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0 ± 3.0 and 6.8 ± 0.7 μM, respectively. The inhibition of papain by mycotoxins (fusaric acid and beauvericin) may indicate a mechanism of Fusarium in the roles of infection process.PURPOSE To assess the diagnostic value of multidetector computed tomography (MDCT) in small bowel obstruction (SBO) patients. METHODS Relevant literature was searched from the Cochrane Library, Pubmed and Embase. The extracted effective data was calculated using the Meta-Disc 1.4 software; statistical heterogeneity was evaluated using Cochran's Q test and I2. RESULTS A total of five articles were selected for the meta-analysis. In addition, the pooled sensitivity, specificity, positive likelihood ratio (PLR), negative likelihood ratio (NLR), as well as the diagnostic odds ratio (DOR) were 0.878 (95% CI 0.822-0.921), 0.807 (95% CI 0.753-0.854), 8.137 (95% CI 2.268-29.192), 0.127 (95% CI 0.040-0.4078) and 72.384 (95% CI 10.841-483.31), respectively. Furthermore, the AUC was 0.9648 with the Q of 0.9116. CONCLUSIONS The data suggest that MDCT is an effective method for diagnosis of SBO.OBJECTIVE Knowledge of CT characteristics of COVID-19 pneumonia might be helpful to the early diagnosis and treatment of patients, and to control the spread of infection. METHODS The chest CT images of the patient were collected to describe the CT manifestations and characteristics, and they were compared with the previous studies. RESULTS Multiple patchy ground-glass opacities (GGOs) were seen in bilateral lung, mostly in subpleural areas. They progressed within 3 days, and nodular GGOs were also seen together with subpleural patchy GGOs. CONCLUSION Our case of COVID-19 pneumonia showed multiple subpleural GGOs in bilateral lung, rapid progression, and it also accompanied nodular GGOs on chest CT. These findings were consistent with the previous reports, and they might be useful for early detection and evaluation of severity of COVID-19 pneumonia.AIMS This study analyses the capability of contrast-enhanced multi-detector computed tomography (MDCT) and spectrum of molecular imaging to characterize typical carcinoids (TCs) of lung and their relationship with Ki-67 index. MATERIALS AND METHODS We analysed 68 patients with histological diagnosis of pulmonary TC, which underwent both MDCT and nuclear molecular imaging (somatostatin receptor scintigraphy/SPECT with 111In-pentetreotide and 18F-FDG-PET/CT) at staging evaluation before surgery. The MDCT scan was reviewed for the following features size, margins, contrast enhancement, presence of calcifications, bronchial obstruction, lymph nodes and metastases. In 111In-pentetreotide SPECT, tumour/non-tumour ratio was measured at 4- and 24-h post-injection and the per cent difference was calculated (T/NT%). FDG uptake was measured as the ratio between lesion SUVmax and liver SUVmean (SUV ratio). All imaging features were correlated between them and with Ki-67 index. RESULTS Forty-four of the 68 lesions (65%) with extra-thorax signs. We found a significant correlation between some MDCT aspects, nuclear medicine features and Ki-67 index. The association of MDCT and nuclear medicine imaging may be useful in predicting proliferative activity and prognosis of lung TCs.Granular corneal dystrophy (GCD) is featured by corneal deposits of transforming growth factor beta-induced gene (TGFBI) mediated by the TGF-β (transforming growth factor-β)/Smad signaling. However, the roles of c-Jun amino-terminal kinase (JNK) pathway in GCD pathogenesis remains unexplored, which was investigated in this study. JNK signaling activation and inhibition in primary corneal fibroblasts were obtained by treatments with anisomycin and SP600125, respectively. Protein abundance and phosphorylation were detected by immunoblotting. PI3K inhibitor Cell viability and apoptosis were analyzed by CCK-8 and flow cytometry respectively. TGFBI deposit and autophagy progression were assessed by immunofluorescence. The results found that JNK1 expression and phosphorylation were greatly increased in corneal tissues from GCD2 patients. JNK signaling activation impaired the viability and promoted apoptosis and autophagy processes in primary corneal fibroblasts, along with Smad2/3 phosphorylation, TGFBI accumulation and Bcl-2 suppression. Autophagy related proteins, such as ATG5 (autophagy related 5), ATG12 (autophagy related 12) and LC3B (microtubule-associated protein 1 light chain 3 beta), were also increased in anisomycin or TGF-β1 treated corneal fibroblasts. However, SP600125 effectively reversed the above effect induced by TGF-β1 treatment in corneal fibroblasts, including the TGF-β-induced autophagy progression. The results suggested that JNK signaling was activated in GCD2 corneal tissues, and it mediated the TGF-β-induced TGFBI protein accumulation and apoptosis of corneal fibroblasts during GCD2 pathogenesis.Vitamin B12 deficiency is a critical problem worldwide and peri-conceptional deficiency of this vitamin is associated with the risk of complex cardio-metabolic diseases. Nutritional perturbations during these stages of development may lead to changes in the fetal epigenome. Using Wistar rat model system, we have earlier shown that low maternal B12 levels are associated with low birth weight, adiposity, insulin resistance, and increased triglyceride levels in the offspring, which might predispose them to the risk of cardio-metabolic diseases in adulthood. In this study, we have investigated the effects of maternal B12 deficiency on genome-wide DNA methylation profile of the offspring and the effect of rehabilitation of mothers with B12 at conception. We have performed methylated DNA immunoprecipitation sequencing of liver from pups in four groups of Wistar rats Control (C), B12-restricted (B12R), B12-rehabilitated at conception (B12RC), and B12-rehabilitated at parturition (B12RP). We have analyzed differentially methylated signatures between the three groups as compared to controls. We have identified a total of 214 hypermethylated and 142 hypomethylated regions in the 10 kb upstream region of transcription start site in pups of B12-deficient mothers, which are enriched in genes involved in fatty acid metabolism and mitochondrial transport/metabolism. B12 rehabilitation at conception and parturition is responsible for reversal of methylation status of many of these regions to control levels suggesting a causal association with metabolic phenotypes. Thus, maternal B12 restriction alters DNA methylation of genes involved in important metabolic processes and influences the offspring phenotype, which is reversed by B12 rehabilitation of mothers at conception.

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