ABSTRACT
The cycle of precipitation change is key to understanding the driving mechanism of the East Asian summer monsoon (EASM). However, the dominant cycles of EASM precipitation revealed by different proxy indicators are inconsistent, leading to the "Chinese 100 kyr problem". In this study, we examine a high-resolution, approximately 350,000-year record from a low-latitude loess profile in China. Our analyses show that variations in the ratio of dithionite-citrate-bicarbonate extractable iron to total iron are dominated by the ~20-kyr cycle, reflecting changes in precipitation. In contrast, magnetic susceptibility varies with the ~100-kyr cycle and may be mainly controlled by temperature-induced redox processes or precipitation-induced signal smoothing. Our results suggest that changes in the EASM, as indicated by precipitation in this region, are mainly forced by precession-dominated insolation variations, and that precipitation and temperature may have varied with different cycles over the past ~350,000 years.
ABSTRACT
BACKGROUND: Liver failure is severe hepatic cellular damage caused by multiple factors that leads to clinical manifestations. Hepatic infiltration by malignancy is rarely reported as a cause of liver failure. CASE PRESENTATION: A 51-year-old male patient was admitted to the Wuhan Union Hospital complaining of bloating and jaundice. He had been diagnosed with polymyositis ten prior and was taking oral glucocorticoids. Physical examination revealed seroperitoneum and icteric sclera; laboratory tests revealed liver dysfunction, a coagulopathy, and negative results for the common causes of liver failure. Moreover, an ascitic tap and bone marrow aspirate and trephine confirmed a metastatic, poorly differentiated adenocarcinoma. These findings indicate that malignant infiltration is the most likely cause of liver failure. Regrettably, the patient refused complete liver and lymph node biopsies and was discharged on day 31. CONCLUSION: Clinicians should consider the possibility of malignant infiltration when approaching a case of liver failure with prodromal symptoms or imaging abnormalities, especially in patients with autoimmune diseases, such as polymyositis.
Subject(s)
Adenocarcinoma , Jaundice , Liver Diseases , Liver Failure , Neoplasms, Unknown Primary , Male , Humans , Middle Aged , Neoplasms, Unknown Primary/complications , Neoplasms, Unknown Primary/diagnosis , Liver Failure/diagnosis , Liver Failure/etiology , Liver Diseases/etiology , Adenocarcinoma/complicationsABSTRACT
BACKGROUND: Colorectal cancer (CRC) represents the third most common malignant tumor in the worldwide. Radiotherapy is the common therapeutic treatment for CRC, but radiation resistance is often encountered. ChIP-seq of Histone H3K27 acetylation (H3K27ac) has revealed enhancers that play an important role in CRC. This study examined the relationship between an active CRC enhancer and claudin-1 (CLDN1), and its effect on CRC radiation resistance. METHODS: The target CRC genes of active enhancers were obtained from public H3K27ac ChIP-seq, and the genes highly expressed in radio-resistant CRC were screened and intersected with enhancer-driven genes. The clinical roles of CLDN1 in radiation resistance were examined using the t-test, standard mean deviation (SMD), summary receiver operating characteristic curve and Kaplan-Meier curves. The co-expressed genes of CLDN1 were calculated using Pearson Correlation analysis, and Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes and Gene Set Variation Analysis (GSVA) analyses were used to examine the molecular mechanisms of CLDN1. RESULTS: Total 13 703 CRC genes were regulated by enhancers using 58 H3K27ac ChIP-seq. Claudin-1 (CLDN1) was enhancer-driven and notably up-regulated in CRC tissues compared to non-CRC controls, with a SMD of 3.45 (95 CI % = .56-4.35). CLDN1 expression was increased in radiation-resistant CRC with a SMD of .42 (95% CI = .16-.68) and an area under the curve of .74 (95% CI = .70-.77). The cell cycle and immune macrophage levels were the most significant pathways associated with CLDN1. CONCLUSION: CLDN1 as an enhancer-regulated gene that can boost radiation resistance in patients with CRC.
