Background: Consumption of ultra-processed foods (UPFs) plays a potential role in the development of obesity and other diet-related noncommunicable diseases (NCDs), but no studies have systematically focused on this. This study aimed to summarize the evidence for the association between UPFs consumption and health outcomes.Methods: A comprehensive search was conducted in PubMed, Embase, and Web of Science to identify all relevant studies. Epidemiological studies were included, and identified studies were evaluated for risk of bias.A narrative review of the synthesized findings was provided to assess the association between UPFs consumption and health outcomes.Results: 20 studies (12 cohort and 8 cross-sectional studies) were included in the analysis, with a total of 334,114 participants and 10 health outcomes. In a narrative review, high UPFs consumption was obviously associated with an increased risk of all-cause mortality, overall cardiovascular diseases, coronary heart diseases, cerebrovascular diseases, hypertension, metabolic syndrome, overweight and obesity, depression, irritable bowel syndrome, overall cancer, postmenopausal breast cancer, gestational obesity, adolescent asthma and wheezing, and frailty. It showed no significant association with cardiovascular disease mortality, prostate and colorectal cancers, gestational diabetes mellitus and gestational overweight.Conclusions: This study indicated a positive association between UPFs consumption and risk of several health outcomes. Large-scale prospective designed studies are needed to confirm our findings.

Background: The SARS‐CoV‐2 pandemic is an ongoing global health emergency. The aim of our study was to investigate the changes of liver function and its clinical significance in COVID‐19 patients.Method: This retrospective, single‐centre study was conducted on 115 confirmed cases of COVID‐19 in Zhongnan hospital of Wuhan University from 18 January 2020 to 22 February 2020. Liver function and related indexes were analysed to evaluate its relationship with disease progression in COVID‐19 patients.Results: Part of the COVID‐19 patients presented with varying degrees of abnormality in liver function indexes. However, the levels of ALT, AST, TBIL, GGT and LDH in COVID‐19 patients were not significantly different when compared with hospitalised community‐acquired pneumonia patients, and the levels of albumin is even significantly higher. The levels of ALT, AST, TBIL, LDH and INR showed statistically significant elevation in severe COVID‐19 cases compared with that in mild cases. However, the clinical significance of the elevation is unremarkable. Majority of severe COVID‐19 patients showed significantly decreasing in albumin level and continuously decreasing in the progress of illness. Most of the liver function indexes in COVID‐19 patients were correlated with CRP and NLR, the markers of inflammation. Logistic regression analysis further identified NLR as the independent risk factor for severe COVID‐19, as well as age.Conclusions: Although abnormalities of liver function indexes are common in COVID‐19 patients, the impairment of liver function is not a prominent feature of COVID‐19, and also may not have serious clinical consequences.

Fifty-two patients with coronavirus disease 2019 (COVID-19) pneumonia were admitted to Zhongnan Hospital of Wuhan University from January 20 to February 28, 2020. The disease was confirmed by detecting SARS-CoV-2 nucleic acid in throat swab samples by using the reverse-transcription polymerase chain reaction assay method. On admission, all patients had a comprehensive laboratory examination, including blood cytology, biochemistry, and inflammatory indicators. Pancreatic injury was defined as any abnormality in amylase (normal range, 0–90 U/L) or lipase (normal range, 0–70 U/L). Serious illness was defined if at least 1 of the following items was present: (1) breathing rate, ≥30/min; (2) pulse oximeter oxygen saturation, ≤93% at rest; or (3) ration of partial pressure of arterial oxygen to fraction of inspired oxygen, ≤300 mm Hg (1 mm Hg = 0.133 kPa). During the hospitalization, each patient had a swab virus test every other day. Negative conversion time of SARS-CoV-2 was defined as the interval between symptom onset and the first of 2 consecutive negative virus test results.

Ferroptosis, a type of cell death triggered by excessive accumulation of iron-dependent lipid peroxidation, possesses an excellent potential in cancer treatment. However, many colorectal cancer (CRC) cell lines are resistant to ferroptosis induced by erastin and RSL3, the classical ferroptotic inducers. Moreover, the underlying mechanism of resistance remains poorly elucidated. This study sought to discover the major factor contributing to ferroptosis resistance in CRC. The study findings will help design strategies for triggering ferroptosis for application in individualized tumor therapy. Here, we show that tetrahydrobiopterin (BH4) determines the sensitivity of CRC cells to ferroptosis induced by erastin. GTP cyclohydrolase-1 (GCH1) is the first rate-limiting enzyme of BH4. Genetic or pharmacological inhibition of GCH1 decreased BH4 and assisted erastin in cell death induction, lipid peroxidation enhancement, and ferrous iron accumulation. BH4 supplementation completely inhibited ferroptotic features resulting from GCH1 knockdown. Unexpectedly, GCH1 knockdown failed to enhance RSL3-induced cell death in CRC. Mechanistically, GCH1 knockdown drastically activated ferritinophagy during erastin treatment rather than RSL3 treatment. Administration of an autophagy inhibitor reversed erastin resistance in GCH1-knockdown cells. GCH1 inhibitor and erastin co-treatment in vivo synergistically inhibited tumor growth in CRC. Overall, our results identified GCH1/BH4 metabolism as a burgeoning ferroptosis defense mechanism in CRC. Inhibiting GCH1/BH4 metabolism promoted erastin-induced ferroptosis by activating ferritinophagy, suggesting that combining GCH1 inhibitors with erastin in the treatment of CRC is a novel therapeutic strategy.

Since the five-year survival rate is less than 5%, pancreatic ductal adenocarcinoma (PDAC) remains the 4th cause of cancer-related death. Although PDAC has been repeatedly researched in recent years, it is still predicted to be the second leading cause of cancer death by year 2030. In our study, the differentially expressed genes in dataset GSE62452 were used to construct a co-expression network by WGCNA. The yellow module related to grade of PDAC was screened. Combined with co-expression network and PPI network, 36 candidates were screened. After survival and regression analysis by using GSE62452 and TCGA dataset, we identified 10 real hub genes (CCNA2, CCNB1, CENPF, DLGAP5, KIF14, KIF23, NEK2, RACGAP1, TPX2 and UBE2C) tightly related to progression of PDAC. According to Oncomine database and The Human Protein Atlas (HPA), we found that all real hub genes were overexpressed in pancreatic carcinoma compared with normal tissues on transcriptional and translational level. ROC curve was plotted and AUC was calculated to distinguish recurrent and non-recurrent PDAC and every AUC of the real hub gene was greater than 0.5. Finally, functional enrichment analysis and gene set enrichment (GSEA) was performed and both of them showed the cell cycle played a vital role in PDAC.