Global, regional, and national burdens of nutritional deficiencies, from 1990 to 2019.

The epidemiological and burden characteristics of nutritional deficiencies (NDs) have been evolving, and it is crucial to identify geographical disparities and emerging trends. This study aimed to analyze the global, regional, and national trends in the burden of NDs over the past 30 years. Data were obtained from the Global Burden of Disease (GBD) 2019 database for the period 1990-2019. The study examined the incidence rates and disability-adjusted life years (DALYs) of NDs at various levels. Globally, the incidence rate of NDs decreased from 2226.2 per 100,000 in 2019 to 2096.3 per 100,000 in the same year, indicating a decline of 5.8%. The average annual percentage change (AAPC) was -0.21 (-0.31 to -0.11). Similarly, DALYs, prevalence, and mortality rates of NDs exhibited significant declines (AAPC = -3.21 [-3.45 to -2.96], AAPC = -0.53 [-0.55 to -0.51], and AAPC = -4.97 [-5.75 to -4.19], respectively). The incidence rate of NDs varied based on age group, gender, cause, and geographical area. Moreover, a negative association was observed between incidence and the sociodemographic index. At the regional level, the South Asia and Sub-Saharan Africa regions had the highest incidence rates of NDs. In conclusion, the global incidence rate of NDs showed a mixed pattern, while the DALY rate consistently declined. Additionally, prevalence and mortality rates of NDs decreased between 1990 and 2019.

The Mediator Med23 controls a transcriptional switch for muscle stem cell proliferation and differentiation in muscle regeneration.

Muscle stem cells (MuSCs) contribute to a robust muscle regeneration process after injury, which is highly orchestrated by the sequential expression of multiple key transcription factors. However, it remains unclear how key transcription factors and cofactors such as the Mediator complex cooperate to regulate myogenesis. Here, we show that the Mediator Med23 is critically important for MuSC-mediated muscle regeneration. Med23 is increasingly expressed in activated/proliferating MuSCs on isolated myofibers or in response to muscle injury. Med23 deficiency reduced MuSC proliferation and enhanced its precocious differentiation, ultimately compromising muscle regeneration. Integrative analysis revealed that Med23 oppositely impacts Ternary complex factor (TCF)-targeted MuSC proliferation genes and myocardin-related transcription factor (MRTF)-targeted myogenic differentiation genes. Consistently, Med23 deficiency decreases the ETS-like transcription factor 1 (Elk1)/serum response factor (SRF) binding at proliferation gene promoters but promotes MRTF-A/SRF binding at myogenic gene promoters. Overall, our study reveals the important transcriptional control mechanism of Med23 in balancing MuSC proliferation and differentiation in muscle regeneration.

The microbiota-gut-brain axis: A crucial immunomodulatory pathway for Bifidobacterium animalis subsp. lactis' resilience against LPS treatment in neonatal rats.

An imbalanced gut microflora may contribute to immune disorders in neonates due to an immature gut barrier. Bacterial toxins, particularly, can trigger the immune system, potentially resulting in uncontrolled gut and systemic inflammation. Previous research has revealed that Bifidobacterium animalis subsp. lactis (B. lactis) could protect against early-life pathogen infections by enhancing the gut barrier. However, the effects of B. lactis on a compromised immune system remain uncertain. Hence, this study concentrated on the immunomodulatory effects and mechanisms of B. lactis in neonatal rats intraperitoneally injected with lipopolysaccharide (LPS), a bacterial toxin and inflammatory mediator. First, B. lactis significantly alleviated the adverse effects induced by LPS on the growth, development, and body temperature of neonatal rats. Second, B. lactis significantly reduced the immune responses and damage induced by LPS, affecting both systemic and local immune responses in the peripheral blood, gut, and brain. Notably, B. lactis exhibited extra potent neuroprotective and neurorepair effects. Our research found that pre-treatment with B. lactis shaped the diverse gut microecology by altering both microbial populations and metabolic biomolecules, closely linked to immunomodulation. Overall, this study elucidated the multifaceted roles of B. lactis in neonatal hosts against pathogenic infection and immune disorder, revealing the existence of the microbiota-gut-brain axis.

Temporal trends in prevalence and disability of chronic kidney disease caused by specific etiologies: an analysis of the Global Burden of Disease Study 2019.

BACKGROUND: The prevalence of disability in CKD is high. In this context the aim of the present study was to assess the  temporal trends of prevalence and disability progression for chronic kidney disease (CKD) caused by specific etiologies. METHODS: Using data from the Global Burden of Diseases Study (GBD) 2019, we examined the age-standardized rates of CKD prevalence and disability-adjusted life-years for different etiologies, including Type 1/2 diabetes mellitus (T1DM/T2DM), glomerulonephritis, and hypertension. We also calculated the average annual percentage changes to assess trends. Additionally, we utilized the joinpoint regression model to identify significant shifts over time. RESULTS: From 1990 to 2019, the global prevalence of CKD due to various etiologies exhibited an overall increasing trend, albeit with fluctuations. Notably, CKD due to T1DM, glomerulonephritis, and hypertension consistently demonstrated a significant upward trend across all continents, while the prevalence of CKD due to T2DM varied across continents. In terms of disability-adjusted life-years, CKD due to T2DM and hypertension exhibited a significant rising trend over the past 30 years. However, changes in age standardized disability-adjusted life-years for CKD due to different etiologies were not consistent across continents, with an upward trend observed in The Americas and a contrasting trend in Asia. Furthermore, both age-standardized prevalence rate and age standardized disability-adjusted life-year trends for CKD varied significantly across 204 countries and territories. Additionally, a negative association was observed between the Socio-demographic Index and the disability progression of CKD. CONCLUSION: The prevalence and disability burden of CKD caused by specific etiologies show substantial heterogeneity worldwide, highlighting significant disparities in the distribution of CKD. It is crucial to implement geographic and personalized strategies in different regions to alleviate the burden of CKD effectively.

Mendelian randomization analysis identifies a genetic casual association between circulating C-reactive protein and intracerebral hemorrhage.

BACKGROUND: The causal effect of C-reactive protein (CRP) on intracerebral hemorrhage (ICH) remains controversial. We discussed the causal association of CRP with ICH based on two-sample Mendelian randomization. METHODS: The data from two genome-wide association studies (GWAS) of European ancestry was extracted, including circulating CRP levels (204,402 individuals) and ICH (1,687 cases and 201,146 controls). The inverse variance weighted (IVW) method was primary tool to evaluate the causal relationship of circulating CRP levels on ICH risk. MR-Egger regression and MR-PRESSO global test were utilized to identify pleiotropy. Heterogeneity was discussed with Cochran's Q test. The leave-one-out analysis explored the reliability of the results. RESULTS: 54 SNPs were identified as instrumental variables (IVs) for circulating CRP levels, and these IVs had no significant horizontal pleiotropy, heterogeneity, or bias. MR analysis demonstrated a causal relationship between elevated circulating CRP levels and decreased risk of ICH (ORIVW = 0.828, 95% CI 0.692-0.992, P = 0.040). CONCLUSION: Elevated circulating CRP levels demonstrated a significant potentially protective causal relationship with risk of ICH.

Expression patterns and immunological characterization of PANoptosis -related genes in gastric cancer.

Background: Accumulative studies have demonstrated the close relationship between tumor immunity and pyroptosis, apoptosis, and necroptosis. However, the role of PANoptosis in gastric cancer (GC) is yet to be fully understood. Methods: This research attempted to identify the expression patterns of PANoptosis regulators and the immune landscape in GC by integrating the GSE54129 and GSE65801 datasets. We analyzed GC specimens and established molecular clusters associated with PANoptosis-related genes (PRGs) and corresponding immune characteristics. The differentially expressed genes were determined with the WGCNA method. Afterward, we employed four machine learning algorithms (Random Forest, Support Vector Machine, Generalized linear Model, and eXtreme Gradient Boosting) to select the optimal model, which was validated using nomogram, calibration curve, decision curve analysis (DCA), and two validation cohorts. Additionally, this study discussed the relationship between infiltrating immune cells and variables in the selected model. Results: This study identified dysregulated PRGs and differential immune activities between GC and normal samples, and further identified two PANoptosis-related molecular clusters in GC. These clusters demonstrated remarkable immunological heterogeneity, with Cluster1 exhibiting abundant immune infiltration. The Support Vector Machine signature was found to have the best discriminative ability, and a 5-gene-based SVM signature was established. This model showed excellent performance in the external validation cohorts, and the nomogram, calibration curve, and DCA indicated its reliability in predicting GC patterns. Further analysis confirmed that the 5 selected variables were remarkably related to infiltrating immune cells and immune-related pathways. Conclusion: Taken together, this work demonstrates that the PANoptosis pattern has the potential as a stratification tool for patient risk assessment and a reflection of the immune microenvironment in GC.

Downregulation of ACC expression suppresses cell viability and migration in the malignant progression of breast cancer.

Exploring new diagnostic biomarkers and molecular targets is of great importance in breast cancer treatment. The present study investigated the effects of acetyl-CoA carboxylase (ACC) expression interference on the malignant progression of breast cancer cells. ACC expression was knocked down using a lentiviral vector and this was verified by quantitative polymerase chain reaction and western blotting. MCF-7 and MDA-MB-231 breast cancer cells were randomly allocated into the following groups: Normal breast cancer cells (control), breast cancer cells transduced with a negative control lentiviral vector and breast cancer cells transduced with an ACC knockdown lentiviral vector. Screening for stable transgenic strains was successful. Cell viability, apoptosis and migration were determined using Cell Counting Kit-8, flow cytometry and scratch test, respectively. The protein expression levels of N-cadherin, Vimentin and Bax were detected by western blotting. In addition, a nude mouse model of subcutaneous metastatic tumor was established using MCF-7 breast cancer cells, and tumor volume was assessed. Furthermore, pathological condition and apoptosis were detected using hematoxylin and eosin, and TUNEL staining, respectively. The protein expression levels of N-cadherin, Vimentin and Bax were detected by western blotting. The in vitro experiments showed that knockdown of ACC expression significantly decreased the viability and migration, and increased the apoptosis of MCF-7 and MDA-MB-231 breast cancer cells. In vivo experiments revealed that ACC knockdown effectively reduced the tumor volume in nude mice, and promoted tumor cell apoptosis. Both in vitro and in vivo experiments showed that ACC knockdown can reduce the protein expression levels of N-cadherin and Vimentin, and increase Bax expression. These findings suggested that downregulation of ACC expression may significantly reduce the malignant progression of breast cancer, and could be considered a potential therapeutic target.

Immunogenic cell death-led discovery of COVID-19 biomarkers and inflammatory infiltrates.

Immunogenic cell death (ICD) serves a critical role in regulating cell death adequate to activate an adaptive immune response, and it is associated with various inflammation-related diseases. However, the specific role of ICD-related genes in COVID-19 remains unclear. We acquired COVID-19-related information from the GEO database and a total of 14 ICD-related differentially expressed genes (DEGs) were identified. These ICD-related DEGs were closely associated with inflammation and immune activity. Afterward, CASP1, CD4, and EIF2AK3 among the 14 DEGs were selected as feature genes based on LASSO, Random Forest, and SVM-RFE algorithms, which had reliable diagnostic abilities. Moreover, functional enrichment analysis indicated that these feature genes may have a potential role in COVID-19 by being involved in the regulation of immune response and metabolism. Further CIBERSORT analysis demonstrated that the variations in the immune microenvironment of COVID-19 patients may be correlated with CASP1, CD4, and EIF2AK3. Additionally, 33 drugs targeting 3 feature genes had been identified, and the ceRNA network demonstrated a complicated regulative association based on these feature genes. Our work identified that CASP1, CD4, and EIF2AK3 were diagnostic genes of COVID-19 and correlated with immune activity. This study presents a reliable diagnostic signature and offers an overview to investigate the mechanism of COVID-19.

Characterization of protein-based risk signature to predict prognosis and evaluate the tumor immune environment in breast cancer.

BACKGROUND: Proteomics profiles have enabled a systematic insight into the prognosis of cancer. This study aimed to establish a valuable protein-based risk signature to assess the prognosis and immune status in patients with breast cancer (BC). METHODS: Protein expression profile, RNA expression data, and clinical information were acquired from The Cancer Genome Atlas (TCGA). The whole cohort was randomly split into two cohorts, one for establishing the risk signature and the other for testing. Univariate Cox analysis and Least absolute shrinkage and selection operator (LASSO) Cox regression were utilized to construct the protein-based risk signature. All cohorts were divided into high- and low-risk groups, which were applied to investigate the clinical relevance, tumor microenvironment, and therapeutic response. RESULTS: The prognostic proteomics signature was established based on prognostic proteins, thus categorizing patients into low-risk and high-risk groups with different prognoses. A predictive nomogram was also developed to predict 1, 3, and 5-year survival possibility for BC patients, and the calibration curves confirmed the predictive significance of this signature. Afterward, the low-risk group displayed higher immune activities, immune checkpoint expression, and immunotherapeutic response. Moreover, GSEA analysis indicated that immune-associated pathways were rich in the low-risk group. Additionally, this prognostic signature demonstrated potential predict significance for chemotherapeutic agents. CONCLUSION: This study established an effective prognostic proteomics signature with reliable predictive performance for survival, immune activity, and drug sensitivity. It might provide a novel perspective into the protein function in BC, and guide the individual treatment strategies for BC patients.

PRR11 is a prognostic biomarker and correlates with immune infiltrates in bladder urothelial carcinoma.

Abnormal proline-rich protein 11 (PRR11) expression is associated with various tumors. However, there are few reports concerning PRR11 with prognostic risk, immune infiltration, or immunotherapy of bladder urothelial carcinoma (BLCA). This study is based on online databases, such as Oncomine, GEPIA, HPA, LinkedOmics, TIMER, ESTIMATE and TISIDB, and BLCA data downloaded from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus, we employed an array of bioinformatics methods to explore the potential oncogenic roles of PRR11, including analyzing the relationship between PRR11 and prognosis, tumor mutational burden (TMB), microsatellite instability, and immune cell infiltration in BLCA. The results depict that PRR11 is highly expressed in BLCA, and BLCA patients with higher PRR11 expression have worse outcomes. In addition, there was a significant correlation between PRR11 expression and TMB and tumor immune infiltration. These findings suggest that PRR11 can be used as a potential marker for BLCA patient assessment and risk stratification to improve clinical prognosis, and its potential regulatory mechanism in the BLCA tumor microenvironment and targeted therapy is worthy of further investigation.

Assessment of the role and mechanism of Bifidobacterium animalis subsp. lactis isolated from neonates' feces in protecting neonatal rats from Salmonella infection.

OBJECTIVES: It is now well known that Bifidobacterium animalis subsp. lactis (B. lactis), an important early-life colonizer of the gut, provides immune-related benefits to infants. The aim of the work is to explore the intraspecific resistance to Salmonella infection of B. lactis isolated from neonatal feces, and to learn more insights into how B. lactis mediates beneficial roles in early-life infection resistance. METHODS: Five strains of B. lactis (NFBAL11/NFBAL23/NFBAL44/NFBAL63/NFBAL92) were screened from fecal samples of neonates born within fifteen days and pretreated neonatal rats prior to infection with Salmonella typhimurium (S. typhimurium) SL1344. The survival rate, fecal occult blood, diarrhea and hepatosplenomegaly were detected to assess the ability of B. lactis to prevent S. typhimurium infection. Furthermore, the structure of mucus layer, gene expression, cytokine levels, antioxidant levels and intestinal microflora composition were detected to explore the mechanism. RESULTS: All strains showed activity against S. typhimurium, with B. lactis NFBAL23 being the most active, followed by NFBAL63 and NFBAL92. And these advantages weren't attained by enhancing physical growth and development. Mechanistically, the neonatal rats treated with B. lactis (NFBAL23/NFBAL63/NFBAL92) had improved intestinal barrier function involving physical, chemical, immune and biological barriers in the face of challenges posed by S. typhimurium. CONCLUSIONS: These findings revealed the intraspecific difference, beneficial roles and mechanisms of action of B. lactis against Salmonella infection early in life, which highlighted the necessity of supplementing appropriate B. lactis, and provided several potential B. lactis candidates for Salmonella infection treatment.

The Diagnostic Value of Coagulation Indicators and Inflammatory Markers in Distinguishing Between Strangulated and Simple Intestinal Obstruction.

BACKGROUND: Intestinal obstruction with strangulation can be life-threating, and it is critical to make an accurate and timely diagnosis for emergency surgery. OBJECTIVE: This was aimed to investigate the value of coagulation indicators and inflammatory markers in distinguishing between strangulated and simple intestinal obstruction. MATERIALS AND METHODS: Fifty-four patients with intestinal obstruction were retrospectively studied. The correlation between coagulation indicators and inflammatory markers with intestinal obstruction was analyzed. Receiver operating characteristic curves were created to assess their ability in discriminative diagnosis. RESULTS: Levels of fibrinogen (Fib), C-reactive protein (CRP), neutrophil ratio, and D-Dimer were significantly greater, while thrombin time was significantly shorter in strangulated intestinal obstruction compared with simple intestinal obstruction. Furthermore, Fib levels in the necrosis subgroup of strangulated intestinal obstruction were significantly higher than those in the ischemia subgroup and simple intestinal obstruction group. The areas under the receiver operating characteristic curve were 0.58 for white blood cells, 0.78 for CRP, and 0.80 for Fib. Using the optimal cutoff values of Fib (3.71 g/L) and CRP (14.54 mg/L), the sensitivity, specificity, positive predictive value, and negative predictive value in discriminating between strangulated intestinal obstruction and simple intestinal obstruction were 51.43%, 100%, 100%, and 52.78% for Fib, and 56.25%, 94.44%, 94.74%, and 54.84% for CRP, respectively. CONCLUSIONS: Fib and CRP demonstrate good performance in predicting strangulation and are indicative of intestinal necrosis and ischemia. The combination of this coagulation indicator and inflammatory marker holds potential for better discrimination between strangulated and simple intestinal obstruction.

Effect of dehydrofluorination reaction on structure and properties of PVDF electrospun fibers.

Piezoelectric nanosensors were prepared with a novel type of dehydrofluorinated poly(vinylidene fluoride) (PVDF) nanofibrous membrane. With the synergistic effect of the dehydrofluorination reaction and applied high voltage electric field, the piezoelectric and energy storage properties of fibrous membranes attained great improvement. It was found that the simultaneous introduction of conjugated double bonds to the backbone of PVDF which was accompanied with the elimination of HF, resulted in the decrease of its molecular weight, solution viscosity and hydrophobicity. The crystalline phase, diameter, piezoelectric and energy storage properties of electro-spun PVDF nanofiber membranes significantly depend on the degree of HF elimination in dehydrofluorinated PVDF. The dehydrofluorinated PVDF with 5 hours of reaction exhibits the highest discharged energy density (W rec) and energy storage efficiency (η), but excessive dehydrofluorination reaction is unfavorable to the energy storage properties. In addition, the dehydrofluorinated PVDF fiber membrane-based nanosensor possesses a larger electrical throughput (open circuit voltage of 30 V, which is three time that of the untreated PVDF), indicating that the introduction of double bonds can also improve the piezoelectric properties of PVDF nanofibers.

BML-111 inhibits EMT, migration and metastasis of TAMs-stimulated triple-negative breast cancer cells via ILK pathway.

Triple-negative breast cancer (TNBC) has a more aggressive phenotype and higher metastasis and recurrence rates than other breast cancer subtypes. The immune microenvironment and hypoxic microenvironment of breast cancer constitute the survival environment of cancer cells, which is an important environment to support cancer cells. LXA4 and its analog, BML-111 is an important regulator of inflammatory cytokines, which provides a possible way for the treatment of inflammatory-related tumors. Here, in the in vitro experiment, we showed that BML-111 could inhibit the EMT and migration of TAMs-stimulated TNBC by down-regulating ILK as well as p-Akt and p-GSK3ß. And it could prevent the formation of breast cancer cell clusters. In the in vivo experiment, BML-111 could inhibit the metastasis of 4T1 breast cancer cells. We also demonstrated that BML-111 could affect macrophages in tumor microenvironment to prevent metastasis. These results showed that BML-111 could be a possible candidate for breast cancer therapy by targeting ILK and TAMs.

SNORA71B promotes breast cancer cells across blood-brain barrier by inducing epithelial-mesenchymal transition.

BACKGROUND: Brain metastasis (BM) is a dreadful complication that significantly impacts the quality of life in breast cancer patients. A key process during brain metastasis is the migration of cancer cells across blood-brain barrier (BBB). However, the role of snoRNAs regulating BBB in BM is still unknown. METHODS: Here SNORic and GEO databases were used to identify differentially expressed snoRNAs between brain metastatic and non-metastatic breast cancer (BC) tissues. The effects of SNORA71B on the capacities of proliferation, migration, invasion, epithelial-mesenchymal transition (EMT), and BBB invasion of BC cells were evaluated by CCK8, transwell, western blot, and BBB model, respectively. RESULTS: SNORA71B was highly expressed in high BM BC tissues and cells compared to low BM BC controls. Survival analysis revealed high expression of SNORA71B was significantly associated with poor PPS and OS in breast cancer patients. ROC curve showed that SNORA71B might act as biomarker for breast cancer. Moreover, SNORA71B significantly promoted proliferation, migration, and invasion of BC cells with different BM abilities. Importantly, SNORA71B promoted the EMT process of low BM BC cells. SNORA71B knockdown inhibited the high BM BC cells across BBB, while EMT activator dramatically abrogated this inhibited effect. CONCLUSIONS: In conclusion, SNORA71B promotes BC cells across the BBB partly via inducing EMT.

[The value of P16/ki67 double labeling, HPV E6/E7 mRNA detection and their combined application in cytological shunt diagnosis of low-grade squamous intraepithelial lesions].

Objective To explore the value of double labeling of P16/ki67, E6/E7 mRNA of human papillomavirus (HPV) and combined detection in shunt diagnosis of low-grade squamous intraepithelial lesions (LSIL) by thin-layer cervical cytology (TCT). Methods The study enrolled 239 patients who underwent colposcopy and biopsy within 4 weeks after primary TCT diagnosis. The remaining cytological samples were double-labeled with P16/ki67 immunocytochemical staining and the HPV E6/E7 mRNA was detected by Panther automatic HPV E6/E7 mRNA detection system. Using SPSS22.0 software, the positive rates of P16/ki67 double-labeling, HPV E6/E7 mRNA and combined detection were analyzed in different cervical lesions, and the positive rates in the same cervical lesions were compared horizontally to evaluate the efficiency of double labeling of P16/ki67, HPV E6/E7 and combined detection in the diagnosis of high-grade squamous intraepithelial lesions (HSIL) and above lesions. Results The diagnostic results of HE staining for the 239 cases of LSIL were 71 cases of chronic cervicitis (29.71%), 143 cases of LSIL (59.83%), 22 cases of HSIL (9.20%) and 3 cases of cervical cancer (1.26%). There were 46 cases of P16+ki67+ lesions (19.25%), 41 cases of ki67+P16- lesions (17.15%), 33 cases of ki67-P16+ lesions (13.81%) and 119 cases of P16-ki67- lesions (49.79%). The positive rates of P16/ki67 double-labeling, HPV E6/E7 mRNA and combined detection increased with the severity of cervical lesions. The positive rate of combined detection was the highest in the HSIL lesions, which was higher than that of P16/ki67 double-labeling and HPV E6/E7 mRNA detection. The sensitivity of combined detection was higher than that of P16/ki67 double-labeling and HPV E6/E7 mRNA detection. The Youden index of joint detection was 0.7850. Conclusion The combined detection of P16/ki67 double labeling, HPV E6/E7 mRNA and HPV E6/E7 mRNA had a certain clinical value in the management of cell LSIL shunt diagnosis. The combined detection significantly improved the sensitivity and Youden index of HSIL and above lesions, while maintaining a high specificity and coincidence rate.

EMT related circular RNA expression profiles identify circSCYL2 as a novel molecule in breast tumor metastasis.

Substantial evidence indicates that circular RNAs (circRNAs) play vital roles in several diseases, especially in cancer development. However, the functions of circRNAs in breast cancer metastasis remain to be investigated. This study aimed to identify the key circRNAs involved in epithelial mesenchymal transition (EMT) of breast cancer and evaluated their molecular function and roles in pathways that may be associated with tumor metastasis. An EMT model was constructed by treating breast cancer cells MCF­7 and MDA­MB­231 with transforming growth factor­ß1. High­throughput RNA sequencing was used to identify the differentially expressed circRNAs in EMT and blank groups of two cells, and reverse transcription­quantitative PCR was used to validate the expression of circSCYL2 in human breast cancer tissues and cells. The effects of circSCYL2 on breast cancer cells were explored by transfecting with plasmids and the biological roles were assessed using transwell assays. EMT groups of breast cancer cells exhibited the characteristics of mesenchymal cells. Furthermore, the present study found that 7 circRNAs were significantly upregulated in both the MCF­7 EMT and MDA­MB­231 EMT groups, while 16 circRNAs were significantly downregulated. The current study identified that circSCYL2 was downregulated in breast cancer tissues and cell lines, and that circSCYL2 overexpression inhibited cell migration and invasion. This study provides expression profiles of circRNAs in EMT groups of breast cancer cells. circSCYL2, which is downregulated in breast cancer tissues and cells, may play an important role in breast cancer EMT progression.

Long noncoding RNA LINC00115 promotes breast cancer metastasis by inhibiting miR-7.

Breast cancer is the second leading cause of cancer-related deaths in women. The long noncoding RNA LINC00115 has been reported to be involved in the poor outcome of patients with breast cancer, but the biological function and underlying mechanism remain unclear. Here, we report that LINC00115 expression is increased in triple-negative breast cancer tissue compared with matched normal tissue, and LINC00115 knockdown suppresses breast cancer cell migration and invasion. Furthermore, we show that LINC00115 directly targets miR-7 and inhibits its expression. LINC00115 also reduces the expression of KLF4, which is a direct target of miR-7 and is involved in breast cancer metastasis. Together, our findings suggest that LINC00115 promotes breast cancer metastasis through modulating the expression of miR-7 and KLF4.

Molecular characteristics of group B Streptococcus isolates from infants in southern mainland China.

BACKGROUND: Invasive group B Streptococcus (GBS) disease in Chinese infants has gradually gained attention in recent years, but the molecular epidemiology of the pathogen is still not well known. METHODS: This multicenter study retrospectively investigated distribution of capsular serotypes, sequence types (STs), and hypervirulent GBS adhesin gene (hvgA) in clinical GBS isolates that caused invasive disease in infants aged < 3 months of age in southern mainland China between January 2013 and June 2016. Genes for antibiotic resistance to tetracycline, erythromycin, and clindamycin were also examined. RESULTS: From a total of 93 GBS isolates taken from 34 early-onset disease (EOD, 0-6 days after birth) and 59 late-onset disease (LOD, 7-89 days after birth) cases, four serotypes were identified: serotypes III (79.6%), Ib (12.9%), Ia (4.3%), and V (3.2%). Serotype III accounted for 73.5% of EOD and 83.1% of LOD and was responsible for 75.5% of cases involving meningitis. Fifteen STs were found, with the majority being ST17 (61.3%), ST12 (7.5%), ST19 (7.5%), and others (23.7%). 96.8% of STs belonged to only five clonal complexes (CCs): CC17 (64.5%), CC10 (12.9%), CC19 (9.7%), CC23 (6.5%), and CC1 (3.2%). The hvgA gene was detected in 66.7% of GBS isolates and 95% of CC17 isolates, all of which were serotype III except one serotype Ib/CC17 isolate. A large proportion of GBS isolates were found to be resistant to tetracycline (93.5%), clindamycin (65.5%), and erythromycin (60.2%). Genes of tetO (74.7%) and tetM (46.0%) were found in tetracycline resistant isolates, linB (24.6%) in clindamycin resistant isolates, and ermB (87.5%) and mefA (3.6%) in erythromycin resistant isolates. CONCLUSION: Our results reveal higher prevalence of serotype III, ST17, CC17, hvgA expressing, and antibiotic resistant GBS isolates than previously reported in southern mainland China. This study provides guidance for appropriate measures of prevention and control to be taken in the future.

Overexpression of long non-coding RNA LINC00982 suppresses cell proliferation and tumor growth of papillary thyroid carcinoma through PI3K-ATK signaling pathway.

Long non-coding RNAs (lncRNAs) have been widely reported that involved in human cancers, including papillary thyroid carcinoma (PTC). The present study aims to investigate the biological role of LINC00982 in PTC. The mRNA expression of LINC00982 in human PTC tissues was detected using qPCR. Moreover, Kaplan-Meier method was performed to analyze the internal relevance between LINC00982 expression and overall survival (OS) rate of patients with PTC. In addition, gain- and loss-of-functions assays were performed to detect the effects of LINC00982 on the cell proliferation and migration in PTC cells. Furthermore, western blot assay was used to measure the alteration expression levels of apoptosis relative proteins and the relative protein involved phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway. Finally, a xenograft model was used to analyze the antitumor role of LINC00982 in vivo Here, we found that LINC00982 was decreased in human PTC tissues. Patients with decreased LINC00982 expression levels had a reduced OS (P=0.0019) compared with those with high LINC00982 expression levels. Overexpression of LINC00982 suppressed the proliferation and migration of BHT101 and B-CPAP cells and promoted cell apoptosis. Knockdown of LINC00982 promoted the proliferation and migration of BHT101 and B-CPAP cells and induced cell apoptosis. Moreover, in vivo assay showed that overexpression of LINC00982 could suppress the growth of PTC. Finally, LINC00982 could regulate the activity of PI3K/AKT signaling pathway in vitro and in vivo Taken together, our findings demonstrated that overexpression of LINC00982 could suppress cell proliferation and induce cell apoptosis by regulating PI3K/AKT signaling pathway in PTC.