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Ongoing top quality improvement of nutrition operations throughout radiotherapy in patients using nasopharyngeal carcinoma.
Moreover, miR-24-3p was identified as a target of NEAT and LRG1 was demonstrated to be a direct target gene of miR-24-3p. Knockdown of NEAT1 or LRG1 significantly suppressed RB cell migration and invasion ability, while the effects were reversed by an miR-24-3p inhibitor. In addition, the downregulation of LRG1 caused by miR-24-3p was restored following the overexpression of NEAT1 in RB cells. It was also demonstrated that NEAT1 knockdown inhibited the epithelial-to-mesenchymal transition (EMT) pathway by inhibiting the expression of LRG via targeting miR-24-3p. In conclusion, the present results suggest that silencing of NEAT1 suppresses cell migration, invasion and the EMT process by downregulating LRG1 expression via sponging miR-24-3p in RB, thus indicating that NEAT1 may be a potential candidate for RB treatment.Proliferation and migration of keratinocytes are major processes of skin wound repair after injury. It has been indicated that microRNAs (miRNAs/miRs) are associated with the proliferation and migration of keratinocytes. However, the mechanism by which miR-185 affects these processes in keratinocytes remains unclear. In the present study, the expression level of miR-185 and peroxisome proliferator-activated receptor β (PPARβ) was examined by reverse transcription-quantitative PCR in HaCaT keratinocytes. Cell proliferation was evaluated using Cell Counting Kit-8 and colony formation assays. selleckchem Western blot analysis was used to detect the levels of cell proliferation, migration and PI3K/AKT signaling pathway-associated proteins. In addition, the migratory capacity of the cells was determined using Transwell assay. The target gene of miR-185 was verified using dual-luciferase reporter assay. The results indicated that overexpression of miR-185 inhibited proliferation, migration and activation of the PI3K/AKT signaling pathway in HaCaT keratinocytes. PPARβ was indicated to be a target of miR-185 and its overexpression promoted the proliferation and migration of HaCaT keratinocytes, while its knockdown exhibited the adverse effects. Furthermore, PI3K inhibitor LY294002 inhibited activation of the PI3K/AKT signaling pathway and decreased the proliferation and migration of HaCaT keratinocytes. In addition, overexpressed PPARβ reversed the suppressive effects of miR-185 overexpression on proliferation, migration and activation of the PI3K/AKT signaling pathway. In conclusion, the results of the present study demonstrated that miR-185 suppressed activation of the PI3K/AKT signaling pathway via targeting PPARβ, thereby regulating proliferation and migration in HaCaT keratinocytes. The present study provided a novel theoretical basis for the use of miR-185 as a target in wound repair.Knee osteoarthritis is caused by a multifactorial imbalance in the synthesis and degradation of knee chondrocytes, subchondral bone and extracellular matrix. Abnormal expression of long non-coding RNAs (lncRNAs) affects the metabolism, synovitis, autophagy and apoptosis of chondrocytes, as well as the production of cartilage matrix. The aim of the present study was to identify novel targets for the treatment of osteoarthritis and to examine the pathogenesis of the disease. The lncRNA expression profiles of seven patients with knee osteoarthritis and six healthy controls were examined by RNA-sequencing. Differentially expressed lncRNAs were selected for bioinformatics analyses, including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment. Reverse transcription-quantitative PCR (RT-qPCR) was used to further investigate the differential expression of the lncRNAs. A total of 23,583 lncRNAs were identified in osteoarthritis cartilage, including 5,255 upregulated and 5,690 downregulated lncRNAs, compared with normal cartilage. Although there were more downregulated lncRNAs compared with upregulated lncRNAs, among the changed lncRNAs (fold-change >6), there were more upregulated lncRNAs compared with downregulated lncRNAs. Several lncRNAs exhibiting differences were identified as potential therapeutic targets in knee osteoarthritis. GO and KEGG pathway analyses were performed for the target genes of the differentially expressed lncRNAs. link2 RT-qPCR validation was performed on three randomly selected upregulated and downregulated lncRNAs. The results of RT-qPCR were consistent with the findings obtained by RNA-sequencing analysis. The findings from the present study may contribute to the diagnosis of osteoarthritis and may predict the development of osteoarthritis. Furthermore, the differentially expressed lncRNAs may aid in the identification of novel candidate targets for the treatment of knee osteoarthritis.Subarachnoid hemorrhage (SAH) is a life-threatening neurological disease. Recently, inflammatory factors have been confirmed to be responsible for the brain damage associated with SAH. Therefore, studying the post-SAH inflammatory reaction may clarify the mechanism of SAH. Mitogen and stress-activated protein kinase 1 (MSK1) causes the phosphorylation of NF-κB and regulates the activity of pro-inflammatory transcription factors. The present study aimed to identify the potential role of MSK1 in inflammation and brain damage development following SAH. A cisterna magna blood injection model was established in Sprague-Dawley rats. Hematoxylin and eosin staining, reverse transcription-quantitative polymerase chain reaction assays and double immunofluorescence staining were used to analyze the role of MSK1, IL-1β and TNF-α in the inflammatory process after SAH. In a model of lipopolysaccharide-induced astrocyte inflammation, the effect of overexpressing MSK1 overexpression was analyzed by western blot analysis. The results demonstrated that MSK1 expression were negatively correlated with TNF-α and IL-1β expression levels, and reached peak levels 2 days after TNF-α and IL-1β. The double immunofluorescence staining results showed that the expression of MSK1 was in the same plane of view as TNF-α and IL-1β in the brain cortex. Furthermore, the in vitro studies indicated that the overexpression of MSK1 inhibited the expression of TNF-α and IL-1β following LPS challenge. These results imply that MSK1 may be involved in the inflammatory reaction following SAH, and may potentially serve as a negative regulator of inflammation.Alongside angiogenesis and lymphangiogenesis, neurogenesis also occurs within the cancer microenvironment. Neurogenesis is a complex process involving multiple factors, among which nerve growth factor (NGF) possesses the dual biological roles of neuron nutrition and axon growth promotion. Thus, NGF might be a key molecule involved in regulating cancer-related neurogenesis, which could play a crucial role in the signal transmission system that controls nerve growth in tumors, and enhances the abilities of migration, invasion and metastasis of tumor cells. The present study aimed to construct differential expression plasmids of NGF, in order to detect whether NGF has a vital role in neurogenesis in breast cancer cells. In the present study, 92 clinical cases of breast cancer were collected and immunohistochemical analysis was performed to verify the existence of neurons in the breast cancer microenvironment. Furthermore, recombinant NGF lentiviral overexpression, knockout and silencing plasmids were constructed, and whether NGF has an effect on neuron growth was preliminarily confirmed, indicating that the successfully constructed plasmids could be used to verify the roles of NGF in cancer-associated neurogenesis.Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may target the central nervous system and several neurological symptoms have been reported in patients with coronavirus disease 2019 (COVID-19). In the present study, a case of a SARS-CoV-2 complicated with meningoencephalitis was reported. Cerebrospinal fluid (CSF) analyses indicated hyperproteinorrachia but the specimen was negative for SARS-CoV-2 RNA. Furthermore, 10 published articles reporting on patients with COVID-19-associated meningitis/encephalitis were reviewed. Patients diagnosed with COVID-19-associated meningitis/encephalitis had diverse clinical neurological manifestations, including consciousness disturbance, epileptic attacks, psychotic syndrome and meningeal irritation signs. CSF tests revealed elevated protein, lymphocytes and cytokines. SARS-CoV-2 may be detected in the CSF of certain cases. Neuroimaging findings included hyperintense signal changes in the white matter and enhancement of meninges on brain MRI. Certain patients responded well to corticosteroid therapy and had a favorable prognosis, while elderly patients tended to have poor outcomes due to multiple organ dysfunction.Since 2003, coronaviruses have caused multiple global pandemic diseases, including severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS) and coronavirus disease 2019 (COVID-19). Clinical and autopsy findings suggest that the occurrence of kidney injury during infection may negatively affect the clinical outcomes of infected patients. The authoritative model predicts that outbreaks of other novel coronavirus pneumonias will continue to threaten human health in the future. The aim of the present systematic review was to summarize the basic knowledge of coronavirus, coronavirus infection-associated kidney injury and the corresponding therapies, in order to provide new insights for clinicians to better understand the kidney involvement of coronavirus so that more effective therapeutic strategies can be employed against coronavirus infection in the future.Classic Bernard-Soulier syndrome (BSS) is a rare form of autosomal recessive disorder that is caused by mutations in the GP1BA gene that encode the GPIb-V-IX complex, a receptor of von Willebrand factor. BSS characterized by macrothrombocytopenia and excessive bleeding. The present study reports a single case (18-month Chinese girl) diagnosed with BSS. The patient suffered mild thrombocytopenia, giant platelets and normal platelet aggregation. In addition, mild bleeding and thrombocytopenia were also indicated in thirteen family members, including the proband and her father. Gene sequence analysis identified a monoallelic missense mutation in GP1BA (c.97T>A), which encodes a p.C33R substitution in the N-terminal domain of glycoprotein (GP)Ibα that may disrupt the protein structure. To the best of our knowledge, this dominant variant has not been reported previously. link3 BSS's autosomal dominant inheritance mode is rarely identified and can be easily misdiagnosed as immune thrombocytopenia. For patients with giant platelets, thrombocytopenia and positive family history, next-generation sequencing for inherited thrombocytopenia, especially disorders that are caused by mutations in glycoprotein Ib-IX-V complex, is required.MicroRNA (miR)-874-3p is a newly identified miRNA that is involved in several pathological processes, including cancer, myocardial infarction, bone formation and erectile dysfunction. However, the role of miR-874-3p in polycystic ovary syndrome (PCOS) and granulosa cell (GC) apoptosis is not completely understood. The present study investigated the expression profile of miR-874-3p in PCOS by reverse transcription- quantitative PCR and the GC apoptosis by flow cytometry analysis. miR-874-3p expression was significantly upregulated in GCs isolated from patients with PCOS compared with patients without PCOS. In addition, miR-874-3p expression was positively correlated with GC apoptosis and testosterone levels in both patients with PCOS and patients without PCOS. Therefore, the present study also aimed to investigate the effects of miR-874-3p on testosterone-induced GC apoptosis. Compared with vehicle-treated GCs, miR-874-3p expression levels were significantly increased in testosterone-treated GCs, which was inhibited by the androgen receptor antagonist flutamide.
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