The evolution and diversification of oakleaf butterflies.

Oakleaf butterflies in the genus Kallima have a polymorphic wing phenotype, enabling these insects to masquerade as dead leaves. This iconic example of protective resemblance provides an interesting evolutionary paradigm that can be employed to study biodiversity. We integrated multi-omic data analyses and functional validation to infer the evolutionary history of Kallima species and investigate the genetic basis of their variable leaf wing patterns. We find that Kallima butterflies diversified in the eastern Himalayas and dispersed to East and Southeast Asia. Moreover, we find that leaf wing polymorphism is controlled by the wing patterning gene cortex, which has been maintained in Kallima by long-term balancing selection. Our results provide macroevolutionary and microevolutionary insights into a model species originating from a mountain ecosystem.

Single-cell sequencing reveals the impact of endothelial cell PIEZO1 expression on thoracic aortic aneurysm.

INTRODUCTION: Thoracic aortic aneurysm (TAA) is a severe vascular disease that threatens human life, characterized by focal dilatation of the entire aortic wall, with a diameter 1.5 times larger than normal. PIEZO1, a mechanosensitive cationic channel, monitors mechanical stimulations in the environment, transduces mechanical signals into electrical signals, and converts them into biological signals to activate intracellular signaling pathways. However, the role of PIEZO1 in TAA is still unclear. METHODS: We analyzed a single-cell database to investigate the expression level of PIEZO1 in TAA. We constructed a conditional knockout mouse model of Piezo1 and used the PIEZO1 agonist Yoda1 to intervene in the TAA model mice established by co-administration of BAPN and ANG-II. Finally, we explored the effect of Yoda1 on TAA in vitro. RESULTS AND DISCUSSION: We observed decreased PIEZO1 expression in TAA at both RNA and protein levels. Single-cell sequencing identified a specific reduction in Piezo1 expression in endothelial cells. Administration of PIEZO1 agonist Yoda1 prevented the formation of TAA. In PIEZO1 endothelial cell conditional knockout mice, Yoda1 inhibited TAA formation by interfering with PIEZO1. In vivo and in vitro experiments demonstrated that the effect of Yoda1 on endothelial cells involved macrophage infiltration, extracellular matrix degradation, and neovascularization. This study highlights the role of PIEZO1 in TAA and its potential as a therapeutic target, providing opportunities for clinical translation.

Novel silicene-mesoporous silica nanoparticles conjugated gemcitabine induced cellular apoptosis via upregulating NF-κB p65 nuclear translocation suppresses pancreatic cancer growthin vitroandin vivo.

Pancreatic cancer's high fatality rates stem from its resistance to systemic drug delivery and aggressive metastasis, limiting the efficacy of conventional treatments. In this study, two-dimensional ultrathin silicene nanosheets were initially synthesized and near-infrared-responsive two-dimensional silicene-mesoporous silica nanoparticles (SMSNs) were successfully constructed to load the clinically-approved conventional pancreatic cancer chemotherapeutic drug gemcitabine. Experiments on nanoparticle characterization show that they have excellent photothermal conversion ability and stability. Then silicene-mesoporous silica nanoparticles loaded with gemcitabine nanoparticles (SMSN@G NPs) were employed in localized photothermal therapy to control pancreatic tumor growth and achieve therapeutic effects. Our research confirmed the functionality of SMSN@G NPs through immunoblotting and apoptotic assays, demonstrating its capacity to enhance the nuclear translocation of the NF-κB p65, further affect the protein levels of apoptosis-related genes, induce the apoptosis of tumor cells, and ultimately inhibit the growth of the tumor. Additionally, the study assessed the inhibitory role of SMSN@G NPs on pancreatic neoplasm growthin vivo, revealing its excellent biocompatibility. SMSN@G NPs have a nice application prospect for anti-pancreatic tumors.

Current Understanding of Timing of Surgical Repair for Ventricular Septal Rupture following Acute Myocardial Infarction.

BACKGROUND: Ventricular septal rupture (VSR) is a mechanical issue that can occur following an acute myocardial infarction (AMI) and has a high mortality rate. It requires a comprehensive, team-based approach for prompt diagnosis and maintaining stable blood flow. While the occurrence of VSR has lessened over the past hundred years and advancements have been made in treatment techniques, the mortality rate within 30 days can still surpass 40 percent. Surgery is the primary treatment method. For patients with stable blood flow, it is generally considered safer to perform surgery 4-6 weeks after the AMI to repair the VSR. However, the timing of surgery for patients with early instability in their blood flow is still a topic of debate. SUMMARY: There is a lack of set criteria and standards to determine the best time for surgery in patients with VSR following an infarction who have unstable blood flow, especially when considering the use of blood circulation support devices and other techniques for maintaining blood flow that are used in clinical settings. KEY MESSAGES: This review outlines the features of different mechanical circulatory support devices utilized in treating VSR, along with the current scoring system designed to direct the treatment approach for VSR patients.

Solibacillus ferritrahens sp. nov., a novel siderophore-producing bacterium isolated from Wumeng Mountain National Nature Reserve in Yunnan Province.

A gram-stain-positive, aerobic, rod-shaped bacterial strain capable of producing siderophores, named YIM B08730T, was isolated from a soil sample collected from Wumeng Mountain National Nature Reserve, Zhaotong City, Yunnan Province. Growth occurred at 10-45 °C (optimum, 35-40 â„ƒ), pH 7.0-9.0 (optimum, 7.0) and in the presence of 0-5 % (w/v) NaCl (optimum, 0-1 %, w/v). A comparative analysis of the 16S rRNA gene sequence (1558 bp) of strain YIM B08730T showed the highest similarity to Solibacillus isronensis JCM 13838T (96.2 %), followed by Solibacillus silvestris DSM 12223T (96.0 %) and Solibacillus kalamii ISSFR-015T (95.4 %). The main polar lipids were diphosphatidylglycerol, phosphatidylglycerol, phosphatidylethanolamine, phosphatidylserine and one unidentified lipid. The main respiratory quinone of strain YIM B08730T was menaquinone 7 (MK-7). The major fatty acids were iso-C15:0 and C16:1ω7c alcohol. The digital DNA-DNA hybridization and average nucleotide identity values between strain YIM B08730T and the reference strain S. isronensis JCM 13838T were 24.8 % and 81.2 %, respectively. The G + C content of the genomic DNA was 37.1 mol%. The genome of the novel strain contained genes associated with the production of siderophores, and it also revealed other functional gene clusters involved in plant growth promotion and soil bioremediation. Based on these phenotypic, chemotaxonomic and phylogenetic analyses, strain YIM B08730T is considered to be a novel species of the genus Solibacillus, for which the name Solibacillus ferritrahens sp. nov. is proposed. The type strain is YIM B08730T (= NBRC 116268T = CGMCC 1.60169T).

Paired protein kinases PRKCI-RIPK2 promote pancreatic cancer growth and metastasis via enhancing NF-κB/JNK/ERK phosphorylation.

BACKGROUND: Protein kinases play a pivotal role in the malignant evolution of pancreatic cancer (PC) through mediating phosphorylation. Many kinase inhibitors have been developed and translated into clinical use, while the complex pathology of PC confounds their clinical efficacy and warrants the discovery of more effective therapeutic targets. METHODS: Here, we used the Gene Expression Omnibus (GEO) database and protein kinase datasets to map the PC-related protein kinase-encoding genes. Then, applying Gene Expression and Profiling Interactive Analysis (GEPIA), GEO and Human Protein Atlas, we evaluated gene correlation, gene expression at protein and mRNA levels, as well as survival significance. In addition, we performed protein kinase RIPK2 knockout and overexpression to observe effects of its expression on PC cell proliferation, migration and invasion in vitro, as well as cell apoptosis, reactive oxygen species (ROS) production and autophagy. We established PC subcutaneous xenograft and liver metastasis models to investigate the effects of RIPK2 knockout on PC growth and metastasis. Co-immunoprecipitation and immunofluorescence were utilized to explore the interaction between protein kinases RIPK2 and PRKCI. Polymerase chain reaction and immunoblotting were used to evaluate gene expression and protein phosphorylation level. RESULTS: We found fourteen kinases aberrantly expressed in human PC and nine kinases with prognosis significance. Among them, RIPK2 with both serine/threonine and tyrosine activities were validated to promote PC cells proliferation, migration and invasion. RIPK2 knockout could inhibit subcutaneous tumor growth and liver metastasis of PC. In addition, RIPK2 knockout suppressed autophagosome formation, increased ROS production and PC cell apoptosis. Importantly, another oncogenic kinase PRKCI could interact with RIPK2 to enhance the phosphorylation of downstream NF-κB, JNK and ERK. CONCLUSION: Paired protein kinases PRKCI-RIPK2 with multiple phosphorylation activities represent a new pathological mechanism in PC and could provide potential targets for PC therapy.

Assessing causality between second-hand smoking and potentially associated diseases in multiple systems: A two-sample Mendelian randomization study.

INTRODUCTION: The global disease burden may be exacerbated by exposure to passive smoking (SHS), with the workplace being a primary location for such exposure. Numerous epidemiological studies have identified SHS as a risk factor for diseases affecting various systems, including cardiovascular, respiratory, immune, endocrine, and nervous systems. The conventional observational study has certain methodological constraints which can be circumvented through a Mendelian randomization (MR) study. Our MR study intends to investigate the causal link between workplace exposure to SHS and the potential associated diseases. METHODS: Summary statistics data involving European participants was sourced from three databases: the UK Biobank, the FinnGen study, and the European Bioinformatics Institute. Genetic variants linked with exposure to SHS in the workplace were identified as instrumental variables. The MR was carried out using inverse variance weighted (IVW), MR-Egger, and weighted median methods. Sensitivity tests were also undertaken within the MR to evaluate the validity of the causality. RESULTS: According to the IVW model, genetically determined atrial fibrillation (AF) and stroke [P= 6.64E-04 and 5.68E-07, odds ratio = 2.030 and 2.494, 95% confidence interval = 1.350,3.051 and 1.743,3.569] were robustly associated with exposure to SHS in the workplace. Suggestive associations were found between workplace SHS and myocardial infarction (MI), asthma, and depression. CONCLUSIONS: The MR study demonstrates that exposure to SHS in the workplace is a significant risk factor for AF and stroke in European individuals. Whether workplace exposure to SHS influences other diseases and the causality between them requires further exploration. IMPLICATIONS: This study explored the causality between exposure to SHS in the workplace and potential associated diseases in multiple systems, including MI, AF, stroke, lung cancer, asthma, allergic disease, type 2 diabetes, and depression, using a MR study. The MR study can circumvent the methodological constraints of observational studies and establish a causal relationship. The two-sample MR analysis provides evidence supporting the causal association of frequent workplace SHS with AF and stroke. Individuals exposed to SHS in the workplace may also have a heightened risk of MI, asthma, and depression. However, whether SHS affects other diseases and the causality between them requires further investigation. To our knowledge, this is the first two-sample MR study to determine the causal relationship between SHS and potential diseases. As exposure to SHS in the workplace is a prevalent issue and may contribute to a global disease burden. The reduction of exposure following the introduction of smoke-free laws has led to a decrease in the admission rate for cardiac events and an improvement in health indicators. It is crucial to further advance smoke-free policies and their implementation.

Pseudomonas subflava sp. nov., a new Gram-negative bacterium isolated from Guishan in Yunnan province, south-west China.

A new Gram-negative, rod-shaped, flagellated bacterium was isolated from soil in the Guishan, Xinping County, Yuxi City, Yunnan Province, China, and named YIM B01952T. Growth occurred at 10-40 °C (optimum, 30 °C), pH 6.0-9.0 (optimum, pH 7.5) and with up to ≤ 5.0% (w/v) NaCl on Tryptic Soy Broth Agar (TSA) plates. Phylogenetic analysis based on the 16S rRNA gene and draft-genome sequence showed that strain YIM B01952T belonged to the genus Pseudomonas, and was closely related to the type strain of Pseudomonas alcaligenes (sequence similarity was 98.8%). The digital DNA-DNA hybridization (dDDH) value between strain YIM B01952T and the parallel strain P. alcaligenes ATCC 14909T was 49.0% based on the draft genome sequence. The predominant menaquinone was Q-9. The major fatty acids were summed feature 8 (C18:1 ω6c and/or C18:1 ω7c), summed feature 3 (C16:1 ω6c and/or C16:1 ω7c) and C16:0. The major polar lipids were phosphatidylethanolamine, diphosphatidylglycerol, and phosphatidylglycerol. The genome size of strain YIM B01952T was 4.341 Mb, comprising 4156 predicted genes with a DNA G + C content of 66.4 mol%. In addition, we detected that strain YIM B01952T had some traditional functional genes (plant growth promotion and multidrug resistance), unique genes through genome comparison and analysis with similar strains. Based on genetic analyses and biochemical characterization, the strain YIM B01952T was identified as a novel species in the genus Pseudomonas, for which the name Pseudomonas subflava sp. nov. is proposed. The type strain is YIM B01952T (=CCTCC AB 2021498T = KCTC 92073T).

Chitinolyticbacter albus sp. Nov., A Novel Chitin-Degrading Bacterium Isolated from Ancient Wood Rhizosphere Soil.

In this study, a novel aerobic mesophilic bacterial strain with capable of degrading chitin, designated YIM B06366T, was isolated and classified. The rod-shaped, Gram-stain-negative, on-spore-forming bacterium originated from rhizosphere soil sample collected in Kunming City, Yunnan Province, southwest PR China. Strain YIM B06366T exhibited growth at temperatures between 20 and 35 °C (optimum, 30 °C) and at pH 6.0-8.0 (optimum, pH 6.0). The analysis of 16S rRNA gene sequence similarity revealed that strain YIM B06366T was most closely related to type strain Chitinolyticbacter meiyuanensis SYBC-H1T (98.9%). Phylogenetic analysis based on genome data indicated that strain YIM B06366T should be assigned to the genus Chitinolyticbacter. The Average Nucleotide Identity (ANI) and digital DNA-DNA Hybridization (dDDH) values between strain YIM B06366T and the reference strain Chitinolyticbacter meiyuanensis SYBC-H1T were 84.4% and 27.7%, respectively. The major fatty acids included Summed Feature 3 (C16:1 ω6c/C16:1 ω7c), Summed Feature 8 (C18:1 ω6c/C18:1 ω7c), and C16:0. The polar lipids were diphosphatidylglycerol, phosphatidylethanolamine, aminophospholipids, and two unidentified phospholipids. The predominant menaquinone was Q-8, and the genomic DNA G + C content was 64.1%. Considering the polyphasic taxonomic evidence, strain YIM B06366T is proposed as a novel species within the genus Chitinolyticbacter, named Chitinolyticbacter albus sp. nov. (type strain YIM B06366T = KCTC 92434T = CCTCC AB 2022163T).

Cohnella mopanensis sp. nov., a new Gram-negative bacterium isolated from soil in Xinping Mountain National Forest Park.

A Gram-stain-negative, aerobic, rod-shaped bacteria strain, named YIM B01951T, was isolated from a forest soil sample collected from Mopan Mountain National Forest Park, Xinping City, Yunnan Province, southwest PR China (101°58'06" N, 23°03'02" E). Growth occurred at 15-40 °C (optimum, 30 °C), pH 5.0-8.0 (optimum, pH 6.5) and with up to ≤ 3.0% (w/v) NaCl on Nutrient Agar plates. The results of 16S rRNA gene sequence similarity analysis showed that strain YIM B01951T was closely related to the type strain of Cohnella arctica M9-62T (96.5%) and Cohnella lupini RLAHU4BT (96.3%). YIM B01951T contains anteiso-C15:0 and iso-C16:0 as the major cellular fatty acids; the main polar lipids are diphosphatidylglycerol (DPG), phosphatidylglycerol (PG), phosphatidylethanolamine (PE), lysylphosphatidylglycerol (PGL) and five aminophospholipids (APL). The MK-7 is the major respiratory quinone and the DNA G + C content is 49.2 mol%. Based on these phenotypic, chemotaxonomic and phylogenetic analyses, strain YIM B01951T is considered to be a novel species of the genus Cohnella, and named Cohnella mopanensis sp. nov. The type strain is YIM B01951T (= NBRC 115331T = KCTC 43370T).

Brevibacillus daliensis sp. nov., Isolated From Soil in Machangqing Nature Reserve.

A new aerobic bacterial strain, designated strain YIM B02290T, was isolated from the soil of Machangqing, Dali city, Yunnan Province, China. Cells were Gram-stain-positive, sporogenous, rod-shaped, and motile with peritrichous flagella. Strain YIM B02290T showed the highest 16S rRNA gene sequence similarity with Brevibacillus laterosporus (97.6%) and Brevibacillus halotolerans (97.6%). The ANI and dDDH values between strain YIM B02290T and the two reference strains Brevibacillus laterosporus LAM00312T and Brevibacillus halotolerans DSM 25T are 72.6% and 72.2%, 20.2% and 19.5% based on the draft genome sequence, respectively. The major cellular fatty acids contain anteiso-C15: 0 and iso-C15: 0. The diagnostic diamino acid of the cell-wall peptidoglycan was meso-diaminopimelic acid. The predominant menaquinone was identified as menaquinone-7. The main polar lipids of strain YIM B02290T were diphosphatidylglycerol, phosphatidylglycerol, phospholipid, phosphatidyl monomethylethanolamine. The genomic DNA G + C content was 40.6 mol%. All results showed that strain YIM B02290T represents a novel species of the genus Brevibacillus, for which the name Brevibacillus daliensis sp. nov. is proposed. The type strain is YIM B02290T (= CCTCC AB 2021094T = CGMCC 1.18802T = KCTC 43376T).

Extracellular CIRP Upregulates Proinflammatory Cytokine Expression via the NF-kappaB and ERK1/2 Signaling Pathways in Psoriatic Keratinocytes.

Psoriasis is a chronic inflammatory skin disease, and elevation of proinflammatory cytokine levels is a critical driver of the pathogenesis of psoriasis. Extracellular cold-inducible RNA-binding protein (eCIRP) has been shown to play a role in various acute and chronic inflammatory diseases. C23, a short peptide derived from CIRP, competitively binds CIRP receptors and reduces damage in inflammatory diseases. However, the effect of eCIRP in psoriasis has not been studied. In the present study, we investigated the role of eCIRP in the expression of proinflammatory cytokines in keratinocytes. Our data show that eCIRP expression was increased in the sera of psoriasis patients and imiquimod- (IMQ-) induced psoriatic mice and cells stimulated with proinflammatory cytokines (IL-1α, IL-17A, IL-22, oncostatin M, and TNF-α; mix M5). Recombinant human CIRP (rhCIRP) promoted the expression of the proinflammatory cytokines TNF-α, IL-6, and IL-8 and the activation of NF-kappaB (NF-κB) and ERK1/2 in cultured keratinocytes. We then found that the above effects of eCIRP could be blocked by C23 in both normal keratinocytes and M5-stimulated psoriatic keratinocytes. In addition, in vivo experiments revealed that C23 could effectively ameliorate IMQ-induced psoriatic dermatitis. TNF-α and IL-6 mRNA expressions were reduced in the skin lesions of mice with C23-treated IMQ-induced psoriasis, and this effect was accompanied by inhibition of the NF-κB and ERK1/2 signaling pathways. In summary, eCIRP plays an important role in the pathogenesis of psoriasis and may become a new target for psoriasis treatment.

Spontaneous Pneumothorax: A Complication of Coronavirus Disease 2019 (COVID-19) Patients.

BACKGROUND: At present, the coronavirus disease 2019 (COVID-19) is spreading all over the world. The occurrence of spontaneous pneumothorax in these patients might be higher than the fact, and we should pay high clinical attention to them. METHOD: Data regarding clinical investigation, laboratory investigation, diagnosis, and treatment measures of 21 COVID-19 patients with spontaneous pneumothorax from January to March of 2020 were collected and analyzed in this study. RESULTS: Seven patients had a history of basic lung diseases. All patients used different methods of oxygen therapy before the occurrence of spontaneous pneumothorax according to the severity of the COVID-19, including 18 patients with ventilator-assisted breathing, 2 patients with bilevel positive airway pressure assisted breathing, and 1 patient with mask oxygen inhalation. All patients were confirmed cases of COVID-19 by chest CT (computed tomography) and virus nucleic acid detection and were found to have spontaneous pneumothorax through physical examination, bedside X-ray, and/or bedside ultrasound. 13 of 21 patients combined with pleural effusion at the same time. All the patients underwent closed thoracic drainage for spontaneous pneumothorax and the pleural effusion, if any. Nine patients died, and 12 patients recovered smoothly. CONCLUSION: Spontaneous pneumothorax might be an overlooked complication of COVID-19 patients and may be associated with poor prognosis.

[Effects and evaluation of different processing and drying methods on components in Paeoniae Radix Alba].

The present study evaluates different processing and drying methods and investigates their effects on the chemical components in Paeoniae Radix Alba via content determination. The fresh medicinal materials of Paeoniae Radix Alba collected from Bozhou of Anhui province were processed(boiled and peeled) and dried(hot air-dried, infrared-dried, and microwave-dried) at different temperatures(40, 50, 60 and 70 ℃), and the 11 components(monoterpene glycosides, polyphenols, tannin, and benzoic acid) in Paeoniae Radix Alba were determined by ultra-performance liquid chromatography coupled to triple quadrupole with electrospray tandem mass spectrometry(UPLC-TQ-MS). Then the compounds in processed and dried samples were analyzed by partial least squares discriminant analysis(PLS-DA) and orthogonal partial least squares discriminant analysis(OPLS-DA), and the contribution rates of differential components were evaluated by variable important in projection(VIP). The results indicated that the samples obtained by different processing and drying methods could be distinguished. Albiflorin, gallic acid, 1,2,3,4,6-pentakis-O-galloyl-ß-D-glucose, and benzoic acid were the common differential components in boiled Paeoniae Radix Alba. Benzoic acid was the common differential component in peeled Paeoniae Radix Alba. Gallic acid was the common differential component in Paeoniae Radix Alba dried by different methods. The samples could not be distinguished after drying at different temperatures due to the lack of common differential components. This study is expected to provide a reference for the selection of processing and drying methods and the optimization of processing parameters.

Long non-coding RNA LINC00467 drives hepatocellular carcinoma progression via inhibiting NR4A3.

Hepatocellular carcinoma (HCC) is a main cause of cancer-related deaths globally. Long non-coding RNAs (lncRNAs) play important roles in diverse cancers. Our previous microarray-based lncRNA profiling showed that LINC00467 was highly expressed in HCC. Here, we further explored the expression, role and functional mechanism of lncRNA LINC00467 in HCC. Our findings revealed that LINC00467 was up-regulated in HCC tissues and HCC cell lines. Increased expression of LINC00467 was positively associated with tumour size and vascular invasion. In vitro functional experiments revealed that LINC00467 accelerated HCC cell proliferation, cell cycle progression and migration and reduced HCC cell apoptosis. In vivo functional assays revealed that LINC00467 drove HCC xenograft growth and HCC cell proliferation and repressed HCC cell apoptosis in vivo. Moreover, LINC00467 inhibited NR4A3 post-transcriptionally via interacting with NR4A3 mRNA to form double-stranded RNA, which was further degraded by Dicer. The expression of NR4A3 was inversely associated with LINC00467 in HCC tissues. Functional rescue assays found that restore of NR4A3 expression blocked the oncogenic roles of LINC00467 in HCC. Taken together, our results demonstrated that lncRNA LINC00467 was a novel highly expressed and oncogenic lncRNA in HCC via inhibiting NR4A3. Targeting LINC00467 or enhancing NR4A3 may be potential therapeutic strategies against HCC.

The effect of growth hormone supplementation in poor ovarian responders undergoing IVF or ICSI: a meta-analysis of randomized controlled trials.

PURPOSE: The aim of this meta-analysis was to evaluate the effect of growth hormone (GH) supplementation in poor responders undergoing in vitro fertilization (IVF) or intracytoplasmic sperm injection (ICSI). METHODS: PubMed, MEDLINE and Cochrane Library databases were searched for the identification of relevant randomized controlled trials. Outcome measures were live birth rate, clinical pregnancy rate, miscarriage rate, cycle cancelation rate, number of retrieved oocytes and total dose of gonadotropin. RESULTS: Fifteen randomized controlled trails (RCTs) involving 1448 patients were eligible for the analysis. GH supplementation improved live birth rate (RR, 1.74; 95% CI, 1.19-2.54), clinical pregnancy rate (RR, 1.65; 95% CI, 1.31-2.08) and retrieved oocytes number (SMD, 0.72; 95% CI, 0.28-1.16), while reducing cancelled cycles rate (RR, 0.62; 95% CI, 0.44-0.85) and dose of Gonadotropin (SMD,-1.05 95% CI, - 1.62 - -0.49) for poor ovarian response patients. Besides, there was no significant difference in the miscarriage rate between GH group and control group. CONCLUSIONS: Based on the limited available evidence, growth hormone supplementation seems to improve IVF/ICSI outcomes for poor ovarian responders. Further randomized controlled trials with large sample sizes are required to clarify the effect of GH adjuvant therapy in the treatment of women with poor ovarian response.

Repression of miR-142-3p alleviates psoriasis-like inflammation by repressing proliferation and promoting apoptosis of keratinocytes via targeting Sema3A.

Psoriasis is a multifactorial, recurring, and chronic inflammatory skin disease characterized by hyperproliferation of keratinocytes. Evidence is rapidly accumulating for the role of microRNAs in psoriasis. The object of the study was to explore the functions and precise mechanism of miR-142-3p in human keratinocyte HaCaT cells in the presence of M5. Here, the results showed that miR-142-3p expression was heightened in HaCaT cells induced by M5. In addition, inhibition of miR-142-3p dramatically restricted cell proliferation and enhanced apoptosis in HaCaT cells exposed to M5, as exemplified by a decrease in the antiapoptotic Bcl-2 protein, concomitant with an increase in the proapoptotic proteins Bax. Moreover, depleting miR-142-3p effectively ameliorated M5-induced inflammation response, as reflected by the attenuation of multiple inflammatory factors. Importantly, Sema3A was identified as an authentic target of miR-142-3p, and indeed regulated by miR-142-3p. Mechanistically, silencing of Sema3A effectively abolished the anti-proliferative, apoptosis-promoting, and anti-inflammatory effects of miR-142-3p inhibition in keratinocytes. Taken together, these data elucidated that repression of miR-142-3p protect HaCaT cells against M5-induced hyper-proliferation and inflammatory injury by suppressing its target Sema3A, implying that the miR-142-3p/Sema3A axis may be a new target for preventing keratinocyte injury process. These findings provide a new and better understanding of the mediating role of miR-142-3p in psoriasis.

miR-338-5p inhibits cell proliferation, colony formation, migration and cisplatin resistance in esophageal squamous cancer cells by targeting FERMT2.

Esophageal cancer is one of the leading causes of cancer death in the male population of Eastern Asia. In addition, esophageal squamous cell carcinoma (ESCC) is the major type of esophageal cancer among the world. Owing to the poor overall 5-year survival rate, novel effective treatment strategies are needed. MicroRNAs are important gene regulators that are dysregulated in many cancer types. In our previous study, we applied next-generation sequencing to demonstrate that miR-338-5p was downregulated in the tumor tissue of patients with versus without recurrence. In this study, we further studied the roles of miR-338-5p in ESCC. The expression of endogenous miR-338-5p was at lower levels in ESCC cells compared with normal cells. Functional assays showed that miR-338-5p reduced cell proliferation, colony formation, migration and cisplatin resistance in an ESCC cell line, CE-81T. Potential target genes of miR-338-5p were identified by microarray and prediction tools, and 31 genes were selected. Among these, Fermitin family homolog 2 (FERMT2) plays an oncogenic role in ESCC, so it was chosen for further study. Luciferase assays showed the direct binding between miR-338-5p and the 3' untranslated region of FERMT2. Silencing of FERMT2 inhibited cell proliferation, colony formation, migration and cisplatin resistance. Pathway analysis revealed that the integrin-linked protein kinase signaling pathway, in which FERMT2 participates, was significantly affected by a miR-338-5p mimic. Our results suggest that miR-338-5p may play an antioncogenic role in ESCC via repressing FERMT2.

CD36- and obesity-associated granulosa cells dysfunction.

Emerging evidence indicates that obesity impairs granulosa cell (GC) function, but the underlying mechanisms remain unclear. Gene expression profiles in GC of non-polycystic ovary syndrome (PCOS) obese (NPO), PCOS obese (PO), PCOS normal weight (PN) and non-PCOS normal weight (NPN) patients were analysed by microarray analysis. Compared with the NPN group, there were 16, 545 and 416 differently expressed genes in the NPO, PO and PN groups respectively. CD36 was the only intersecting gene, with greater than two fold changes in expression between the NPO versus NPN and PO versus NPN comparisons, and was not present in the PN versus NPN comparison. In addition, levels of CD36 protein were higher in GC from obese than normal weight patients. Furthermore, CD36 overexpression in a GC line inhibited cell proliferation, as determined by the cell counting kit-8 (CCK8) test, promoted cell apoptosis, as determined by flow cytometry, and inhibited the secretion of oestradiol by depositing triglyceride in cells and increasing cellular lipid peroxide levels. These adverse effects were reduced by sulfo-N-succinimidyloleate, a specific inhibitor of CD36. Together, the findings of this study suggest that obesity with and without PCOS should be regarded as separate entities, and that CD36 overexpression in GC of obese patients is one of the mechanisms by which obesity impairs GC function.

Long non-coding RNA CRNDE promotes the proliferation, migration and invasion of hepatocellular carcinoma cells through miR-217/MAPK1 axis.

Hepatocellular carcinoma (HCC) is an invasive malignant tumour and the second major cause of cancer-related deaths over the world. CRNDE and miR-217 are non-coding RNAs which play critical roles in cell growth, proliferation, migration. Mitogen-activated protein kinase 1 (MAPK1) also participates in cancer cell process. Hence, this study aimed at investigating the effect of CRNDE on migration and invasion of HCC and figuring out the role of miR-217 and MAPK1 in this process. The overexpression of CRNDE was demonstrated by a microarray-based lncRNA profiling study. CRNDE expression in HCC was verified by qRT-PCR. MTT assay and BrdU staining were applied to detect cell proliferation level. Transwell assay was utilized to examine cell migration and invasiveness abilities. Wound healing assay was performed for further exploration of cell migration capacity. MiR-217 was predicted by bioinformatics. The dual luciferase reporter assay was performed to corroborate the targeting relationship between CRNDE, miR-217 and MAPK1. MAPK1, the downstream target of miR-217, was predicted using bioinformatics and was further confirmed by qRT-PCR and Western blot. The interaction between CRNDE, miR-217 and MAPK1 was studied by qRT-PCR, Western blot, MTT, BrdU, transwell assay and wound healing assay. CRNDE was up-regulated in HCC tissues and HCC cell lines. The high expression of CRNDE facilitated cell proliferation, migration and invasion, while the inhibited one affected on the contrary. MiR-217, negatively correlated with CRNDE expression, was the target of CRNDE and was more lowly expressed in HCC. With the high expression of miR-217, HCC cell proliferation, migration and invasion were suppressed. MAPK1, the possible target of miR-217, was negatively correlated with miR-217 but positively correlated with CRNDE and had the same effect in HCC formation process as CRNDE. Long non-coding RNA CRNDE promotes the proliferation, migration and invasion of HCC cells through miR-217/MAPK1 axis.