Human NESG1 (CCDC19) gene was originally isolated in our laboratory from human nasopharynx tissue. However, the biological and clinical significances of this gene remain largely unknown. In this report, two errors in the originally submitted sequence of human NESG1 gene were found, and the open reading frame sequence of NESG1 (Accession number: NM_012337.1) was revised and updated in the NCBI database (Accession number: NM_012337.2). The antibody raised against the revised sequence of NESG1 detected a single band of 66 kD in human nasopharynx tissues. NESG1 transcripts were specifically expressed in the nasopharynx epithelium. Expression of NESG1 transcripts and protein was downregulated or absent in nasopharyngeal carcinoma (NPC) tissues and cell lines in comparison to that in the normal nasopharynx tissues. The levels of NESG1 protein were significantly greater in the low-grade NPC tissues than that in the high-grade NPC tissues. Induced expression of NESG1 in otherwise NESG1-negative 5-8F cells not only significantly decreased cell proliferation, G1-S phase transition, but also markedly inhibited the ability of cell migration and invasion as well as in vivo tumorigenesis. Furthermore, NESG1 also significantly regulated the expression of cell cycle regulator CCNA1 and p21. Our findings first provided evidence that NESG1 may act as a tumor suppressor by inhibiting cell proliferation, invasion and migration of NPC cells.

BackgroundThe aim of the present study was to analyze the expression of eukaryotic translation initiation factor 4 gamma 1 (EIF4G1) in nasopharyngeal carcinoma (NPC) and its correlation with clinicopathologic features, including patients' survival time.MethodsUsing real-time PCR, we detected the expression of EIF4G1 in normal nasopharyngeal tissues, immortalized nasopharyngeal epithelial cell lines NP69, NPC tissues and cell lines. EIF4G1 protein expression in NPC tissues was examined using immunohistochemistry. Survival analysis was performed using Kaplan-Meier method. The effect of EIF4G1 on cell invasion and tumorigenesis were investigated.ResultsThe expression levels of EIF4G1 mRNA were significantly greater in NPC tissues and cell lines than those in the normal nasopharyngeal tissues and NP69 cells (P < 0.001). Immunohistochemical analysis revealed that the expression of EIF4G1 protein was higher in NPC tissues than that in the nasopharyngeal tissues (P < 0.001). In addition, the levels of EIF4G1 protein in tumors were positively correlated with tumor T classification (P = 0.039), lymph node involvement (N classification, P = 0.008), and the clinical stages (P = 0.003) of NPC patients. Patients with higher EIF4G1 expression had shorter overall survival time (P = 0.019). Multivariate analysis showed that EIF4G1 expression was an independent prognostic indicator for the overall survival of NPC patients. Using shRNA to knock down the expression of EIF4G1 not only markedly inhibited cell cycle progression, proliferation, migration, invasion, and colony formation, but also dramatically suppressed in vivo xenograft tumor growth.ConclusionOur data suggest that EIF4G1 can serve as a biomarker for the prognosis of NPC patients.

Background. Although intravenous immunoglobulin (IVIG) is expected to prevent coronary artery abnormalities of Kawasaki disease (KD) in the acute phase, the timing and effectiveness of IVIG remain to be determined. The association of timing of IVIG administration in KD patients with coronary artery abnormalities is evaluated in this cohort study. Methods. We systematically studied KD patients from two participating institutions between 2015 and 2017. To reveal the effectiveness of IVIG treatment, these patients were classified into four groups regarding the time of IVIG treatment. Primary outcome was coronary artery abnormalities by echo at diagnosis and 12 months follow-up; secondary outcomes included inflammatory markers. Results. A total of 1281 patients were included in this study. The best time of IVIG treatment cut-off values in 12 months follow-up for predicting coronary artery abnormalities was days 7.5 of illness onset. According to the best time of IVIG treatment cut-off values, all patients were classified into 4 groups. Group 1 was defined as earlier IVIG treatment administration on days ≤4 of the illness ( n = 77 ). Group 2 was defined with days 5-7 ( n = 817 ), group 3 with days 8-10 ( n = 249 ), group 4 with days >10 ( n = 138 ). A greater proportion of IVIG-resistant KD patients were group 4 than the other three groups, and there were significant differences ( p < 0.05 ). The incidence of coronary artery lesions (CALs) and coronary artery aneurysms (CAAs) in group 3 and group 4 was higher than that in group 1 ( p < 0.05 ) and group 2 ( p < 0.05 ) during a 12-month follow-up. Additionally, the incidence of CALs in group 1 was higher than that in group 2 but without statistical significance ( p > 0.05 ). The OR was significantly higher for those who started IVIG administration more than 7 days from the onset was positively associated with the occurrence of CALs (OR, 5.3; 95% CI, 2.0-13.9) and CAAs (OR, 13.5; 95% CI, 2.9-14.1) 12 months after initial onset. Multivariate regression revealed that the timing of IVIG treatment and IVIG-resistance was independent risk factors of CALs. Conclusions. IVIG treatment less than 7 days after illness onset are found to be sufficient for preventing developing coronary artery abnormalities in KD patients. Earlier IVIG treatment administration within 4 days may not increase the higher incidence of coronary artery abnormalities and IVIG resistance (Chinese Clinical Trial Registry:ChiCTR1800015800).

Talaromyces marneffei (TM) infection is rarely seen in clinical practice, and its pathogenesis may be related to deficiency in antifungal immune function. Human caspase recruitment domain-containing protein 9 (CARD9) is a key molecule in fungal immune surveillance. There have been no previous case reports of TM infection in individuals with CARD9 gene mutations. Herein, we report the case of a 7-month-old Chinese boy who was admitted to our hospital with recurring cough and fever with a papular rash. A blood culture produced TM growth, which was confirmed by metagenomic next-generation sequencing. One of the patient’s sisters had died of TM septicaemia at 9 months of age. Whole exome sequencing revealed that the patient had a complex heterozygous CARD9 gene mutation with a c.1118G&gt;C p.R373P variation in exon 8 and a c.610C&gt;T p.R204C variation in exon 4. Based on the culture results, voriconazole antifungal therapy was administered. On the third day of antifungal administration, his temperature dropped to within normal range, the rash gradually subsided, and the enlargement of his lymph nodes, liver, and spleen improved. Two months after discharge, he returned to the hospital for a follow-up examination. His general condition was good, and no specific abnormalities were detected. Oral voriconazole treatment was continued. Unexplained TM infection in HIV-negative individuals warrants investigation for immune deficiencies.

Introduction: Clostridium difficile infection (cdi) often occurs with long-term and irregular use of antibiotics. Patients with tumors receiving both antibiotics and chemotherapy are at a high risk of cdi. The symptoms of cdi vary but can include diarrhea, hypovolemia, electrolyte imbalance, hypoproteinemia, toxic megacolon, gastrointestinal tract perforation, disseminated intravascular coagulation, sepsis, and other lethal complications. Here, we report a rare clinical manifestation associated with cdi in a child with lymphoma presenting with massive hydrothorax and ascites. Case Presentation: A 6-year-old girl who was on chemotherapy for lymphoma presented with fever and was treated with intravenous broad-spectrum antibiotics 3 days before admission to our hospital. On the day before admission, she developed abdominal distension and diarrhea. After admission, broad-spectrum antibiotic therapy was initiated, and her hydrothorax and ascites were drained. An initial extensive microbiological evaluation revealed no pathogens, and laboratory tests and imaging studies of the pleural and peritoneal effusions revealed no evidence of cancer. The initial culture results for C. difficile were negative. The patient was diagnosed with CDI only after a positive test result for C. difficile toxin B gene and a repeated stool culture test revealed CDI. Intravenous antibiotics were suspended and replaced with oral vancomycin and Saccharomyces boulardii, which resulted in successful treatment and a good post-discharge outcome. Conclusions: Massive hydrothorax and ascites are rare manifestations associated with CDI. CDI can occur in individuals with risk factors such as those undergoing broad-spectrum antibiotic therapy.