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The DEGs in the SAH‑associated modules were associated with Gene Ontology biological processes such as 'regulation of programmed cell death', 'apoptosis' and 'immune response'. The subsequent lncRNA‑mRNA regulatory network included seven upregulated lncRNAs [HCG27, ZNFX1 antisense RNA 1, long intergenic non‑protein coding RNA (LINC)00265, murine retrovirus integration site 1 homolog‑antisense RNA 1, cytochrome P450 1B1‑AS1, LINC01347 and LINC02193] and 375 DEGs. Functional enrichment analysis and screening in the Comparative Toxicogenomics Database demonstrated that SAH‑associated DEGs, including neutrophil cytosolic factor (NCF)2 and NCF4, were enriched in 'chemokine signaling pathway' (hsa04062), 'leukocyte transendothelial migration' (hsa04670) and 'Fc gamma R‑mediated phagocytosis' (hsa04666). The upregulated lncRNAs and genes, including NCF2 and NCF4, in patients with IA rupture‑induced SAH indicated their respective potentials as anti‑inflammatory therapeutic targets.Sepsis is a serious clinical condition characterized by systemic inflammation. The long noncoding RNA (lncRNA) highly upregulated in liver cancer (HULC) was validated to partake in the development of sepsis. The present study aimed to investigate the potential mechanism of HULC in lipopolysaccharide (LPS)‑induced sepsis. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blot analysis was employed to examine the expression of HULC, microRNA (miR)‑128‑3p, Rac family small GTPase 1 (RAC1) and pro‑inflammatory factors [IL‑6, TNF‑α, intercellular adhesion molecule (ICAM1) and vascular cell adhesion molecule (VCAM1)] in the serum of patients with sepsis or LPS‑induced human dermal microvascular endothelial cells (HMEC‑1). Flow cytometry and western blot assays were performed to detect cell apoptosis. The targeted relationship among HULC, miR‑128‑3p and RAC1 was confirmed by a dual‑luciferase reporter assay, RNA binding protein immunoprecipitation (RIP) assay and RNA pull‑down assay. HULC and RAC1 were found to be upregulated, and miR‑128‑3p was downregulated in the serum of patients with sepsis and LPS‑stimulated HMEC‑1 cells. LPS promoted apoptosis and inflammation, which were decreased by silencing of HULC. HULC targeted miR‑128‑3p and negatively regulated its expression. HULC knockdown protected HMEC‑1 cells from LPS‑induced injury by upregulating miR‑128‑3p. RAC1 was a target of miR‑128‑3p, and gain of RAC1 also relieved the silencing of HULC‑mediated suppressive effects on apoptosis and inflammation in LPS‑stimulated HMEC‑1 cells. In conclusion, HULC knockdown partially reversed LPS‑induced sepsis via the regulation of miR‑128‑3p/RAC1 axis.The altered expression of glycan antigens has been reported during cervix transformation, demonstrating increased mRNA levels of certain glycogenes. Human papillomavirus (HPV) is the aetiological agent of cervical cancer. High risk HPV E5 is considered an oncogene and has been implicated in cell transformation. E6 and E7 HPV oncoproteins modify the expression of certain glycogenes. The role of the E5 HPV protein in glycogene expression changes has not yet been reported. The aim of the present study was to determine the effects of HPV16 E5 oncoprotein on glycogene expression. For these, a microarray assay was performed using the HaCaT cell line and altered glycogenes were identified. The mRNA levels of certain glycogenes were determined via reverse transcription‑quantitative PCR (RT‑qPCR). Using in silico analysis, the present study identified that glycosylation pathways were altered by E5. Microarray analysis revealed alterations in certain glycogenes, including the upregulation of ST6GAL1, ST3GAL3, CHST2 and MANBA, and the downregulation of UGT2B15, GALNT11, NDST2 and UGT1A10. Increased mRNA levels were confirmed via RT‑qPCR for sialyltransferases genes. Additionally, in silico analysis was performed to identify glycosylation networks altered in the presence of the E5 oncoprotein. The analysis revealed that E5 could modify glycan sialylation, the N‑glycosylation pathway, keratan sulfate and glycosaminoglycan synthesis. Isoproterenol sulfate agonist To the best of our knowledge, the current study was the first to determine the role of the HPV16 E5 oncoprotein in glycogene expression changes. The results indicated that increased sialyltransferase mRNA levels reported in pre‑malignant and malignant cervical tissues could be the result of E5 oncoprotein expression. The results provide a possible role of HPV infection on glycosylation changes reported during cervix transformation.The discovery, introduction and clinical use of prognostic and diagnostic biomarkers has significantly improved outcomes for patients with various illnesses, including bladder cancer (BC) and other bladder‑related diseases, such as benign bladder dysfunction and interstitial cystitis (IC). Several sensitive and noninvasive clinically relevant biomarkers for BC and IC have been identified. Metabolomic‑ and lipidomic‑based biomarkers have notable clinical potential in improving treatment outcomes for patients with cancer; however, there are also some noted limitations. This review article provides a short and concise summary of the literature on metabolomic and lipidomic biomarkers for BC and IC, focusing on the possible clinical utility of profiling metabolic alterations in BC and IC.Bronchial asthma poses a serious threat to human health. Previous studies have documented the role of long non‑coding RNAs (lncRNAs) in asthma. However, the molecular mechanism underlying bronchial asthma remains unclear. The aim of the present study was to evaluate the role of the lncRNA Opa‑interacting protein 5 antisense RNA1 (OIP5‑AS1) in the house dust mite‑induced inflammatory response in human bronchial epithelial cells. BEAS‑2B cells were treated with Dermatophagoides pteronyssinus peptidase 1 (Der p1) to establish an in vitro model of asthma. OIP5‑AS1 expression levels increased in BEAS‑2B cells following Der p1 treatment, while microRNA (miR)‑143‑3p was downregulated. Additionally, the levels of the pro‑inflammatory factors tumor necrosis factor‑α, interleukin (IL)‑6 and IL‑8 were measured, and apoptosis was evaluated following OIP5 silencing. OIP5‑AS1 knockdown reduced the inflammatory response and apoptosis in BEAS‑2B cells. Furthermore, using dual luciferase reporter assays and co‑transfection experiments, it was demonstrated that the function of OIP5‑AS1 was mediated by miR‑143‑3p. miR‑143‑3p overexpression attenuated the Der p1‑induced inflammatory response and apoptosis of BEAS‑2B cells by targeting high mobility group box 1 (HMGB1). In summary, OIP5‑AS1 exacerbated Der p1‑induced inflammation and apoptosis in BEAS‑2B cells by targeting miR‑143‑3p via HMGB1.In order to improve the water solubility of the volatile oils extracted from Flos magnoliae (FM) and Centipeda minima (CM), they were prepared as a microemulsion (ME), which were then used in the development of an FM and CM volatile oil ME for the treatment of allergic rhinitis (AR). ME was prepared by phase inversion emulsification, and the prescription factors such as emulsifier, co‑emulsifier, oil phase, Km, which represents the ratio of the mass of emulsifier to that of the co‑emulsifier, and preparation factors such as temperature affecting the formation of the ME were selected according to the formation area of ME in a pseudo‑ternary phase diagram. The quality of the ME was evaluated based on its appearance, particle size, Zeta potential and stability. The content of eucalyptol in ME was determined by gas chromatography‑mass spectrometry (GC‑MS). The cumulative permeability of the ME within 24 h was measured with a transdermal diffusion tester. The results revealed that the best formula for preparation of the ME was as follows Castor oil polyoxyethylene ether (EL‑40) was the emulsifier; the co‑emulsifier was anhydrous ethanol; the Km was 21; the mixed phase of volatile oil and isopropyl myristate with mass ratio of 11 was used as oil phase; and the preparation temperature was 25˚C. The content of eucalyptol in the ME was 2.57 mg/g, and the cumulative permeability of the ME in 24 h was significantly increased compared with that of the reference oil solution. The appearance of the ME was uniform, and the solution was transparent. In conclusion, compared with traditional preparations, FM and CM volatile oil ME is a novel, improved and more effective preparation for the treatment of AR.Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide. Ubiquitin‑specific protease 12 (USP12) is specifically upregulated in the tumor tissues of patients with HCC compared with the corresponding adjacent normal tissues. However, the relationship between USP12 and the growth of HCCs is not fully understood. In the present study, USP12 was knocked down in HCC cell lines to investigate its effects on proliferation and apoptosis. The results showed that USP12‑knockdown could inhibit the proliferation and promote apoptosis in HCC cell lines. Flow cytometry analysis also showed that USP12 could induce cell cycle arrest at the G2/M stage. In vivo experiments showed that USP12‑knockdown could suppress tumor growth in mice, and immuno‑blotting revealed that USP12 could induce G2/M arrest through the cyclin dependent kinase 1/cyclinB1 axis, and trigger apoptosis via the p38/mitogen‑activated protein kinase pathway. These data strongly indicate that USP12 is a potential target for the treatment of HCC.Tissue damage in diabetes is at least partly due to elevated reactive oxygen species production by the mitochondrial respiratory chain during hyperglycemia. Sustained hyperglycemia results in mitochondrial dysfunction and the abnormal expression of mitochondrial genes, such as NADH Ubiquinone oxidoreductase subunit A13 (NDUFA13). Metformin, an AMP‑activated protein kinase (AMPK) activator, protects cardiomyocytes from oxidative stress by improving mitochondrial function; however, the exact underlying mechanisms are not completely understood. The aim of the present study was to investigated the molecular changes and related regulatory mechanisms in the response of H9C2 cardiomyocytes to metformin under high glucose conditions. H9C2 cells were subjected to CCK‑8 assay to assess cell viability. Reactive oxygen species generation was measured with DCFH‑DA assay. Western blotting was used to analyze the expression levels of NDUFA13, AMPK, p‑AMPK and GAPDH. Reverse transcription‑quantitative PCR was used to evaluate the expression levels of mitochondrial genes and transcription factors. It was observed that metformin protected H9C2 cardiomyocytes by suppressing high glucose (HG)‑induced elevated oxidative stress. In addition, metformin stimulated mitochondrial biogenesis, as indicated by increased expression levels of mitochondrial genes (NDUFA1, NDUFA2, NDUFA13 and manganese superoxide dismutase) and mitochondrial biogenesis‑related transcription factors [peroxisome proliferator‑activated receptor‑gamma coactivator‑1α, nuclear respiratory factor (NRF)‑1, and NRF‑2] in the metformin + HG group compared with the HG group. Moreover, metformin promoted mitochondrial NDUFA13 protein expression via the AMPK signaling pathway, which was abolished by pretreatment with the AMPK inhibitor, Compound C. The results suggested that metformin protected cardiomyocytes against HG‑induced oxidative stress via a mechanism involving AMPK, NDUFA13 and mitochondrial biogenesis.