcinoma tissue specimens were also collected, which were later used to construct tissue microarrays. The expression of XPC and IFN-γ in cancer tissues and in paraneoplastic tissues was detected using immunohistochemistry. The prognosis and overall survival of patients were determined through telephone follow-up. The results showed a positive correlation between expression of XPC and IFN-γ in NSCLC. Additionally, high expression of both markers was associated with a favorable prognosis in patients with NSCLC. The aforementioned findings suggest that the expression of XPC and IFN-γ has prognostic value in clinical practice and is expected to become a marker for clinical application.

IncRNA AC004943.2 regulates miR-135a-5p and PTK2/P13K axis to promote laryngeal squamous cell carcinoma progression.

Long noncoding RNAs (lncRNAs) are involved in regulatory processes in laryngeal squamous cell carcinoma (LSCC) at posttranscriptional epigenetic modification level. Yet, the function and underlying mechanism behind lncRNA AC004943.2 in LSCC is still obscure. Therefore, the potential role of AC004943.2 in LSCC progression was investigated. The expression of gene or protein was tested by real-time quantitative polymerase chain reaction and western blot. MTT, colony formation, wound healing, and transwell experiments were applied to detect LSCC cell viability, proliferation, migration and invasion, respectively. The interaction among AC004943.2, miR-135a-5p, and protein tyrosine kinase 2 (PTK2) were analyzed by bioinformatics prediction and luciferase assay. AC004943.2 was highly expressed in LSCC cells compared with normal human bronchial epithelial cells, while miR-135a-5p was lowly expressed. AC004943.2 knockdown or miR-135a-5p overexpression inhibited LSCC cell viability, proliferation, migration and invasion. Mechanistically, AC004943.2 increased PTK2 expression in LSCC cells by sponging miR-135a-5p. Furthermore, miR-135a-5p knockdown inverted the inhibitory effect of AC004943.2 silencing on LSCC cell malignant behaviors. MiR-135a-5p upregulation attenuated the PTK2/PI3K pathway to inhibit progression of LSCC. AC004943.2 facilitated the cancerous phenotypes of LSCC cells by activating the PTK2/PI3K pathway through targeting miR-135a-5p, which furnished a therapeutic candidate for LSCC treatment.

Mg2+ addition: Unlocking optimized treatment performance and anti-fouling property in microalgal-bacterial membrane bioreactors.

While microalgal-bacterial membrane bioreactors (microalgal-bacterial MBRs) have risen as an important technique in the realm of sustainable wastewater treatment, the membrane fouling caused by free microalgae is still a significant challenge to cost-effective operation of the microalgal-bacterial MBRs. Addressing this imperative, the current study investigated the influence of magnesium ion (Mg2+) addition on the biological dynamics and membrane fouling characteristics of the laboratory-scale submerged microalgal-bacterial MBRs. The results showed that Mg2+, important in augmenting photosynthetic process, yielded a biomass concentration of 2.92 ± 0.06 g/L and chlorophyll-a/MLSS (mixed liquor suspended solids) of 33.95 ± 1.44 mg/g in the RMg (Mg2+ addition test group). Such augmentation culminated in elevated total nitrogen and phosphorus removal efficiencies, clocking 81.73 % and 80.98 % respectively in RMg. Remarkably, despite the enhanced microalgae activity and concentration in RMg, the TMP growth rate declined by a significant 46.8 % compared to R0. Detailed characterizations attributed reduced membrane fouling of RMg to a synergy of enlarged floc size and reduced EPS contents. This transformation is intrinsically linked to the bridging action of Mg2+ and its role in creating a non-stressed ecological environment for the microalgal-bacterial MBR. In conclusion, the addition of Mg2+ in the microalgal-bacterial MBR appears an efficient approach, improving the efficiency of pollutant treatment and mitigating fouling, which potentially revolutionizes cost-effective applications and propels the broader acceptance of microalgal-bacterial MBRs. It also of great importance to promote the development and application of microalgal-bacterial wastewater treatment technology.

Semantic embedding based online cross-modal hashing method.

Hashing has been extensively utilized in cross-modal retrieval due to its high efficiency in handling large-scale, high-dimensional data. However, most existing cross-modal hashing methods operate as offline learning models, which learn hash codes in a batch-based manner and prove to be inefficient for streaming data. Recently, several online cross-modal hashing methods have been proposed to address the streaming data scenario. Nevertheless, these methods fail to fully leverage the semantic information and accurately optimize hashing in a discrete fashion. As a result, both the accuracy and efficiency of online cross-modal hashing methods are not ideal. To address these issues, this paper introduces the Semantic Embedding-based Online Cross-modal Hashing (SEOCH) method, which integrates semantic information exploitation and online learning into a unified framework. To exploit the semantic information, we map the semantic labels to a latent semantic space and construct a semantic similarity matrix to preserve the similarity between new data and existing data in the Hamming space. Moreover, we employ a discrete optimization strategy to enhance the efficiency of cross-modal retrieval for online hashing. Through extensive experiments on two publicly available multi-label datasets, we demonstrate the superiority of the SEOCH method.

Harnessing diurnal dynamics: Deciphering the interplay of light cycles on algal-bacterial membrane bioreactors.

Light profoundly modulates the algal-bacterial membrane bioreactor (algal-bacterial MBR) performance. Yet, its outdoor deployment grapples with the inherent diurnal cycle of sunlight, engendering suboptimal light conditions. The adaptability of such systems to these fluctuating light conditions and their implications for practical outdoor applications remained an under-explored frontier. In response, this study meticulously scrutinized two laboratory-scale algal-bacterial MBRs under varying light regimes: a 24-h continuous and a 12-h cyclic illumination. Over 70 days, continuous illumination was observed to yield superior biomass production and total nitrogen and total phosphorus removal efficiencies compared to its cyclic counterpart. Contrarily, when focusing on membrane fouling, the 12-h cyclic illumination exhibited lower membrane fouling. The spectral analyses coupled with adhesion ability evaluation, traced the enhanced membrane fouling under continuous illumination to the elevated organics and heightened adhesive properties of the flocs. Given the tangible benefits of reduced membrane fouling and the potential harnessing of solar radiation, the 12-h cyclic illumination emerges as an economically astute operational paradigm for algal-bacterial MBRs. The significance of this study is to promote the application of algal-bacterial MBR in sewage treatment and provide robust support for the development of green technology in the future.

Optimizing aeration intensity to enhance self-flocculation in algal-bacterial symbiosis systems.

Effectuating optimal wastewater treatment via algae-bacterial symbiosis (ABS) systems necessitates the precise selection of aeration intensity. This study pioneers an in-depth investigation into the interplay of aeration intensity on the microalgal-bacterial consortia's self-flocculation efficacy and the overall treatment performance within ABS systems. The research provides evidence for a direct association between aeration intensity and biomass proliferation, indicating enhanced pollutant removal efficiency with escalated intensities (1.0 and 1.5 L min-1), though the variance lacks statistical significance. The peak self-flocculation efficacy of the microalgal-bacterial consortium (82.39% at 30 min) was manifested at an aeration intensity of 1.0 L min-1. The meticulous analysis of biomass properties showed the complexity of self-flocculation capacity in the consortium, which involves a dynamic interplay of several pivotal factors, including floc size, zeta potential, and EPS content. In situations where these factors pose conflicting influences, the determining factor emerges as the dominant influencer. In this study, the optimal aeration intensity was identified as 1 L min-1, shedding light on the critical threshold for ABS system operation. This study not only enriches the understanding of microalgal-bacterial wastewater treatment mechanisms but also fosters innovative strategies to enhance the performance of such systems.

Sulindac selectively induces autophagic apoptosis of GABAergic neurons and alters motor behaviour in zebrafish.

Nonsteroidal anti-inflammatory drugs compose one of the most widely used classes of medications, but the risks for early development remain controversial, especially in the nervous system. Here, we utilized zebrafish larvae to assess the potentially toxic effects of nonsteroidal anti-inflammatory drugs and found that sulindac can selectively induce apoptosis of GABAergic neurons in the brains of zebrafish larvae brains. Zebrafish larvae exhibit hyperactive behaviour after sulindac exposure. We also found that akt1 is selectively expressed in GABAergic neurons and that SC97 (an Akt1 activator) and exogenous akt1 mRNA can reverse the apoptosis caused by sulindac. Further studies showed that sulindac binds to retinoid X receptor alpha (RXRα) and induces autophagy in GABAergic neurons, leading to activation of the mitochondrial apoptotic pathway. Finally, we verified that sulindac can lead to hyperactivity and selectively induce GABAergic neuron apoptosis in mice. These findings suggest that excessive use of sulindac may lead to early neurodevelopmental toxicity and increase the risk of hyperactivity, which could be associated with damage to GABAergic neurons.

Quantifying interfacial interactions for improved membrane antifouling: A novel approach using triangulation and surface element integration method.

To gain a thorough understanding of interfacial behaviors such as adhesion and flocculation controlling membrane fouling, it is necessary to simulate the actual membrane surface morphology and quantify interfacial interactions. In this work, a new method integrating the rough membrane morphology reconstruction technology (atomic force microscopy (AFM) combining with triangulation technique), the surface element integration (SEI) method, the extended Derjaguin-Landau-Verwey-Overbeek (XDLVO) theory, the compound Simpson's approach, and the computer programming was proposed. This new method can exactly mimic the real membrane surface in terms of roughness and shape, breaking the limitation of previous fractal theory and Gaussian method where the simulated membrane surface is only statistically similar to the real rough surface, thus achieving a precise description of the interfacial interactions between sludge foulants and the real membrane surface. This method was then applied to assess the antifouling propensity of a polyvinylidene fluoride (PVDF) membrane modified with Ni-ZnO particles (NZPs). The simulated results showed that the interfacial interactions between sludge foulants in a membrane bioreactor (MBR) and the modified PVDF-NZPs membrane transformed from an attractive force to a repulsive force. The phenomenon confirmed the significant antifouling propensity of the PVDF-NZPs membrane, which is highly consistent with the experimental findings and the interfacial interactions described in previous literature, suggesting the high feasibility and reliability of the proposed method. Meanwhile, the original programming code of the quantification was also developed, which further facilitates the widespread use of this method and enhances the value of this work.

Advanced Membrane Technologies for Wastewater Treatment and Recycling.

In the face of the ever-growing severe problem of water scarcity, wastewater reuse, recycling and resource recovery are increasingly recognized as crucial part of the solution [...].

The metallic compound promotes primordial follicle activation and ameliorates fertility deficits in aged mice.

Background: Aged women and premature ovarian insufficiency (POI) patients have residual dormant primordial follicles that are hard to be activated through a physiological process. However, there are no effective and safe drugs to help them. Methods: We used the in vitro culture model of newborn mouse ovaries to identify the drugs that promote primordial follicle activation and study its mechanisms. It was verified by in vivo injection model of newborn mice and in vitro culture model of human ovarian tissue. In addition, we used the aged mice as a low infertility model to verify the effects of primordial follicle activation, and fertility by drugs. Results: Eleven metallic compounds activated mouse primordial follicles, and the five most effective compounds were selected for further study. Thapsigargin (TG), CrCl3, MnCl2, FeCl3 and ZnSO4 increased the levels of the glycolysis-related proteins (glucose transporter type 4, GLUT4; hexokinase 1, HK1; pyruvate kinase M2, PKM2; phosphofructokinase, liver type, PFKL), phosphorylated mammalian target of rapamycin (p-mTOR) in cultured mouse ovaries. The compound-promoted p-mTOR levels could be completely blocked by 2-DG (the inhibitor of glycolysis). The compounds also increased the levels of phosphorylated protein kinase B (p-Akt). TG-, CrCl3- and FeCl3-promoted p-Akt levels, but not MnCl2- and ZnSO4- promoted p-Akt levels, could be completely blocked by ISCK03 (the inhibitor of proto-oncogenic receptor tyrosine kinase, KIT). The injection of newborn mice with the compounds also activated primordial follicles and increased the levels of the glycolysis-related proteins, p-mTOR, and p-Akt. The oral administration of the compounds in adolescent and aged mice promoted primordial follicle activation, and had no obvious side effect. Importantly, ZnSO4 also increased ovulated oocytes, oocyte quality and offspring in aged mice. Furthermore, the compounds promoted human primordial follicle activation and increased the levels of the glycolysis-related proteins, p-mTOR, and p-Akt. Conclusion: The metallic compounds activate primordial follicles through the glycolysis-dependent mTOR pathway and/or the PI3K/Akt pathway, and the oral administration of ZnSO4 enhances fertility in aged mice. We suggest that these metallic compounds may be oral drugs to ameliorate fertility deficits in aged women and POI patients.

RA-RAR signaling promotes mouse vaginal opening through increasing ß-catenin expression and vaginal epithelial cell apoptosis.

BACKGROUND: Retinoic acid (RA) plays important role in the maintenance and differentiation of the Müllerian ducts during the embryonic stage via RA receptors (RARs). However, the function and mechanism of RA-RAR signaling in the vaginal opening are unknown. METHOD: We used the Rarα knockout mouse model and the wild-type ovariectomized mouse models with subcutaneous injection of RA (2.5 mg/kg) or E2 (0.1 µg/kg) to study the role and mechanism of RA-RAR signaling on the vaginal opening. The effects of Rarα deletion on Ctnnb1 mRNA levels and cell apoptosis in the vaginas were analyzed by real-time PCR and immunofluorescence, respectively. The effects of RA on the expression of ß-catenin and apoptosis in the vaginas were analyzed by real-time PCR and western blotting. The effects of E2 on RA signaling molecules were analyzed by real-time PCR and western blotting. RESULTS: RA signaling molecules were expressed in vaginal epithelial cells, and the mRNA and/or protein levels of RALDH2, RALDH3, RARα and RARγ reached a peak at the time of vaginal opening. The deletion of Rarα resulted in 25.0% of females infertility due to vaginal closure, in which the mRNA (Ctnnb1, Bak and Bax) and protein (Cleaved Caspase-3) levels were significantly decreased, and Bcl2 mRNA levels were significantly increased in the vaginas. The percentage of vaginal epithelium with TUNEL- and Cleaved Caspase-3-positive signals were also significantly decreased in Rarα-/- females with vaginal closure. Furthermore, RA supplementation of ovariectomized wild-type (WT) females significantly increased the expression of ß-catenin, active ß-catenin, BAK and BAX, and significantly decreased BCL2 expression in the vaginas. Thus, the deletion of Rarα prevents vaginal opening by reducing the vaginal ß-catenin expression and epithelial cell apoptosis. The deletion of Rarα also resulted in significant decreases in serum estradiol (E2) and vagina Raldh2/3 mRNA levels. E2 supplementation of ovariectomized WT females significantly increased the expression of RA signaling molecules in the vaginas, suggesting that the up-regulation of RA signaling molecules in the vaginas is dependent on E2 stimulation. CONCLUSION: Taken together, we propose that RA-RAR signaling in the vaginas promotes vaginal opening through increasing ß-catenin expression and vaginal epithelial cell apoptosis.

Caloric restriction remodels the hepatic chromatin landscape and bile acid metabolism by modulating the gut microbiota.

BACKGROUND: Caloric restriction (CR) has been known to promote health by reprogramming metabolism, yet little is known about how the epigenome and microbiome respond during metabolic adaptation to CR. RESULTS: We investigate chromatin modifications, gene expression, as well as alterations in microbiota in a CR mouse model. Collectively, short-term CR leads to altered gut microbial diversity and bile acid metabolism, improving energy expenditure. CR remodels the hepatic enhancer landscape at genomic loci that are enriched for binding sites for signal-responsive transcription factors, including HNF4α. These alterations reflect a dramatic reprogramming of the liver transcriptional network, including genes involved in bile acid metabolism. Transferring CR gut microbiota into mice fed with an obesogenic diet recapitulates the features of CR-related bile acid metabolism along with attenuated fatty liver. CONCLUSIONS: These findings suggest that CR-induced microbiota shapes the hepatic epigenome followed by altered expression of genes responsible for bile acid metabolism.

USP21 contributes to the aggressiveness of laryngeal cancer cells by deubiquitinating and stabilizing AURKA.

Laryngeal cancer is a usual malignant tumor of the head and neck. The role and mechanism of deubiquitinase USP21 in laryngeal cancer are still unclear. We aimed to explore whether USP21 affected laryngeal cancer progress through deubiquitinating AURKA. USP21 and AURKA levels were evaluated by qRT-PCR and Western blot. Kaplan-Meier analysis was conducted by survival package. MTT was performed to detect cell proliferation. The wound healing assay was applied to evaluate cell migration. Transwell was used to measure cell invasion. Co-IP and GST-pull down determined the interaction between USP21 and AURKA. In addition, AURKA ubiquitination levels were analyzed. USP21 was signally elevated in laryngeal cancer tissues and cells. USP21 level in clinical stages III-IV was higher than that in clinical stages I-II, and high levels of USP21 were highly correlated with poor prognosis in laryngeal cancer. USP21 inhibition suppressed AMC-HN-8 and TU686 cell proliferation, migration and invasion. Co-IP and GST-pull down confirmed the interaction between USP21 and AURKA. Knockdown of USP21 markedly increased the ubiquitination level of AURKA, and USP21 restored AURKA activity through deubiquitination. In addition, overexpression of AURKA reversed the effects of USP21 knockdown on cell growth, migration, and invasion. USP21 stabilized AURKA through deubiquitination to promote laryngeal cancer progression.

The Mature COC Promotes the Ampullary NPPC Required for Sperm Release from Porcine Oviduct Cells.

Porcine spermatozoa are stored in the oviductal isthmus after natural mating, and the number of spermatozoa is increased in the oviductal ampulla when the mature cumulus-oocyte complexes (COCs) are transferred into the ampulla. However, the mechanism is unclear. Herein, natriuretic peptide type C (NPPC) was mainly expressed in porcine ampullary epithelial cells, whereas its cognate receptor natriuretic peptide receptor 2 (NPR2) was located on the neck and the midpiece of porcine spermatozoa. NPPC increased sperm motility and intracellular Ca2+ levels, and induced sperm release from oviduct isthmic cell aggregates. These actions of NPPC were blocked by the cyclic guanosine monophosphate (cGMP)-sensitive cyclic nucleotide-gated (CNG) channel inhibitor l-cis-Diltiazem. Moreover, porcine COCs acquired the ability to promote NPPC expression in the ampullary epithelial cells when the immature COCs were induced to maturation by epidermal growth factor (EGF). Simultaneously, transforming growth factor-ß ligand 1 (TGFB1) levels were dramatically increased in the cumulus cells of the mature COCs. The addition of TGFB1 promoted NPPC expression in the ampullary epithelial cells, and the mature COC-induced NPPC was blocked by the transforming growth factor-ß type 1 receptor (TGFBR1) inhibitor SD208. Taken together, the mature COCs promote NPPC expression in the ampullae via TGF-ß signaling, and NPPC is required for the release of porcine spermatozoa from the oviduct isthmic cells.

Early-life bisphenol AP exposure impacted neurobehaviors in adulthood through microglial activation in mice.

Bisphenol AP (BPAP), a structural analog of bisphenol A (BPA), has been widely detected in environment and biota. BPAP was reported to interfere with hormone and metabolism, while limited data were available about its effects on neurobehavior, especially exposure to it during early-life time. A mouse model of early-life BPAP exposure was established to evaluate the long-term neurobehaviors in offspring. Collectively, early-life BPAP exposure caused anxiety-like behaviors and impaired learning and memory in adult offspring. Through brain bulk RNA-sequencing (RNA-seq), we found differential expressed genes were enriched in pathways related to behaviors and neurodevelopment, which were consistent with the observed phenotype. Besides, single-nucleus RNA-sequencing (snRNA-seq) showed BPAP exposure altered the transcriptome of microglia in hippocampus. Mechanistically, BPAP exposure induced inflammations in hippocampus through upregulating Iba-1 and activating the microglia. In addition, we observed that BPAP exposure could activate peripheral immunity and promote proportion of macrophages and activation of dendritic cells in the offspring. In conclusion, early-life exposure to BPAP impaired neurobehaviors in adult offspring accompanied with excessive activation of hippocampal microglia. Our findings provide new clues to the underlying mechanisms of BPAP's neurotoxic effects and therefore more cautions should be taken about BPAP.

Covalent Organic Frameworks: The Rising-Star Platforms for the Design of CO2 Separation Membranes.

Membrane-based carbon dioxide (CO2 ) capture and separation technologies have aroused great interest in industry and academia due to their great potential to combat current global warming, reduce energy consumption in chemical separation of raw materials, and achieve carbon neutrality. The emerging covalent organic frameworks (COFs) composed of organic linkers via reversible covalent bonds are a class of porous crystalline polymers with regular and extended structures. The inherent structure and customizable organic linkers give COFs high and permanent porosity, short transport channel, tunable functionality, and excellent stability, thereby enabling them rising-star alternatives for developing advanced CO2 separation membranes. Therefore, the promising research areas ranging from development of COF membranes to their separation applications have emerged. Herein, this review first introduces the main advantages of COFs as the state-of-the-art membranes in CO2 separation, including tunable pore size, modifiable surfaces property, adjustable surface charge, excellent stability. Then, the preparation approaches of COF-based membranes are systematically summarized, including in situ growth, layer-by-layer stacking, blending, and interface engineering. Subsequently, the key advances of COF-based membranes in separating various CO2 mixed gases, such as CO2 /CH4 , CO2 /H2 , CO2 /N2 , and CO2 /He, are comprehensively discussed. Finally, the current issues and further research expectations in this field are proposed.

Mitigation of protein fouling by magnesium ions and the related mechanisms in ultrafiltration process.

Although protein is an important membrane foulant in the water body that may be significantly affected by the coexisting common cation magnesium (Mg2+), the effect of Mg2+ on protein fouling is rarely reported. In this context, this study selected bovine serum albumin (BSA) as the model foulant, and investigated its fouling characteristics at different Mg2+ concentrations (0-100 mM). Filtration tests showed that the protein fouling can be significantly mitigated by adding Mg2+, and the specific filtration resistance (SFR) of pure BSA (3.56 × 1014 m kg-1) was at least 5 times that of BSA-Mg2+ solutions (0.5-100 mM). In addition, an optimal Mg2+ concentration exists, which can achieve the lowest BSA SFR. A series of characterizations indicated that the main contributors to the differences in BSA SFR were the changes in BSA adhesion capacity and the thickness and structure of the foulant layer. Basically, the above results were attributed to the hydration repulsion effect of Mg2+, which prevented tight adhesion of foulants to the membrane. Moreover, the lowest BSR SFR at 1 mM Mg2+ was achieved not only by the hydration repulsion effect but also by the particle size compression due to the conformational change of BSA molecules. This combined effect led to the lowest foulant retention on the membrane surface and delivered to the lowest SFR. This study conducts a thorough inspection into the specific effect of Mg2+ on protein fouling and provides a fresh insight into protein fouling control in the UF process.

Salt-like transcription factor 4 promotes laryngeal cancer progression through transcriptional activation of ubiquitin-specific protease 21 to stabilize Yin Yang 1.

Laryngeal cancer (LC) is a rare and challenging clinical problem. Our aim was to investigate the mechanism of salt-like transcription factor 4 (SALL4) in LC. LC tissue and paracancerous tissue were collected. Relative mRNA or protein levels were measured by quantitative real-time polymerase chain reaction or Western blot. MTT, wound healing, and transwell assay were performed to evaluate cell proliferation, migration and invasion. The binding relationship between SALL4 and USP21 promoter was verified by dual-luciferase assay and ChIP. Co-IP and glutathione-S-transferase (GST)-pull down were performed to measure the protein interaction between USP21 and YY1. Additionally, YY1 ubiquitination level was analyzed. It was found that SALL4 mRNA and SALL4 protein levels were elevated in LC clinical tissues and various LC cells. Knockdown of SALL4 inhibited epithelial-mesenchymal transition (EMT) of LC cells. USP21 was transcriptionally activated by SALL4. Co-IP and GST-pull down confirmed USP21 interacted with YY1. USP21 protected YY1 from degradation through deubiquitination. Furthermore, overexpression of USP21 reversed the effect of knockdown of SALL4 on YY1 and EMT in LC cells. In general, SALL4 facilitated EMT of LC cells through modulating USP21/YY1 axis.

High propensity of membrane fouling and the underlying mechanisms in a membrane bioreactor during occurrence of sludge bulking.

While sludge bulking often occurring in activated sludge processes generally leads to serious membrane fouling in membrane bioreactors (MBR), the underlying causes are still unclear. In this study, fouling behaviors of a MBR operated at stages of normal and sludge bulking were compared, and the fouling mechanisms of the different behaviors were explored. It was found that, the MBR could be stably operated in normal stage without membrane cleaning for about 60 days, whereas, daily membrane cleaning had to be carried out when operated in sludge bulking stage. The bulking sludge possessed a rather high specific filtration resistance (SFR) of about 1.36×1014 m·kg-1, which is over 5.33 times than that of the normal sludge. A series of characterizations demonstrated that the bulking sludge had rather lower dewaterability, smaller particle size, higher fractal dimension, higher viscosity, abundant filamentous bacteria and different functional groups of extracellular polymer sustains (EPS). It was suggested that microbial community transition was responsible for the occurrence of sludge bulking, further affecting membrane fouling. Based on these characterizations, it was reported that adhesion propensity (indicated by the thermodynamic interaction) of the bulking sludge to the membrane surface is about 3.6 times than that of the normal sludge. It was proposed that, extra force should be provided to offset a chemical potential gap caused by foulant layer structure transition during sludge bulking in order to sustain filtration of the bulking sludge, resulting in extremely high SFR. This study offered deep thermodynamic mechanisms of MBR fouling during occurrence of sludge bulking.

The oocyte cumulus complex regulates mouse sperm migration in the oviduct.

As the time of ovulation draws near, mouse spermatozoa move out of the isthmic reservoir, which is a prerequisite for fertilization. However, the molecular mechanism remains unclear. The present study revealed that mouse cumulus cells of oocytes-cumulus complexes (OCCs) expressed transforming growth factor-ß ligand 1 (TGFB1), whereas ampullary epithelial cells expressed the TGF-ß receptors, TGFBR1 and TGFBR2, and all were upregulated by luteinizing hormone (LH)/human chorionic gonadotropin (hCG). OCCs and TGFB1 increased natriuretic peptide type C (NPPC) expression in cultured ampullae via TGF-ß signaling, and NPPC treatment promoted spermatozoa moving out of the isthmic reservoir of the preovulatory oviducts. Deletion of Tgfb1 in cumulus cells and Tgfbr2 in ampullary epithelial cells blocked OCC-induced NPPC expression and spermatozoa moving out of the isthmic reservoir, resulting in compromised fertilization and fertility. Oocyte-derived paracrine factors were required for promoting cumulus cell expression of TGFB1. Therefore, oocyte-dependent and cumulus cell-derived TGFB1 promotes the expression of NPPC in oviductal ampulla, which is critical for sperm migration in the oviduct and subsequent fertilization.