Gene Reports最新文献

This study sequenced and assembled the mitochondrial genome of the rare dragonfly species Libellula melli, and submitted the results to the NCBI GenBank database, obtaining the accession number PP588458. The mitochondrial genome spans a total length of 15,149 bp, encompassing 13 protein-coding genes (PCGs), 22 tRNA genes, 2 rRNA genes, and a control region or D-loop. Of these, 25 genes and segments are located on the heavy strand (H-strand), while the remaining 13 reside on the light strand (L-strand). The nucleotide composition of the L. melli mitochondrial genome exhibits a prominent AT bias (AT = 73.3 %), with T, C, A, and G bases comprising 34.5 %, 15.6 %, 38.8 %, and 11.1 % respectively, displaying a positive AT skew of 0.059. Among the 13 PCGs, the primary start codons are ATT, ATG, and TTG, while the primary stop codons are TAA, with instances of TA(C) and T(AT) also observed. RSCU analysis reveals that the most frequently used codon is UUA, with an RSCU value of 3.75, encoding leucine (Leu). The secondary structures of the proteins encoded by the 13 PCGs generally exhibit a trend of α-helix > random coil > extended strand > β-turn. Phylogenetic analysis uncovers the phylogenetic relationships of L. melli within the reported Libellulidae species, revealing (((((((L. melli + L. quadrimaculata) + L. angelina) + ((O. chrysis + O. glaucum) + O. albistylum)) + ((C. servilia servilia + T. virginia) + N. fulvia) + (L. albifrons + S. eroticum)) + (P. flavescens + T. aurora)) + (D. phaon + H. croceus)) + (B. contaminate + P. zonata)). This study provides insights into the mitochondrial genome and its characteristics of this rare dragonfly species, contributing to our understanding of the intricate evolutionary relationships within the Odonata order. The data obtained serve as a foundation for further exploration of the complex phylogenetic relationships among dragonfly insects.

Objective

To screen the key genes of patients with premature ovarian insufficiency (POI) by bioinformatics analysis, study the pathological mechanism of POI and predict the potential therapeutic targets.

Methods

The WGCNA algorithm was used to establish a weighted gene co-expression network, and the data downloaded from the GEO database was used to identify the relevant hub genes of premature ovarian insufficiency (GSE39501), and the relevant genes of premature ovarian insufficiency downloaded from the HMDD database were intersected to identify the key genes using Cytoscape and verified for their differential expression by QRT-PCR and Western Blot (WB) to verify their differential expression.

Results

A total of 20 expression modules were identified by WGCNA, and the Firebricks module was found to be highly correlated with premature ovarian insufficiency after correlation coefficient screening. 1666 up-regulated genes and 1617 down-regulated genes were screened by differential analysis in the GSE39501 dataset, and a total of 12 co-expressed genes were localized after taking the intersections with related genes in the POI of the HMD database, which were validated by QRT PCR and Western Blot (WB). Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, and found that they mainly affect the MAPK signaling pathway and VEGF signaling pathway. The top three key genes, VEGFB, PEDF and SERP1NF1, were then localized by Cytoscape, and finally the opposite expression trends of VEGF and PEDF were verified by WB and QRT-PCR experiments.

Conclusion

The key genes VEGFB, PEDF and SERP1NF1 may be the potential biological markers of POI, and the imbalance of PEDF and VEGF may lead to the development of POI, which needs to be verified by further experiments.

Breast cancer is the most common cancer among women worldwide. Early detection and treatment are essential to improve patient outcomes and reduce mortality. Fibroblasts play a significant role in breast cancer development. Fibroblasts can be activated and influenced by cancer cells, leading to their identification as cancerassociated fibroblasts (CAFs), which are essential for tumor progression. In breast cancer, CAFs, as the main population of the tumor microenvironment, play a vital role and control several biological processes through non-coding RNAs(ncRNA) and signaling pathways. NcRNAs, such as long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), function as epigenetic regulators to control gene expression. Several studies have suggested that ncRNAs interfere in regulating tumor initiation and progression and can be used as biomarkers and therapeutic targets in different cancer types. Exosomes are extracellular vesicles that interact between fibroblasts and cancer cells. Exosomes derived from CAFs can influence breast cancer cells. Cancer cellderived exosomes may promote CAF phenotype, and CAF-derived exosomes transport miRNAs, lncRNAs, and several other substances, promoting breast cancer cell proliferation, migration, invasion, and angiogenesis, making them a potential therapeutic target. Despite little knowledge of the underlying functions of lncRNAs and miRNAs in CAFs, this review investigates how these ncRNAs cross-talk between tumor cells and CAFs.

Signaling molecules secreted during bone fracture healing stimulate molecular and cellular changes to promote healing and tissue regeneration. Molecular characterization of cytokines and growth factors can provide insight into their function and potential application as biologics or drug targets for bone tissue regeneration. Previous studies have identified the expression of IL1B, IL6, IL34, IGF1, ANGPT1, and TGFB3 during osteogenic differentiation and facture healing. In this study, we evaluated the transcriptome of adipose-derived mesenchymal stromal cells (AMSCs) following stimulation with these biological factors and examined their role in osteogenic differentiation. Stimulation of AMSCs with recombinant human (rh)-IL1B led to the largest gene expression changes compared to the other signaling factors including 1411 induced and 541 repressed genes (>2-fold). Rh-IL1B regulated genes included inflammatory (IL1B, IL6, CCL2) and osteogenic (BMP2, RUNX2, TWIST2) genes. Rh-IL1B also induced the expression of BMP2 in bone marrow-derived mesenchymal stromal cells (BMSCs) and bone digest cells. Although no changes in osteogenic differentiation of AMSCs was observed, low concentrations of rh-IL1B (0.1 ng/mL) promoted alkaline phosphatase activity of differentiated bone digest cells. Further, rh-IL1B significantly induced the secretion of BMP2 from these cells. Together this data provides insight into the molecular function of fracture-associated biological factors.

Psoriasis is a chronic relapsing inflammatory disease of the skin that affects almost 2–3 % population worldwide. The current treatment strategies include palliative therapeutics targeting the inflammatory pathways that do not completely cure the lesioned skin. The molecular cues in the hyper-proliferative and aberrantly differentiated keratinocytes of the psoriatic lesioned skin remain unknown. Through an integrative in-silico approach, we have analyzed human psoriatic skin samples from 3 RNA-Seq and 3 microarray datasets to identify 340 differentially expressed genes (DEGs). Further, these DEGs were analyzed using gene ontology enrichment, KEGG pathways, and protein-protein interaction networks for their role in disease pathology and the identification of hub genes. The expression of the hub genes was validated in a preclinical murine model of psoriasiform dermatitis. Finally, the ten hub genes were assessed for their drugability, which revealed 74 drugs targeting 7 hub genes (CCNA2, TOP2A, BIRC5, RRM2, CDK1, AURKA, and CCNB1) that can be repurposed for psoriasis treatment. This study provides an understanding of psoriasis pathophysiology and suggests key molecular biomarkers as therapeutic targets for effective mitigation of the disease.

Multidrug resistant (MDR) Escherichia coli causing diarrhea and the spread of antibiotic resistance genes as well as virulence genes through aquatic MDR strains represent a major clinical concern worldwide. In this study, we examined the virulence gene contents and prevalence of multidrug resistance among Escherichia coli strains isolated from diarrheal patients and aquatic environment of Bangladesh. Clinical isolates from Mathbaria and environmental isolates from Dhaka (freshwater and wastewater) and Chittagong (marine-water) in Bangladesh were included. Herein, antibiotic resistance was examined using the disc diffusion method, while the screening of virulence genes was conducted through PCR assay. The results showed a high prevalence of multidrug resistance (MDR) among clinical isolates, with 90.91 % exhibiting MDR. Erythromycin resistance was observed in all clinical isolates, while mecillinam showed 100 % sensitivity. Significant resistance was also seen for ampicillin, azithromycin, and sulfamethoxazole-trimethoprim (>70 %) in clinical isolates. Among environmental isolates, 87.64 % were identified as MDR, with high resistance rates for erythromycin, ampicillin, and azithromycin. Geographic variations in resistance patterns were observed between Dhaka and Chittagong, with higher resistance in Dhaka for certain antibiotics such as Gentamycin (CN), Tetracycline (TE), Ciprofloxacin (CIP), Ampicillin (AMP), Cefixime (CFM), Mecillinam (MEL). Virulence gene prevalence differed between clinical and environmental isolates, with entero-toxigenic E. coli (ETEC) being dominant in clinical samples and Entero-invasive E. coli (EIEC) in environmental samples. Younger patients had significantly higher occurrence of virulence genes than older ones. No significant gender biasness was observed for the prevalence of antibiotic resistance and virulence. Comparative analysis showed Rampura isolates had the highest resistance and Mirpur isolates had the highest virulence gene prevalence. Results from sewerage samples showed significantly higher antibiotic resistance compared to river water isolates. In Chittagong, significant difference in resistance was noticed for the samples from Chatkhil and Patenga 1 zones, while virulence gene prevalence did not vary significantly. Overall, this study highlights the preponderance of MDR in clinical E. coli isolates and substantial antibiotic resistance and virulence genes in environmental isolates, particularly in non-coastal water sources. Therefore, effective antibiotic stewardship programs are crucial to combat resistance in clinical and environmental settings in Bangladesh.

Background

Despite recent advances in our knowledge of genetic contributions to the highly variable sickle cell disease (SCD) phenotype, our understanding of genetic factors associated with pain sensitivity in SCD remains limited. Previous studies investigated specific variants in single candidate genes and their association with SCD pain variability. The primary aim of the current study was to expand the genes and polymorphisms tested to discover new risk genes (polymorphisms) associated with central sensitization for individuals with SCD.

Methods

Adults with sickle cell disease (n = 59, Mage = 36.8 ± 11.5, 65.8 % female) underwent quantitative sensory testing to examine central sensitization and general pain sensitivity. Participants reported average crisis and non-crisis pain intensities weekly using a 0–100 scale, and provided salivary samples for genotyping. The Hardy-Weinberg equilibrium was verified for controls, and allele distributions were tested with chi-square and odds ratio tests. The Benjamini-Hochberg procedure was used to control for false discovery rate. Regression analyses and Wilcoxon tests were used to test associations for normally distributed and skewed data, respectively.

Results

Central sensitization and general pain sensitivity were not associated with hemoglobin genotype (Ps > 0.05). Of 4145 SNPs tested, following false discovery rate adjustments, 11 SNPs (rs11575839, rs12185625, rs12289836, rs1493383, rs2233976, rs3131787, rs3739693, rs4292454, rs4364, rs4678, rs6773307) were significantly associated with central sensitization, and one SNP (rs7778077) was significantly associated with average weekly non-crisis pain. No SNPs were associated with general pain sensitivity.

Conclusions

These findings provide insights into genetic variants association with average non-crisis pain and central sensitization for individuals with SCD, and may provide support for genetic predictors of heightened pain experience within SCD.

Termites heavily depend on the gut microbiota to process a broad spectrum of biological reactions; therefore, influencing the gut microbiota is a crucial strategy for managing their infestation. Prior research has focused on the effects of entomopathogenic agents and antibiotics. However, there is a dearth of studies examining the impact of Chitin Synthesis Inhibitors (CSIs) on the gut microbiome. Therefore, this study aimed to characterize the gut microbiota in both untreated control and CSIs bait treated of Coptotermes gestroi (lower termite), Globitermes sulphureus and Macrotermes gilvus (higher termites) by amplifying V3 to V4 hypervariable region using 16S rRNA metagenomic in Illumina Miseq platform. Among all samples, the abundance of bacteria in higher termites was observed to be greater than in lower termite, and the abundance of bacteria in CSIs bait-treated samples is higher than in untreated control samples. This presumably due to established symbiont relationship with the pre-existing bacteria and archaea and divergence of dietary pattern. On the other hand, the gut microbiome also proved to highly susceptible to CSIs bait treatment hence, the upregulated after the bait treatment.

Blastocystis sp. is a protozoan parasite commonly found in the gastrointestinal tract of humans and various animals, including livestock. This study aimed to assess the prevalence, subtypes (STs) distribution, and zoonotic transmission potential of Blastocystis sp. in livestock in southwestern Iran. A cross-sectional study was conducted, and fecal samples were collected from cattle and sheep in Shiraz, the capital city of Fars province. Molecular analysis was conducted to amplify a specific fragment from the SSU rRNA gene through PCR and sequencing to detect Blastocystis.sp. and identify the related STs in the livestock population. This study identified a relatively low occurrence of Blastocystis sp. in cattle (8 %; 4/50) and sheep (6 %; 3/50). Nonetheless, different zoonotic STs were found in these animals. In cattle, ST10 accounted for 50 % (2/4), ST1 for 25 % (1/4), and ST3 for 25 % (1/4) of the cases. In sheep, 66.7 % (2/3) and 33.3 % (1/3) of the positive isolates were classified as ST10 and ST3, respectively. Blastocystis sp. was more common in young animals and females, as well as in diarrheal samples (P > 0.05). The findings suggest a significant risk of zoonotic transmission of Blastocystis sp. from livestock to humans in the region. Although this small-scale research was not suitable for firm epidemiological conclusions, it underscores the importance of monitoring and implementing control measures to prevent zoonotic transmission of Blastocystis sp. from livestock to humans in southwestern Iran, highlighting the need for further research to better understand the epidemiology and public health implications of this parasite.

Background

Gliomas are brain tumours categorised into low-grade (I and II) and high-grade (III and IV). Unfortunately, patients with high-grade gliomas have a poor prognosis, which is why researchers are working to improve their management. One crucial area of study is the understanding of glioma tumorigenesis and progression. Recent research has shown that long non-coding RNAs (lncRNAs) play a potential role in this process.

Material and methods

We evaluated the expression of SNHG18, HOXA11-AS, MEG3, and MDC1-AS1 in 150 paraffin tissue block samples, including 37 low-grade gliomas, 58 high-grade gliomas, and 55 non-tumoural tissues. After RNA extraction and complementary DNA synthesis (cDNA), we used probe-based qPCR to evaluate the lncRNA expression level, followed by statistical analyses.

Results

The qRT-PCR analysis revealed differential expression patterns of lncRNAs in tumour tissues compared to controls. In low-grade tumours, SNHG18 and HOXA11-AS were upregulated (SNHG18: 1.78 ± 0.21, p < 0.001; HOXA11-AS: 1.24 ± 0.60, p < 0.001), while MEG3 and MDC1-AS1 were downregulated (MEG3: 0.72 ± 0.17, p < 0.001; MDC1-AS1: 0.24 ± 0.18, p < 0.001). In high-grade tumours, SNHG18 and HOXA11-AS were further upregulated (SNHG18: 3.16 ± 0.88, p < 0.001; HOXA11-AS: 3.83 ± 0.82, p < 0.001), and MEG3 and MDC1-AS1 remained downregulated (MEG3: 0.49 ± 0.29, p < 0.001; MDC1-AS1: 0.15 ± 0.09, p < 0.001). The bioinformatic-based study conveyed that the alteration in lncRNAs expression leads to dysregulation of RNA Polymerase II, which is observed in glioblastoma.

Conclusion

Our results suggest that SNHG18 and HOXA11-AS (up-regulated) may act as oncogenes in high-grade gliomas. In contrast, the downregulation of MEG3 and MDC1-AS1 in high-grade gliomas could be related to tumour suppressor properties. Therefore, it could be assumed that the expression levels of these lncRNAs may serve as potential biomarkers for diagnostic and therapeutic purposes.