Circ_0060967 facilitates proliferation, migration, and invasion of non-small-cell lung cancer cells by sponging miR-660-3p/UBN2.

Growing evidence has implied that circular RNAs (circRNAs) are involved in multiple tumors progression. This study firstly uncovered the function of circ_0060967 in non-small-cell lung cancer (NSCLC) progression. Quantitative real-time polymerase chain reaction was employed to monitor circ_0060967, miR-660-3p, and ubinuclein-2 (UBN2) mRNA expression in clinical tissues and cell lines. Cell counting kit-8 assay, 5-ethynyl-20-deoxyuridine assay, and Transwell assay were recruited to research cells viability, proliferation, migration, and invasion. BALB/c nude mice were applied to perform in vivo study. Fluorescence in situ hybridization was adopted to explore the subcellular location of circ_0060967 in NSCLC cells. Dual luciferase reporter gene assay and RNA pull-down assay were utilized to identify the interaction among circ_0060967, miR-660-3p, and UBN2. Western blot was employed for UBN2 protein expression investigation in NSCLC cells. Immunohistochemistry was utilized to research UBN2 protein expression in clinical tissues and xenograft tumor tissues. Circ_0060967 was aberrantly over-modulated in NSCLC tissues and cells. High circ_0060967 expression implied grim prognosis. Loss of circ_0060967 weakened NSCLC cells viability, proliferation, migration, invasion, and in vivo growth. Circ_0060967 was mainly distributed in the cytoplasm of NSCLC cells. Down-modulated miR-660-3p and up-regulated UBN2 were found in NSCLC patients. miR-660-3p was sponged by circ_0060967 and it directly targeted UBN2. miR-660-3p down-modulation rescued the suppression of circ_0060967 loss on NSCLC cells viability, proliferation, migration, and invasion. Circ_0060967 facilitated NSCLC progression by enhancing UBN2 expression via sponging miR-660-3p. It might be a promising target for NSCLC treatment.

A meta-analysis of the prognostic impact of tissue golgi protein 73 (tGP73) in hepatocellular carcinoma.

INTRODUCTION: To date, an increasing number of studies have revealed that GP73 may have prognostic value in liver cancer. However, most of the studies evaluated serum GP73, and the results regarding the prognostic value of tGP73 in liver cancer are still controversial. Therefore, in this meta-analysis, we aimed to determine whether tGP73 has any prognostic value in patients with HCC. MATERIALS AND METHODS: Relevant publications were searched for in PubMed, EMBASE, OVID, the Cochrane Library, and the Web of Science databases up to March 2023. The hazard ratio (HR) or odds ratio (OR) with corresponding 95% confidence intervals (95% CIs) of eligible studies were assessed by fixed-effects or random-effects models. In addition, subgroup analyses were conducted to investigate the possible causes of heterogeneity, and publication bias analysis was also performed to assess the reliability of the meta-analysis results. RESULTS: A total of 10 studies were included. These studies included 1569 HCC patients, and a meta-analysis was performed. The results of our meta-analysis showed that higher GP73 expression levels were significantly associated with poorer OS (HR = 1.87, 95% CI: 1.41-2.48, P < 0.0001, I2 = 58%). However, there was no significant correlation between high GP73 expression and disease-free survival (DFS) (HR: 1.43, 95% CI: 0.93-2.33, P = 0.100). In addition, abnormal GP73 expression was also related to higher tumour tissue differentiation grade (OR = 3.03, 95% CI = 2.01-4.57, P < 0.0001, I2 = 89%), later tumour stage (OR = 5.89, 95% CI = 2.31-14.99, P < 0.0001, I2 = 0%), vascular invasion (OR = 1.72, 95% CI = 1.12-2.64, P = 0.010, I2 = 0%), multiple tumours (OR = 2.44, 95% CI = 1.37-3.68, P = 0.001, I2 = 44%) and early postoperative tumour recurrence (OR = 1.92, 95% CI = 1.10-3.28, P = 0.020, I2 = 62%). CONCLUSIONS: The meta-analysis showed that the overexpression of GP73 may be related to a poor prognosis of HCC, and it may also have a predictive effect on the invasion and metastasis of HCC.

Characterization of the genomic and transcriptional structure of chicken NRG4 gene.

Neuregulin 4 (NRG4) is an important adipocytokine, which plays crucial roles in maintaining energy balance, regulating glucose and lipid metabolism, and preventing non-alcoholic fatty liver disease in mammals. At present, the genomic organization, transcript and protein isoforms of human NRG4 gene have been fully explored. Previous studies in our laboratory have shown that the NRG4 gene is expressed in chicken adipose tissue, but the chicken NRG4 (cNRG4) genomic structure, transcript and protein isoforms are still unknown. To this end, in this study, the genomic and transcriptional structure of the cNRG4 gene were systematically investigated using rapid amplification of cDNA ends (RACE) and reverse transcription-polymerase chain reaction (RT-PCR). The results showed that the coding region (CDS) of the cNRG4 gene was small, but it had a very complex transcriptional structure characterized by multiple transcription start sites, alternative splicing, intron retention, cryptic exons, and alternative polyadenylation, thus leading to production of four 5?UTR isoforms (cNRG4 A, cNRG4 B, cNRG4 C, and cNRG4 D) and six 3?UTR isoforms (cNRG4 a, cNRG4 b, cNRG4 c, cNRG4 d, cNRG4 e, and cNRG4 f) of the cNRG4 gene. The cNRG4 gene spanned 21,969 bp of genomic DNA (Chr.10:3,490,314~3,512,282) and consisted of 11 exons and 10 introns. Compared with the cNRG4 gene mRNA sequence (NM_001030544.4), two novel exons and one cryptic exon of the cNRG4 gene were identified in this study. Bioinformatics analysis, RT-PCR, cloning and sequencing analysis showed that the cNRG4 gene could encode three protein isoforms (cNRG4-1, cNRG4-2 and cNRG4-3). This study lays a foundation for further research on the function and regulation of the cNRG4 gene.

An effective method to reduce lymphatic drainage post-lateral cervical lymph node dissection of differentiated thyroid cancer: a retrospective analysis.

BACKGROUND: Lymph or chyle leak (LL/CL) is severe complications after lateral cervical lymph node dissection (LLND), mainly due to iatrogenic injury of the lymphatic duct. Efficient and well-operated methods to reduce postoperative drainage are still lacking. This was a feasibility study to evaluate a new method of preventing LL/CL compared to conventional treatment. METHOD: We retrospectively analyzed 20 consecutive patients who used the "pedicled omohyoid flap covering (POFC)" method during LLND from January 2019 to December 2021 in our center as an observation group. Another 20 consecutive patients used the conventional method during LLND in this period as a control group. The clinical and pathological features of the two groups were compared, and the related factors that affected postoperative lymphatic drainage were analyzed with Cox proportional hazards models. RESULTS: The drainage volume per 24 h and the incidence of LL/CL in the control group were both higher than that in the observation group (all P < 0.05), and the number of lymph nodes dissected in the IV region > 10 and the use of the POFC method were the independent risk factors that significantly affected the incidence of LL/CL post LLND (all P < 0.05). CONCLUSIONS: POFC is a safe and useful method for reducing drainage and preventing LL/CL post-LLND, especially for patients with heavy metastasis of the lymph nodes in the IV region.

Studies on the Performance of Molar Porous Root-Analogue Implant by Finite Element Model Simulation and Verification of a Case Report.

PURPOSE: The aim of this study was to evaluate the effect of porous layer thickness in a 3-dimensionally printed 1-piece molar porous root-analogue implant (RAI) on the biomechanical properties of the peri-implant bone and the clinical efficacy of one such implant in a patient. MATERIALS AND METHODS: Three RAIs with different superficial porous layer thicknesses (0.5 mm, 1 mm, and fully porous) were designed and assembled using a mandible model and then solidified to obtain 3 finite elements models, denoted A, B, and C. Finite element analysis was performed to analyze the stress on the solid and porous structures of the RAIs and the stress and strain experienced by the bone surrounding the implant. RAIs were fabricated by selective laser melting. An unrepairable molar in a single patient was selected for replacement. An RAI was designed and prepared and then implanted into the alveolar bone immediately after minimally invasive extraction of the damaged tooth. Definitive restorations were placed after a 3-month period of uninterrupted healing. RESULTS: The stress concentration observed in the 3 types of RAI was principally between the solid and porous interface contact points, with maximum stress on the solid and porous structures smaller than that of the respective yield strength. The introduction of a porous structure on the surface of the RAIs increased peri-implant bone stress, which increased with thickness of the porous layer. The 3-dimensionally printed porous RAI exhibited excellent initial stability immediately after implantation. After continual observation for 6 months, it was found that bone surrounding the root had infiltrated into the RAI, achieving good osseointegration. CONCLUSIONS: Stress shielding can be reduced by decreasing the elastic modulus of the implant, with the interface between implant and bone allowing more appropriate stress conduction. A 1-piece porous RAI fabricated using 3-dimensional printing establishes a new indication for immediate implantation after extraction.

A Trio-RhoA-Shroom3 pathway is required for apical constriction and epithelial invagination.

Epithelial invagination is a common feature of embryogenesis. An example of invagination morphogenesis occurs during development of the early eye when the lens placode forms the lens pit. This morphogenesis is accompanied by a columnar-to-conical cell shape change (apical constriction or AC) and is known to be dependent on the cytoskeletal protein Shroom3. Because Shroom3-induced AC can be Rock1/2 dependent, we hypothesized that during lens invagination, RhoA, Rock and a RhoA guanine nucleotide exchange factor (RhoA-GEF) would also be required. In this study, we show that Rock activity is required for lens pit invagination and that RhoA activity is required for Shroom3-induced AC. We demonstrate that RhoA, when activated and targeted apically, is sufficient to induce AC and that RhoA plays a key role in Shroom3 apical localization. Furthermore, we identify Trio as a RhoA-GEF required for Shroom3-dependent AC in MDCK cells and in the lens pit. Collectively, these data indicate that a Trio-RhoA-Shroom3 pathway is required for AC during lens pit invagination.

Balanced Rac1 and RhoA activities regulate cell shape and drive invagination morphogenesis in epithelia.

Epithelial bending is a central feature of morphogenesis in animals. Here we show that mutual antagonism by the small Rho GTPases Rac1 and RhoA determines cell shape, tissue curvature, and invagination activity in the model epithelium of the developing mouse lens. The epithelial cells of the invaginating lens placode normally elongate and change from a cylindrical to an apically constricted, conical shape. RhoA mutant lens placode cells are both longer and less apically constricted than control cells, thereby reducing epithelial curvature and invagination. By contrast, Rac1 mutant lens placode cells are shorter and more apically restricted than controls, resulting in increased epithelial curvature and precocious lens vesicle closure. Quantification of RhoA- and Rac1-dependent pathway markers over the apical-basal axis of lens pit cells showed that in RhoA mutant epithelial cells there was a Rac1 pathway gain of function and vice versa. These findings suggest that mutual antagonism produces balanced activities of RhoA-generated apical constriction and Rac1-dependent cell elongation that controls cell shape and thus curvature of the invaginating epithelium. The ubiquity of the Rho family GTPases suggests that these mechanisms are likely to apply generally where epithelial morphogenesis occurs.

Risk factors, prognostic factors, and nomograms for distant metastases in patients with gastroenteropancreatic neuroendocrine tumors: a population-based study.

Background: Patients with gastroenteropancreatic neuroendocrine tumors (GEP-NETs) have a poor prognosis for distant metastasis. Currently, there are no studies on predictive models for the risk of distant metastasis in GEP-NETs. Methods: In this study, risk factors associated with metastasis in patients with GEP-NETs in the Surveillance, Epidemiology, and End Results (SEER) database were analyzed by univariate and multivariate logistic regression, and a nomogram model for metastasis risk prediction was constructed. Prognostic factors associated with distant metastasis in patients with GEP-NETs were analyzed by univariate and multivariate Cox, and a nomogram model for prognostic prediction was constructed. Finally, the performance of the nomogram model predictions is validated by internal validation set and external validation set. Results: A total of 9145 patients with GEP-NETs were enrolled in this study. Univariate and multivariate logistic analysis demonstrated that T stage, N stage, tumor size, primary site, and histologic types independent risk factors associated with distant metastasis in GEP-NETs patients (p value < 0.05). Univariate and multivariate Cox analyses demonstrated that age, histologic type, tumor size, N stage, and primary site surgery were independent factors associated with the prognosis of patients with GEP-NETs (p value < 0.05). The nomogram model constructed based on metastasis risk factors and prognostic factors can predict the occurrence of metastasis and patient prognosis of GEP-NETs very effectively in the internal training and validation sets as well as in the external validation set. Conclusion: In conclusion, we constructed a new distant metastasis risk nomogram model and a new prognostic nomogram model for GEP-NETs patients, which provides a decision-making reference for individualized treatment of clinical patients.

A self-organized sandwich structure of chromium nitride for ultra-long lifetime in liquid sodium.

The development of fast neutron reactors with improved efficiency and sustainability, being a tangible solution to the large-scale utilization of nuclear energy, serves as a critical step prior to the commercialization of fusion energy. These reactors use liquid metal coolants, which can weaken the durability of metallic components. Conventional design of protective coatings counts upon thermodynamics, which often overlooks the kinetic factors such as structural evolutions, resulting in deteriorated coating properties. Herein, we present a novel interface-engineering strategy involving the control of the phase transformation direction and interface diffusion reaction. Through iterations of self-organization, desired surfaces and interfaces can be achieved for materials used in harsh environments. Specifically, a CrN-coated steel sample with an interfacial Cr layer was designed and fabricated. After ultra-long (up to 6000 h) immersion in liquid sodium, the CrN/Cr coating structure was converted into a sandwich Cr2N/CrN/Cr2N structure dynamically. As a consequence, the coating system exhibited enhanced properties, namely increased surface hardness (by ∼36%), reduced coefficient of friction (by ∼13%), and enhanced interfacial adhesion (by ∼37%). Thus, the proposed strategy can guide the future design of robust coatings with ultra-long service life in harsh environments.

AQP1 Deficiency Drives Phthalate-Induced Epithelial Barrier Disruption through Intestinal Inflammation.

Di-2-ethylhexyl phthalate (DEHP) is frequently used as a plasticizer to enhance the plasticity and durability of agricultural products, which pose adverse effects to human health and the environment. Aquaporin 1 (AQP1) is a main water transport channel protein and is involved in the maintenance of intestinal integrity. However, the impact of DEHP exposure on gut health and its potential mechanisms remain elusive. Here, we determined that DEHP exposure induced a compromised duodenum structure, which was concomitant with mitochondrial structural injury of epithelial cells. Importantly, DEHP exposure caused duodenum inflammatory epithelial cell damage and strong inflammatory response accompanied by activating the TLR4/MyD88/NF-κB signaling pathway. Mechanistically, DEHP exposure directly inhibits the expression of AQP1 and thus leads to an inflammatory response, ultimately disrupting duodenum integrity and barrier function. Collectively, our findings uncover the role of AQP1 in phthalate-induced intestinal disorders, and AQP1 could be a promising therapeutic approach for treating patients with intestinal disorders or inflammatory diseases.

Phthalate drives splenic inflammatory response via activating HSP60/TLR4/NLRP3 signaling axis-dependent pyroptosis.

As the most produced phthalate, di-(2-ethylhexyl) phthalate (DEHP) is a widely environmental pollutant primarily used as a plasticizer, which cause the harmful effects on human health. However, the impact of DEHP on spleen and its underlying mechanisms are still unclear. Pyroptosis is a novel form of cell death induced by activating NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasomes and implicated in pathogenesis of numerous inflammatory diseases. The current study aimed to explore the impact of DEHP on immune inflammatory response in mouse spleen. In this study, the male ICR mice were treated with DEHP (200 mg/kg) for 28 days. Here, DEHP exposure caused abnormal pathohistological and ultrastructural changes, accompanied by inflammatory cells infiltration in mouse spleen. DEHP exposure arouse heat shock response that involves increase of heat shock proteins 60 (HSP60) expression. DEHP also elevated the expressions of toll-like receptor 4 (TLR4) and myeloid differentiation protein 88 (MyD88) proteins, as well as the activation of NF-κB pathway. Moreover, DEHP promoted NLRP3 inflammasome activation and triggered NLRP3 inflammasome-induced pyroptosis. Mechanistically, DEHP drives splenic inflammatory response via activating HSP60/TLR4/NLRP3 signaling axis-dependent pyroptosis. Our findings reveal that targeting HSP60-mediated TLR4/NLRP3 signaling axis may be a promising strategy for inflammatory diseases treatment.

Phthalates Induce Neurotoxicity by Disrupting the Mfn2-PERK Axis-Mediated Endoplasmic Reticulum-Mitochondria Interaction.

Di-(2-ethylhexyl) phthalate (DEHP), as the most common phthalate, has been extensively used as a plasticizer to improve the plasticity of agricultural products, which pose severe harm to human health. Mitochondrial dynamics and endoplasmic reticulum (ER) homeostasis are indispensable for maintaining mitochondria-associated ER membrane (MAM) integrity. In this study, we aimed to explore the effect of DEHP on the nervous system and its association with the ER-mitochondria interaction. Here, we showed that DEHP caused morphological changes, motor deficits, cognitive impairments, and blood-brain barrier disruption in the brain. DEHP triggered ER stress, which is mainly mediated by protein kinase R-like endoplasmic reticulum kinase (PERK) signaling. Moreover, DEHP-induced mitofusin-2 (Mfn2) downregulation results in imbalance of the mitochondrial dynamics. Interestingly, DEHP exposure impaired MAMs by inhibiting the Mfn2-PERK interaction. Above all, this study elucidates the disruption of the Mfn2-PERK axis-mediated ER-mitochondria interaction as a phthalate-induced neurotoxicity that could be potentially developed as a novel therapy for neurological diseases.

Pax6-dependent Shroom3 expression regulates apical constriction during lens placode invagination.

Embryonic development requires a complex series of relative cellular movements and shape changes that are generally referred to as morphogenesis. Although some of the mechanisms underlying morphogenesis have been identified, the process is still poorly understood. Here, we address mechanisms of epithelial morphogenesis using the vertebrate lens as a model system. We show that the apical constriction of lens epithelial cells that accompanies invagination of the lens placode is dependent on Shroom3, a molecule previously associated with apical constriction during morphogenesis of the neural plate. We show that Shroom3 is required for the apical localization of F-actin and myosin II, both crucial components of the contractile complexes required for apical constriction, and for the apical localization of Vasp, a Mena family protein with F-actin anti-capping function that is also required for morphogenesis. Finally, we show that the expression of Shroom3 is dependent on the crucial lens-induction transcription factor Pax6. This provides a previously missing link between lens-induction pathways and the morphogenesis machinery and partly explains the absence of lens morphogenesis in Pax6-deficient mutants.

Analysis of EIF4G1 in ethnic Chinese.

BACKGROUND: Eukaryotic translation initiation factor 4-gamma 1 (EIF4G1) gene mutations have recently been reported in autosomal dominant, late-onset Parkinson's disease (LOPD). We carried out genetic analysis to determine the prevalence of EIF4G1 variants in an ethnic Chinese population and to better understand the association between EIF4G1 and PD. METHODS: We conducted a comprehensive genetic analysis of EIF4G1 in a cohort of 29 probands of autosomal dominant, LOPD families. Polymerase chain reaction (PCR) analysis and sequencing was carried out of the entire EIF4G1 exonic regions and exon-intron boundaries. Specific mutation and exonic variants were chosen for further sequencing in a case-control study including 503 sporadic PD and 508 healthy controls. Statistical significance was analyzed by the Chi-square test. RESULTS: Our analysis revealed three exonic variants (rs2230571, rs13319149 and rs2178403) and eight intronic variants across the entire EIF4G1 gene. No reported mutations were detected in EIF4G1 exonic regions. The synonymous coding variant rs2230571 in exon 27 and the eight intronic variants were not used for further sequencing, but the specific mutation c.3614G > A (p.R1205H) and the two nonsynonymous variants (rs13319149 and rs2178403) were chosen for further analysis in a case-control study. None of the 503 sporadic PD or 508 healthy controls carried p.R1205H, and there was no statistical significance in rs2178403 genotype or allele frequencies in EIF4G1 between the PD cases and the healthy controls (p = 0.184 and p = 0.774, respectively; Chi-square test). The rs13319149 genotype in all PD cases and healthy controls was GG. CONCLUSIONS: Our data indicate that in an ethnic Chinese population, the pathogenic mutation p.R1205H in EIF4G1 is not common and that EIF4G1 exonic variants rs2178403 and rs13319149 are not associated with PD. EIF4G1 does not appear to be a frequent cause of PD in this ethnic Chinese population.

[Using in-situ reflectance to monitor the chlorophyll concentration in the surface layer of tidal flat].

An optical monitoring method is proposed for the rapid, non destructive measurements of chlorophyll concentration (Chl-a) in the surface sediments of emerged tidal flat, and it can be further applied in remote sensing work. Hyperspectral reflectance of intertidal sediments were measured in day time at the tidal flats of the Sishili Bay, the Northern Yellow Sea, and surface sediments (3 mm) were sampled for the in-door measurements of Chl-a. On the basis of the reflectance at 650, 675 and 700 nm, the indices of normalized difference index of microbenthos (NDI-MPB) and trough depth (T-depth) were proposed for the measurements of microphytobenthos biomass. T-depth can be used to remove the linear background spectral noises and indicate the existence of microphytobenthos; Good linear relationship was observed between NDI-MPB and Chl-a content in sediments (2.22-49.36 mg x m(-2), r > 0.99), which may be used to monitor the biomass of microphy to benthos.

Predictive value for mortality of left ventricular wall thickness in dilated cardiomyopathy.

AIMS: The purpose of this study was to explore the predictive value of wall thickness measured by cardiac magnetic resonance (CMR) for all-cause mortality in dilated cardiomyopathy (DCM) patients. METHODS AND RESULTS: DCM patients who underwent CMR and completed the regular follow-up were included in this study. The left ventricular end-diastolic diameter (LVDd), left ventricular end-diastolic volume (LVEDV), left ventricular posterior wall thickness (PWT), interventricular septum thickness (IVST), left ventricular ejection fraction, and left ventricular mass (LVM) were measured by CMR. The presence and extent of late gadolinium enhancement (LGE) were also assessed. The relative posterior wall thickness (RWTPW ) and relative interventricular septum wall thickness (RWTIVS ) were defined by the following equations: RWTPW  = (2 × PWT)/LVDd, and RWTIVS  = (2 × IVST)/LVDd. All patients received regular telephone and outpatient follow-up. The primary endpoint was all-cause mortality. A total of 161 patients were enrolled in this study, including 126 (78.3%) males. The mean age was 52.3 ± 13.6 years. During the median follow-up of 47 months (interquartile range 32-57 months), 41 (24.8%) patients died. Compared with the non-death group, LVDd (75.2 ± 11.9 vs. 70.5 ± 8.8 mm; P = 0.025) was greater in the death group, while PWT [5.2 mm (3.7-6.8) vs. 6.9 mm (5.3-8.6); P < 0.001], IVST [8.2 mm (6.5-9.5) vs. 9.3 mm (7.4-10.5); P = 0.005], RWTPW [0.15 (0.11-0.19) vs. 0.20 (0.15-0.25); P < 0.001], RWTIVS [0.22 (0.17-0.26) vs. 0.26 (0.22-0.31); P < 0.001], and LVM/LVEDV ratio (0.5 ± 0.2 vs. 0.7 ± 0.2 g/mL; P < 0.001) were lower. The presence of LGE [LGE(+)] was more frequent in the death group (75.6% vs. 58.3%; P = 0.048). However, the LGE extent was not significantly different between the two groups [4 (1-7) vs. 2 (0-6); P = 0.096]. Multivariate Cox regression analysis showed that PWT [hazard ratio (HR) 0.086, 95% confidence interval (CI) 0.665-0.976; P < 0.05] and RWTPW (HR 0.001, 95% CI 0.000-0.502; P < 0.05) were independent predictors of all-cause death. In contrast, IVST, RWTIVS , and the presence of LGE were not clearly associated with death. CONCLUSIONS: PWT measured by CMR is an independent predictor of all-cause mortality in DCM patients. However, there was no significant correlation between septum wall thickness and mortality.

Cdc42- and IRSp53-dependent contractile filopodia tether presumptive lens and retina to coordinate epithelial invagination.

The vertebrate lens provides an excellent model with which to study the mechanisms required for epithelial invagination. In the mouse, the lens forms from the head surface ectoderm. A domain of ectoderm first thickens to form the lens placode and then invaginates to form the lens pit. The epithelium of the lens placode remains in close apposition to the epithelium of the presumptive retina as these structures undergo a coordinated invagination. Here, we show that F-actin-rich basal filopodia that link adjacent presumptive lens and retinal epithelia function as physical tethers that coordinate invagination. The filopodia, most of which originate in the presumptive lens, form at E9.5 when presumptive lens and retinal epithelia first come into close contact, and have retracted by E11.5 when invagination is complete. At E10.5--the lens pit stage--there is approximately one filopodium per epithelial cell. Formation of filopodia is dependent on the Rho family GTPase Cdc42 and the Cdc42 effector IRSp53 (Baiap2). Loss of filopodia results in reduced lens pit invagination. Pharmacological manipulation of the actin-myosin contraction pathway showed that the filopodia can respond rapidly in length to change inter-epithelial distance. These data suggest that the lens-retina inter-epithelial filopodia are a fine-tuning mechanism to assist in lens pit invagination by transmitting the forces between presumptive lens and retina. Although invagination of the archenteron in sea urchins and dorsal closure in Drosophila are known to be partly dependent on filopodia, this mechanism of morphogenesis has not previously been identified in vertebrates.

6-Fluoro-1H-indole-3-carb-oxy-lic acid.

In the title compound, C(9)H(6)FNO(2), all the non-H atoms are approximately coplanar, the carb-oxy O atoms deviating by 0.0809 and -0.1279 Šfrom the indole plane. In the crystal, O-H⋯O hydrogen bonds link the mol-ecules into dimers which are linked via N-H⋯O hydrogen bonds and π-π inter-actions [centroid-centroid distance = 3.680 (2) Å].

Lncrna FGD5-AS1 Aggravates Myocardial Ischemia-Reperfusion Injury by Sponging Mir-129-5p.

Background: LncRNA FGD5-AS1 regulates the pathogenesis of many human diseases. We aimed to elucidate the function of lncRNA FGD5-AS1 and the regulatory mechanism of lncRNA FGD5-AS1/miR-129-5p in myocardial ischemia-reperfusion (I/R) injury. Methods: Myocardial I/R injury mice model and H/R treated H9c2 cells were established. RT-qPCR and Western blot analysis were used to detect the mRNA and protein expression. Cell viability was detected by MTT assay. Dual luciferase reporter assay was applied to confirm the relationship between lncRNA FGD5-AS1 and miR-129-5p. Results: LncRNA FGD5-AS1 was upregulated in myocardial I/R injury mice models and H/R treated H9c2 cells. Functionally, knockdown of lncRNA FGD5-AS1 promoted cell viability and inhibited apoptosis in H/R treated H9c2 cells. In addition, lncRNA FGD5-AS1 directly targets miR-129-5p. Upregulation of lncRNA FGD5-AS1 weakened the protective effect of miR-129-5p on myocardial I/R injury. Conclusion: LncRNA FGD5-AS1 aggravates myocardial I/R injury by downregulating miR-129-5p.

Does authoritarianism necessarily stifle creativity? The role of discipline-focused authoritarian leadership.

A burgeoning body of research has shown that authoritarian leadership (AL) embodies the characteristics of "light" and "dark," meaning that it does not always have a negative impact on employees' creative activities. However, studies explaining this potential positive effect are insufficient. To extend the AL and creativity literature, we draw on self-determination theory and event system theory, and elicit discipline-focused AL and appointment event criticality to examine whether, when, and how authoritarian leaders affect employee creativity positively. With time-lagged data collected from 435 employees and their direct leaders in China, we found that discipline-focused AL has an indirect positive effect on employee creativity through creative self-efficacy. Additionally, appointment event criticality strengthens the positive relationship between discipline-focused AL and creative self-efficiency, and the indirect impact of discipline-focused AL on employee creativity through creative self-efficiency. The theoretical and practical implications are discussed.