Abstract. Anillin actin binding protein (ANLN) is a biomarker of cancer progression and is overexpressed in lung adenocarcinoma. The aim of the present study was to investigate the role of ANLN protein and RNA in the development of lung adenocarcinoma. The ANLN protein sequence was downloaded from The National Centre for Biotechnology information, RNA sequencing (RNA-seq) data was obtained from The Cancer Genome Atlas database. All immunohistochemical staining pictures were adapted from the Human Protein Atlas. PyMOL software was employed to predict protein functional changes in response to mutations. Gene Set Enrichments Analysis was employed for pathway analysis. The results indicated that ANLN experiences genetic change and overexpression at the RNA and protein levels in patients with lung adenocarcinoma. Kaplan-Meier survival curve analysis revealed significant differences between high and low RNA-seq expression levels in ANLN, and patients exhibiting higher expression of ANLN had a relatively poor prognosis. Pathway analysis demonstrated that ANLN was involved in developmental processes via the regulation of nuclear division' pathway. In conclusion, ANLN has potential for use as a diagnostic and prognostic biomarker to diagnoseand predict the outcome of lung adenocarcinoma. IntroductionAccording to 2015 statistics, lung cancer is considered to be the most common type of cancer and the leading cause of cancer-associated mortality in China (1). Similar statistics have been observed worldwide, with lung cancer being diagnosed in 1.8 million people in 2012, resulting in 1.6 million cases of mortality, rendering it the most common cause of cancer-associated mortality in men and the second most common in women (2). Adenocarcinoma is the most common form of lung cancer, originating in peripheral lung tissue and causing almost 40% all lung cancer cases (3). The most important risk factor associated with lung adenocarcinoma is tobacco smoking. Obtaining a reliable diagnosis and identifying prognostic markers for lung cancer remains a challenge.The anillin actin binding protein (ANLN) gene is located on chromosome 7p14.2, and encodes a protein consisting of 1,124 amino acids that form 4 structural domains, including a myosin-and actin-binding domain, a RhoA-binding domain and a C-terminal pleckstrin homology domain (4,5). The ANLN protein is located in the nucleus, cytoplasm, cytoskeleton, cleavage furrow and cell cortex, and is expressed in adult placenta, testis, and the spinal cord, and in numerous fetal organs (6). ANLN was initially characterized as a human homologue of anillin, a Drosophila actin-binding protein that is present in the cortex following breakdown of the nuclear envelope, and in the cleavage furrow during cytokinesis (7). Anillin serves an important role in cell-cycle progression and in the assembly of the actin and myosin contractile ring that separates daughter cells (6). Importantly, anillin has been demonstrated to be a substrate of the anaphase-promoting complex/cyclosome (APC/C), a typeof ub...
BACKGROUND: Community-acquired pneumonia (CAP) in autoimmune diseases (AID)-induced immunocompromised host (ICH) had a high incidence and poor prognosis. However, only a few studies had determined the clinical characteristics of these patients. Our study was to explore the characteristics and predictors of mortality in CAP patients accompanied with AID-induced ICH. METHODS: From 2013 to 2018, a total of 94 CAP patients accompanied with AID-induced ICH, admitted to Emergency Department of Zhongshan Hospital, Fudan University, were enrolled in this study. Clinical data and the risk regression estimates of repeated predictors were evaluated by generalized estimating equations (GEEs) analysis. An open-cohort approach was used to classify patient's outcomes into the survival or non-survival group. RESULTS: The hospital mortality of patients with CAP occurring in AID-induced ICH was 60.64%. No significant differences were found with respect to clinical symptoms and lung images between survival and non-survival groups, while renal insufficiency and dysfunction of coagulation had higher proportions in non-survival patients (P<0.05). Both noninvasive ventilation (NIV) and invasive mechanical ventilation (IMV) were performed more frequently in non-survival group (P< 0.05). By the multivariate GEEs analysis, the repeated measured longitudinal indices of neutrophilto-lymphocyte ratio (NLR) (odds ratio [OR]=1.055, 95% confidence interval [95%CI] 1.025-1.086), lactate dehydrogenase (LDH) (OR=1.004, 95%CI 1.002-1.006) and serum creatinine (sCr) (OR=1.018, 95%CI 1.008-1.028), were associated with a higher risk of mortality. CONCLUSION: The CAP patients in AID-induced ICH had a high mortality. A signifi cant relationship was demonstrated between the factors of NLR, LDH, sCr and mortality risk in these patients.
Background Secondary nosocomial infections, which are commonly caused by carbapenem-resistant Klebsiella pneumoniae (CRKP) and vancomycin-resistant Enterococcus faecium (VRE), often develop in septic patients. This study aimed to identify the origin of secondary systemic pathogens and reveal the underlying mechanism of infection. Methods In this prospective, observational case–control study, a total of 34 septic patients, 33 non-septic intensive care unit (ICU) patients and 10 healthy individuals serving as controls were enrolled. Three hundred and twelve fecal samples were collected and subjected to 16S rRNA gene amplicon sequencing. Metagenome sequencing was performed to identify the homology between dominant CRKP or VRE in the intestine and pathogens isolated from secondary infectious sites. C57/BL mice were established as pseudo germ-free animal model by pretreatment with broad-spectrum antibiotics for two weeks. Results The abundance and diversity of the gut microbiota in septic patients was drastically decreased one week after ICU admission, potentially leading to the enrichment of antibiotic-resistant bacteria, such as CRKP. Furthermore, secondary bloodstream and abdominal infections caused by CRKP or VRE in septic patients occurred after intestinal colonization with the predominant bacterial species. Genomic analysis showed that bacteria isolated from secondary infection had high homology with the corresponding predominant intestinal opportunistic pathogens. In addition, animal model experiments validated the hypothesis that the administration of antibiotics caused the enrichment of CRKP and VRE among the intestinal microbiota, increasing the likelihood of permeation of other tissues and potentially causing subsequent systemic infection in pseudo germ-free mice. Conclusion Our study indicated that the pathogens causing secondary infection in septic patients might originate from the intestinal colonization of pathogens following broad-spectrum antibiotic treatment.
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