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Early diagnosis of serious bacterial infections (SBI) is important for improving outcome of morbidity and mortality in children. A systematic review was conducted to examine if shivering had any value in diagnosing serious bacterial infection. We split our population (0-18 years old) into two categories depending on the presence of a known malignancy. The databases of Medline, Embase, Cinahl, and Web of Science were searched from inception until July 2019. The quality was assessed with the QUADAS-2 tool. Two by two tables were created, extracting the number of true positive (TP), true negative (TN), false positive (FP), and false negative (FN) regarding shivering and SBI, by 2 authors independently. Sensitivity, specificity, likelihood ratios, and their 95% confidence intervals were calculated using the MetaDATA Shiny app. In a population with known malignancy, we found a +LR of 3.47 (95% CI 2.58-4.36) for a serious bacterial infection when shivering was present, implying an increase of 25-30% possibility for a serious bacterial infection. In children without malignancy, diagnostic accuracy of shivering was poor.Conclusion Shivering is of limited use to diagnose serious bacterial infection in children without malignancy. Nevertheless, in children with known malignancy, it can be useful as an alarm signal. What is Known • In the NICE guidelines for febrile illness in children, "shivering" is considered as an intermediate risk factor ("amber" sign) for a serious illness. • A systematic literature search conducted in 2007 investigating the correlation between shivering in a febrile child and the presence of a serious bacterial infection could include only one study. What is New • Based on the results of this systematic review, shivering has little diagnostic value in children without malignancy but can be useful as an alarm sign of serious bacterial infection in children with known malignancy. • In case of absence of shivering, serious bacterial infection cannot be ruled out.The present study aimed to investigate whether microRNA (miR)‑31 exerted therapeutic potential in allergic rhinitis (AR) and to explore its underlying mechanism. Firstly, the expression levels of miR‑31 were detected by reverse transcription‑quantitative PCR in the nasal mucosa of patients and mice. Subsequently, an ovalbumin (OVA)‑induced animal model of AR was constructed. Allergic symptom score, histopathological characteristics, OVA‑specific immunoglobulin E (IgE) titers, and T‑helper (Th)1 and Th2 cell‑related cytokine levels were analyzed in OVA‑sensitized mice, miR‑31‑overexpressing mice, miR‑negative control mice and control mice. Furthermore, interleukin (IL)‑13‑stimulated nasal epithelial cells (NECs) were used to assess the effects of miR‑31 on the production of IL‑13‑induced inflammatory cytokines and mucin 5AC by performing western blotting and ELISA. The expression levels of miR‑31 were significantly decreased in the nasal mucosa of the AR group compared with those in the control group. Moreover, upregulation of miR‑31 markedly attenuated sneezing and nasal rubbing events, reduced nasal eosinophil infiltration and goblet cell hyperplasia, and decreased the levels of OVA‑specific IgE and Th2‑related cytokines. In addition, subsequent experiments showed that upregulation of miR‑31 inhibited IL‑13 receptor α1 chain expression and signal transducer and activator of transcription 6 phosphorylation in NECs. Furthermore, miR‑31 suppressed IL‑13‑induced expression of thymic stromal lymphopoietin, granulocyte‑macrophage colony‑stimulating factor, eotaxin and mucin 5AC in NECs. In conclusion, these data revealed that miR‑31 could ameliorate AR by suppressing IL‑13‑induced nasal epithelial inflammatory responses, and thus may serve as a novel therapeutic target for AR.The purpose of the present study was to identify aberrantly expressed genes for gallbladder cancer based on the annotation analysis of microarray studies and to explore their potential functions. Differential gene expression was investigated in cholesterol polyps, gallbladder adenoma and gallbladder cancer using microarrays. Subsequently, microarray results were comprehensively analyzed. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed to determine the affected biological processes or pathways. Differentially expressed genes (DEGs) of cholesterol polyps, gallbladder adenoma and gallbladder cancer were identified. Following comprehensive analysis, 14 genes were found to be differentially expressed in the gallbladder wall of both gallbladder cancer and gallbladder adenoma. The 20 most significantly upregulated genes were only upregulated in the gallbladder wall of gallbladder cancer, but not in the gallbladder wall of cholesterol polyps and gallbladder adenoma. In addition, 182 DEGs were upregulated in the gallbladder wall of gallbladder adenoma compared with the gallbladder wall of cholesterol polyps. A total of 20 most significant DEGs were found in both the tumor and gallbladder wall of gallbladder cancer. In addition, the most significant DEGs that were identified were only upregulated in the tumor of gallbladder cancer. GO and KEGG analysis indicated that the aforementioned DEGs could participate in numerous biological processes or pathways associated with the development of gallbladder cancer. The present findings will help improve the current understanding of tumorigenesis and the development of gallbladder cancer.Calcitonin gene‑related peptide (CGRP) is the predominant neurotransmitter located in sensory nerves. This peptide is extensively distributed in central and peripheral tissues. CGRP causes relaxation of cardiovascular smooth muscle cells and confers protection against ischaemic myocardium and cardiac remodeling. The pharmacological effects of nitroglycerine and rutaecarpine have been demonstrated to be associated with an increase in the synthesis and release of CGRP. Guanosine 5'-monophosphate In the gastrointestinal tissues, CGRP participates in the regulation of gastrointestinal function, and exerts protective effects on gastric mucosa. Rutaecarpine, capsaicin and its derivatives, such as evodiamine, decrease gastric mucosal damage induced by several factors, including increased synthesis and release of CGRP. Taken together, this review focuses on the pharmacological effects of several CGRP related canonical drugs and suggests that synthesis and secretion of CGRP exhibit significant therapeutic effects in the occurrence and development of cardiovascular and gastrointestinal diseases.Rheumatic heart disease (RHD) is an autoimmune disease caused by rheumatic fever following group A hemolytic streptococcal infection and primarily affects the mitral valve. RHD is currently a major global health problem. However, the exact pathological mechanisms associated with RHD‑induced cardiac valve damage remain to be elucidated. The endothelial‑mesenchymal transition (EndMT) serves a key role in a number of diseases with an important role in cardiac fibrosis and the activin/Smad2 and 3 signaling pathway is involved in regulating the EndMT. Nevertheless, there are no studies to date, to the best of the authors' knowledge, investigating the association between RHD and EndMT. Thus, the aim of the current study was to investigate the potential role of EndMT in cardiac valve damage and assess whether activin/Smad2 and 3 signaling was activated during RHD‑induced valvular injury in a rat model of RHD induced by inactivated Group A streptococci and complete Freund's adjuvant. Inflammation and fibrosis were asB 1, ZEB2, α‑SMA and COL1A1) were significantly increased in the RHD group. These results suggested that the activin/Smad2 and 3 signaling pathway was activated during the development of valvular damage caused by RHD and that the EndMT is involved in RHD‑induced cardiac valve damage.Our understanding of the skeletal system has been expanded upon the recognition of several neural pathways that serve important roles in bone metabolism and skeletal homeostasis, as bone tissue is richly innervated. Considerable evidence provided by , animal and human studies have further elucidated the importance of a host of hormones and local factors, including neurotransmitters, in modulating bone metabolism and osteo‑chondrogenic differentiation, both peripherally and centrally. Various cells of the musculoskeletal system not only express receptors for these neurotransmitters, but also influence their endogenous levels in the skeleton. As with a number of physiological systems in nature, a neuronal pathway regulating bone turnover will be neutralized by another pathway exerting an opposite effect. These neuropeptides are also critically involved in articular cartilage homeostasis and pathogenesis of degenerative joint disorders, such as osteoarthritis. In the present Review, data on the role of several neuronal populations in nerve‑dependent skeletal metabolism is examined, and the molecular events involved are explored, which may reveal broader relationships between two apparently unrelated organs.Astragaloside (AST) is derived from the Chinese herb , and studies have demonstrated that it promotes differentiation of bone marrow‑derived mesenchymal stem cells (BMSCs). To the best of our knowledge, however, the functions of the component AST‑IV in osteogenesis have not previously been elucidated. The present study aimed to verify the effects of AST‑IV in osteogenesis. First, the proliferation and differentiation status of human BMSCs incubated with AST‑IV were analysed and compared with a control (no AST‑IV treatment). In order to determine the involvement of the glycogen synthase kinase (GSK)3β signalling pathway in AST‑IV, overexpression and inhibition of GSK3β was induced during incubation of BMSCs with AST‑IV. In order to investigate how neuronal growth factor (NGF) contributes to BMSCs differentiation, BMSCs were co‑incubated with an anti‑NGF antibody and AST IV, and then levels of osteogenesis markers were assessed. The results demonstrated for the first time that AST‑IV contributed to BMSCs differentiation. Furthermore, the GSK3β/β‑catenin signalling pathway was revealed to be involved in AST‑IV‑induced osteogenesis; moreover, AST‑IV accelerated differentiation by enhancing the expression levels of NGF. In summary, the present study demonstrated that AST‑IV promotes BMSCs differentiation, thus providing a potential target for the treatment of osteoporosis.Colorectal cancer (CRC) is one of the primary causes of cancer‑associated mortality worldwide. However, the potential molecular mechanism of CRC progression remains unknown. Long non‑coding RNA small nucleolar RNA host gene 20 (SNHG20) has been demonstrated to be involved in the development and progression of a variety of tumors, including CRC. However, the involvement of SNHG20 in CRC progression remains unclear. The aim of the present study was to investigate the functional role and molecular mechanism of SNHG20 in CRC progression. In the present study, SNHG20 expression was found to be significantly upregulated in CRC tissues and cell lines. Association analysis indicated that high SNHG20 expression was significantly association with greater tumor size (P=0.014), tumor invasion depth (P=0.019), positive lymph node status (P=0.022), distant metastasis (P=0.017) and advanced tumor node metastasis stage (P=0.038). Loss‑of‑function experiments indicated that SNHG20 knockdown could significantly suppress proliferation, migration and invasion in vitro.