Synergistic bioremediation of petroleum-contaminated soil using immobilized consortium of Rhodococcus rhodochrous and Bacillus subtilis laccase.

Petroleum-contaminated soil represents a significant environmental and public health challenge on a global scale. Microbial bioremediation has shown potential, yet the role of enzymes in enhancing petroleum degradation remains underexplored. In this study, the synergistic effects of Rhodococcus rhodochrous (R.rh) and Bacillus subtilis-derived laccase (BsLac) was investigated in the remediation of petroleum-contaminated soil. Immobilized R.rh (PSIMRH) and BsLac (ADIMLac) exhibited higher petroleum degradation rates than their free state, achieving 78.3% and 56.3% degradation in liquid systems, respectively. The combined treatment of PSIMRH and ADIMLac demonstrated a synergistic effect on petroleum degradation, achieving 43.6% with a maximum degradation constant of 0.0335 d-1, representing a 202.7% improvement over untreated soil. PSIMRH enhanced petroleum degradation through microbial metabolism, while ADIMLac accelerated the initial breakdown of complex hydrocarbons into simpler, more bioavailable ones via enzymatic oxidation, providing growth substrates for microbes and significantly improving petroleum degradation rates. The microbial analysis revealed an increase abundance of known petroleum-degrading bacterial genera, including Rhodococcus, Lysobacter, Micromonospora, and Streptomyces. However, the presence of BsLac appeared to reduce the competitive advantage of Rhodococcus, promoting the proliferation of indigenous strains like Lysobacter and Streptomyces. These results suggest that enzyme-microbe synergy can enhance the bioremediation process by altering microbial community dynamics and accelerating petroleum degradation. This study attempts to remediate petroleum-contaminated pollution with the combined use of strains and enzymes, providing a new approach for the remediation of other pollution problems.

USP14 inhibition promotes DNA damage repair and represses ovarian granulosa cell senescence in premature ovarian insufficiency.

BACKGROUND: Premature ovarian insufficiency (POI) is a condition characterized by a substantial decline or loss of ovarian function in women before the age of 40. However, the pathogenesis of POI remains to be further elucidated, and specific targeted drugs which could delay or reverse ovarian reserve decline are urgently needed. Abnormal DNA damage repair (DDR) and cell senescence in granulosa cells are pathogenic mechanisms of POI. Ubiquitin-specific protease 14 (USP14) is a key enzyme that regulates the deubiquitylation of DDR-related proteins, but whether USP14 participates in the pathogenesis of POI remains unclear. METHODS: We measured USP14 mRNA expression in granulosa cells from biochemical POI (bPOI) patients. In KGN cells, we used IU1 and siRNA-USP14 to specifically inhibit USP14 and constructed a cell line stably overexpressing USP14 to examine its effects on DDR function and cellular senescence in granulosa cells. Next, we explored the therapeutic potential of IU1 in POI mouse models induced by D-galactose. RESULTS: USP14 expression in the granulosa cells of bPOI patients was significantly upregulated. In KGN cells, IU1 treatment and siUSP14 transfection decreased etoposide-induced DNA damage levels, promoted DDR function, and inhibited cell senescence. USP14 overexpression increased DNA damage, impaired DDR function, and promoted cell senescence. Moreover, IU1 treatment and siUSP14 transfection increased nonhomologous end joining (NHEJ), upregulated RNF168, Ku70, and DDB1, and increased ubiquitinated DDB1 levels in KGN cells. Conversely, USP14 overexpression had the opposite effects. Intraperitoneal IU1 injection alleviated etoposide-induced DNA damage in granulosa cells, ameliorated the D-galactose-induced POI phenotype, promoted DDR, and inhibited cell senescence in ovarian granulosa cells in vivo. CONCLUSIONS: Upregulated USP14 in ovarian granulosa cells may play a role in POI pathogenesis, and targeting USP14 may be a potential POI treatment strategy. Our study provides new insights into the pathogenesis of POI and a novel POI treatment strategy.

Enhancing the performance of mode-pairing quantum key distribution by wavelength division multiplexing.

Mode-pairing quantum key distribution (MP-QKD) holds great promise for the practical implementation of QKD in the near future. It combines the security advantages of measurement device independence while still being capable of breaking the Pirandola-Laurenza-Ottaviani-Banchi bound without the need for highly demanding phase-locking and phase-tracking technologies for deployment. In this work, we explore optimization strategies for MP-QKD in a wavelength-division multiplexing scenario. The simulation results reveal that incorporation of multiple wavelengths not only leads to a direct increase in key rate but also enhances the pairing efficiency by employing our novel pairing strategies among different wavelengths. As a result, our work provides a new avenue for the future application and development of MP-QKD.

Novel method for identifying the heaviest QED atom.

QED atoms are composed of unstructured and point-like lepton pairs bound together by the electromagnetic force. The smallest and heaviest QED atom is formed by a τ+τ- pair. Currently, the only known atoms of this type are the e+e- and µ+e- atoms, which were discovered 64 years ago and remain the sole examples found thus far. We demonstrate that the Jτ (τ+τ- atom with JPC=1--) atom signal can be observed with a significance larger than 5σ including both statistical and systematic uncertainties, via. the process e+e-→X+Y-Ɇ (X,Y=e,µ,π,K, or ρ, and Ɇ is the missing energy due to unobserved neutrinos) with 1.5ab-1 data taken around the τ pair production threshold. The τ lepton mass can be measured with a precision of 1 keV with the same data sample. This is within one year's running time of the proposed super tau-charm facility in China or super charm-tau factory in Russia.

Advanced oxidation protein products attenuate the autophagy-lysosome pathway in ovarian granulosa cells by modulating the ROS-dependent mTOR-TFEB pathway.

Oxidative stress dysfunction has recently been found to be involved in the pathogenesis of premature ovarian insufficiency (POI). Previously, we found that advanced oxidation protein products (AOPPs) in plasma were elevated in women with POI and had an adverse effect on granulosa cell proliferation. However, the mechanism underlying the effects of AOPPs on autophagy-lysosome pathway regulation in granulosa cells remains unclear. In this study, the effect of AOPPs on autophagy and lysosomal biogenesis and the underlying mechanisms were explored by a series of in vitro experiments in KGN and COV434 cell lines. AOPP-treated rat models were employed to determine the negative effect of AOPPs on the autophagy-lysosome systems in vivo. We found that increased AOPP levels activated the mammalian target of rapamycin (mTOR) pathway, and inhibited the autophagic response and lysosomal biogenesis in KGN and COV434 cells. Furthermore, scavenging of reactive oxygen species (ROS) with N-acetylcysteine and blockade of the mTOR pathway with rapamycin or via starvation alleviated the AOPP-induced inhibitory effects on autophagy and lysosomal biogenesis, suggesting that these effects of AOPPs are ROS-mTOR dependent. The protein expression and nuclear translocation of transcription factor EB (TFEB), the key regulator of lysosomal and autophagic function, were also impaired by the AOPP-activated ROS-mTOR pathway. In addition, TFEB overexpression attenuated the AOPP-induced impairment of autophagic flux and lysosomal biogenesis in KGN and COV434 cells. Chronic AOPP stimulation in vivo also impaired autophagy and lysosomal biogenesis in granulosa cells of rat ovaries. The results highlight that AOPPs lead to impairment of autophagic flux and lysosomal biogenesis via ROS-mTOR-TFEB signaling in granulosa cells and participate in the pathogenesis of POI.

Resveratrol prevents age-related heart impairment through inhibiting the Notch/NF-κB pathway.

Resveratrol (RSV) is a natural polyphenol compound found in various plants that has been shown to have potential benefits for preventing aging and supporting cardiovascular health. However, the specific signal pathway by which RSV protects the aging heart is not yet well understood. This study aimed to explore the protective effects of RSV against age-related heart injury and investigate the underlying mechanisms using a D-galactose-induced aging model. The results of the study indicated that RSV provided protection against age-related heart impairment in mice. This was evidenced by the reduction of cardiac histopathological changes as well as the attenuation of apoptosis. RSV-induced cardioprotection was linked to a significant increase in antioxidant activity and mitochondrial transmembrane potential, as well as a reduction in oxidative damage. Additionally, RSV inhibited the production of pro-inflammatory cytokines such as interleukin-1ß (IL-1ß) and tumor necrosis factor-α (TNF-α). Furthermore, the expression of toll-like receptor 4 (TLR4), nuclear factor kappa-B p65 (NF-κB p65), and notch 1 protein were inhibited by RSV, indicating that inhibiting the Notch/NF-κB pathway played a critical role in RSV-triggered heart protection in aging mice. Moreover, further data on intestinal function demonstrated that RSV significantly increased short-chain fatty acids (SCFAs) in intestinal contents and reduced the pH value in the feces of aging mice. RSV alleviated aging-induced cardiac dysfunction through the suppression of oxidative stress and inflammation via the Notch/NF-κB pathway in heart tissue. Furthermore, this therapeutic effect was found to be associated with its protective roles in the intestine.

Predicting stroke and myocardial infarction risk in Takayasu arteritis with automated machine learning models.

Few models exist for predicting severe ischemic complications (SIC) in patients with Takayasu arteritis (TA). We conducted a retrospective analysis of 703 patients with TA from January 2010 to December 2019 to establish an SIC prediction model for TA. SIC was defined as ischemic stroke and myocardial infarction. SIC was present in 97 of 703 (13.8%) patients with TA. Common iliac artery, coronary artery, internal carotid artery, subclavian artery, vertebral artery, renal artery involvement, chest pain, hyperlipidemia, absent pulse, higher BMI, vascular occlusion, asymmetric blood pressure in both upper limbs, visual disturbance, and older age were selected as predictive risk factors. Considering both discrimination and calibration performance, the Weighted Subspace Random Forest model was the most optimal model, boasting an area under the curve of 0.773 (95% confidence interval [0.652, 0.894]) in the validation cohort. Effective models for predicting SIC in TA may help clinicians identify high-risk patients and make targeted interventions.

Photoswitchable Enantioselective and Helix-Sense Controlled Living Polymerization.

A pair of enantiomeric photoswitchable PdII catalysts, alkyne-PdII /LR-azo and alkyne-PdII /LS-azo , were prepared via the coordination of alkyne-PdII and azobenzene-modified phosphine ligands LR-azo and LS-azo . Owing to the cis-trans photoisomerization of the azobenzene moiety, alkyne-PdII /LR-azo and alkyne-PdII /LS-azo exhibited different polymerization activities, helix-sense selectivities, and enantioselectivities during the polymerization of isocyanide monomers under irradiation of different wavelength lights. Furthermore, the achiral isocyanide monomer A-1 could be polymerized efficiently using alkyne-PdII /LR-azo under dark condition in a living/controlled manner. Further, it generated single right-handed helical poly-A-1m (LR-azo ), confirmed by the circular dichroism spectra and atomic force microscopy images. However, the polymerization of A-1 almost could not be initiated under 420 nm light in identical conditions of dark condition. Moreover, the photoswitchable catalyst alkyne-PdII /LR-azo exhibited high enantioselectivity for the polymerization of the racemates of L-1 and D-1, respectively. D-1 was polymerized preferentially under dark condition with a D-1/L-1 rate ratio of 70, yielding single right-handed polyisocyanides. Additionally, reversible enantioselectivity was observed under 420 nm light using alkyne-PdII /LR-azo , and the calculated polymerization rate ratio of L-1/D-1 was 57 because of the isomerization of the azobenzene moiety of the catalyst. Furthermore, alkyne-PdII /LS-azo showed opposite enantioselectivity and helix-sense selectivity during the polymerization of the racemates of L-1 and D-1.

Successful pregnancy and delivery in a female with pituitary stalk interruption syndrome following in vitro fertilization and embryo transfer: A case report and literature review.

Pituitary stalk interruption syndrome (PSIS) in female patients is mainly characterized by short stature, primary amenorrhea, absent or incomplete sexual maturation, and infertility. Successful pregnancies among these patients are rare. In this report, we describe a successful pregnancy and delivery in a 28-year-old Chinese woman with PSIS following in vitro fertilization and embryo transfer. The patient exhibited typical symptoms, including multiple pituitary hormone deficiency, typical triad signs in magnetic resonance imaging (MRI), undetectable serum gonadotropins and estradiol levels, and invisible antral follicles in both ovaries. During the first attempted controlled ovarian hyperstimulation cycle, 14 oocytes were retrieved and six embryos were acquired. Artificial endometrial preparation and frozen-thawed embryo transfer were performed, resulting in a clinical pregnancy after the transfer of a day 5 blastocyst. The patient was closely monitored throughout the pregnancy and multiple hormone dosages were modulated accordingly. She delivered a healthy boy by elective cesarean section, and the newborn developed normally during a 1-year follow-up period. This is the first report of a successful live birth in a woman with PSIS achieved through in vitro fertilization and frozen-thawed embryo transfer. A literature review on this topic is also presented.

Novel Tu translation elongation factor, mitochondrial (TUFM) homozygous variant in a consanguineous family with premature ovarian insufficiency.

Premature ovarian insufficiency (POI) is a clinical syndrome of ovarian dysfunction characterized by cessation of menstruation occurring before the age of 40 years. The genetic causes of idiopathic POI remain unclear. Here we recruited a POI patient from a consanguineous family to screen for potential pathogenic variants associated with POI. Genetic variants of the pedigree were screened using whole-exome sequencing analysis and validated through direct Sanger sequencing. A homozygous variant in TUFM (c.524G>C: p.Gly175Ala) was identified in this family. TUFM (Tu translation elongation factor, mitochondrial) is a nuclear-encoded mitochondrial protein translation elongation factor that plays a critical role in maintaining normal mitochondrial function. The variant position was highly conserved among species and predicted to be disease causing. Our in vitro functional studies demonstrated that this variant causes decreased TUFM protein expression, leading to mitochondrial dysfunction and impaired autophagy activation. Moreover, we found that mice with targeted Tufm variant recapitulated the phenotypes of human POI. Thus, this is the first report of a homozygous pathogenic TUFM variant in POI. Our findings highlighted the essential role of mitochondrial genes in folliculogenesis and ovarian function maintenance.

Elevated cell-free mitochondria DNA level of patients with premature ovarian insufficiency.

BACKGROUND: Premature ovarian insufficiency (POI) patients present with a chronic inflammatory state. Cell-free mitochondria DNA (cf-mtDNA) has been explored as a reliable biomarker for estimating the inflammation-related disorders, however, the cf-mtDNA levels in POI patients have never been measured. Therefore, in the presenting study, we aimed to evaluate the levels of cf-mtDNA in plasma and follicular fluid (FF) of POI patients and to determine a potential role of cf-mtDNA in predicting the disease progress and pregnancy outcomes. METHODS: We collected plasma and FF samples from POI patients, biochemical POI (bPOI) patients and control women. Quantitative real-time PCR was used to measure the ratio of mitochondrial genome to nuclear genome of cf-DNAs extracted from the plasma and FF samples. RESULTS: The plasma cf-mtDNA levels, including COX3, CYB, ND1 and mtDNA79, were significantly higher in overt POI patients than those in bPOI patients or control women. The plasma cf-mtDNA levels were weakly correlated with ovarian reserve, and could not be improved by regular hormone replacement therapy. The levels of cf-mtDNA in FF, rather than those in plasma, exhibited the potential to predict the pregnancy outcomes, although they were comparable among overt POI, bPOI and control groups. CONCLUSIONS: The increased plasma cf-mtDNA levels in overt POI patients indicated its role in the progress of POI and the FF cf-mtDNA content may hold the value in predicting pregnancy outcomes of POI patients.

Boosting the performance of loss-tolerant measurement-device-independent quantum key distribution.

Measurement-device-independent quantum key distribution can remove all possible detector side channels, and is robust against state preparation flaws when further combined with the loss-tolerant method. However, the secure key rate in this scenario is relatively low, thus hindering its practical application. Here, we first present a four-intensity decoy-state protocol where the signal intensity is modulated only in Z basis for key generation while the decoy intensities are modulated in both Z and X bases for parameter estimation. Moreover, we adopt collective constraint and joint-study strategy in statistical fluctuation analysis. We have also experimentally demonstrated this protocol and the result indicates high performance and good security for practical applications.

Plasma metabolomic characterization of premature ovarian insufficiency.

BACKGROUND: Premature ovarian insufficiency (POI) patients are predisposed to metabolic disturbances, including in lipid metabolism and glucose metabolism, and metabolic disorders appear to be a prerequisite of the typical long-term complications of POI, such as cardiovascular diseases or osteoporosis. However, the metabolic changes underlying the development of POI and its subsequent complications are incompletely understood, and there are few studies characterizing the disturbed metabolome in POI patients. The aim of this study was to characterize the plasma metabolome in POI by using ultrahigh-performance liquid chromatography-mass spectrometry (UHPLC-MS/MS) metabolomics and to evaluate whether these disturbances identified in the plasma metabolome relate to ovarian reserve and have diagnostic value in POI. METHODS: This observational study recruited 30 POI patients and 30 age- and body mass index (BMI)-matched controls in the Center for Reproductive Medicine, Department of Gynecology and Obstetrics, Nanfang Hospital, Southern Medical University, from January 2018 to October 2020. Fasting venous blood was collected at 9:00 am on days 2-4 of the menstrual cycle and centrifuged for analysis. An untargeted quantitative metabolomic analysis was performed using UHPLC-MS/MS. RESULTS: Our study identified 48 upregulated and 21 downregulated positive metabolites, and 13 upregulated and 48 downregulated negative metabolites in the plasma of POI patients. The differentially regulated metabolites were involved in pathways such as caffeine metabolism and ubiquinone and other terpenoid-quinone biosynthesis. Six metabolites with an AUC value > 0.8, including arachidonoyl amide, 3-hydroxy-3-methylbutanoic acid, dihexyl nonanedioate, 18-HETE, cystine, and PG (16:0/18:1), were correlated with ovarian reserve and thus have the potential to be diagnostic biomarkers of POI. CONCLUSION: This UHPLC-MS/MS untargeted metabolomics study revealed differentially expressed metabolites in the plasma of patients with POI. The differential metabolites may not only be involved in the aetiology of POI but also contribute to its major complications. These findings offer a panoramic view of the plasma metabolite changes caused by POI, which may provide useful diagnostic and therapeutic clues for POI disease.

Effect of Sugar and Milk Powder Addition on the Mechanical Properties and Texture of Chocolate.

In order to investigate how the addition of two common ingredients in chocolate, sugar and milk powder, affects the mechanical properties of solid chocolate, uniaxial compression tests and wedge fracture tests were carried out using four ratios of chocolate as the experimental material. Mechanical properties such as Young's modulus and fracture toughness were directly correlated with textural properties such as hardness, elasticity, and brittleness. The results show that adding sugar increases Young's modulus and fracture toughness of chocolate, while milk powder is the opposite. In equal amounts of both, sugar played a more substantial role. In combination with the properties exhibited by chocolate in the above tests, data from creep tests were collected to improve the classical Bingham model and develop a new constitutive model for predicting the mechanical behaviour of solid chocolate with different ratios of added sugar and milk powder. The new four-component constitutive model allows for a more accurate fit to the creep test data and this work provides some suggestions for making different tasting chocolates by adjusting the addition of ingredients.

Study of differential proteomics in granulosa cells of premature ovarian insufficiency (POI) and the roles and mechanism of RAC1 in granulosa cells.

In the present study, we focused on characterizing the proteome in granulosa cells in patients with biochemical premature ovarian insufficiency (bPOI) in order to identify differential proteins and investigate the fundamental mechanisms of POI. A total of 2688 proteins were identified based on the data-independent acquisition method, and 70 differentially expressed proteins were significant. Bioinformatic analyses, including gene expression pattern analysis, gene ontology enrichment analysis, Kyoto Encyclopedia of Genes and Genomes pathway analysis, and Search Tool for the Retrieval of Interacting Genes/Proteins analysis, revealed discrete modules and the underlying molecular mechanisms in bPOI. Importantly, we observed that Ras-related C3 botulinum toxin substrate 1 (RAC1) was downregulated in the granulosa cells of bPOI. Low expression of RAC1 may affect the development process of POI by affecting the proliferation, apoptosis, and hormone synthesis of granulosa cells. Downregulation of RAC1 expression in the KGN and COV434 cells inhibited cell proliferation, blocked cells in the G1/G0 phase, and promoted apoptosis. Western blot results showed that ß-catenin and cyclin D1 in the KGN and COV434 cells transfected with RAC1-siRNA were downregulated, while P21 and Bax were upregulated. Knocking down RAC1 in the KGN cells or adding the RAC1 enzyme inhibitor to the human luteinized granulosa cells (hLGC) inhibited the synthesis of E2, and the expression of aromatase and follicle-stimulating hormone receptor (FSHR) was reduced.

Measurement-device-independent quantum key distribution with insecure sources.

Measurement-device-independent quantum key distribution (MDI-QKD) can remove all detection side channels but still makes additional assumptions on sources that can be compromised through uncharacterized side channels in practice. Here, we combine a recently proposed reference technique to prove the security of MDI-QKD against possible source imperfections and/or side channels. This requires some reference states and an upper bound on the parameter that describes the quality of the sources. With this formalism we investigate the asymptotic performance of single-photon sources, and the results show that the side channels have a great impact on the key rates.

Effect of gelatin content and oral processing ability on vitamin C release in gummy jelly.

In order to investigate the factors affecting the release of vitamin C (VC) in gummy jelly during oral processing, four levels of gelatin (3%, 6%, 9% and 12%) were selected and a bionic chewing robot was employed in chewing experiments. Textural profile analysis showed the hardness of gummy jelly increased from 91.7 N to 198.8 N when the gelatin content was raised from 3 to 12%. Single factor chewing experiment showed that the release of VC was positively correlated with chewing frequency (Fchew) and chewing strain (STchew), while negatively correlated with gelatin content, chewing speed (SPchew) and volume of saliva (Vsaliva). Orthogonal chewing experiment showed that the priority of the factors affected the release of VC was following: STchew > Fchew > SPchew > Vsaliva. Multivariate linear regression analysis proposed a model to predict the amount of VC released and the goodness-of-fit of the model was 95.7%. The amount of VC released was the highest under the combination of Fchew 12 times, STchew 100%, Vsaliva 2 ml and SPchew 40 times/min. The optimal amount of gelatin addition was 6%. This study provided an effective reference for the formula design and chewing mode optimization of gummy jelly.

Advanced Oxidation Protein Products Induce G1/G0-Phase Arrest in Ovarian Granulosa Cells via the ROS-JNK/p38 MAPK-p21 Pathway in Premature Ovarian Insufficiency.

The mechanism underlying the role of oxidative stress and advanced oxidation protein products (AOPPs) in the aetiology of premature ovarian insufficiency (POI) is poorly understood. Here, we investigated the plasma AOPP level in POI patients and the effects of AOPPs on granulosa cells both in vitro and in vivo. KGN cells were treated with different AOPP doses, and cell cycle distribution, intracellular reactive oxygen species (ROS), and protein expression levels were measured. Sprague-Dawley (SD) rats were treated daily with PBS, rat serum albumin, AOPP, or AOPP+ N-acetylcysteine (NAC) for 12 weeks to explore the effect of AOPPs on ovarian function. Plasma AOPP concentrations were significantly higher in both POI and biochemical POI patients than in controls and negatively correlated with anti-Müllerian hormone and the antral follicle count. KGN cells treated with AOPP exhibited G1/G0-phase arrest. AOPP induced G1/G0-phase arrest in KGN cells by activating the ROS-c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (MAPK)-p21 pathway. Pretreatment with NAC, SP600125, SB203580, and si-p21 blocked AOPP-induced G1/G0-phase arrest. In SD rats, AOPP treatment increased the proportion of atretic follicles, and NAC attenuated the adverse effects of AOPPs in the ovary. In conclusion, we provide mechanistic evidence that AOPPs may induce cell cycle arrest in granulosa cells via the ROS-JNK/p38 MAPK-p21 pathway and thus may be a novel biomarker of POI.

Let-7e modulates the proliferation and the autophagy of human granulosa cells by suppressing p21 signaling pathway in polycystic ovary syndrome without hyperandrogenism.

Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disorder in reproductive-aged women, and its pathogenesis is still under debate. Recent studies suggest crucial roles for microRNAs (miRNAs) in PCOS development. The let-7 family miRNAs constitute the most abundant miRNAs in human granulosa cells (GCs), and plays an important role in follicular development. However, research on the let-7e implications of the non-hyperandrogenic (non-HA) phenotype remains unclear. This study aimed at determining the role of let-7e in the progression of PCOS. We performed quantitative real-time PCR to examine the levels of let-7e in fifty-two non-HA PCOS patients and fifty-two controls. A receiver operating characteristic (ROC) curve were used to reveal the diagnostic value of let-7e in non-HA PCOS. Using an immortalized human granulosa cell line, KGN, we investigated the influence of let-7e on cell proliferation and autophagy. Our data substantiated the expression of let-7e was significantly increased in non-HA PCOS group, and associated with an increased antral follicle count. The ROC curve indicated a major separation between non-HA PCOS group and the control group. Let-7e knockdown suppressed cell proliferation and enhanced cell autophagy by activating p21 pathway. Conversely, let-7e overexpression promoted cell proliferation and inhibited cell autophagy by suppressing p21 pathway. Our results indicate that increased let-7e levels in non-HA PCOS GCs may contribute to excessive follicular activation and growth, thereby involving in the pathogenesis of PCOS. Let-7e may thus be a potential therapeutic target in non-HA PCOS.

Experimental three-state measurement-device-independent quantum key distribution with uncharacterized sources.

Measurement-device-independent quantum key distribution (MDI-QKD) removes all detector side-channel attacks and guarantees a promising way for remote secret keys sharing. Several proof-of-principal experiments have been demonstrated to show its security and practicality. However, these practical implementations demand mostly, for example, perfect state preparation or completely characterized sources to ensure security, which are difficult to realize with prior art. Here, we investigate a three-state MDI-QKD using uncharacterized sources, with the simple requirement that the encoding state is bidimensional, which eliminates security threats from both the source flaws and detection loopholes. As a demonstration, a proof-of-principal experiment over 170 km transmission distance based on Faraday-Michelson interferometers is achieved, representing, to the best of our knowledge, the longest transmission distance recorded under the same security level.