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Chloroplast RNA splicing and ribosome maturation (CRM) domain proteins are a family of plant-specific proteins associated with RNA binding. In this study, we have conducted a detailed characterization of a novel rice CRM gene (LOC_Os04g39060) mutant, yl4, which showed yellow-green leaves at all the stages, had fewer tillers, and had a decreased plant height. Map-based cloning and CRISPR/Cas9 editing techniques all showed that YL4 encoded a CRM domain protein in rice. In addition, subcellular localization revealed that YL4 was in chloroplasts. YL4 transcripts were highly expressed in all leaves and undetectable in roots and stems, and the mutation of YL4 affected the transcription of chloroplast-development-related genes. This study indicated that YL4 is essential for chloroplast development and affects some agronomic traits.
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OBJECTIVE: To characterize the traumatic brain injury profile and its associated risk factors in homeless individuals in Santa Clara County, CA. DESIGN: Observational cohort study SETTING: : Two homeless shelter health clinics in Santa Clara County, CA PARTICIPANTS: Currently or recently homeless individuals seeking health care at two homeless shelter health clinics between August 2013 and May 2014. INTERVENTIONS: Not applicable MAIN OUTCOME MEASURES: Demographics, traumatic brain injury incidence and characteristics RESULTS: Findings indicate that TBI history in the homeless population is higher (79.7%) than the general population (12%). Almost half of the population (49.2%) reported that their TBI occurred before the age of 18. 68.2% of participants reported sustaining a TBI with loss of consciousness. TBI due to violence (60%) was lower in this cohort compared to other homeless cohorts but was the main cause of injury regardless of age. Alcoholism was a risk factor for having more TBIs. No differences in TBI profile were found between genders. CONCLUSION: Our findings underscore the need for more research on the lifetime risk factors associated with TBI to prevent and reduce the number of brain injuries in homeless populations.
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Laryngeal squamous cell carcinoma (LSCC) is a prevalent human cancer with a complex pathogenesis that remains incompletely understood. Here, we unveil a long non-coding RNA (lncRNA) associated with LSCC tumorigenesis and progression. LOC730101 exhibits significant overexpression in human LSCC tissues, and elevated LOC730101 levels correlate with malignant clinicopathological characteristics. Moreover, we demonstrate that LOC730101 is encapsulated into exosomes in an hnRNPA2B1-dependent manner, serving as a promising plasma biomarker for discriminating LSCC patients from healthy individuals (AUC = 0.92 with 89.36% sensitivity and 86.36% specificity). Exosomes derived from LSCC cells enhance the viability, DNA synthesis rate, and invasiveness of normal nasopharynx epithelial cells, with pronounced effects observed upon LOC730101 overexpression. Additionally, exosomal LOC730101 promotes tumor growth in vivo. Mechanistically, exosomal LOC730101 internalization by normal nasopharynx epithelial cells leads to increased H3K4me3 levels on the p38 MAPK gamma (p38γ) promoter via direct interaction with hnRNPA2B1. This interaction activates p38γ transcription, ultimately driving LSCC tumorigenesis. Collectively, our findings uncover a novel exosomal lncRNA that mediates communication between normal and LSCC cells during LSCC carcinogenesis, suggesting that targeting LOC730101 may represent a promising therapeutic strategy for LSCC treatment.
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Carcinogenèse , Exosomes , Tumeurs du larynx , ARN long non codant , Humains , Exosomes/métabolisme , ARN long non codant/génétique , ARN long non codant/métabolisme , Tumeurs du larynx/anatomopathologie , Tumeurs du larynx/métabolisme , Tumeurs du larynx/génétique , Animaux , Lignée cellulaire tumorale , Carcinogenèse/génétique , Mâle , Ribonucléoprotéine nucléaire hétérogène du groupe A-B/métabolisme , Ribonucléoprotéine nucléaire hétérogène du groupe A-B/génétique , Souris , Femelle , Souris nude , Régulation de l'expression des gènes tumoraux , Adulte d'âge moyen , Prolifération cellulaire , Carcinome épidermoïde/anatomopathologie , Carcinome épidermoïde/métabolisme , Carcinome épidermoïde/génétique , Souris de lignée BALB CRÉSUMÉ
BACKGROUND: Metastasis is the leading cause of mortality in patients with colorectal cancer (CRC) and angiogenesis is a crucial factor in tumor invasion and metastasis. Long noncoding RNAs (lncRNAs) play regulatory functions in various biological processes in tumor cells, however, the roles of lncRNAs in CRC-associated angiogenesis remain to be elucidated in CRC, as do the underlying mechanisms. METHODS: We used bioinformatics to screen differentially expressed lncRNAs from TCGA database. LOC101928222 expression was assessed by qRT-PCR. The impact of LOC101928222 in CRC tumor development was assessed both in vitro and in vivo. The regulatory mechanisms of LOC101928222 in CRC were investigated by cellular fractionation, RNA-sequencing, mass spectrometric, RNA pull-down, RNA immunoprecipitation, RNA stability, and gene-specific m6A assays. RESULTS: LOC101928222 expression was upregulated in CRC and was correlated with a worse outcome. Moreover, LOC101928222 was shown to promote migration, invasion, and angiogenesis in CRC. Mechanistically, LOC101928222 synergized with IGF2BP1 to stabilize HMGCS2 mRNA through an m6A-dependent pathway, leading to increased cholesterol synthesis and, ultimately, the promotion of CRC development. CONCLUSIONS: In summary, these findings demonstrate a novel, LOC101928222-based mechanism involved in the regulation of cholesterol synthesis and the metastatic potential of CRC. The LOC101928222-HMGCS2-cholesterol synthesis pathway may be an effective target for diagnosing and managing CRC metastasis.
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Cholestérol , Tumeurs colorectales , Néovascularisation pathologique , ARN long non codant , ARN messager , Animaux , Humains , Mâle , Souris , , Lignée cellulaire tumorale , Cholestérol/métabolisme , Tumeurs colorectales/génétique , Tumeurs colorectales/anatomopathologie , Tumeurs colorectales/métabolisme , Régulation de l'expression des gènes tumoraux , Hydroxymethylglutaryl-coA synthase/génétique , Hydroxymethylglutaryl-coA synthase/métabolisme , Néovascularisation pathologique/génétique , Néovascularisation pathologique/métabolisme , Néovascularisation pathologique/anatomopathologie , ARN long non codant/génétique , ARN long non codant/métabolisme , ARN messager/génétique , ARN messager/métabolismeRÉSUMÉ
High-definition transcranial direct current stimulation (HD-tDCS) is a non-invasive brain stimulation technique that has been shown to be safe and effective in modulating neuronal activity. The present study investigates the effect of anodal HD-tDCS on haptic object perception and memory through stimulation of the lateral occipital complex (LOC), a structure that has been shown to be involved in both visual and haptic object recognition. In this single-blind, sham-controlled, between-subjects study, blindfolded healthy, sighted participants used their right (dominant) hand to perform haptic discrimination and recognition tasks with 3D-printed, novel objects called "Greebles" while receiving 20 min of 2 milliamp (mA) anodal stimulation (or sham) to the left or right LOC. Compared to sham, those who received left LOC stimulation (contralateral to the hand used) showed an improvement in haptic object recognition but not discrimination-a finding that was evident from the start of the behavioral tasks. A second experiment showed that this effect was not observed with right LOC stimulation (ipsilateral to the hand used). These results suggest that HD-tDCS to the left LOC can improve recognition of objects perceived via touch. Overall, this work sheds light on the LOC as a multimodal structure that plays a key role in object recognition in both the visual and haptic modalities.
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Lobe occipital , , Stimulation transcrânienne par courant continu , Humains , Mâle , Femelle , Lobe occipital/physiologie , Jeune adulte , Adulte , Stimulation transcrânienne par courant continu/méthodes , /physiologie , Méthode en simple aveugle , Perception du toucher/physiologie , /physiologie , Latéralité fonctionnelle/physiologieRÉSUMÉ
PURPOSE: Mastering intracorporeal suturing is challenging in the evolution from conventional to laparoscopic bariatric surgery. Among various techniques competing for superiority in overcoming this hurdle, we focus on exploring the potential of barbed sutures through a meta-analysis that compares outcomes to those of conventional non-barbed sutures in bariatric surgery. MATERIALS AND METHODS: We conducted a comprehensive search on PubMed, Scopus, and Embase to identify studies comparing barbed sutures with non-barbed sutures in bariatric surgeries, focusing on outcomes such as operative time, suturing time, postoperative complications, and hospital stay. The statistical analysis was carried out using RStudio version 4.3.2. Heterogeneity was assessed using the Cochrane Q test and I2 statistics. RESULTS: Incorporating data from 11 studies involving a total of 27,442 patients, including 3,516 in the barbed suture group across various bariatric surgeries, our analysis demonstrates a significant reduction in suturing time (mean difference -4.87; 95% CI -8.43 to -1.30; p < 0.01; I2 = 99%) associated with the use of barbed sutures. Specifically, in Roux-en-Y gastric bypass, we observed a significant decrease in operative time (mean difference -12.11; 95% CI -19.27 to -4.95; p < 0.01; I2 = 93%). Subgroup analyses and leave-one-out analyses consistently supported these findings. Furthermore, we found that the mean body mass index did not significantly predict the mean difference in operative time outcome. No significant differences emerged in hospital stay or postoperative complications, including leak, bleeding, stenosis, and bowel obstruction (p > 0.05). CONCLUSION: Our study findings address barbed sutures as a potential alternative for laparoscopic intracorporeal suturing in bariatric surgery.
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Chirurgie bariatrique , Obésité morbide , Durée opératoire , Complications postopératoires , Techniques de suture , Matériaux de suture , Humains , Chirurgie bariatrique/méthodes , Complications postopératoires/épidémiologie , Obésité morbide/chirurgie , Résultat thérapeutique , Durée du séjour/statistiques et données numériques , Laparoscopie/méthodes , Femelle , Mâle , AdulteRÉSUMÉ
Effective project planning and management in the global software development landscape relies on addressing major issues like cost estimation and effort allocation. Timely estimation of software development is a critical focus in software engineering research. With the industry increasingly relying on diverse teams worldwide, accurate estimation becomes vital. Software size serves as a common measure for costs and schedules, but advanced estimation methods consider various variables, such as project purpose, personnel expertise, time and efficiency constraints, and technology requirements. Estimating software costs involve significant financial and strategic commitments, making it crucial to address complexity and versatility related to cost drivers. To achieve enhanced accuracy and convergence, we employ the cuckoo algorithm in our proposed NFDLNN (Neuro Fuzzy Logic and Deep Learning Neural Networks) model. Through extensive validation with industrial project data, using Function Point Analysis as the algorithmic models, our NFA model demonstrates high accuracy in software cost approximation, outperforming existing methods insights of MRE of 3.33, BRE of 0.13, and PI of 74.48. Our research contributes to improved project planning and decision-making processes in global software development endeavours.
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Long non-coding RNA (lncRNA) is a novel emerging type of competitive endogenous RNA (ceRNA) that performs key functions in multiple biological processes. However, little is known about the roles of lncRNA under hypoxia stress in fish. Here, vascular endothelial growth factor-Aa (vegfaa) was cloned in rainbow trout (Oncorhynchus mykiss), with the complete cDNA sequence of 2914â¯bp, encoding 218 amino acids. The molecular weight of the protein was approximately 25.33â¯kDa, and contained PDGF and VEGF_C domains. Time-course and spatial expression patterns revealed that LOC110520012 was a key regulator of rainbow trout in response to hypoxia stress, and LOC110520012, miR-206-y and vegfaa exhibited a ceRNA regulatory relationship in liver, gill, muscle and rainbow trout liver cells treated with acute hypoxia. Subsequently, the targeting relationship of LOC110520012 and vegfaa with miR-206-y was confirmed by dual-luciferase reporter analysis, and overexpression of LOC110520012 mediated the inhibition of miR-206-y expression in rainbow trout liver cells, while the opposite results were obtained after LOC110520012 silencing with siRNA. We also proved that vegfaa was a target of miR-206-y in vitro and in vivo, and the vegfaa expression and anti-proliferative effect on rainbow trout liver cells regulated by miR-206-y mimics could be reversed by LOC110520012. These results suggested that LOC110520012 can positively regulate vegfaa expression by sponging miR-206-y under hypoxia stress in rainbow trout, which facilitate in-depth understanding of the molecular mechanisms of fish adaptation and tolerance to hypoxia.
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Prolifération cellulaire , Foie , microARN , Oncorhynchus mykiss , ARN long non codant , Facteur de croissance endothéliale vasculaire de type A , Animaux , Oncorhynchus mykiss/génétique , microARN/génétique , ARN long non codant/génétique , Facteur de croissance endothéliale vasculaire de type A/génétique , Facteur de croissance endothéliale vasculaire de type A/métabolisme , Prolifération cellulaire/effets des médicaments et des substances chimiques , Foie/effets des médicaments et des substances chimiques , Hypoxie/génétique , Néovascularisation physiologique/effets des médicaments et des substances chimiques , Néovascularisation physiologique/génétique ,RÉSUMÉ
BACKGROUND AND OBJECTIVE: Non-small cell lung cancer (NSCLC) is a pernicious tumor with high incidence and mortality rates. The incidence rate of NSCLC increases with age and poses a serious danger to human health. The aim of this study was to determine the mechanism by which (-)-epicatechin (EC) alleviates NSCLC. METHODS: Twenty-four pairs of NSCLC tissues and cancer-adjacent tissues were collected, and A549 and H460 radiotherapy-resistant strains were generated by repeatedly irradiating A549 and H460 cells with dose-gradient X-rays. Radiotherapy-resistant H460 cells were successfully injected subcutaneously into the left dorsal side of nude mice at a dose of 1 × 105 to establish an NSCLC animal model. The levels of interrelated genes and proteins were detected by RTâqPCR and Western blotting, and cell proliferation and apoptosis were evaluated by CCKâ8 assay, Transwell assay, flow cytometry, and TUNEL staining. RESULTS: LOC107986454 was highly expressed in NSCLC patients, while miR-143-3p was expressed at low levels and was negatively correlated with LOC107986454. Functionally, EC promoted autophagy and apoptosis induced by radiotherapy, restrained cell proliferation and migration, and ultimately enhanced the radiosensitivity of NSCLC cells. A downstream mechanistic study showed that EC facilitated miR-143-3p expression by inhibiting LOC107986454 and then restraining the expression of EZH2, which ultimately facilitated autophagy and apoptosis in cancer cells, inhibited proliferation and migration, and enhanced the radiosensitivity of NSCLC cells. CONCLUSION: EC can enhance the radiosensitivity of NSCLC cells by regulating the LOC107986454/miR-143-3p/EZH2 axis.
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BACKGROUND: The thalamus system plays critical roles in the regulation of reversible unconsciousness induced by general anesthetics, especially the arousal stage of general anesthesia (GA). But the function of thalamus in GA-induced loss of consciousness (LOC) is little known. The thalamic reticular nucleus (TRN) is the only GABAergic neurons-composed nucleus in the thalamus, which is composed of parvalbumin (PV) and somatostatin (SST)-expressing GABAergic neurons. The anterior sector of TRN (aTRN) is indicated to participate in the induction of anesthesia, but the roles remain unclear. This study aimed to reveal the role of the aTRN in propofol and isoflurane anesthesia. METHODS: We first set up c-Fos straining to monitor the activity variation of aTRNPV and aTRNSST neurons during propofol and isoflurane anesthesia. Subsequently, optogenetic tools were utilized to activate aTRNPV and aTRNSST neurons to elucidate the roles of aTRNPV and aTRNSST neurons in propofol and isoflurane anesthesia. Electroencephalogram (EEG) recordings and behavioral tests were recorded and analyzed. Lastly, chemogenetic activation of the aTRNPV neurons was applied to confirm the function of the aTRN neurons in propofol and isoflurane anesthesia. RESULTS: c-Fos straining showed that both aTRNPV and aTRNSST neurons are activated during the LOC period of propofol and isoflurane anesthesia. Optogenetic activation of aTRNPV and aTRNSST neurons promoted isoflurane induction and delayed the recovery of consciousness (ROC) after propofol and isoflurane anesthesia, meanwhile chemogenetic activation of the aTRNPV neurons displayed the similar effects. Moreover, optogenetic and chemogenetic activation of the aTRN neurons resulted in the accumulated burst suppression ratio (BSR) during propofol and isoflurane GA, although they represented different effects on the power distribution of EEG frequency. CONCLUSION: Our findings reveal that the aTRN GABAergic neurons play a critical role in promoting the induction of propofol- and isoflurane-mediated GA.
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Anesthésie générale , Conscience , Neurones GABAergiques , Isoflurane , Propofol , Propofol/pharmacologie , Isoflurane/pharmacologie , Animaux , Neurones GABAergiques/effets des médicaments et des substances chimiques , Neurones GABAergiques/physiologie , Souris , Conscience/effets des médicaments et des substances chimiques , Conscience/physiologie , Mâle , Électroencéphalographie , Anesthésiques par inhalation/pharmacologie , Noyaux antérieurs du thalamus/effets des médicaments et des substances chimiques , Noyaux antérieurs du thalamus/physiologie , Souris de lignée C57BL , Souris transgéniques , Anesthésiques intraveineux/pharmacologie , Protéines proto-oncogènes c-fos/métabolisme , OptogénétiqueRÉSUMÉ
BACKGROUND: Skeletal muscle development and fat deposition have important effects on meat quality. The study of regulating skeletal muscle development and fat deposition is of great significance in improving the quality of carcass and meat. In the present study, whole transcriptome sequencing (including RNA-Seq and miRNA-Seq) was performed on the longissimus dorsi muscle (LDM) of Jinfen White pigs at 1, 90, and 180 days of age. RESULTS: The results showed that a total of 245 differentially expressed miRNAs were screened in any two comparisons, which may be involved in the regulation of myogenesis. Among them, compared with 1-day-old group, miR-22-5p was significantly up-regulated in 90-day-old group and 180-day-old group. Functional studies demonstrated that miR-22-5p inhibited the proliferation and differentiation of porcine skeletal muscle satellite cells (PSCs). Pearson correlation coefficient analysis showed that long non-coding RNA (lncRNA) LOC106505926 and CXXC5 gene had strong negative correlations with miR-22-5p. The LOC106505926 and CXXC5 were proven to promote the proliferation and differentiation of PSCs, as opposed to miR-22-5p. In terms of mechanism, LOC106505926 functions as a molecular sponge of miR-22-5p to modulate the expression of CXXC5, thereby inhibits the differentiation of PSCs. In addition, LOC106505926 regulates the differentiation of porcine preadipocytes through direct binding with FASN. CONCLUSIONS: Collectively, our results highlight the multifaceted regulatory role of LOC106505926 in controlling skeletal muscle and adipose tissue development in pigs and provide new targets for improving the quality of livestock products by regulating skeletal muscle development and fat deposition.
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Différenciation cellulaire , Lipogenèse , microARN , Développement musculaire , ARN long non codant , Animaux , ARN long non codant/génétique , Développement musculaire/génétique , Suidae , microARN/génétique , microARN/métabolisme , Lipogenèse/génétique , Différenciation cellulaire/génétique , Prolifération cellulaire , Cellules satellites du muscle squelettique/métabolisme , Cellules satellites du muscle squelettique/cytologie , Muscles squelettiques/métabolisme , Muscles squelettiques/croissance et développement , Cellules cultivéesRÉSUMÉ
Dieting is theorized as a risk factor for loss-of-control (LOC)-eating (i.e., feeling a sense of lack of control while eating). Support for this association has largely relied on retrospective self-report data, which does not always correlate with objectively assessed eating behavior in youth. We hypothesized that during a laboratory-based LOC-eating paradigm, children and adolescents who reported current (at the time of the visit) dieting would consume meals consistent with LOC-eating (greater caloric intake, and intake of carbohydrates and fats, but less intake of protein). Participants were presented with a buffet-style meal and instructed to "Let yourself go and eat as much as you want." Current dieting (i.e., any deliberate change to the amount or type of food eaten to influence shape or weight, regardless of how effective the changes are) was assessed via interview. General linear models were adjusted for fat mass (%), lean mass (kg), height, sex, protocol, race and ethnicity, pre-meal hunger and minutes since consumption of a breakfast shake. Of 337 participants (Mage 12.8 ± 2.7y; 62.3 % female; 45.7 % non- Hispanic White and 26.1 % non-Hispanic Black; MBMIz 0.78 ± 1.11), only 33 (9.8 %) reported current dieting. Current dieting was not significantly associated with total energy intake (F = 1.63, p = .20, ηp2 = 0.005), or intake from carbohydrates (F = 2.45, p = .12, ηp2 = 0.007), fat (F = 2.65, p = .10, ηp2 = 0.008), or protein (F = 0.39, p = .53, ηp2 = 0.001). Contrary to theories that dieting promotes LOC-eating, current dieting was not associated with youth's eating behavior in a laboratory setting. Experimental approaches for investigating dieting are needed to test theories that implicate dieting in pediatric LOC-eating.
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Ration calorique , Comportement alimentaire , Humains , Femelle , Mâle , Ration calorique/physiologie , Adolescent , Comportement alimentaire/psychologie , Enfant , Régime amaigrissant/psychologie , Sang-froid/psychologie , Repas/psychologieRÉSUMÉ
The evaluation of nanoparticles (NPs) cytotoxicity is crucial for advancing nanotechnology and assessing environmental pollution. However, existing methods for NPs cytotoxicity evaluation suffer from limited accuracy and inadequate information content. In the study, we developed a novel detection platform that enables the identification of cellular carbonyl metabolites at the organ level. The platform is integrated with a cell co-culture lung organ chip (LOC) and a micropillar concentrator. Notably, our work represents the successful measurement of the amounts of cellular metabolites on LOC system. The volatile carbonyl metabolites (VCMs) generated by cells exposure to various types of NPs with different concentrations were captured and detected by high-resolution mass spectrometry (MS). Compared with conventional cell viability and reactive oxygen species (ROS) analysis, our method discerns the toxicological impact of NPs at low concentrations by analyzed VCM at levels as low as ppb level. The LOC system based metabolic gas detection confirmed that low concentrations of NPs have a toxic effect on the cell model, which was not reflected in the fluorescence detection, and the effect of NP material is more significant than the size effect. Furthermore, this method can distinguish different NPs acting on cell models through cluster analysis of multiple VCMs.
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Laboratoires sur puces , Poumon , Nanoparticules , Composés organiques volatils , Humains , Poumon/cytologie , Poumon/métabolisme , Poumon/effets des médicaments et des substances chimiques , Composés organiques volatils/analyse , Composés organiques volatils/métabolisme , Nanoparticules/composition chimique , Nanoparticules/toxicité , Survie cellulaire/effets des médicaments et des substances chimiques , Cellules A549 , Espèces réactives de l'oxygène/métabolisme , Espèces réactives de l'oxygène/analyse , Systèmes microphysiologiquesRÉSUMÉ
For the treatment of human immunodeficiency virus (HIV)-infected patients, the regular assessment of the immune status is indispensable. The quantification of CD4+ T lymphocytes in blood by gold standard optical flow cytometry is not point-of-care testing (POCT) compatible. This incompatibility is due to unavoidable pre-analytics, expensive and bulky optics with limited portability, and complex workflow integration. Here, we propose a non-optical, magnetic flow cytometry (MFC) workflow that offers effortless integration opportunities, including minimal user interaction, integrated sample preparation and up-concentration, and miniaturization. Furthermore, we demonstrate immunomagnetic CD4+ T lymphocyte labeling in whole blood with subsequent quantification using sheath-less MFC. Showing linearity over two log scales and being largely unimpaired by hematocrit, evidence is provided for POCT capabilities of HIV patients.
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BACKGROUND: Long non-coding RNAs (lncRNAs) are involved in many key bioprocesses, including the occurrence and development of rheumatoid arthritis (RA). We aimed to analyze the association of genetic variants of long non-coding RNA LOC553103 and its peripheral blood mononuclear cells (PBMC) expression with RA. METHODS: We enrolled 457 RA patients and 551 healthy controls and conducted a case-control study to analyze the relationship between LOC553103 gene rs272879 and the susceptibility of RA by TaqMan single nucleotide polymorphism genotyping. Among them, we sampled 92 cases and 92 controls, respectively, to detect the PBMC level of LOC553103 using quantitative real-time polymerase chain reaction technology. We explored the association between LOC553103 rs272879 and its PBMC expression levels in 71 RA patients. Mann-Whitney, Chi-square, and Spearman correlation analysis were used for statistical analysis and P-value <.05 was considered statistically significant. RESULTS: The genotype frequency of LOC553103 rs272879 CC was increased, and CG was decreased in RA patients compared to the control group (χ2 = 6.772, P = .034). The LOC553103 expression level in PBMC of RA patients was downregulated compared to healthy control (Z = -4.497, P < .001). Moreover, negative correlations were observed between the PBMC level of LOC553103 and erythrocyte sedimentation rate (rs = -0.262, P = .018), white blood cell count (rs = -0.382, P = .004), platelet (rs = -0.293, P = .030), and disease activity score in 28 joints (rs = -0.271, P = .016) in RA patients. CONCLUSIONS: This study provides the first evidence supporting an association between LOC553103 gene polymorphisms and susceptibility of RA and a relationship of PBMC level of LOC553103 with clinical manifestations and laboratory indicators of RA patients.
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Granulosa cells (GCs) are essential for follicular development, and long non-coding RNAs (LncRNAs) are known to support the maintenance of this process and hormone synthesis in mammals. Nevertheless, the regulatory roles of these lncRNAs within sheep follicular GCs remain largely unexplored. This study delved into the influence of a Loc105611671, on the proliferation and steroid hormone synthesis of sheep ovarian GCs and the associated target genes in vitro. Cell Counting Kit-8 (CCK-8) gain-of-function experiments indicated that overexpression of Loc105611671 significantly boosted GCs proliferation, along with estrogen (E2) and progesterone (P4) levels. Further mechanistic scrutiny revealed that Loc105611671 is primarily localized within the cytoplasm of ovarian granulosa cells and engages in molecular interplay with CDC42. This interaction results in the upregulation of CDC42 protein expression. Moreover, it was discerned that increased CDC42 levels contribute to augmented proliferation of follicular granulosa cells and the secretion of E2 and P4. Experiments involving co-transfection elucidated that the concurrent overexpression of CDC42 and Loc105611671 acted synergistically to potentiate these effects. These findings provide insights into the molecular underpinnings of fecundity in ovine species and may inform future strategies for enhancing reproductive outcomes.
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Long noncoding RNA (lncRNAs) are involved in the pathogenesis of ulcerative colitis (UC). Moxibustion, a traditional Chinese medicine, can improve symptoms in patients with UC and reduce intestinal inflammation in rats with UC. However, it remains unclear whether the ameliorative effect of moxibustion on intestinal mucosal inflammation in UC is related to lncRNAs. Thirty-two rats were randomly assigned to four groups: normal control, UC, moxibustion (MOX), and sulfasalazine (SASP). The UC rat model was induced by administering 4% dextran sulfate sodium (DSS) in drinking water. Rats in the moxibustion group underwent bilateral Tianshu (ST25) moxibustion using the herbs-partition moxibustion method. Rats in the sulfasalazine group received SASP solution via gavage twice daily for seven consecutive days. Our results revealed that, compared with the UC group [2.00 (1.00, 2.50)], the DAI score [0.25 (0.00, 0.50)] was significantly lower in the MOX group (P < 0.05). Compared with the UC group [13.00 (11.25, 14.00)], the histopathological score [5.50 (4.00, 7.75)] was significantly lower in the MOX group (P < 0.05). In addition, the CMDI and macroscopic scores were decreased in the MOX group (P < 0.05). Moxibustion significantly decreased the protein expression of inflammatory factors TNF-α, IFN-γ, and IL-1ß in the colonic tissues of UC rats (P <0.05), thereby suppressing the inflammatory response. Moreover, moxibustion exerted a regulatory influence on colon lncRNA and mRNA expression profiles, upregulating LOC108352929 and downregulating Phf11 in rats with UC (P <0.05). Moxibustion also led to a reduction in the expression and colocalization of Phf11 and NF-κB in the colons of UC rats. Moreover, knockdown of LOC108352929 in rat enteric glial cells demonstrated a significant upregulation of TNF-α mRNA expression (P <0.05). In summary, these data illustrate that moxibustion effectively ameliorates DSS-induced colonic injury and inflammation while exerting regulatory control over the lncRNA-mRNA co-expression network in UC rats. Collectively, the in vivo and in vitro studies suggested that LOC108352929-Phf11 may serve as a potential biological marker for moxibustion in the treatment of UC.
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Cisplatin resistance remains a persistent challenge in cervical cancer (CC) treatment. Molecular biomarkers have garnered attention for their association with cisplatin resistance in various diseases. Long non-coding RNAs (lncRNAs) exert significant influence on CC development. This study explores the role of LOC644656 in regulating cisplatin resistance in CC. Parental and cisplatin-resistant CC cells underwent cisplatin treatment. Functional assays assessed cell proliferation and apoptosis under different conditions. RNA pull-down with mass spectrometry, along with literature review, elucidated the interaction between LOC644656, ZNF143, and E6-AP. Mechanistic assays analyzed the relationship between different factors. RT-qPCR and western blot quantified RNA and protein levels, respectively. In vivo models validated E6-AP's function. Results revealed LOC644656 overexpression in cisplatin-resistant CC cells, exacerbating cell growth. LOC644656 recruited ZNF143 to activate E6-AP transcription, promoting cisplatin resistance in CC. In conclusion, LOC644656 positively modulates E6-AP expression via ZNF143-mediated transcriptional activation, contributing to cisplatin resistance in CC.
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Cisplatine , Résistance aux médicaments antinéoplasiques , microARN , Transactivateurs , Ubiquitin-protein ligases , Tumeurs du col de l'utérus , Femelle , Humains , Lignée cellulaire tumorale , Prolifération cellulaire , Cisplatine/usage thérapeutique , Régulation de l'expression des gènes tumoraux , microARN/métabolisme , ARN , Transactivateurs/métabolisme , Activation de la transcription , Tumeurs du col de l'utérus/traitement médicamenteux , Tumeurs du col de l'utérus/génétique , Ubiquitin-protein ligases/métabolismeRÉSUMÉ
Background: Newer minimally invasive techniques have supplanted laparotomy and thoracotomy for management of hiatal hernias. Limited data exists on outcomes after robotic hiatal hernia repair without mesh despite the increasing popularity of this approach. We report our high-volume experience with durable robotic hiatal hernia repair with gastric fundoplication without mesh. Methods: A retrospective review was conducted on patients with type I-IV hiatal hernias who underwent an elective robotic-assisted repair from 2016 to 2019 using a novel technique of approximating the hiatus with running barbed absorbable (V-locTM) suture and securing it with interrupted silk sutures. Main outcomes included length of stay, readmission rate, and recurrence rate. Results: A total of 144 patients were reviewed. The average age of the patient was 61 years. Most of the patients were female [95 females (66%) to 49 males], and the average body mass index (BMI) was 29.96 kg/m2. The average operating time was 173 minutes (standard deviation 62 minutes). The average length of stay in the hospital was 2 days, and 89% of patients went home within the first 3 days. Ten patients (6.9%) were readmitted within 30 days, there were no mortalities in 30 days, and there were 6 (4.2%) recurrences on follow up requiring reoperation. Conclusions: Elective robotic hiatal hernia repair with fundoplication and primary closure of the hiatus with V-locTM and nonabsorbable suture without mesh is safe and effective. The robotic approach has similar operative times, lengths of stay, and complications compared to nationally published data on laparoscopic hiatal hernia repairs.
RÉSUMÉ
Heat stroke (HS) is a severe medical condition characterized by a systemic inflammatory response that may precipitate multi-organ dysfunction, with a particular predilection for inducing profound central nervous system impairments. We aim to employ bioinformatics techniques for the retrieval and analysis of genes associated with heat stroke-induced neurological damage. We performed a comprehensive analysis of the GSE64778 dataset from the Sequence Read Archive, resulting in the identification of 1178 significantly differentially expressed genes (DEGs). We retrieved 2914 genes associated with heat stroke from the GeneCards database and 2377 genes associated with heat stroke from the Comparative Toxicogenomics Database (CTD). The intersection of the top 300 DEGs in the GSE64778 dataset intersected with the search results of GeneCards and CTD, yielding 25 final candidates for DEGs associated with heat stroke. Gene Ontology functional annotation results indicated that the target genes were mainly involved in apoptosis, stress response, and negative regulation of cellular processes and function in processes such as protein dimerization and protein binding. The Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis revealed a predominant enrichment of candidate target genes within the PI3K-AKT signaling pathway. Subsequent protein-protein interaction network analysis highlighted HSP90aa1 as a central gene, indicating its pivotal role by possessing the highest number of edges among the genes enriched in the PI3K-AKT signaling pathway. Quantitative reverse transcription-polymerase chain reaction analysis performed on blood samples from patients validated the expression of Hsp90aa1 in individuals exhibiting early neurological damage in HS, consistent with the findings from the mRNA bioinformatics analysis. Additionally, the bioinformatics analysis of the upstream microRNAs (miRNAs) regulating HSP90aa1 and the target miRNAs associated with candidate long non-coding RNAs (lncRNAs) identified three lncRNAs, eight miRNAs, and one mRNA in the regulatory network. The DIANA Tools database and algorithms were employed for pathway enrichment and correlation analysis, revealing a significant association between LOC102547734 and MIR-206-3p, with the latter being identified as a target binding site Moreover, the analysis unveiled a correlation between MIR-206-3p and HSP90aa1, implicating the latter as a potential target binding site within the regulatory network.