ABSTRACT
Introduction: Cervical cancer (CC) is the fourth most common malignant tumor in term of in incidence and mortality among women worldwide. The tricarboxylic acid (TCA) cycle is an important hub of energy metabolism, networking one-carbon metabolism, fatty acyl metabolism and glycolysis. It can be seen that the reprogramming of cell metabolism including TCA cycle plays an indispensable role in tumorigenesis and development. We aimed to identify genes related to the TCA cycle as prognostic markers in CC. Methods: Firstly, we performed the differential expressed analysis the gene expression profiles associated with TCA cycle obtained from The Cancer Genome Atlas (TCGA) database. Differential gene list was generated and cluster analysis was performed using genes with detected fold changes >1.5. Based on the subclusters of CC, we analysed the relationship between different clusters and clinical information. Next, Cox univariate and multivariate regression analysis were used to screen genes with prognostic characteristics, and risk scores were calculated according to the genes with prognostic characteristics. Additionally, we analyzed the correlation between the predictive signature and the treatment response of CC patients. Finally, we detected the expression of ench prognostic gene in clinical CC samples by quantitative polymerase chain reaction (RT-qPCR). Results: We constructed a prognostic model consist of seven TCA cycle associated gene (ACSL1, ALDOA, FOXK2, GPI, MDH1B, MDH2, and MTHFD1). Patients with CC were separated into two groups according to median risk score, and high-risk group had a worse prognosis compared to the low-risk group. High risk group had lower level of sensitivity to the conventional chemotherapy drugs including cisplatin, paclitaxel, sunitinib and docetaxel. The expression of ench prognostic signature in clinical CC samples was verified by qRT-PCR. Conclusion: There are several differentially expressed genes (DEGs) related to TCA cycle in CC. The risk score model based on these genes can effectively predict the prognosis of patients and provide tumor markers for predicting the prognosis of CC.
ABSTRACT
Background: Necrotizing enterocolitis (NEC) is a devastating gastrointestinal emergency with significant mortality and morbidity rates. A subset of patients progressed rapidly and underwent surgical intervention within a short period. This study aimed to establish a model to predict the rapid progression of NEC in preterm neonates. Methods: A retrospective study was conducted to review neonates with NEC between December 2015 and April 2019 at the Guangzhou Women and Children's Medical Center. Rapidly progressive NEC was defined as the need for surgical intervention or death within 48â h of NEC onset. Patients were divided into two groups: rapidly progressive NEC (RP-NEC) and non-rapidly progressive NEC (nRP-NEC). Data on demographics, perinatal characteristics, examination variables, and radiographic findings at onset were collected. Results: A total of 216 preterm neonates with NEC were included in the study, of which 64 had RP-NEC and 152 had nRP-NEC. The mortality rates of patients with RP-NEC and nRP-NEC were 32.8% and 3.28%, respectively. Male sex (p-value, adjusted odds ratio [95% confidence interval]: 0.002, 3.43 [1.57, 7.53]), portal venous gas (0.000, 8.82 [3.73, 20.89]), neutrophils <2.0 × 109/L (0.005, 4.44 [1.59, 12.43]), pH <7.3 (7.2 ≤ pH < 7.3) (0.041, 2.95 [1.05, 8.31]), and pH <7.2 (0.000, 11.95 [2.97, 48.12]) at NEC onset were identified as independent risk factors for RP-NEC. An established model that included the four risk factors presented an area under the curve of 0.801 with 83% specificity and 66% sensitivity. Conclusion: Among preterm neonates with NEC, a significantly higher mortality rate was observed in those with rapid progression. It is recommended that close surveillance be performed in these patients, and we are confident that our established model can efficiently predict this rapid progression course.
ABSTRACT
Infectious hypodermal and haematopoietic necrosis virus (IHHNV) is a major viral pathogen in cultured penaeid shrimp. IHHNV has many hosts, mainly including crustaceans. It has recently been reported that Procambarus clarkii can be infected by IHHNV. In the present study, we studied the hepatopancreas of P. clarkii by transcriptome high-throughput sequencing to analyze the response of P. clarkii to IHHNV infection. After de novo assembly, there were 400,340,760 clean reads. A total of 237 differentially expressed genes (DEGs) were obtained, including 77 significantly up-regulated unigenes and 160 significantly down-regulated ones. The expression levels of 12 immune-related DEGs were validated by qRT-PCR, substantiating the reliability of RNA-Seq results. The enrichment analysis of DEGs showed that the immune-related pathways were closely related to apoptosis and phagocytosis. Moreover, a large number of pathways related to metabolic function were down-regulated, suggesting that IHHNV infection might affect the growth of P. clarkii.
