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+ miR-195 inhibitor group (p<0.05). The above results demonstrated that the protein expressions of TLR4 and NF-κB in macrophages could be markedly inhibited by si-TLR4, but be promoted by si-TLR4 + miR-195 inhibitor. CCK-8 assay demonstrated that the proliferation ability of macrophages was remarkably weaker in miR-195 mimics group than NC group (p<0.001). Furthermore, it was also significantly weaker in si-TLR4 + miR-195 inhibitor group than si-TLR4 group (p<0.05).
MiR-195 reduces the release of inflammatory factors and inhibits the proliferation of macrophages through targeting TLR4 and blocking the NF-κB pathway, thereby alleviating the symptoms of DN rats.
MiR-195 reduces the release of inflammatory factors and inhibits the proliferation of macrophages through targeting TLR4 and blocking the NF-κB pathway, thereby alleviating the symptoms of DN rats.
Coronary artery bypass grafting (CABG) seems to present a powerful trigger of oxidative stress (OS) and acute inflammatory response. This study aimed to estimate the effects of off-pump coronary artery bypass (OPCAB) grafting on the OS that is commonly observed in patients undergoing operation under cardiopulmonary bypass (CPB). Additionally, we aimed to examine the relationship between and paraoxonase 1 (PON1) activity and the degree of stenosis, severity and complexity of the atherosclerotic lesions, estimated by SYNTAX score (SS).
Study group of 107 patients scheduled for CABG were divided into CPB and OPCAB group. Blood samples for OS markers measurement were collected at six-time intervals before skin incision (t1), immediately after surgery (t2), 6h (t3), 24h (t4), 48h (t5) and 96h after cessation of the operation and surgical trauma (t6). SS was calculated.
A significant decrease in lipid hydroperoxides (LOOH) and advanced oxidation protein products (AOPP) levels after both types of surgeries wer postoperative complications.
The aim of this study was to review evidence to determine whether "pure" chronic obstructive pulmonary disease (COPD) patients without a history of asthma differ in the clinical characteristics, severity of airflow limitation, and clinical outcomes compared to patients with Asthma-COPD Overlap Syndrome (ACOS).
An electronic search was performed in the MEDLINE, EMBASE, SCOPUS and Web of Science databases to identify comparing the clinical characteristics and outcomes between ACOS and "pure" COPD. The included studies were subjected to meta-analysis and risk of bias assessment using ROBINS-E tool. Eleven observational studies were included.
The results of the meta-analysis showed increased expression of lung function parameters like forced expiration volume (FEV) at 1 secmean difference (MD) 2.36; 95% CI [0.05,4.66] ; p=0.004; I2= 72% and clinical symptoms in terms of fever Relative Risk (RR) 0.34, p<0.0001, wheezing RR 0.39, p<0.0001 and dyspnea RR 0.53, p<0.0001. The comorbidities assocs with a varying degree of clinical symptoms.
Bronchopulmonary dysplasia (BPD) is one of the most common chronic lung diseases in infants, but the ways to prevent and treat BPD are still very limited. We tried to find an effective method for treating BPD by studying the effect of fibroblast growth factor 18 (FGF18) on hyperoxia-induced lung injury in mice.
We placed newborn mice in high-oxygen environment (60-70%) and collected mouse lung tissue for histological examination at 3, 7, 14 and 21 days after birth. The correlation between FGF18 and BPD was studied by analyzing the expression of FGF18 in mouse lung tissue. In addition, we used exogenous FGF18 to stimulate primary mouse type II alveolar epithelial cells (AECs II), and detected changes in oxidative stress, inflammation and NF-κB signaling pathway activity of AECs II to analyze the effects of FGF18 on AECs II.
From the 7th day after the birth of the mouse, the lung tissue of the hyperoxia-induced mice suffered significant lung injury relative to the control group. The expression of FGF18 in lung tissue induced by hyperoxia was lower than that in the control group. Cell viability of AECs II stimulated by exogenous FGF18 increased, and FGF18 also reduced oxidative stress and inflammation levels of AECs II and inhibited the AECs II injury caused by hyperoxia. NF-κB signaling pathway activity in hyperoxia-induced lung increased, while exogenous FGF18 could reduce the expression and phosphorylation of NF-κB p65 in AECs II.
Hyperoxia-induced lung injury was accompanied by a decrease in FGF18. FGF18 can reduce oxidative stress and inflammation levels of AECs II by inhibiting the NF-κB signaling pathway, thereby reducing hyperoxia-induced cell injury.
Hyperoxia-induced lung injury was accompanied by a decrease in FGF18. FGF18 can reduce oxidative stress and inflammation levels of AECs II by inhibiting the NF-κB signaling pathway, thereby reducing hyperoxia-induced cell injury.
Different types of vasculitis can occur in patients with inflammatory bowel disease [IBD], but large vessels vasculitis seems to be the most prevalent. Indeed, the presence of both Crohn's disease [CD] and Takayasu's arteritis [TAK] has previously been reported, with higher prevalence in young women between the second and the third decade of life. This article aims to provide clinicians with an accurate picture of the most common clinical features and current treatment strategy for patients with both CD and TAK.
We described the coexistence of CD and TAK in three young women and also performed an extensive literature review about the association of these two immune-related disorders. Research on PubMed server was performed typing the terms "Takayasu's arteritis and inflammatory bowel disease", "Takayasu's arteritis and Crohn's disease", and "Takayasu's arteritis and Ulcerative colitis".
Although the association of CD with TAK is uncommon, due to the severity of both diseases, concomitance in the same patient may significantly complicate the diagnostic and therapeutic work-up. In addition, since TAK can compromise intestinal vasculature, it may possibly exacerbate the clinical course of patients with IBD. All patients we reported underwent surgery due to IBD complications and two of them started biological therapy with different outcomes.
Early detention of these conditions has a great importance for both gastroenterologists and immunologists, for ensuring a tailored multidisciplinary management, possibly in order to identify a common therapy for these two immune-related disorders.
Early detention of these conditions has a great importance for both gastroenterologists and immunologists, for ensuring a tailored multidisciplinary management, possibly in order to identify a common therapy for these two immune-related disorders.
Biliary and hyperlipidemic acute pancreatitis (AP) has become the second most common AP in China. Currently, AP is exclusively diagnosed as biliary or hyperlipidemic AP. However, as suggested by some reports, biliary and hyperlipidemic AP might coexist in a single patient. Moreover, acute lipotoxicity was shown to regulate the severity of biliary AP in the mouse model. Thus, whether these two etiologies coexist in AP patients and potentially worsen the clinical course remains unclear. To elucidate the clinical feature of a new complex type of acute pancreatitis with both biliary and hyperlipidemic etiologies.
This retrospective study included AP patients who were admitted into our department within 7 days after the onset of the disease. 267 AP patients were enrolled in this study and were classified as BAP (biliary acute pancreatitis, n=153), HLAP (hyperlipidemic acute pancreatitis, n=65) and BHAP (biliary-hyperlipidemic acute pancreatitis, n=49). All the enrolled patients met the classification criteria more severe clinical course of the disease and have worse prognosis than single-etiology BAP or HLAP patients in the early stage of AP (within 7 days). It should be recognized as a new etiological type named biliary-hyperlipidemic acute pancreatitis (BHAP).
Patients with both biliary and hyperlipidemic etiologies suffer from more severe clinical course of the disease and have worse prognosis than single-etiology BAP or HLAP patients in the early stage of AP (within 7 days). It should be recognized as a new etiological type named biliary-hyperlipidemic acute pancreatitis (BHAP).
The purpose of this study was to establish a nomogram for predicting the severity of acute pancreatitis (AP) and verify its predictive value.
A total of 571 AP patients received by Ordos Central Hospital from January 2015 to December 2018 were included in this study. According to the 2012 Revised Atlanta classification, the included subjects were classified into severe AP (SAP) group and non-severe AP (NSAP) group [including patient with mild AP (MAP) and moderately SAP (MSAP)]. The baseline characteristics, imageological data and pathological data within 24 h after the disease onset between the two groups were analyzed using One-way analysis of variance (one-way ANOVA). R language was used for establishing a predictive nomogram, whose performance was verified by clinical data of 150 AP cases collected from December 2018 to December 2019.
One-way ANOVA shows that SAP and NSAP patients show significant differences in sex, calcium ions, creatinine, neutrophils ratio, lymphocytes ratio and eosinophils ratio (p<0.05). A predictive nomogram was accordingly established using the six indicators. Validation on this predictive nomogram showed high internal validation concordance index (C-index) of 0.69 (95% CI, 0.64-0.74), and high external validation C-index of 0.71 (95% CI, 0.67-0.76).
This nomogram can be used as a clinical tool to predict the severity of SAP.
This nomogram can be used as a clinical tool to predict the severity of SAP.The aim of this study was to analyze the clinical features of a Rubinstein-Taybi syndrome (RSTS) case with neonatal glaucoma. We also wanted to explore the manifestation of the disease in combination with genotype-phenotype correlation. For DNA extraction we used 2 ml peripheral blood, collected from the child and parents. The extracted genomic DNA was used for clinical exome sequencing. A 38-day old baby boy was diagnosed with congenital glaucoma on the third day after birth with symptoms, including choking milk, feeding difficulties and slow weight gain. He was admitted to the neonatology department because of lung infection. The clinical exome sequencing showed that the child has a c.2368C>T heterozygous mutation in exome 13 in CREBBP (cAMP responsive element binding protein) while his parents have no such mutation. Combining genetic data with the clinical features, this infant was diagnosed with RSTS. This is the first report of RSTS caused by a c. 2368C>T mutation in CREBBP. RSTS is an extremely rare disease with extensive clinical manifestations. It is highly overlapped with other syndromes which makes the diagnosis difficult. RSTS is easy to be missed or misdiagnosed due to the lack of specific clinical manifestations during the neonatal period. Neonatal specialists need to enhance their awareness and recognition of this condition, and use genetic testing as an effective tool in order to finalize their diagnosis.
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