A colorimetric sensor based on 4-MPBA Au@AgNPs for accurately identification of EnshiYulu tea grade.

Enshi Yulu green tea (ESYL) is the most representative traditional steamed green tea in Enshi, Hubei. Different ESYL grades exhibit distinct flavors, tastes, and prices. In this study, a visual sensor based on 4-MPBA Au@AgNPs was developed for the rapid and accurate identification of ESYL grades. The recognition mechanism involved the binding of 4-MPBA Au@AgNPs with polyphenolic compounds in ESYL to form borate esters and the conversion of Ag+ to Ag0, with the generated Ag0 depositing on the surface of 4-MPBA Au@AgNPs. The results showed that the sensor can amplify the color differences of different grades of ESYL. The visual results were also validated by the partial least squares discriminant analysis model, demonstrating an enhancement in recognition accuracy from 68.2 % to 95.5 % compared to the original extraction solution. The colorimetric sensor developed in this study is expected to provide a new approach for traceability research of other foods.

LKB1 regulates autophagy through AMPK/TOR signaling pathway to alleviate the damage caused by Vibrio alginolyticus infection.

LKB1 (liver kinase B1) is a key upstream kinase of AMPK and plays an important role in various cellular activities. While the function and mechanism of LKB1 have been widely reported in the study of tumor, there are few reports on its role in bacterial infectious diseases, especially in shrimp. In the present study, molecular characterization revealed that LvLKB1 has an open reading frame (ORF) of 1266 bp encoding 421 amino acids with a molecular weight of about 48 KDa, including the kinase region, N-terminal regulatory domain and C-terminal regulatory domain. LvLKB1 in hepatopancreas and hemocytes was significantly upregulated after infection with Vibrio alginolyticus (V. alginolyticus). After silencing LvLKB1 gene in Litopenaeus vannamei (L. vannamei) and artificially infecting V. alginolyticus, the survival rate of L. vannamei was significantly decreased. Subsequently, it was found that the expression of inflammatory factors in hepatopancreas and hemocytes of shrimp was up-regulated, and the expression of lipid oxidation factors was decreased after silencing LKB1, leading to the phenomenon of lipid accumulation in hepatopancreas. In order to explore the mechanism, autophagy levels of shrimp were detected after silencing LKB1, which showed that autophagy levels in hepatopancreas and hemocytes were significantly reduced. Further studies conclusively showed that silencing LvLKB1 inhibited AMPK phosphorylation induced by V. alginolyticus infection, thereby activating TOR pathway and inhibiting autophagy in shrimp. These results indicate that LvLKB1 regulates autophagy through AMPK/TOR signaling pathway to alleviate the damage caused by V. alginolyticus infection.

Neonatal sequential organ failure assessment score within 72†h after delivery reliably predicts bronchopulmonary dysplasia in very preterm infants.

Background: The neonatal sequential organ failure assessment (nSOFA) score is an operational definition of organ dysfunction employed to predict sepsis-associated mortality. However, the relationship between the nSOFA score and bronchopulmonary dysplasia (BPD) has not been investigated clearly. This study evaluates whether the nSOFA score within 72 h after delivery could be used to predict the occurrence of BPD in very preterm infants. Methods: In this retrospective, single-center cohort study, preterm infants born between 2019 and 2021 were investigated, the nSOFA score was calculated from medical records after admission to the neonatal intensive care unit (NICU) within 72 h after delivery, and the peak value was used for calculation. A logistic regression model was used to evaluate the relationship between the nSOFA score and BPD. Propensity score matching and subgroup analysis were performed to verify the reliability of the results. Results: Of 238 infants meeting the inclusion criteria, 93 infants (39.1%) were diagnosed with BPD. The receiver operating characteristic curve of the nSOFA score in predicting BPD was 0.790 [95% confidence interval (CI): 0.731-0.849]. The logistic regression model showed that an increment of one in the nSOFA score was related to a 2.09-fold increase in the odds of BPD (95% CI: 1.57-2.76) and 6.36-fold increase when the nSOFA score was higher than 1.5 (95% CI: 2.73-14.79). Conclusions: The nSOFA score within 72 h after delivery is independently related to BPD and can be used to identify high-risk infants and implement early interventions.

Association of obesity with high retears and complication rates, and low functional scores after rotator cuff repair: a systematic review and meta-analysis.

BACKGROUND: Obesity influences the outcomes of orthopedic surgeries such as total knee arthroplasty and spinal surgery. However, the effect of obesity on the outcomes of rotator cuff repair is unknown. This systematic review and meta-analysis aimed to examine the effect of obesity on rotator cuff repair outcomes. METHODS: PubMed, EMBASE, Web of Science, and Cochrane Library databases were searched to identify relevant studies published from their inception till July 2022. Two reviewers independently screened titles and abstracts using the specified criteria. Articles were included if they indicated the effect of obesity on rotator cuff repair and the related outcomes after surgery. Review Manager 5.4.1 software was used to perform statistical analysis. RESULTS: Thirteen articles involving 85,497 patients were included. Obese patients had higher retear rates than nonobese patients (odds ratio [OR] 2.58, 95% confidence interval [CI] 1.23-5.41, P = .01), lower American Shoulder and Elbow Surgeons scores (mean difference [MD]: -3.59, 95% CI: -5.45 to [-1.74]; P = .0001), higher visual analog scale for pain (mean difference: 0.73, 95% CI: 0.29-1.17; P = .001), higher reoperation rates (OR 1.31, 95% CI 1.21-1.42, P < .00001), and higher rates of complications (OR 1.57, 95% CI 1.31-1.87, P = .000). Obesity did not affect the duration of surgery (MD: 6.03, 95% CI: -7.63 to 19.69; P = .39) or external rotation of the shoulder (MD: -1.79, 95% CI: -5.30 to 1.72; P = .32). CONCLUSION: Obesity is a significant risk factor for retear and reoperation after rotator cuff repair. Furthermore, obesity increases the risk of postoperative complications and leads to lower postoperative American Shoulder and Elbow Surgeons scores and higher shoulder visual analog scale for pain.

Mechanism of Notch Signal Regulating Alveolar Epithelial Cell Autophagy after Infection with Klebsiella Pneumoniae.

BACKGROUND: The Notch signaling pathway regulates various cellular processes, including cell growth, inflammation response, and autophagy, thereby participating in the occurrence and development of various diseases. The present study aimed to investigate the molecular mechanism of Notch signaling in regulating alveolar type II epithelial cell viability and autophagy after Klebsiella pneumonia (KPN) infection. METHODS: KPN-infected human alveolar type II epithelial cells A549 (ACEII) were constructed. The autophagy inhibitor 3-methyladenine (3-MA) and Notch1 signaling inhibitor (DAPT) were used to pretreat A549 cells for 24 hours, 48 hours, and 72 hours before KPN infection. Real-time fluorescent quantitative PCR (qRT-PCR) and western blot assays were applied to detect the mRNA and protein expressions of LC3 and Notch1, respectively. ELISA was used to detect the levels of INF-γ, TNF-α, and IL-1ß in the cell supernatants. RESULTS: The results showed that KPN-infected A549 cells presented significantly upregulated Notch1 and autophagy-related protein LC3 levels, along with increased IL-1ß, TNF-α, INF-γ levels in a time-dependent manner. Autophagy inhibitor 3-methyladenine (3-MA) counteracted the promotive effects of LC3 and inflammatory cytokine levels in KPN-infected A549 cells; however, 3-MA did not influence Notch1 level. Notch1 inhibitor DAPT could suppress Notch1 and LC3 levels, thereby inhibiting inflammation response in KPN-treated A549 cells in a time-dependent way. CONCLUSIONS: KPN infection can activate the Notch signaling pathway and induce autophagy in type Ⅱ alveolar epithelial cells. Inhibiting the Notch signaling pathway may restrain KPN-induced A549 cell autophagy and inflammation response, shedding new insights for the treatment of pneumonia.

PPAR-γ activation promotes xenogenic bioroot regeneration by attenuating the xenograft induced-oxidative stress.

Xenogenic organ transplantation has been considered the most promising strategy in providing possible substitutes with the physiological function of the failing organs as well as solving the problem of insufficient donor sources. However, the xenograft, suffered from immune rejection and ischemia-reperfusion injury (IRI), causes massive reactive oxygen species (ROS) expression and the subsequent cell apoptosis, leading to the xenograft failure. Our previous study found a positive role of PPAR-γ in anti-inflammation through its immunomodulation effects, which inspires us to apply PPAR-γ agonist rosiglitazone (RSG) to address survival issue of xenograft with the potential to eliminate the excessive ROS. In this study, xenogenic bioroot was constructed by wrapping the dental follicle cells (DFC) with porcine extracellular matrix (pECM). The hydrogen peroxide (H2O2)-induced DFC was pretreated with RSG to observe its protection on the damaged biological function. Immunoflourescence staining and transmission electron microscope were used to detect the intracellular ROS level. SD rat orthotopic transplantation model and superoxide dismutase 1 (SOD1) knockout mice subcutaneous transplantation model were applied to explore the regenerative outcome of the xenograft. It showed that RSG pretreatment significantly reduced the adverse effects of H2O2 on DFC with decreased intracellular ROS expression and alleviated mitochondrial damage. In vivo results confirmed RSG administration substantially enhanced the host's antioxidant capacity with reduced osteoclasts formation and increased periodontal ligament-like tissue regeneration efficiency, maximumly maintaining the xenograft function. We considered that RSG preconditioning could preserve the biological properties of the transplanted stem cells under oxidative stress (OS) microenvironment and promote organ regeneration by attenuating the inflammatory reaction and OS injury.

Exosomal DNAJB11 promotes the development of pancreatic cancer by modulating the EGFR/MAPK pathway.

Pancreatic ductal adenocarcinoma (PDAC) is a malignant tumor with invasive and metastatic characteristics and poor prognosis. Intracellular protein homeostasis is associated with invasion and metastasis of pancreatic cancer, but the specific molecular mechanism remains unclear. Our previous studies have revealed that DNAJB11, a key protein in protein homeostasis, is secreted by exosomes in the supernatant of dissociated pancreatic cancer cells with high metastasis. The results from transcriptome sequencing and co-immunoprecipitation (Co-IP)-based liquid chromatography with tandem mass spectrometry (LC-MS/MS) showed that depletion of DNAJB11 levels could increase HSPA5 expression and induce endoplasmic reticulum stress through the PRKR-like endoplasmic reticulum kinase signaling pathway in pancreatic cancer cells. Furthermore, exosomal DNAJB11 promoted cell development of PC cells in vitro and in vivo. In addition, exosomal DNAJB11 could regulate the expression of EGFR and activate the downstream MAPK signaling pathway. Clinical blood samples were collected to evaluate the potential of exosome DNAJB11 as a diagnostic biomarker and therapeutic target for the treatment of pancreatic cancer. This study could provide a new theoretical basis and potential molecular targets for the treatment of pancreatic cancer.

Andrographolide promote the growth and immunity of Litopenaeus vannamei, and protects shrimps against Vibrio alginolyticus by regulating inflammation and apoptosis via a ROS-JNK dependent pathway.

Vibrio alginolyticus (V. alginolyticus) is one of the major pathogens causing mass mortality of shrimps worldwide, affecting energy metabolism, immune response and development of shrimps. In the context of the prohibition of antibiotics, it is necessary to develop a drug that can protect shrimp from V. alginolyticus. Andrographolide (hereinafter called Andr), a traditional drug used in Chinese medicine, which possesses diverse biological effects including anti-bacteria, antioxidant, immune regulation. In this study, we investigated the effect of Andr on growth, immunity, and resistance to V. alginolyticus infection of Litopenaeus vannamei (L. vannamei) and elucidate the underlying molecular mechanisms. Four diets were formulated by adding Andr at the dosage of 0 g/kg (Control), 0.5 g/kg, 1 g/kg, and 2 g/kg in the basal diet, respectively. Each diet was randomly fed to one group with three replicates of shrimps in a 4-week feeding trial. The results showed that dietary Andr improved the growth performance and non-specific immune function of shrimps. L. vannamei fed with Andr diets showed lower mortality after being challenged by V. alginolyticus. After 6 h of V. alginolyticus infection, reactive oxygen species (ROS) production, tissue injury, apoptosis, expression of inflammatory factors (IL-1 ß and TNFα) and apoptosis-related genes (Bax, caspase3 and p53) were increased in hemocytes and hepatopancreas, while feeding diet with 0.5 g/kg Andr could inhibit the increase. Considering that JNK are important mediators of apoptosis, we examined the influence of Andr on JNK activity during V. alginolyticus infection. We found that Andr inhibited JNK activation induced by V. alginolyticus infection on L. vannamei. The ROS scavenger N-acetyl-l-cysteine (NAC) suppressed V. alginolyticus-induced inflammation and apoptosis, suggesting that ROS play an important role in V. alginolyticus-induced inflammation and apoptosis. Treated cells with JNK specific activator anisomycin, the inflammation and apoptosis inhibited by Andr were counteracted. Collectively, Andr promote the growth and immunity of L. vannamei, and protects shrimps against V. alginolyticus by regulating inflammation and apoptosis via a ROS-JNK dependent pathway. These results improve the understanding of the pathogenesis of V. alginolyticus infection and provide clues to the development of effective drugs against V. alginolyticus.

Use of magnetic resonance elastography to gauge meningioma intratumoral consistency and histotype.

OBJECTIVE: To determine whether tumor shear stiffness, as measured by magnetic resonance elastography, corresponds with intratumoral consistency and histotype. MATERIALS AND METHODS: A total of 88 patients with 89 meningiomas (grade 1, 74 typical [13 fibroblastic, 61 non-fibroblastic]; grade 2, 12 atypical; grade 3, 3 anaplastic) were prospectively studied, each undergoing preoperative MRE in conjunction with T1-, T2- and diffusion-weighted imaging. Contrast-enhanced T1-weighted sequences were also obtained. Tumor consistency was evaluated as heterogeneous or homogenous, and graded on a 5-point scale intraoperatively. MRE-determined shear stiffness was associated with tumor consistency by surgeon's evaluation and whole-slide histologic analyses. RESULTS: Mean tumor stiffness overall was 3.81+/-1.74 kPa (range, 1.57-12.60 kPa), correlating well with intraoperative scoring (r = 0.748; p = 0.001). MRE performed well as a gauge of tumor consistency (AUC = 0.879, 95 % CI: 0.792-0.938) and heterogeneity (AUC = 0.773, 95 % CI: 0.618-0.813), significantly surpassing conventional MR techniques (DeLong test, all p < 0.001 after Bonferroni adjustment). Shear stiffness was independently correlated with both fibrous content (partial correlation coefficient = 0.752; p < 0.001) and tumor cellularity (partial correlation coefficient = 0.547; p < 0.001). MRE outperformed other imaging techniques in distinguishing fibroblastic meningiomas from other histotypes (AUC = 0.835 vs 0.513 âˆ¼ 0.634; all p < 0.05), but showed limited ability to differentiate atypical or anaplastic meningiomas from typical meningiomas (AUC = 0.723 vs 0.616 âˆ¼ 0.775; all p > 0.05). Small (<2.5 cm, n = 6) and intraventricular (n = 2) tumors displayed inconsistencies between MRE and surgeon's evaluation. CONCLUSIONS: The results of this prospective study provide substantial evidence that preoperative evaluation of meningiomas with MRE can reliably characterize tumor stiffness and spatial heterogeneity to aid neurosurgical planning.

Preclinical investigation of artesunate as a therapeutic agent for hepatocellular carcinoma via impairment of glucosylceramidase-mediated autophagic degradation.

Artesunate (ART) has been indicated as a candidate drug for hepatocellular carcinoma (HCC). Glucosylceramidase (GBA) is required for autophagic degradation. Whether ART regulates autophagic flux by targeting GBA in HCC remains to be defined. Herein, our data demonstrated that the dramatic overexpression of GBA was significantly associated with aggressive progression and short overall survival times in HCC. Subsequent experiments revealed an association between autophagic activity and GBA expression in clinical HCC samples, tumor tissues from a rat model of inflammation-induced HCC and an orthotopic mouse model, and human HCC cell lines. Interestingly, probe labeling identified GBA as an ART target, which was further verified by both a glutathione-S-transferase pulldown assay and surface plasmon resonance analysis. The elevated protein expression of LC3B, the increased numbers of GFP-LC3B puncta and double-membrane vacuoles, and the enhanced expression of SQSTM1/p62 indicated that the degradation of autophagosomes in HCC cells was inhibited by ART treatment. Both the in vitro and in vivo data revealed that autophagosome accumulation through targeting of GBA was responsible for the anti-HCC effects of ART. In summary, this preclinical study identified GBA as one of the direct targets of ART, which may have promising potential to inhibit lysosomal autophagy for HCC therapy.

Pellino2 accelerate inflammation and pyroptosis via the ubiquitination and activation of NLRP3 inflammation in model of pediatric pneumonia.

BACKGROUND: Mycoplasma pneumoniae pneumonia (MPP) is a common and frequently-occurring disease in pediatrics. This study aims to via unveiling the novel effects and mechanisms of Pellino2 in model of pediatric pneumonia. MATERIALS AND METHODS: Male infancy C57BL/6 mice were injected with 2 mg/kg of LPS (Sigma-Aldrich Merck KGaA). THP-1 cells were induced with LPS and ATP. RESULTS: The expression of Pellino2 mRNA and protein in patients with pediatric pneumonia or mice with pediatric pneumonia were reduced. Pellino2 accelerated lung injury and expanded inflammation and pyroptosis in lung tissue of pediatric pneumonia in vivo and vitro model. Furthermore, the inhibition of Pellino2 reduced lung injury and weakened inflammation and pyroptosis in lung tissue of pediatric pneumonia in vivo and vitro model. Pellino2 protein catenated NLRP3 protein, and Pellino2 promoted ubiquitination and activation of NLRP3 inflammation in model of pediatric pneumonia. Pellino2 accelerate inflammation and pyroptosis in model of pediatric pneumonia by NLRP3. CONCLUSIONS: These results suggest that Pellino2 accelerate inflammation and pyroptosis via the induction of ubiquitination and activation of NLRP3 inflammation in model of pediatric pneumonia, Pellino2 may serve as a potential approach for the treatment of pediatric pneumonia and other inflammatory diseases.

MYC drives autophagy to adapt to stress in Penaeus vannamei.

MYC proto-oncogene (MYC), a first oncogenic nuclear transcription factor isolated from the human genome, belongs to the helix loop helix/leucine zipper protein family (bHLHzip). MYC plays an important part in the process of various physiological and biochemical of vertebrate, such as cell growth, proliferation, cycle, and autophagy. However, its molecular regulation mechanism and function in invertebrates are still unclear. In this study, a novel transcription factor MYC gene was screened, cloned, and characterized from Penaeus vannamei. The open reading frame of PvMYC was 1593bp, encode a polypeptide of 530 amino acids with molecular weight of 58.5 kDa, and a theoretical PI of 5.75. The results of tissue distribution showed that PvMYC was constitutively expressed in all detected tissues, and highest expression in hepatopancreas. The expression level of PvMYC up-regulated significantly and responded to low temperature stress by nuclear ectopic after low temperature stress. Overexpression of PvMYC in shrimp hemocytes negatively regulated the expression of Beclin-1 and reduced the conversion from LC3I to LC3II, yet p62 was decreased significantly. Meanwhile, RAPA eliminated the inhibition of autophagy caused by overexpression of PvMYC. ROS levels and autophagy flux showed the similar trend under low temperature stress after silencing PvMYC. The expression levels of Beclin-1, key ATG gene and LC3II increased significantly, while p62 decreased significantly under the same conditions. In addition, the Total hemocyte count (THC) decreased sharply, and accelerated the injury of hepatopancreas under low temperature stress after silencing PvMYC. Collectively, these results suggest that PvMYC has vital role in the cold adaptation mechanism of P. vannamei by negatively regulating autophagy.

Nemo-like kinase (NLK) gene regulates apoptosis via the p53 signaling pathway in Litopenaeus vannamei under low-temperature stress.

The Nemo-like kinase (NLK) is an important serine/threonine-protein kinase in many signaling pathways. However, its function in crustaceans, such as shrimps, is still poorly understood and needs to be further explored. In the present study, the full-length cDNA of NLK from Litopenaeus vannamei (LvNLK) was cloned. The full-length LvNLK cDNA has 2497 bp, including an open reading frame (ORF) of 1524 bp encoding a protein with 507 amino acids and a predicted molecular mass of 56.1 kDa. Phylogenetic analysis revealed that LvNLK shared high similarities with NLK from other known species. Low-temperature stress markedly upregulated the expression of LvNLK. Its overexpression in hemocytes suppressed the expression of BCL2-associated X (Bax) and tumor protein P53 (p53) in vitro. Meanwhile, the BCL2 apoptosis regulator (Bcl-2), MDM2 proto-oncogene (MDM2), and Yin Yang 1 (YY1) were upregulated. Moreover, LvNLK silencing in vivo increased the susceptibility of shrimps to low-temperature stress. The generation of ROS and the rate of hemocyte apoptosis also increased when LvNLK was silenced. Additionally, qPCR results indicated that LvNLK might participate in apoptosis via the p53 signaling pathway in vitro and in vivo. These results suggested that LvNLK is indispensable for the environmental adaptation of L. vannamei. Our current findings also demonstrated that NLK is evolutionarily conserved in crustaceans and provided insights into the environmental adaptation of invertebrates.

Transcriptome analysis of Pacific white shrimp (Litopenaeus vannamei) hepatopancreas challenged by Vibrio alginolyticus reveals lipid metabolic disturbance.

Vibrio alginolyticus is a devastating bacterial pathogen of Pacific white shrimp (Litopenaeus vannamei), which often causes acute hepatopancreatic necrosis syndrome (AHPNS) and early mortality syndrome (EMS). Elucidation of molecular mechanisms of L. vannamei in responding to infection is essential for controlling the epidemic. In the present study, transcriptomic profiles of L. vannamei hepatopancreas were explored by injecting with PBS or V. alginolyticus. Hepatopancreas morphology of L. vannamei was also assessed. The result reveals that compared with the hepatopancreas of PBS group, the storage cells (R-cell), secretory cells (B-cell) and star-shaped polygonal structures of the lumen were disappeared and necrotic after challenged by V. alginolyticus at 24 h. Transcriptome data showed that a total of 314 differential expression genes were induced by V. alginolyticus, with 133 and 181 genes up- and down-regulated, respectively. These genes were mainly associated with lysosome pathway, glycerophospholipid metabolism, drug metabolism-other enzymes, cysteine and methionine metabolism, aminoacyl-tRNA biosynthesis and PPAR signal pathway. Among these pathways, the lysosome pathway, glycerophospholipid metabolism and PPAR signal pathway were both related with lipid metabolism. Therefore, we detected the lipid accumulation in hepatopancreas by Oil Red O staining, TG and CHOL detection and the relative mRNA expression of several lipid metabolism related genes in the hepatopancreas of shrimp after challenge to V. alginolyticus. The present data reveals that lipids from the L. vannamei are nutrient sources for the V. alginolyticus and define the fate of the infection by modulating lipid homeostasis. These findings may have important implication for understanding the L. vannamei and V. alginolyticus interactions, and provide a substantial dataset for further research and may deliver the basis for preventing the bacterial diseases.

TBC domain family 7-like enhances the tolerance of Penaeus vannamei to ammonia nitrogen by the up-regulation of autophagy.

TBC domain family 7 (TBC1D7) is one of the subunits of tuberous sclerosis complex (TSC) and an important regulator of autophagosome biogenesis. However, the function of TBC1D7 is not fully understood in crustaceans. In the present study, TBC1D7 was identified from Penaeus vannamei. The complete coding sequence of PvTBC1D7 was of 960 bp encoding a predicted polypeptide of 319 amino acids with one conserved TBC domain, which shared high similarity with TBC1D7 of that other species. The mRNA of PvTBC1D7 was highly expressed in hemocyte and hepatopancreas, and the PvTBC1D7 protein was localized specifically in the cytoplasm of hemocyte of shrimp. Besides, PvTBC1D7 was co-localized with PvTSC1 in the cytoplasm of shrimp, indicating that there might existed a binding relationship between PvTBC1D7 and PvTSC1. During the ammonia nitrogen stress, the mRNA transcripts of PvTBC1D7 were significantly upregulated in hemocyte, hepatopancreas, and gill. Functionally, overexpression of PvTBC1D7 in vitro restored the inhibition to autophagy caused by chloroquine (CLQ) and increased the autophagy level, while the silencing of PvTBC1D7 could inhibit the autophagy. More importantly, after interfering with PvTBC1D7, the autophagy level decreased significantly both in hepatopancreas and hemocyte of P. vannamei, the mRNA expression of PvmTOR was increased remarkably with the significantly decrease of autophagy-related genes (PvATG12 and PvATG14). And the reduction of PvTBC1D7 remarkably exacerbated the damage of hepatopancreas, increased the accumulation of ROS, and reduced the survival proportion of shrimp under ammonia nitrogen stress. Altogether, these results indicated that PvTBC1D7 might positively regulate the autophagy by stabilizing the negative regulation of mTOR by TSC complex, reduce the oxidative stress damage and improve shrimp ammonia nitrogen tolerance.

Electrochemical Behavior and Interfacial Delamination of a Polymer-Coated Galvanized Steel System in Acid Media.

The degradation behavior of polymer coatings is essential for their protective performance under various corrosive environments. Herein, electrochemical impedance spectroscopy (EIS) is employed to study the corrosion behavior and interfacial delamination of a polymer-coated metal system exposed to 0.1, 0.5, and 1 mol/L H2SO4 solutions at 50 °C. The electrochemical impedance spectra are analyzed using different equivalent circuits to derive the time dependence of the parameters of the coating, delaminated area, and interfacial processes. The phase angle at 10 Hz (θ10 Hz) is not appropriate in the case of higher delamination area ratio α, while θ10 kHz provides a rapid approach to evaluate the degradation of polymer-coated metal systems. The frequency of the phase angle at -45° (f -45°) leads to a wrong evaluation for higher α and can be no longer viewed as the breakpoint frequency. The frequency f p obtained by the changing rate of phase angle (CRPA) method is proposed to monitor the coating degradation and determine the breakpoint frequency with the consideration of dispersive number n. The frequency f EIS derived from fitting EIS spectra shows a good agreement with f p, which can contribute to clarify the evolution in the process of degradation.

Identification of prognosis-related molecular subgroups based on DNA methylation in pancreatic cancer.

BACKGROUND: Pancreatic cancer (PC) is one of the most lethal and aggressive cancer malignancies. The lethality of PC is associated with delayed diagnosis, presence of distant metastasis, and its easy relapse. It is known that clinical treatment decisions are still mainly based on the clinical stage and pathological grade, which are insufficient to determine an appropriate treatment. Considering the significant heterogeneity of PC biological characteristics, the current clinical classificatory pattern relying solely on classical clinicopathological features identification needs to be urgently improved. In this study, we conducted in-depth analyses to establish prognosis-related molecular subgroups based on DNA methylation signature. RESULTS: DNA methylation, RNA sequencing, somatic mutation, copy number variation, and clinicopathological data of PC patients were obtained from The Cancer Genome Atlas (TCGA) dataset. A total of 178 PC samples were used to develop distinct molecular subgroups based on the 4227 prognosis-related CpG sites. By using consensus clustering analysis, four prognosis-related molecular subgroups were identified based on DNA methylation. The molecular characteristics and clinical features analyses based on the subgroups offered novel insights into the development of PC. Furthermore, we built a risk score model based on the expression data of five CpG sites to predict the prognosis of PC patients by using Lasso regression. Finally, the risk score model and other independent prognostic clinicopathological information were integrative utilised to construct a nomogram model. CONCLUSION: Novel prognosis-related molecular subgroups based on the DNA methylation signature were established. The specific five CpG sites model for PC prognostic prediction and the derived nomogram model are effective and intuitive tools. Moreover, the construction of molecular subgroups based on the DNA methylation data is an innovative complement to the traditional classification of PC and may contribute to precision medicine development, therapeutic efficacy prediction, and clinical decision guidance.

Surgical Treatment for Asymptomatic Congenital Pulmonary Airway Malformations in Children: Waiting or Not?

INTRODUCTION: Infection is undoubtedly the most important factor in influencing the timing and surgical strategy of congenital pulmonary airway malformation (CPAM) surgery. However, there have been no studies on the optimal timing of surgery for patients based on the probability of infection. The aim of this study was performed to explore the optimal timing of surgery of CPAM in children from the risk of infection. MATERIALS AND METHODS: The correlation of age distribution and pulmonary infection of 237 children diagnosed by pathology from January 2012 to January 2020 in Guangzhou Women and Children's Medical Center were analyzed retrospectively. We defined the cases with preoperative computed tomographic findings of infection, pathological findings of large number of neutrophils, tissue cells, and abscess formation as the infection group. RESULTS: The rate of infection in patients less than 2 years old was significantly lower than in patients over 2 years old (11.4% vs. 45.7%, p < 0.001). And the pulmonary lobectomy rate of patients with infection (29.0%) was significantly higher than in noninfected patients (17.2%) and whole patients (36.3%), p = 0.033. Patients with infection lose more blood during surgery (noninfected patients: 81.76 ± 13.14 mL, infected patients: 145.10 ± 25.39 mL, p = 0.027). The univariate analysis revealed that the infection rate of patients over 2 years old was 3.084 times that of patients ≤2 years old (odds ratio [OR]: 3.084, 95% confidence interval [CI]: 1.196-7.954; p = 0.020). The infection rate of CPAM types III and IV patients is lower than types I and II (OR: 0.531, 95% CI: 0.307-0.920; p = 0.024). CONCLUSION: In consideration of the high risk of infection, lower minimally invasive surgery rate, an increased rate of pulmonary lobectomy, and more blood loss in patients over 2 years old, our study also supports early surgical treatment. Therefore, we suggest that for asymptomatic patients with CPAM I and CPAM II, surgical treatment should be performed when they are less than 2 years old, providing more options for surgical strategies and monitoring of CPAM patients.

Increasing of FKBP9 can predict poor prognosis in patients with prostate cancer.

BACKGROUND: FK506 binding protein 9 (FKBP9) has been reported and identified for a long time, but its relationship with cancer is rarely studied. For example, the role of FK506 binding protein 9 in prostate cancer (PCa) is still unclear. Therefore, we decided to detect the expression level of FKBP9 in PCa and explore its clinical significance. METHODS: The expression level of FKBP9 protein was detected by immunohistochemistry. In addition, it was demonstrated by high-throughput sequencing of mRNA levels in the TCGA (cancer genome atlas) dataset of 499 patients. Kaplan-meier analysis and Cox proportional hazard regression model were used to evaluate the relationship between FKBP9 expression and survival in prostate cancer patients. RESULTS: The expression of FKBP9 was localized in the cytoplasm, which in normal prostate tissues was obviously lower than that in PCa tissues (P = 0.001). High expression of FKBP9 was related with lymph node metastasis (P = 0.022) and distant metastasis (P = 0.028). Kaplan-Meier survival analysis revealed that the BCR-free survival of PCa patients with high FKBP9 level was significantly shortened (P=0.041). CONCLUSIONS: FKBP9 may be a cancer promoter that enhances PCa progression, and the level of FKBP9 may be used as an independent precursor of PCa patients.

ERα and Wnt/ß­catenin signaling pathways are involved in angelicin­dependent promotion of osteogenesis.

Reports of the ameliorative effect of angelicin on sex hormone deficiency­induced osteoporosis have highlighted this compound as a candidate for the treatment of osteoporosis. However, the molecular mechanisms of action of angelicin on osteoblast differentiation have not been thoroughly researched. The aim of the present study was to evaluate the effect of angelicin on the proliferation, differentiation and mineralization of rat calvarial osteoblasts using a Cell Counting Kit­8, alkaline phosphatase activity and the expression of osteogenic genes and proteins. Treatment with angelicin promoted the proliferation, matrix mineralization and upregulation of osteogenic marker genes including collagen type I α 1 and bone γ­carboxyglutamate in fetal rat calvarial osteoblasts. Furthermore, angelicin promoted the expression of ß­catenin and runt related transcription factor 2, which serve a vital role in the Wnt/ß­catenin signaling pathway. Consistently, the osteogenic effect of angelicin was attenuated by the use of a Wnt inhibitor. Moreover, angelicin increased the expression of estrogen receptor α (ERα), which also serves a key role in osteoblast differentiation. Taken together, these results demonstrated that angelicin may promote osteoblast differentiation through activation of ERα and the Wnt/ß­catenin signaling pathway.